Laurence D. Chalem

Inspirational Authors and their Works on Diabetes and Nutrition

2022-04-28T04:49:00.044-07:00

Gary Taubes’ article entitled, "What If It’s All Been a Big Fat Lie?" literally changed my life.

A $700,000+ advance and five years later, he completed the book Good Calories, Bad Calories, (New York: Anchor Books, 2007, 2008), another life changer, available free of charge here and here. His other books include Why we get Fat and What to do about It (New York: Alfred A. Knopf, 2016), The Case Against Sugar (New York: Alfred A. Knopf, 2016), and The Case for Keto: Rethinking Weight Control and the Science and Practice of Low-Carbohydrate, High-Fat Eating (New York: Alfred A. Knopf, 2020).

Available free of charge online, you could read his article entitled, "How a Fatally, Tragically, Flawed Paradigm has Derailed the Science of Obesity," and, on the subject of gout, this thought provoking article.

Dr. Richard K. Bernstein, the first diabetic patient to monitor his own blood sugar many decades ago, is considered by many to be the go-to diabetes doctor. His is an interesting story and you can learn about it and his teachings in the two books The Diabetes Solution (New York: Little, Brown and Company, 1997, 2007, 2011), and The Diabetes Diet: Dr. Bernstein's Low-Carbohydrate Solution (New York: Little, Brown & Company, 2008). He has written other books such as Beating Diabetes Type 2: 1000+ Answers Your Doctor May Not Know or Tell You (New York: Diabetes in Control, LLC, 2016), Dr. Bernstein’s Secrets to Normal Blood Sugars (For Type 1 Diabetes, Volume 1) (New York: Diabetes in Control, LLC, 2005), Diabetes Type II: Living a Long, Healthy Life Through Blood Sugar Normalization (1st ed., Prentice Hall Trade, 1981, 1990), and Diabetes: The GlucograF Method for Normalizing Blood Sugar (New York: Crown/Tarcher, 1984).

One of the most influential books in the world of nutrition is Nutrition and Physical Degeneration, (Current: Price-Pottenger Nutrition Foundation; 8th edition, January 1, 2009; originally published in 1939) by Weston A. Price. It changed my life and influenced most of the current authors on the subject.

Stephen Phinney, MD, PhD, and Jeff Volek, PhD, RD, collaborated on a couple of impactful books, The Art and Science of Low Carbohydrate Performance (Beyond Obesity LLC, 2012) and The Art and Science of Low Carbohydrate Living (Beyond Obesity, LLC, 2011). With the backing of investor Sami Inkinen, they launched the successful Type II diabetes treatment healthcare company Virta.

Dr. Eric Westman. Short and to the point, see his article entitled, "Is Dietary Carbohydrate Essential for Human Nutrition?" He’s written more than 90 other articles that you could search online and read. In conjunction with the two above writers, he co-authored The New Atkins for a New You (Fireside/Simon & Schuster, 2010). His newest book, End Your Carb Confusion (Victory Belt Publishing, 2020), is also worth a read. Dr. Westman is the co-founder of Adapt Your Life® and Adapt Your Life® Academy, an Associate Professor of Medicine at Duke University Health System and the Director of the Duke Keto Medicine Clinic in Durham, North Carolina.

Nina Teicholz’ book, The Big Fat Surprise (New York: Simon & Schuster, 2014), reviews thousands of scientific studies and documents the politics and personalities dominating the last 50 years in nutrition policy, to get behind the flip-flopping headlines and explain some basic truths about nutrition science. She has also written more than twenty articles which can be read here.

On fasting, one must read the works of Dr. Jason Fung, which include Life in the Fasting Lane (Vancouver: HarperCollins, 2020), The Complete Guide to Fasting (Canada: Victory Belt Publishing Inc., 2016), The Diabetes Code (Vancouver: Graystone Books, 2018), The Obesity Code (Vancouver: Graystone Books, 2016), and The Cancer Code (New York: HarperCollins, 2020). He also hosts the helpful Fasting Method Blog.

Laurence is neither a doctor nor medical practitioner. Neither this blog nor this website should be considered medical or healthcare information or advice. Mr. Chalem is simply providing experiential information as a user and buyer of treatment options. For more information about him, please feel free to visit www.diabetesspeaker.com.

Laurence has neither received nor will he receive any kind of remuneration from the authors, agents, or sales channels of the above.

Glycosis (CA: Sugarless Books, 2010), a novel by Laurence Chalem

2019-06-11T21:17:00.001-07:00

Book cover and video summary of Glycosis (CA: Sugarless Books, 2010), a novel by Laurence Chalem.

Available on Amazon.com here.

Chapters will be available to read via links to the right.

Psychosis (sī-kō’sĭs) noun; Psychotic (sī-kŏt’ĭk) adjective
(1) Abnormal condition of the mind.
(2) A severe mental disorder, with or without organic damage, characterized by derangement of personality and loss of contact with reality causing deterioration of normal social functioning.

Psycho (sī’kō) noun
A slang word for a person who is psychotic.

Glycosis (glī-kō’sĭs) noun; Glycotic (glī-kŏt’ĭk) adjective
(1) Abnormal condition of sugar in the body.
(2) A physical disorder comprised of too much glucose in the blood (BG). Although low BG is acutely more serious, high BG can lead to complications such as extreme hunger and thirst, fat, muscle or bone loss, frequent urination, depression, dementia, agitation, lethargy, loss of vision, loss of sensation, immune suppression, renal failure, liver and cardiovascular disease, gangrene, coma and death.
(3) Quantifiable maladaptation to carbohydrate(s). Example: if a species that uses glucose as its sole energy source is forced to consume a different carbohydrate instead, the survival rate would serve as the measure of adaptation or maladaptation to that fare. The lower the survival rate, the more the species as a whole is maladapted, the higher the glycosis. In omnivores, glycosis manifests as various afflictions.

Glyco (glī’kō) noun
(1) The chemical prefix for sweetness or sugar.
(2) A slang word for a person who is glycotic.

The Diabetes Industry is Ripe for Disruption

2018-04-19T10:40:00.000-07:00

And it has been for some time.

If we plot carbohydrate consumption from low to high on the y-axis, and pharmaceutical—one or more of the many insulins, metformin, etc.–consumption from low to high on the x-axis, we can see all possible combinations of expected patient results on the following matrix:

When exo- or endogenous insulin—and/or insulin sensitivity—is low, and carbohydrate consumption is high, the patient may present with the classical triad of type one diabetes symptoms: polyuria, polydipsia, and polyphagia: respectively, frequent urination, increased thirst and consequent increased fluid intake, and increased appetite. Other manifestations may include weight loss despite normal or increased eating, irreducible fatigue, and changes in the shape of the lenses of the eyes or sorbitol accumulation, resulting in vision changes.

Patients may also present with diabetic ketoacidosis (DKA), an extreme state of metabolic dysregulation characterized by the smell of acetone on the patient's breath; a rapid, deep breathing known as Kussmaul breathing; nausea; vomiting and abdominal pain; and an altered state of consciousness or arousal, such as hostility and mania or, equally, confusion and lethargy. In severe DKA, coma may follow, progressing to death.

Surrounding this cell on the matrix is hyperglycemia, both to the right, when carbohydrates consumed are high and exo- or endogenous insulin is moderate—but not enough to cover the load—and below, when a decrease in carbohydrates is consumed, but still not offset enough by insulin.

In the middle of the chart, where one eats a moderate amount of carbohydrates and injects a moderate amount of bolus insulin, lies the typical diabetes treatment. “Eat a balanced diet and learn to adjust your insulin accordingly” is the principal treatment that is followed here. It is possible to attain near-normal A1c levels with this approach, however, normal weight, blood pressure, not to mention time and resources spent in the process may prove unsustainable. There must be a better way.

Furthermore, this area of the table is fraught with negative consequences at nearly all adjacent and opposite borders. Not enough insulin puts one in hyperglycemia territory both to the left and above. Not enough carbohydrate, and one finds themselves hypoglycemic to the right and below.

At the other extreme, when injected insulin is high, and carbohydrates consumed are too low, severe hypoglycemia could result, necessitating a visit from the local paramedics when subsequent low blood glucose causes unconsciousness. If not attended to quickly, coma and death could occur within minutes.

Too, if carbohydrates and insulin injected are high, the result is a hypo-hyperglycemic swing—a rollercoaster ride if you will—of great magnitude, where the patient is constantly adjusting carbohydrate and insulin loads to offset their blood sugar.

But look what happens when both carbohydrates and pharmaceuticals consumed are as low as possible. At the far lower-left cell of the matrix, one doesn’t eat a great many non-structural carbohydrates, and, subsequently, does not need to, say, inject much insulin as a result. In this case, one can achieve a normal blood sugar concentration and enjoy the benefits of a normal life, with more energy than previously, stable or decreasing body weight, and less anxiety not having to think about whether one has ingested the correct amount of chemicals. And testing can be reduced to once a day, in the morning, to validate their successful treatment, i.e., whether their morning BG is in the 70-110 mg/dL range. This home base is where thriving begins.

At the zero bolus-insulin and near-zero carbohydrate home, you may thrive for a long, long time. There are three major centenarian studies going on around the world. See the New England Centenarian Study Website, the Georgia Centenarian Study Article, the Georgia Centenarian Study Youtube Video; and the Okinawa Centenarian Study Website. According to Dr. Ron Rosedale back in 1999:

“They are trying to find the variable that would confer longevity among this group of people who live to be 100 years old. Why do centenarians become centenarians? Why are they so lucky? Is it because they have low cholesterol, exercise a lot and live a healthy, clean life?

What researchers are finding from these major centenarian studies is that there is hardly anything in common among these people. They have high cholesterol and low cholesterol, some exercise and some don't, some smoke, some don't. Some are nasty as can be, some nice and calm and some are ornery. But, they all have relatively low sugar for their age, and they all have low triglycerides for their age. And, they all have relatively low insulin…The way to treat virtually all of the so-called chronic diseases of aging is to treat insulin itself.” See “Insulin and its Metabolic Effects,” by Dr. Ron Rosedale, presented at Designs for Health Institute's BoulderFest, August, 1999. Full online Article.

Although the use of exogenous insulin as a treatment to mitigate the effects of carbohydrate consumption was innovative, exciting, and promising nearly a century ago, its use has become—save on the acutely serious hyperglycemic—grotesquely over-prescribed with the knowledge that carbohydrates are non-essential and that, in the case of T2 diabetics, the problem is initially more of insulin resistance than of insulin production.

For more about the non-essentiality of carbohydrates, see Dr. Eric Westman’s article entitled, “Is dietary carbohydrate essential for human nutrition?” here. For more about insulin resistance, see this full online article.

A remarkable picture develops when you take those three yellow-highlighted cells from the above figure and place them on two different axes, one a continuum of complexity from low to high, and the other, a continuum of knowledge, skills, and tools, again, from low to high.

The y-axis, complexity, relates to the treatment—medication and nutrition—and lifestyle a person implements or recommends. Regarding the x-axis, knowledge, skills, and tools, it could be looked at from two perspectives; one, from a diabetic’s perspective, where the focus is on their knowledge and skills as it relates to implementing advice from a third-party or self-directed behavior, and another, from the perspective of a third-party’s knowledge and skills, be it friend, relative, caregiver, nutritionist, nurse, or doctor. Treatment efficiency and effectiveness in either case is also measured.

The lowest complexity matched with the lowest skill and knowledge will result in a diabetic on the brink. It is quite easy for them to eat carbohydrates at will and develop the hyperglycemic symptoms of full-blown diabetes: polyuria, glycosuria, polydipsia, polyphagia, ketoacidosis, weight loss, etc., culminating in shortened life span. Patient knowledge about diabetes may be non-existent, and they will likely seek out medical attention for help, though, unfortunately, some don’t or for many reasons even if they do, helpful advice is not available. Acquaintances will also most likely notice the change in persona or appearance, and they too will make it a point to tell the person that something is wrong.

“Diabetes Managed” represents a diabetic trying to follow the instructions and advice of his or her general practitioner, though both are influenced by a wide variety of stakeholders with oftentimes divergent self-interests. Influencers in the medical advice providing supply chain may include:

· Acquaintances, co-workers, family, friends

· American Diabetes Association (ADA) and other associations/foundations. See especially the ADA’s 2018 Standards of Medical Care in Diabetes.

· Educators

· Endocrinologists. See the Consensus Statement by the American Association of Clinical Endocrinologists and American College of Endocrinology on the Comprehensive Type 2 Diabetes Management Algorithm - 2018 Executive Summary, especially the Disclosures on page 103.

· Food manufacturers and marketers

· Medical doctors

· Medical schools

· Nurses

· Nutritionists. Dietetic Associations referred to the public by the USDA include the Academy of Nutrition and Dietetics (FKA the American Dietetic Association), the British Dietetic Association, Dietitians of Canada, Dietitians Association of Australia, the International Confederation of Dietetic Associations, et al. For links see Dietetic Associations.

· Pharmaceutical companies. See for example Dr. Aseem Malhotra’s appeal to the European Parliament, Brussels, April, 2018. Youtube Video.

· Popular internet sites, print and TV media

· Reference media such as the Physician’s Desk Reference, which was formerly a commercially published compilation of manufacturers' prescribing information on prescription drugs, updated annually. While originally designed to provide physicians with the full legally mandated information relevant to writing prescriptions, widely available in libraries and bookstores, widely used by other medical specialists, and in significant part valuable to consumers, it was financially supported in part by pharmaceutical manufacturing corporations which created the drugs listed within its pages. Now it is published only online by ConnectiveRx, and the website is here.

· Researchers. Most research findings are false for most research designs and for most fields. See Ioannidis JPA. Why Most Published Research Findings Are False. PLoS Medicine. 2005;2(8):e124. doi:10.1371/journal.pmed.0020124. Full online article.

· United States Department of Agriculture. See USDA Dietary Guidelines.

· World Health Organization. See their 2016 Global Report on Diabetes.

To the uninitiated, each influencer may seem well-intentioned and sincere; but, by default, advocates of each group act in their own perceived best interests, based upon their knowledge and skill, which may in turn be based upon the state of information available at their time of training or education. Or, they may have conflicting interests, having received benefits from other constituencies. For example, surveys conducted in 2004 and again in 2009 showed that more than three-quarters of doctors had at least one type of financial relationship with a drug or medical device company. (See Campbell EG, Rao SR, DesRoches CM, et al. Physician Professionalism and Changes in Physician-Industry Relationships From 2004 to 2009. Arch Intern Med. 2010;170(20):1820–1826. doi:10.1001/archinternmed.2010.383. Full online article.)

And many of the above influencers have significant power. In fact, some have a near-absolute advantage in the marketplace—the ability to influence behavior without question or pause—leaving the buyer of an optimal diabetes treatment treating their diabetes sub-optimally, i.e., carbohydrate and pharmaceutical intensive.

And the results? Perhaps an HbA_1c at or below 7%, weight gain, increasing blood pressure, too much time spent counting carbohydrates and measuring insulin doses, anxiety caused by constantly wondering whether or not too much or too little carbohydrates were eaten or insulin dosed, the ever present chance of hypo- or hyper-glycemia, constant blood sugar testing, and the list goes on. “Diabetes Managed” may not achieve optimal results for the patient; but, for other stakeholders, it may bring and keep customers longer.

Although the science behind pharmaceuticals that may limit the amount of glycogen released from the liver or that bind to receptors allowing channel membranes to open so that glucose may cross is remarkable, it is based upon two assumptions: (1) that carbohydrates are an essential majority part of the diet, and/or (2) that through education, a patient cannot, will not, or should not keep from consuming them. Remove those key assumptions, and the house of cards from which that remarkable science is based comes toppling down.

Caveat emptor. “Diabetes Managed” may be the first natural step for diabetics to enter—a complex medical-advice-providing system—in progression of their self-treatment, but it doesn’t have to be.

As knowledge about diabetes and its optimal treatment increases, trusted advisers and patients alike will choose a less-complex method, one that transcends diabetes by avoiding the root cause of symptoms and complications—non-structural carbohydrates—and replacing those carbohydrates in the diet with real food sources of fat and protein, resulting in benefits such as healthy weight loss, normal blood pressure, etc.; in short, leading to a longer, happier, healthier life.

To transcend diabetes requires reduced carbohydrate consumption to near zero, with emphasis on a combination of fats and protein. It is orders of magnitude less complex, less worrisome, and less risky than counting carbohydrates and matching it with doses of insulin or other pharmaceuticals. It is simple. And it should be the first approach in diabetes treatment. See Feinman, Richard, et al. (2014). Dietary carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base. Nutrition. 31. 10.1016/j.nut.2014.06.011. Full online article.

When the blood sugar function is optimized this way, then, a new, refreshing meaning to the words of Frederick G. Banting, largely credited for the idea behind the work which led to the discovery of insulin, becomes evident:

“…with the relief of the symptoms of the disease…the pessimistic, melancholy diabetic becomes optimistic and cheerful.”

This last quote is from the conclusion of Frederick G. Banting, Nobel Lecture, September 15, 1925, The Nobel Prize in Physiology or Medicine 1923. Full online article. That prize for the discovery of insulin was actually divided between Frederick G. Banting and John J. R. Macleod. The choice of this combination of Laureates has been much debated ever since the prize was awarded. Thus, for instance, Banting shared his part of the prize amount with his younger coworker Charles Best. See the article August Krogh and the Nobel Prize to Banting and Macleod.

Essential Diabetes Leadership

2015-06-17T17:27:00.000-07:00

“Why in this stultifying and needless conflict between reason and tradition, it should be so easy to believe the incredible and so difficult to accept the obvious, is a riddle which is not flattering to contemplate.”[1]

F. J. COLE, 1944

In ESSENTIAL DIABETES LEADERSHIP (2011), the hypothesis and proof that a ketogenic—high fat, adequate protein, low-carbohydrate—diet for diabetics, as part of an overall BG optimization model, supports a long, happy, healthy life in general, I included specifics from six of the twelve total systems: the (1) circulatory, (2) digestive, (3) endocrine, (4) excretory, (5) nervous, (6a) skeletal (teeth), and (7a) integumentary (gingiva: the gums).[2]

Regarding the (5) nervous system, which includes the sense organs and vestibular system, the last endnote of the “Epilogue” provided supporting evidence for the use of a ketogenic diet in the successful treatment of epilepsy. Since there’s more to the nervous system, and to the diseases of, than forty different kinds of epilepsy, this blog suggests a couple other information sources.

Reminiscent of Dr. Weston Price, we find a brave treatise written by another dentist. First published in 2001, then condensed in 2005, ALZHEIMER’S SOLVED, by Dr. Henry Lorin, proffers a thoroughly researched theorem—his book references over 2,500 scientific articles—that better explains the data and observations than any other work on the subject: “It is indeed possible for a person to have blood cholesterol levels that are too low.”[3] Reading through his manuscript, that conclusion is inescapable.

From aging to xanthomas, Dr. Lorin’s theorem in ALZHEIMER’S SOLVED unifies seemingly diverse conditions such as AIDS, Alzheimer’s disease, brain surgery, Cushing’s disease, dementia, depression, Down syndrome, epilepsy, head injury, HIV, osteoporosis, Parkinson’s disease, vasculitis, and others, with his remarkably simple deduction that amyloid—beta amyloid plaques—“is the body’s temporary substitute for cholesterol molecules. Amyloid is to be used as a short-term ‘bandage’ for cell membranes until more cholesterol is provided.”[4] Should that cholesterol, for whatever reason, be withheld, nearly all the aforementioned diseases inevitably become terminal. Dr. Lorin summarizes his diet—beyond important micronutrients such as vitamin D—quite eloquently in one sentence: “The easiest and most natural way to do this [preventing and treating most of the described diseases] is by eating foods that contain cholesterol, while minimizing the consumption of foods that are primarily carbohydrates (starches).”[5]

You may also be interested in reading THE BRAIN TRUST PROGRAM (2007), by Larry McCleary, MD, which accessibly describes the important component parts of the nervous system, then delivers a striking contrast to all the also-ran diet-brain books published on how to best support them through diet. Although he doesn’t outright advocate a low-carbohydrate diet, his 7-day menu plan sure does resemble one.[6] A person with diabetes would simply need to skimp further on the fruit and minimal multigrain bread and crackers mentioned.

Here I could discuss the (8) muscular system in detail, but so much data exists on low-carbohydrate diets and exercise physiology, overlapping some with the (9) respiratory system—and I reprinted with permission much of the material written by Professor Emeritus Robert S. Horn on the subject in my first book—that, although tempting, I shall not rehearse the subject here, other than to say that Stephen D. Phinney provides great additional insight.

In “Ketogenic Diets and Physical Performance,” which contains many good sources for further reading, Dr. Phinney states in the Abstract that “impaired physical performance is a common but not obligate result of a low carbohydrate diet. Lessons from traditional Inuit culture indicate that time for adaptation, optimized sodium and potassium nutriture, and constraint of protein to 15–25 % of daily energy expenditure allow unimpaired endurance performance despite nutritional ketosis.”[7]

And he concludes:

“Both observational and prospectively designed studies support the conclusion that submaximal endurance performance can be sustained despite the virtual exclusion of carbohydrate from the human diet. Clearly this result does not automatically follow the casual implementation of dietary carbohydrate restriction, however, as careful attention to time for keto-adaptation, mineral nutriture, and constraint of the daily protein dose is required. Contradictory results in the scientific literature can be explained by the lack of attention to these lessons learned (and for the most part now forgotten) by the cultures that traditionally lived by hunting. Therapeutic use of ketogenic diets should not require constraint of most forms of physical labor or recreational activity, with the one caveat that anaerobic (i.e., weight lifting or sprint) performance is limited by the low muscle glycogen levels induced by a ketogenic diet, and this would strongly discourage its use under most conditions of competitive athletics.”[8]

Based upon Dr. Phinney’s work, my blood glucose model, of which I proudly presented in the chapter entitled “The Way Things Ought To Be (Part I),” recommended frequent, light exercise.

If you were thinking that I would now go over each of remaining five human organ systems (five because I’m including the skeletal system proper, the bones, and the integumentary system proper, the skin, hair and nails), I have a shocker for you: the medical literature world is predominantly data- and theorem-light—more, ignorant—about how macronutrients, not just vitamins and minerals, but how macronutrients—fats, proteins, and carbohydrates—and, specifically, a low-carbohydrate, medium-protein, high-fat diet, affect all but one of the remaining systems.

True, we know how the use of sugar per se affects nearly every organ system; two accessible books on the subject that you may find interesting are LICK THE SUGAR HABIT (2001) and SUICIDE BY SUGAR (2009), both by Nancy Appleton, PhD.[9] By the way, these books remind me of an experiment on dogs performed by an ex-physician about two hundred years ago. Let me share this brief story.

“In 1816, in an attempt to understand the biological value of certain foodstuffs, Francois Magendie—a child of revolutionary Paris and a former physician—set out to observe the effects of a restricted diet. He was particularly interested in what role nitrogen has to play in digestion. The answer he got back, after ten years of painstaking work was none at all: ‘As so often in research,’ Magendie wrote, with what bitterness we may imagine, ‘unexpected results had contradicted every reasonable expectation.’ But in the pursuit of this knowledge, Magendie had stumbled upon a striking, if unpleasant discovery: he had found that he was able to starve his experimental dogs to death on diets that should, on the face of it, have given them all the energy they needed for life.

By his own account, Magendie ‘placed a small dog about three years old upon a diet exclusively of pure refined sugar with distilled water for drink; he had both ad libitum.’ By the third week the animal, already weakened, lost its appetite, and developed small ulcers in the centre of each cornea. The ulcers spread, and then the corneas liquefied. Shortly afterwards, the dog died.

Magendie tried other nutritious foods. ‘Everyone knows that dogs can live very well on bread alone,’ he confidently asserted—but when he put this to the test, he found that ‘a dog does not live above fifty days.’ The most calorific foods in Magendie’s pantry—wheat gluten, starches, sugar, olive oil—were not enough for life. This was totally unexpected. There was something missing—something available only as part of a varied diet—but what?”[10]

Turns out that it was vitamin A, isolated a hundred years later by two American teams, that was needed to keep the eyes from liquefying, though not enough to save the life. The addition of whole milk to the diet saved the life; no, not of the dog, but of children, soldiers, waifs and strays suffering from xerophthalmia in the years preceding the isolation of vitamin A. Of course, even then, experiments—on dogs, children, waifs, or strays—were not performed in the reverse to prove that you don’t need the sugar. Carbohydrates have been considered essential since the dawn of agriculture.

“That transition from hunting and gathering to agriculture is generally considered a decisive step in our progress, when we at last acquired the stable food supply and leisure time prerequisite to the great accomplishments of modern civilization. In fact, careful examination of that transition suggests another conclusion: for most people the transition brought infectious diseases, malnutrition, and a shorter life span. For human society in general it worsened the relative lot of women and introduced class-based inequality. More than any other milestone along the path from chimpanzeehood to humanity, agriculture inextricably combines causes of our rise and our fall.”[11]

Back to organ systems. As I was saying, we know how sugar by itself negatively affects many organs and organ systems, but little is known about how any specific diet permutation affects the (7b) integumentary (skin, hair and nails), (9) respiratory, (10) lymphatic, (11) immune,[12] or (12) reproductive system. Now, it surely can be inferred that, if we forgo the bolus insulin and carbohydrates, and eat just fat and protein, with type 1s only adding basal insulin, and we live a long, happy, healthy life, then all other organ systems must be doing just fine. But such circumstantial evidence doesn’t necessarily prove that they’re healthy in the court of public opinion, let alone in science. Unlike in evolution versus creationism, where, thankfully, evolution has been upholded,[13] no action has been brought against any carbohydrate-espousing proponent, by any low-carbohydrate proponent, in any jurisdiction. Thus, we have no precedent, no ruling, no adjudication, based upon any evidence, for or against any diet, from any court of law. Not that the vegans haven’t tried.[14]

We live today in an environment similar to that initially championed by John Washington Butler,[15] except, instead of its realization deriving from a law forbidding public school teachers from denying the Biblical account of man’s origin, we now navigate through an environment emotionally charged by a low-fat dogma; those that pray to it and live by its code do so influenced by the trinity of politics—playing into the public perceptions that they themselves or their forebearers created—faith and commerce, not science, serving it best by ensuring its promulgation into clinical practice guidelines, research, education, news and fixed media. This dogma, however, unlike the Butler Act, is enforced not just in public schools, but across nearly all demographics. Maybe by the time the 18^th edition of this book is published, a precedent will be set upholding low-carbohydrate diets in a court of law, the above organ systems will be covered in more detail, and I will be able to provide a robust summary.

There is some information about how diet affects the (12) reproductive system, but most sources highlight the role of calories, not how any specific combination of macronutrients affects the reproductive system. At first glance, learning that a low-carbohydrate, ketogenic diet led to significant improvement in weight, percent free testosterone, and fasting insulin in women with obesity and Polycystic Ovary Syndrome (PCOS) over a 24 week period, it sounds like we can put one in the win column for a low-carbohydrate diet best supporting the reproductive system. Alas, PCOS is considered an endocrine disorder.[16]

Which really leaves only one organ system that I didn’t cover. Well, half of one.

The (6b) Skeletal (bone) system, beyond studies about the correlation between osteoporosis and calcium, is supported by a low-carbohydrate diet in “The Effect of a Low-Carbohydrate Diet on Bone Turnover,” by J. D. Carter, F. B. Vasey, and J. Valeriano. Here, the authors set out to determine whether or not a low-carbohydrate diet would lead to increased bone turnover. Thirty patients (15 study subjects and 15 controls) were recruited for this 3-month study. The 15 patients on the diet were instructed to consume less than 20 g of carbohydrates per day for the 1st month and then less than 40 g per day for months 2 and 3. Control subjects had no restrictions on their diet. And the conclusion? “Although the patients on the low-carbohydrate diet did lose significantly more weight than the controls did, the diet did not increase bone turnover markers compared with controls at any time point. Further, there was no significant change in the bone turnover ratio compared with controls.”[17]

In what could be classified as the only compendium devoted to the relationship between the skeletal system and diet, NUTRITION AND BONE HEALTH (2004) doesn’t advocate any particular diet, although it does include an article—the book is a collection of independently written articles—describing both the plate model of the UK and the pyramid model of the US.[18] The authors used these models as an assumption of diet; that, and a reference to fat leading to heart disease, without quoting any specific, credible evidence in defense of either. As you read more and more health, diet, medical, reference books and articles, you’ll find support of those two concepts without evidence common faults.[19] Mark Twain understated it best when he said “Be careful about reading health books. You could die of a misprint.”

However, if I could choose one quote from the book to best embody its entirety, it is that “bone health is not a mononutrient issue.”[20] Some specific examples include:

· “An inadequate intake of calcium and an inadequate level of vitamin D, alone and in combination, influence calcium-regulating hormone levels. Deficiency of either nutrient results in reduced calcium absorption and a lower circulating ionized concentration. The latter stimulates the secretion of parathyroid hormone (PTH), a potent bone-resorbing agent. Over time, a small increase in the circulating level of PTH leads to measurable and significant bone loss and increased risk of fracture.”[21]

· “Vitamin A deficiency is characterized by xerophthalmia, night blindness, cessation of growth, and increased susceptibility to infections. On the other side, very vitamin A intake might affect, among others, bone and bone metabolism, as it has long been known. High vitamin A intake seems to accelerate bone loss.”[22]

· “Fluorine is an indispensable trace element and plays a role in normal development and maintenance of the skeleton and teeth. As is true for other essential trace elements, deficiency or excess has clinical consequences: intakes below the recommended daily dose result in growth and development retardation, whereas long-term high intake leads to hyperostosis or even severe skeletal sclerosis.”[23]

Low-fat endorsing as it may be perceived, one article clearly supports the use of fat in promoting bone health: “Dairy products are complex, containing many essential nutrients, and thus their effects on bone health are likely more that can be accounted for by any single constituent and the totality of their effects may be more than the sum of parts.”[24]

But more interesting is the book’s discussion on fruits and vegetables:

· “The approach of using food groups to examine the relationship between diet and disease is an appropriate and logical approach to examining the relationship between diet and osteoporosis. There is somewhat remarkable agreement among countries as to the proportions with which we should be eating food groups. The data suggest that milk and milk products (as providers of more than 50% of total dietary calcium) and fruit and vegetables are beneficial to bone health across the age ranges, although clearly more work on fracture reduction is required.”[25]

· “Only two large population-based studies have examined the specific impact of dietary “quality”/food groups directly on indices of bone health, namely, the Aberdeen Prospective Osteoporosis Screening Study (APOSS) and the Framingham Offspring Study. Cluster analysis on 904 women (mean age 54 yr.), pre-, peri-, and postmenopausal, showed that a number of food groups, including fried foods, cakes, processed meats, and puddings, were associated with worsening hip bone loss…”[26]

· “These data support the findings of both the original APOSS baseline study and the older Framingham cohort and indicate that a high fruit and vegetable intake is protective to the skeleton, whereas high candy consumption is associated with lower bone mass, regardless of gender. These data also suggest that a high intake of fatty, sugary foods is detrimental to bone health around the time of menopause.”[27]

This last quote conflicts with one of the most interesting cohort studies I’ve seen on the subject. In “Food Choices and Coronary Heart Disease: A Population Based Cohort Study of Rural Swedish Men with 12 Years of Follow-up,” by Sara Holmberg, Anders Thelin, and Eva-Lena, the authors concluded: “Daily intake of fruit and vegetables was associated with a lower risk of coronary heart disease when combined with a high dairy fat consumption, but not when combined with a low dairy fat consumption. Choosing wholemeal bread or eating fish at least twice a week showed no association with the outcome.”[28]

As with other nutritional controversies, we find the unifying answer to whether or not it’s fruits and vegetables per se or in combination with other foods that reduces heart or bone disease risk from Gary Taubes, and here he delivers the last words: “As a matter of logic, though, it doesn’t necessarily imply that the lack of vitamins are caused by the lack of fresh fruits and vegetables…It’s possible that eating easily digestible carbohydrates and sugars increases our need for vitamins that we would otherwise derive from animal products in sufficient quantities.”[29] “There is an increased need for these vitamins when more carbohydrate in the diet is consumed.”[30]

[1] In its original context, this quote refers to the 17^th century comparative anatomist Tyson, who “Nevertheless after carefully reviewing the evidence which demonstrated conspiculously that the porpoise must be a mammal, Tyson nowhere has the courage to declare that it is not a fish, for once attaching more importance to habitat than to structure. He says he should like to think it was a mammal, but further than that he did not go.” See Cole, F.J. A History of Comparative Anatomy: From Aristotle to the Eighteenth Century. London: Macmillan & Co. Ltd., 1944, p. 202.

[2] There are three main approaches to studying anatomy: systemic, regional, and clinical. Systemic anatomy is the study of the body as a series of organ systems. Although systemic anatomy textbooks typically cover all the human organ systems, they may group them differently, into from six to many more organ systems. This grouping difference is based on writers’ specialty, preference and style, and editors’ formatting concerns. Complicating the issue, some organ systems share significant functional overlap. For instance, the nervous and endocrine system both operate via a shared organ, the hypothalamus; thus the two systems are sometimes combined and studied as the neuroendocrine system. And the vestibular system, in fact all sense organs, are often covered in sections on the nervous system. The musculoskeletal system combines two as one; textbooks frequently include the immune with the lymphatic system.

The publication of Andreas Vesalius’s De Humani Corporis Fabrica in 1543 ushered a new era in the history of medicine and marked the beginning of modern anatomy. This first anatomy book of 659 pages detailed six human systems: (1) skeletal, (2) muscles and ligaments, (3) circulatory, (4) cerebral and peripheral nerves, (5) abdominal and thoracic organs, and (6) brain and organs of special senses. See Persaud, T.V.N. A History of Anatomy: The Post-Vesalian Era. Springfield, IL: Charles C. Thomas Publisher, Ltd., 1997.

In the classic work Anatomy of the Human Body (Philadelphia: Lea & Febiger, 1918), Henry Gray (1827-1861, smallpox) posthumously grouped the various systems of the human body into the following six headings: “(1) Osteology—the bony system or skeleton, (2) Syndesmology—the articulations or joints, (3) Myology—the muscles. With the description of the muscles it is convenient to include that of the fasciæ which are so intimately connected with them, (4) Angiology—the vascular system, comprising the heart, blood vessels, lymphatic vessels, and lymph glands, (5) Neurology—the nervous system. The organs of sense may be included in this system, and (6) Splanchnology—the visceral system. Topographically the viscera form two groups, viz., the thoracic viscera and the abdomino-pelvic viscera. The heart, a thoracic viscus, is best considered with the vascular system. The rest of the viscera may be grouped according to their functions: (a) the respiratory apparatus; (b) the digestive apparatus; and (c) the urogenital apparatus. Strictly speaking, the third subgroup should include only such components of the urogenital apparatus as are included within the abdomino-pelvic cavity, but it is convenient to study under this heading certain parts which lie in relation to the surface of the body, e.g., the testes and the external organs of generation.” The work, thoroughly revised and re-edited by Warren H. Lewis (New York: Bartleby.com, 2000) is available online at http://www.bartleby.com/107/.

“The shortcomings of existing anatomical textbooks probably impressed themselves upon Henry Gray when he was still a student at St. George’s Hospital Medical School, near London’s Hyde Park Corner, in the mid 1840’s. He began thinking about creating a new anatomy textbook a decade later, while war was being fought in the Crimea. New legislation was being planned which would establish the General Medical Council (1858) to regulate professional education and standards.

Gray shared the idea for the new book with a gifted artistic colleague on the teaching staff at St. George’s, Dr. Henry Vandyke Carter, in November, 1855. Neither was interested in producing a pretty book, or an expensive one. Their purpose was to supply an affordable, accurate teaching aid for students like their own, who might soon be required to operate on soldiers injured at Sebastopol or on some other battlefield. The book they planned together was a practical one, designed to encourage youngsters to study anatomy, help them pass exams, and assist them as budding surgeons.

The book Gray and Carter created, Anatomy: Descriptive and Surgical, published by JW Parker & Son, appeared in August, 1858, to immediate acclaim.” (Condensed from Stranding, 2005, p. xvii).

The thirty-ninth edition of Gray’s Anatomy: The Anatomical Basis of Clinical Practice (Edited by Susan Stranding, et al., New York: Elsevier Churchill Livingstone, 2005), an enormous reference book consisting of 1,627 pages, “…is radically different from earlier editions because the body is described in regions rather than in systems. In the real world, the editorial team for the 39^th edition decided that a book which would be of the greatest benefit to practicing clinicians should mirror their daily practice and describe anatomy in the way in which they use it, i.e., regionally.” However, it too describes six systems: the (1) nervous, (2) blood, lymphoid tissues and haemopoiesis (red and white blood cells), (3) musculoskeletal, (4) smooth muscle and the cardiovascular and lymphatic, (5) skin and its appendages, and (6) endocrine. Basic structure and function of cells, integrating cells into tissues, embryogenesis, prenatal and neonatal growth are also covered. Following the systemic overview, this compendium then describes seven sections: (1) neuroanatomy, (2) head and neck, (3) back and macroscopic anatomy of the spinal cord, (4) pectoral girdle and upper limb, (5) thorax, (6) abdomen and pelvis, and (7) pelvic girdle and lower limb.

A recent textbook, Principles of Anatomy and Physiology, by Professors Gerard J. Tortora and Bryan Derrickson (New Jersey: John Wiley & Sons, Inc., 12^th edition, 2009) describes eleven systems of the human body: the (1) integumentary, (2) skeletal, (3) muscular, (4) nervous, (5) endocrine, (6) cardiovascular, (7) digestive, (8) urinary, (9) lymphatic and immunity, (10) respiratory, and (11) reproductive system. In what seems like the authors proudly going the extra mile, this textbook advocates a high-carbohydrate, low-fat diet in support of optimum health: “…many experts recommend the following distribution of calories: 50-60% from carbohydrates, with less than 15% from simple sugars; less than 30% from fats (triglycerides are the main type of dietary fat), with no more than 10% as saturated fats; and about 12-15% from proteins.” (See page 1006).

[3] See Lorin, Henry. Alzheimer’s Solved (Condensed Edition). South Carolina: BookSurge, LLC, 2005, p. 5.

[4] Ibid, p. 94.

[5] Ibid, p. 225.

[6] See McCleary, Larry. The Brain Trust Program. New York: Penguin Group (USA) Inc., 2007, pages 97-93.

[7] See “Ketogenic Diets and Physical Performance,” by Stephen D Phinney. Nutrition & Metabolism 2004, 1:2. doi: 10.1186/1743-7075-1-2. Available online at http://www.nutritionandmetabolism.com/content/1/1/2. Retrieved on 12/10/09.

[8] Ibid.

[9] Dr. Appleton lists “146 Reasons Why Sugar Is Ruining Your Health,” on her website at http://www.nancyappleton.com/NA144reasons.html. Retrieved on 12/10/09.

[10] See Ings, Simon. A Natural History of Seeing: The Art & Science of Vision. New York: W.W. Norton & Company, 2008, p. 65.

[11] See Diamond, Jared. The Third Chimpanzee: The Evolution and Future of the Human Animal. New York: Harper Perennial, 1992, p. 139

[12] “Whether diet may influence autoimmunity has been the subject of many unsolved debates. Interestingly, growing evidence indicates a large overlap between the mechanisms controlling tolerance to dietary antigens and autoimmunity. See “Autoimmunity and Diet,” by Cerf-Bensussan N. Nestle Nutr Workshop Ser Pediatr Program. 2009;64:91-9; discussion 99-104, 251-7. Available online at http://www.ncbi.nlm.nih.gov/pubmed/19710517?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=43. Retrieved on 12/11/09.

The use of omega-3 polyunsaturated fat—fish oil—has been known in small doses to aid the immune system. See “Dietary Fatty Acids and the Immune System,” by Calder PC. Lipids 1999; 34:S137-S140. Available online at http://www.springerlink.com/content/0195rt84xr947wvt/fulltext.pdf. Retrieved on 12/13/09.

[13] As of 2009, proponents of evolution are 18-0 in US court cases. Although State v. Scopes (1925), the first and most famous court case, resulted in a loss for Scopes, who was then fined $100, the verdict was eventually set aside due to a technicality on appeal to the Supreme Court of Tennessee. The most recent case, Tammy Kitzmiller, et al. v. Dover Area School District, et al. (2005) was the first direct challenge brought in the United States federal courts against a public school district that required the presentation of intelligent design as an alternative to evolution as an “explanation of the origin of life.” The plaintiffs successfully argued that intelligent design is a form of creationism, and that the school board policy thus violated the Establishment Clause of the First Amendment to the United States Constitution. The Decision of the Court in the matter of Kitzmiller, et al. v. Dover Area School District, et al., is available online at http://www.talkorigins.org/faqs/dover/kitzmiller_v_dover_decision.html. Retrieved on 12/10/09. For good background information and further references, see http://en.wikipedia.org/wiki/Kitzmiller_v._Dover_Area_School_District. Retrieved on 12/10/09.

[14] In 2006, Wilson Elser attorneys won a significant victory in US District Court, Southern District of New York, by securing the dismissal of a case charging the Atkins book and food products were defective and dangerous under product liability laws. The case involved a Florida man, and the lawsuit was commensed on the plaintiff’s behalf by the Physicians Committee for Responsible Medicine, which publically advocates a vegan (no meat, no dairy, no fish) lifestyle and has long been an opponent of the Atkins diet, attacking it as unhealthy. Southern District Judge Denny Chin said the suit must be dismissed because the Atkins book and food products are not defective or dangerous under product liability law. See the archives of the Wilson Elser Moskowitz Edelman & Dicker LLP law firm online at http://www.wilsonelser.com/files/repository/Nextrounddietlit_FallWinter20042005.pdf and http://www.wilsonelser.com/files/repository/LeghornAtkins_Dec2006.pdf. Both retrieved on 12/14/09.

[15] John Washington Butler (1875 – 1952) was an American farmer and a member of the Tennessee House of Representatives. He is most noted for introducing the Butler Act, which prohibited teaching of evolution in public, i.e., state, schools, and which was challenged in the Scopes Trial. The Butler Act was a 1925 Tennessee law forbidding public school teachers from denying the Biblical account of man’s origin. It was enacted as Tennessee Code Annotated Title 49 (Education) Section 1922. The law also prevented the teaching of the evolution of man from lower orders of animals in place of the Biblical account. However, the law did not prohibit the teaching of evolutionary theory for other species of plants or animals. The Butler Act was Introduced in the Tennessee House of Representatives as House Bill No. 185 by John Washington Butler on January 21, 1925; it passed the House on January 28, 1925 (Yeas: 71; Nays: 5); it passed the Senate on March 13, 1925 (Yeas: 24; Nays: 6); signed into law by Governor Peay on March 21, 1925; repealed on September 1, 1967 by Chapter No. 237, House Bill No. 48. See the Wikipedia article titled “Butler Act,” available online at http://en.wikipedia.org/wiki/Butler_Act. Retrieved on 12/15/09.

[16] See “The Effects of a Low-Carbohydrate, Ketogenic Diet on the Polycystic Ovary Syndrome: A Pilot Study,” by John C Mavropoulos, William S Yancy, Juanita Hepburn, and Eric C Westman. Nutrition & Metabolism 2005, 2:35. doi: 10.1186/1743-7075-2-35. Available online at http://www.nutritionandmetabolism.com/content/2/1/35. Retrieved on 12/10/09.

[17] See “The Effect of a Low-Carbohydrate Diet on Bone Turnover,” by J. D. Carter, F. B. Vasey, and J. Valeriano. Osteoporos Int (2006) 17: 1398–1403. doi: 10.1007/s00198-006-0134-x. Available online at http://www.springerlink.com/content/ej54l85238623l57/. Retrieved on 12/10/09.

[18] See “Food Groups and Bone Health,” by Susan A. New. In: Nutrition and Bone Health. Edited by M.F. Holick and B. Dawson-Hughes. New Jersey: Humana Press Inc., 2004.

[19] For a summary of the issues involved, see “Toward A Policy Agenda On Medical Research Funding: Results Of A Symposium,” by Robert I. Field, Barbara J. Plager, Rebecca A. Baranowski, Mary Anne Healy and Margaret L. Longacre. Health Affairs, 22, no. 3 (2003): 224-230. doi: 10.1377/hlthaff.22.3.224. Available online at http://content.healthaffairs.org/cgi/content/full/22/3/224. Retrieved on 12/13/09.

[20] See “Sodium, Potassium, Phosphorous, and Magnesium,” by Robert P. Heany. In: Nutrition and Bone Health. Edited by M.F. Holick and B. Dawson-Hughes. New Jersey: Humana Press Inc., 2004, p. 327.

[21] See “Calcium and Vitamin D for Bone Health in Adults,” by Bess Dawson-Hughes. In: Nutrition and Bone Health. Edited by M.F. Holick and B. Dawson-Hughes. New Jersey: Humana Press Inc., 2004, p. 197.

[22] See “Vitamin A and Bone Health,” by Peter Burckhardt. In: Nutrition and Bone Health. Edited by M.F. Holick and B. Dawson-Hughes. New Jersey: Humana Press Inc., 2004.

[23] See “Fluoride and Bone Health,” by Johann D. Ringe. In: Nutrition and Bone Health. Edited by M.F. Holick and B. Dawson-Hughes. New Jersey: Humana Press Inc., 2004, p.345.

[24] See “Food Groups and Bone Health,” by Susan A. New. In: Nutrition and Bone Health. Edited by M.F. Holick and B. Dawson-Hughes. New Jersey: Humana Press Inc., 2004, p. 237.

[25] Ibid, p. 245.

[26] Ibid, pages 236-237.

[27] Ibid, p. 237. See also the following: Macdonald HM, New SA, Grubb DA, Goloden MHN, Reid DM. “Impact of Food Groups on Perimenopausal Bone Loss.” In: Burckhardt P, Dawson-Hughes B, Heaney RP, eds. Nutritional Aspects of Osteoporosis 2000 (4^th International Symposium on Nutritional Aspects of Osteoporosis, Switzerland, 1997). Challenges of Modern Medicine. Ares-Serono, Academic, New York, 2001, pp. 399-408; Tucker KL, Chen H, Hannan MT, et al. “Bone Mineral Density and Dietary Patterns in Older Adults: the Framingham Osteoporosis Study.” Am J Clin Nutr 2002; 76:245-252; New SA, Bolton-Smith C, Grubb DA, Reid DM. “Nutritional Influences on Bone Mineral Density: a Cross-Sectional Study in Premenopausal Women.” Am J Clin Nutr 1997; 65:1831-1839; New SA, Robins Sp, Campbell MK, et al. “Dietary Influence on Bone Mass and Bone Metabolism: Further Evidence of a Positive Link Between Fruit and Vegetable Consumption and Bone Health?” Am J Clin Nutr 2000; 71:142-151; & Tucker KL, Hannan MT, Chen H, Cupples A, Wilson PWF, Kiel DP. “Potassium and Fruit & Vegetables are Associated with Greater Bone Mineral Density in Elderly Men and Women.” Am J Clin Nutr 1999; 69:727-736. Op cit. ”Food Groups and Bone Health,” by Susan A. New. In: Nutrition and Bone Health. Edited by M.F. Holick and B. Dawson-Hughes. New Jersey: Humana Press Inc., 2004, p. 237.

[28] The authors followed coronary heart disease morbidity and mortality in a cohort of rural men (N = 1,752) participating in a prospective observational study. Dietary choices were assessed at baseline with a 15-item food questionnaire. 138 men were hospitalized or deceased owing to coronary heart disease during the 12 year follow-up. See “Food Choices and Coronary Heart Disease: A Population Based Cohort Study of Rural Swedish Men with 12 Years of Follow-up,” by Sara Holmberg, Anders Thelin, and Eva-Lena Stiernström. Int. J. Environ. Res. Public Health 2009, 6, 2626-2638; doi: 10.3390/ijerph6102626. Available online at http://www.mdpi.com/1660-4601/6/10/2626/pdf. Retrieved on 12/13/09.

[29] See Taubes, Gary. Good Calories, Bad Calories. First Anchor Books Edition. New York: Anchor Books, 2008, p. 322.

[30] Ibid, p. 325. As it relates specifically to vitamin C, Gary Taubes states: “The vitamin C molecule is similar in configuration to glucose and other sugars in the body. It is shuttled from the bloodstream into the cells by the same insulin-dependent transport system used by glucose. Glucose and vitamin C compete in this cellular-uptake process, like strangers trying to flag down the same taxicab simultaneously. Because glucose is greatly favored in the contest, the uptake of vitamin C by cells is “globally inhibited” when blood sugar levels are elevated. In effect, glucose regulates how much vitamin C is taken up by the cells…In other words, there is significant reason to believe that the key factor determining the level of vitamin C in our cells and tissues is not how much or little we happen to be consuming in our diet, but whether the starches and refined carbohydrates in our diet serve to flush vitamin C out of our system, while simultaneously inhibiting the use of what vitamin C we do have.”

The Non-Corrupt Diabetes Association

2015-04-02T23:27:00.003-07:00

Disappointed with the leadership provided by diabetes organizations around the world, I have founded my own group, the Non-Corrupt Diabetes Association.

A little about me.

The better world I seek is one in which diabetics, regardless of type, aren’t told to eat carbohydrates. Diabetes is, after all, the inability to process carbohydrates. Yet nearly all health providers in general, and diabetes organizations specifically, advocate a diet consisting primarily of carbohydrates. Why? Well, there are millions of reasons why; the American Diabetes Association, the most influential diabetes treatment guidelines author, receives millions of dollars a year from pharmaceutical companies. The World Diabetes Foundation was founded and receives 90% of their yearly funding from Novo Nordisk, which makes most of its $100,000,000,000 DKK yearly income from diabetes care. What diet do you suppose they advocate?

Let me spell it out for you: true, a type one diabetic will have to take some insulin to control their blood sugar regardless of their diet, however, the more carbohydrates they eat, the more insulin they will have to take. The unfortunate reality of this disappointing conflict of interest is that the de facto customers of the ADA, WDF, and others, are insulin manufacturers, not diabetics.

And while the Juvenile Diabetes Research Foundation does not provide diet or treatment advice to diabetics, its chapters are free to fund their events as they see fit. Here's a picture of a recent JDRF promotion. Does that seem right to you?

There are some people that do well eating carbohydrates and taking matching insulin doses. But the vast majority of diabetics would be better served by not raising their blood sugar to begin with by not eating carbohydrates, or severely restricting them, hence, taking much less insulin. It isn’t illegal, immoral, or unethical, but it is a conflict of interest to take money from manufacturers, let alone treatment providers, and then turn around and recommend their products to patients.

To that end, I’ve founded the Non-Corrupt Diabetes Association which makes a difference in the lives of diabetics and their loved ones without regard to third parties. There are zero conflicts of interest. Feel free to join the group on Facebook.

For more information please feel free to read a past blog post, a book I wrote, or posts on the Facebook site.

Best wishes… - lc

Supermassive Black Holes and the DCCT

2015-02-20T10:50:00.001-08:00

[Author's note: this article is from the chapter by the same name from the book ESSENTIAL DIABETES LEADERSHIP. The DCCT is the most influential study to date investigating the use of insulin in the treatment of diabetes, but it is based upon a faulty assumption. DCCT stands for the Diabetes Control and Complications Trial, and this article details a metaphor. If you're not metaphorically-oriented, please feel free to skip to the last few paragraphs to find out why black holes are so fitting a metaphor for the DCCT.]

“I know that most men—not only those considered clever, but even those who are very clever and capable of understanding the most difficult scientific, mathematical, or philosophic, problems—can seldom discern even the simplest and most obvious truth if it be such as obliges them to admit the falsity of conclusions they have formed, perhaps with much difficulty—conclusions of which they are proud, which they have taught to others, and on which they have built their lives.”

LEO TOLSTOY, What is Art?, 1896

When a star runs out of nuclear fuel, it will collapse. If the core, or central region, of the star has a mass that is greater than three suns, no known nuclear forces can prevent the core from forming a deep gravitational warp in space called a black hole. A black hole is a dense, compact object whose gravitational pull is so strong that—within a certain distance of it—nothing can escape, not even light. Black holes are thought to result from the collapse of certain very massive stars at the ends of their evolution.[1]

A black hole does not have a surface in the usual sense of the word. There is simply a region, or boundary, in space around a black hole beyond which we cannot see. This boundary is called the event horizon.[2]

Anything that passes beyond the event horizon is doomed to be crushed as it descends ever deeper into the gravitational well of the black hole. No visible light, nor X-rays, nor any other form of electromagnetic radiation, nor any particle, no matter how energetic, can escape. The radius of the event horizon, proportional to the mass, is very small, only 30 kilometers for a non-spinning black hole with the mass of 10 Suns.[3]

Can astronomers see a black hole? Not directly. The only way to find one is to use circumstantial evidence. Observations must imply that a sufficiently large amount of matter is compressed into a sufficiently small region of space so that no other explanation is possible. For stellar black holes, this means observing the orbital acceleration of a star as it orbits its unseen companion in a double or binary star system.[4]

Searching for black holes is tricky business. One way to locate them has been to study X-ray binary systems. These systems consist of a visible star in close orbit around an invisible companion star which may be a neutron star or black hole. The companion star pulls gas away from the visible star.[5]

As this gas forms a flattened disk, it swirls toward the companion. Friction caused by collisions between the particles in the gas heats them to extreme temperatures and they produce X-rays that flicker or vary in intensity within a second.[6]

Many bright X-ray binary sources have been discovered in our galaxy and nearby galaxies. In about ten of these systems, the rapid orbital velocity of the visible star indicates that the unseen companion is a black hole. The X-rays in these objects are produced by particles very close to the event horizon. In less than a second after they give off their X-rays, they disappear beyond the event horizon.[7]

However, not all the matter in the disk around a black hole is doomed to fall into the black hole. In many black hole systems, some of the gas escapes as a hot wind that is blown away from the disk at high speeds. Even more dramatic are the high-energy jets that radio and X-ray observations show exploding away from some stellar black holes. These jets can move at nearly the speed of light in tight beams and travel several light years before slowing down and fading away.[8]

Do black holes grow when matter falls into them? Yes, the mass of the black hole increases by an amount equal to the amount of mass it captures. The radius of the event horizon also increases by about 3 kilometers for every solar mass that it swallows. A black hole in the center of a galaxy, where stars are densely packed, may grow to the mass of a billion Suns and become what is known as a supermassive black hole.[9]

The X-ray spectrum (see inset) of a binary star system consisting of a black hole and a normal star indicates that turbulent winds of multimillion degree gas are swirling around the black hole. As the illustration shows, much of the hot gas is spiraling inward toward the black hole, but about 30 percent is blowing away.

The temperature and intensity of the winds imply that powerful magnetic fields must be present. These magnetic fields, likely carried by the gas flowing from the companion star, create magnetic turbulence that generates friction in the gaseous disk and drive winds from the disk that carry momentum outward as the gas falls inward. Magnetic friction also heats the gas in the inner part of the disk to X-ray emitting temperatures. Image credit: Illustration: NASA/CXC/M.Weiss; X-ray Spectrum: NASA/CXC/U.Michigan/J.Miller et al.

Recently Chandra* has found evidence that black holes with masses of about a thousand Suns can be formed in dense star clusters by processes that are not yet understood.[10]

Kitty Ferguson, in her accessible book on black holes entitled Prisons of light: Black Holes, explains that a black hole is not the destiny of all suns:

“In the late 1920s, Subrahmanyan Chandrasekhar, a young Indian physicist then at the University of Cambridge, calculated that is a star’s mass is less than 1.4 times the mass of our sun, gravity will not be able to overpower this exclusion principle repulsion among the electrons. The star shrinks and becomes a white dwarf, but, because of the exclusion principle, it shrinks no further. That star will not become a black hole. We now call this mass of 1.4 solar masses the “Chandrasekhar limit.” Only in a star whose mass is more than the Chandrasekhar limit will gravity overcome the exclusion principle among the electrons and be the victor in this second competition.”[11]

Supermassive black holes with the mass of many millions of stars are thought to lie at the center of most large galaxies. The evidence comes from optical and radio observations which show a sharp rise in the velocities of stars or gas clouds orbiting the centers of galaxies. High orbital velocities mean that something massive is creating a powerful gravitational field which is accelerating the stars. X-ray observations indicate that a large amount of energy is produced in the centers of many galaxies, presumably by the in-fall of matter into a black hole.[12]

How could a supermassive black hole form in the center of a galaxy? One idea is that an individual star-like black hole forms and swallows up enormous amounts of matter over the course of millions of years to produce a supermassive black hole. Another possibility is that a cluster of starlike black holes forms and eventually merges into a single, supermassive black hole. Or, a single large gas cloud could collapse to form a supermassive black hole.[13]

Recent research, including results from Chandra suggests that galaxies and their black holes do not grow steadily, but in fits and starts. In the beginning of a growth cycle, the galaxy and its central black hole are accumulating matter. The energy generated by the jets that accompany the growth of the supermassive black hole eventually brings the infall of matter and the growth of the galaxy to a halt. The activity around the central black hole then ceases because of the lack of a steady supply of matter, and the jets disappear. Millions of years later the hot gas around the galaxy cools and resumes falling into the galaxy, initiating a new season of growth.[14]

Admittedly, this is a cursory introduction to the subject. If you are interested as much as I am in learning where, why, and how we are, let alone what else is out there, you would be best served by reviewing much more information.

A quick search on the Library of Congress returned 390 books written on black holes, and, surprisingly, only 9 on supermassive black holes. In addition to Kitty Ferguson’s book cited above, see Gravity’s Fatal Attraction: Black Holes in the Universe, by Mitchell Begelman and Martin Rees (New York: Scientific American Library, 1996). For a particularly good history underlying Chandrasekhar’s anticipation of the existence of black holes, and the clash of personalities at the time of his discoveries, see Empire of the Stars: Obsession, Friendship, and Betrayal in the Quest for Black Holes, by Arthur I. Miller (New York: Houghton Mifflin Company, 2005).

See also The Black Hole at the Center of our Galaxy, by Fulvio Melia (New Jersey: Princeton University Press, 2003). In addition, you could read any book by Stephen Hawking[15] to gather a better understanding of our existence and that of black holes. These works include: A Brief History of Time (Tenth Anniversary Edition, New York: Bantam Books, 1996), Black Holes and Baby Universes and Other Essays (New York: Bantam Books, 1994) and The Theory of Everything: The Origin and Fate of the Universe (Beverly Hills, CA: New Millennium Press, 2002).

Two books worth mentioning that are not focused on black holes, but, nevertheless, are worth your reading time because they answer so many questions, and even propose others, are The Origins of the Future: Ten Questions for the Next Ten Years, by John Gribbin (New Haven, CT: Yale University Press, 2006), and Just Six Numbers: The Deep Forces that Shape the Universe, by Martin Rees (New York: Basic books, 2000). Both are written accessibly for the lay reader like me, and both do a good job of putting things—the universe—into perspective. That we exist at all is the result of some very fine tuning, and that the search for answers inevitably leads to more questions, ad infinitum.

And, of course, I cannot leave the subject of black holes and supermassive black holes without mentioning the 19,100,000 and 1,360,000 individual results, respectively, when performing a search on GOOGLE.

This composite NASA image of the spiral galaxy M81, located about 12 million light years away, includes X-ray data from the Chandra X-ray Observatory, optical data from the Hubble Space Telescope, infrared data from the Spitzer Space Telescope and ultraviolet data from GALEX. The inset shows a close-up of the Chandra image. At the center of M81 is a supermassive black hole that is about 70 million times more massive than the Sun. A new study using data from Chandra and ground-based telescopes, combined with detailed theoretical models, shows that the supermassive black hole in M81 feeds just like stellar mass black holes, with masses of only about ten times that of the Sun. This discovery supports the implication of Einstein's relativity theory that black holes of all sizes have similar properties, and will be useful for predicting the properties of a conjectured new class of black holes.

The supermassive black hole in M81 generates energy and radiation as it pulls gas in the central region of the galaxy inwards at high speed. Therefore, the model that Markoff and her colleagues used to study the black holes includes a faint disk of material spinning around the black hole. This structure would mainly produce X-rays and optical light. A region of hot gas around the black hole would be seen largely in ultraviolet and X-ray light. A large contribution to both the radio and X-ray light comes from jets generated by the black hole. Multiwavelength data is needed to disentangle overlapping sources of light.

Image Credit: X-ray: NASA/CXC/Wisconsin/D.Pooley and CfA/A.Zezas; Optical: NASA/ESA/CfA/A.Zezas; UV: NASA/JPL-Caltech/CfA/J.Huchra et al.; IR: NASA/JPL-Caltech/CfA

The illustration above depicts a supermassive black hole ripping apart a star and consuming a portion of it, a long-predicted astronomical event confirmed by NASA's Chandra and the European Space Agency’s XMM-Newton X-ray Observatories.

Astronomers believe a doomed star came too close to a giant black hole after being thrown off course by a close encounter with another star. As it neared the enormous gravity of the black hole, the star was stretched by tidal forces until it was torn apart. This discovery provides crucial information about how these black holes grow and affect surrounding stars and gas.

Illustration: NASA/CXC/M.Weiss

Having read my brief overview, and perhaps endeavored to read a few of the aforementioned cited books, you are now as much of an expert on black holes as I, and we are ready to develop a couple of metaphors, then apply our learning to find an optimal solution to our diabetes conundrum.

There are stellar black holes and supermassive black holes.

Stellar black holes in the realm of diabetes include the use of fiber and carbohydrates in the diet. Carbohydrates have typically been restricted in diabetes diets throughout the century, and only recently has it been such a controversial topic. For example, in “General Treatment of Diabetes,” (1970), written by D. A. Pyke, M.D., F.R.C.P., the author states:

“The only important recent advance in the dietary treatment of diabetes is that it has now been widely agreed that diets should be reckoned in 10 g. carbohydrate portions and that, except in the obese, fat and protein need not be restricted. Control of diabetes, even in the obese, is often achieved by carbohydrate restriction alone, before there is any weight reduction. Though it may be a useful encouragement to a fat patient to lose weight that this will control his diabetes, this is in fact seldom essential; the important measure is carbohydrate restriction.”[16]

The above article is in sharp contrast to numerous biased articles written in the decades previous, and after, such as “Low-Fat Diet and Therapeutic Doses of Insulin in Diabetes Mellitus,” (1955), where the author, Inder Singh states assuredly that:

“There is no indication that healthy people taking a diet rich in carbohydrates are especially liable to diabetes; in fact numerous observations show improvement of carbohydrate tolerance following its greater intake.”[17]

That conclusion was based on a study of 80 “insulin-sensitive” diabetics, but if you were to see the actual BG levels of those studied, you would be aghast at how high they were. Of the 80 people studied, 25 started with relatively normal BG levels, but the majority of them had starting BG levels over 125, with some in the 200, 300, and 400 mg/dL range, and one even starting at 600. By the end of the glucose tolerance test, that individual was at 1,000.[18]

Clearly, the standards back in 1955 weren’t quite so high. Let us turn to 1976, however, when the high-carbohydrate diet was gaining some momentum. In “Beneficial Effects of a High Carbohydrate, High Fiber Diet on Hyperglycemic Diabetic Men,” (1976), the authors, Tae G. Kiehm, M.D., James W. Anderson, M.D., and Kyleen Ward, R.D., state the following:

“A “diabetic” diet is an essential feature in the treatment of diabetes and traditionally this diet has been restricted in carbohydrate.[19] Although recently it has been recommended that the carbohydrate content of the diabetic diet be increased,[20] no data are available that provide compelling evidence for increasing the carbohydrate content of the diabetic diet. However, several studies[21] suggest that a high-carbohydrate may be beneficial in treating some patients. Because diets containing 75 to 85% of calories as carbohydrate have been associated with improved glucose metabolism of normal individuals and patients with mild diabetes, we have studied the therapeutic utility of a 75% carbohydrate diet in treating diabetic patients requiring either insulin or oral hypoglycemic agents.”[22]

Here is a summary of that study:

“High carbohydrate diets rich in dietary fiber were fed to 13 hyperglycemic diabetic men; five men required 15 to 28 units of insulin per day, five men required sulfonylureas, and three men required 50 to 55 units of insulin. All 13 men were fed weight maintaining American Diabetic Association diets containing 43% of calories as carbohydrates for 1 week and then were fed 75% carbohydrate diets with 15 g. of crude dietary fiber for approximately 2 weeks. After 2 weeks on the 75% carbohydrate diet, sulfonylureas were discontinued in all five men, insulin was discontinued in four men and decreased from 28 to 15 units in 1 man from the group requiring less than 30 units per day. Fasting plasma glucose values were significantly lower (P<0.001)* in all 10 men. However, insulin requirements and fasting plasma glucose values were not changed in the three men requiring 40 to 55 units of insulin. Fasting serum cholesterol values were significantly (P<0.001) lower and mean fasting serum triglyceride values were 15% lower on the high carbohydrate diet than on the American Diabetic Association diet in these 13 men. Thus a high carbohydrate diet with generous amounts of fiber may be the treatment of choice of diabetic patients requiring sulfonylureas or less than 30 units of insulin per day.”[23]

In “High-Carbohydrate Diets and Insulin-Dependent Diabetics,” (1979), by R W Simpson, J I Mann, J Eaton, R D Carter, and T D Hockaday, the authors concluded: “Thus several measures of carbohydrate and lipid metabolism appear to be more satisfactory when patients receive a HC [High-Carbohydrate] diet, which is an acceptable alternative to that still recommended to most insulin-requiring patients.”[24]

In “A high Carbohydrate Leguminous Fibre Diet Improves All Aspects of Diabetic Control,” (1981), by Simpson HC, Simpson RW, Lousley S, Carter RD, Geekie M, Hockaday TD, and Mann JI, the authors concluded that “a diet high in complex carbohydrate and leguminous fibre improves all aspects of diabetic control, and continued use of a low carbohydrate diet no longer appears justified.”[25]

In “Digestible Carbohydrate—an Independent Effect on Diabetic Control in Type 2 (Non-Insulin-Dependent) Diabetic Patients?” (1982), by H. C. R. Simpson, R. D. Carter, S. Lousley, and J. I. Mann, the authors stated that “Many studies have shown high carbohydrate, high fibre diets to benefit diabetic control, the improvement being attributed mainly to an effect of fibre,” without footnote identifying any of those studies. And they concluded “These results indicate that a diet rich in carbohydrate, but restricted in fibre, does not cause overall deterioration of diabetic control or lipid metabolism in stable Type 2 diabetic patients, and suggest that digestible carbohydrate has an effect on basal blood glucose independent of fibre.”[26]

In “What Carbohydrate Foods Should Diabetics Eat?” (1984), by JI Mann, the author stated:

“…Epidemiological evidence suggested that the standard diabetic diet, low in carbohydrate and relatively high in fat, might actually increase the risk of cardiovascular disease, the most frequent cause of death among diabetics. Furthermore, several studies suggested that diets relatively high in fibre rich carbohydrate reduced hyperglycemia in diabetic patients. Though there remains some disagreement about the precise quantity of carbohydrate which should be included in the diabetic diet, the diabetic associations of many Western countries, including the United States, Britain, Canada, Australia, and Finland, have affirmed the importance in the management of diabetes and recommend an increase in unrefined carbohydrate (especially fibre rich carbohydrate) with a reduction in the fat intake.”[27]

Further in the article, he asks two fundamental questions:

“Does this mean that wholemeal bread and potato should be eliminated from or at least discouraged in the diabetic diet, or that suitability of foods for the diabetic may in future be determined in the laboratory?

The answer to both questions must be no, at least in the light of present knowledge. Wholemeal bread and potatoes have formed a substantial part of several experimental diets which have over weeks or months shown an appreciable improvement in diabetic control.”[28]

He concludes this article with the following statement, subtly insinuating that it’s not a diabetic’s diet that should drive the insulin use, but, rather, it’s the prescribed exogenous insulin use that should drive the diet:

“Finally, every commentary on dietary advice for diabetics should restate the most important principles: energy intake should be adjusted to maintain the ideal body weight and in the insulin dependent diabetic a regular meal pattern should be established to match the injected insulin.[29]

But are these studies credible? Hardly. Dr. Uffe Ravnskov points out Jim Mann’s conflicts of interest in his latest book. He writes:

“All [these] studies were co-authored by Jim Mann, a professor in Human Nutrition and Medicine at the University of Otago, a WHO expert in nutrition and the main advisor for the Sugar Research Advisory Service (SRAS), an information service established in 2002 and funded by the New Zealand Sugar Company with the aim ‘to encourage appropriate use and enjoyment of sugar as part of a healthy and balanced diet.’ Jim Mann is also the main author of the European guidelines for the treatment and prevention of diabetic patients. But you will look in vain for any information about the author’s possible competing interests in that paper or in his other publications.”[30]

We find more answers, especially those centered on what it means to be insulin resistant, in Gary Taubes’s discussion of geneticist James Neel, the thrifty-gene hypothesis creator that would later reject his own idea. Focused on what constitutes insulin resistance, Gary Taubes wrote that “Neel suggested three scenarios of these insulin-secretory responses that could constitute a pre-disposition to obesity and/or type 2 diabetes—each of which, he wrote, would be a physiological ‘response to the excessive glucose pulses that result from the refined carbohydrates/over-alimentation of many civilized diets.’”[31] Of those three scenarios, one stands out as coming closest to reality:

“Here an appropriate amount of insulin is secreted in response to the “excessive glucose pulses” of a modern meal, and the response of the muscle cells to the insulin is also appropriate. The defect is in the relative sensitivity of muscle and fat cells to the insulin. The muscle cells become insulin-resistant in response to the “repeated high levels of insulinemia that result from excessive ingestion of highly refined carbohydrates and/or over-alimentation,” but the fat cells fail to compensate. They remain stubbornly sensitive to insulin. So, as Neel explained, the fat tissue accumulates more and more fat, but “mobilization of stored fat would be inhibited.” Now the accumulation of fat in the adipose tissue drives the vicious cycle.

This scenario is the most difficult to sort out clinically, because when these investigators measure insulin resistance in humans they invariably do so on a whole body level, which is all the existing technology allows. Any disparities between the responsiveness of fat and muscle tissue to insulin cannot be measured. This is critical, because for the past thirty-five years the American Diabetes Association has recommended that diabetics eat a diet relatively rich in carbohydrates based on the notion that this makes them more sensitive to insulin, at least temporarily, so the diet appears to ameliorate the diabetes. This effect was initially reported in 1971, by the University of Washington endocrinologists Edwin Bierman and John Brunzell, who then waged a lengthy and successful campaign to persuade the American Diabetes Association to recommend that diabetics eat more carbohydrates rather than less. If Neel’s third scenario is correct, however, a likely explanation for why carbohydrate-rich diets appear to facilitate blood-sugar control after meals is that they increase the insulin sensitivity of the fat cells specifically, while the muscle tissue remains insulin-resistant.”[32]

Here might be the opportune time to tell the tale of James Van Gundia Neel (March 22, 1915 – February 1, 2000) and his refinement.[33]

James Neel, a professor of Human Genetics at the University of Michigan Medical School, proposed the “thrifty genotype” hypothesis in 1962 in his paper “Diabetes Mellitus: A ‘Thrifty’ Genotype Rendered Detrimental by ‘Progress’?” Neel intended the paper to provoke further contemplation and research on the possible evolutionary and genetic causes of diabetes among populations that had only recently come into regular contact with Westerners.[34]

The genetic paradox Neel sought to address was this: diabetes conferred a significant reproductive, and thus evolutionary, disadvantage to anyone who had it; yet the populations Neel studied had diabetes in such high frequencies that a genetic predisposition to develop diabetes seemed plausible. Neel sought to unravel the mystery of why genes that promote diabetes had not been naturally-selected out of the population's gene pool.[35]

Neel proposed that a genetic predisposition to develop diabetes was adaptive to the feast and famine cycles of Paleolithic human existence, allowing humans to fatten rapidly and profoundly during times of feast in order that they might better survive during times of famine.[36]

While Neel considered the “thrifty genotype” notion worth further investigation, he also proposed in 1962, yet did not develop until years later, a counter-hypothesis. namely that “this frequency of obesity and diabetes is a relatively recent phenomenon” in which case the question would become “what changes in the environment are responsible for the increase?”[37]

In the decades following the publications of his first paper on the “thrifty genotype” hypothesis, Neel investigated the frequency of diabetes and, increasingly, obesity in a number of other populations, and, as a proper scientist, sought out observations that might disprove or discount his “thrifty gene” hypothesis.

Neel's further investigations cast doubt on the “thrifty genotype” hypothesis. If a propensity to develop diabetes were an evolutionary adaptation, then diabetes would have been a disease of long standing in those populations currently experiencing a high frequency of diabetes. However, Neel found no evidence of diabetes among these populations earlier in the century.[38] And when he tested younger members of these populations for glucose intolerance—which might have indicated a predisposition for diabetes—he found none.[39]

In 1989, Neel published a review of his further research based on the “thrifty genotype” hypothesis and in the Introduction noted the following: “The data on which that rather soft hypothesis was based has now largely collapsed.”[40] However, this sentence clearly could only be applied to his original hypothesis, because later in the same paper where he continued to refine his concepts, Neel noted “...the concept of a “thrifty genotype” remains as viable as when first advanced...” He went on to advance that the thrifty genotype concept be thought of in the context of a “compromised” genotype that effects several other metabolically-related diseases.

This refinement is actually just a return by Neel to the alternative hypothesis to which he had alluded twenty years earlier—that modern, very-high levels of obesity and diabetes among formerly native populations were a relatively recent phenomenon most likely caused by changes in diet. Given that some “thrifty gene” populations, like the Inuit, experienced a rise in obesity and diabetes in conjunction with a reduction of the proportion of fat and protein in their diets, Neel surmised that the dietary causes of obesity and diabetes lay in carbohydrate consumption, “specifically the use of highly refined carbohydrate.”[41]

The central premise of the thrifty gene hypothesis—that famines were common and severe enough to select for thrifty genes has been recently challenged.[42] Many of the populations that later developed high rates of obesity and diabetes appeared to have no discernible history of famine or starvation (for example, Pacific Islanders whose “tropical-equatorial islands had luxuriant vegetation all year round and were surrounded by lukewarm waters full of fish.”).[43] Moreover, one of the most significant problems for the “thrifty gene” idea is that it predicts that modern hunter gatherers should get fat in the periods between famines. Yet data on the body mass index of hunter-gatherer and subsistence agriculturalists clearly show that between famines they do not deposit large fat stores.[44]

We return now to see that Gary Taubes provides the last word on carbohydrates when he states:

“It is not the case, despite public-health recommendations to the contrary, that carbohydrates are required in a healthy human diet. Most nutritionists still insist that a diet requires 120 to 130 grams of carbohydrates, because this is the amount of glucose that the brain and central nervous system will metabolize when the diet is carbohydrate rich. But what the brain uses and what it requires are two different things. Without carbohydrates in the diet, the brain and central nervous system will run on ketone bodies, converted from dietary fat and from the fatty acids released by the adipose tissue; on glycerol, also released from the fat tissue with the breakdown of triglycerides into free fatty acids; and on glucose, converted from the protein in the diet. Since a carbohydrate-restricted diet, unrestricted in calories, will, by definition, include considerable fat and protein, there will be no shortage of fuel for the brain. Indeed, this is likely to be the fuel mixture that our brains evolved to use, and our brains seem to run more efficiently on this fuel mixture than they do on glucose alone. (A good discussion of the rationale for a minimal amount of carbohydrates in the diet can be found in the 2002 Institute of Medicine [IOM] report, Dietary Reference Intakes. The IOM sets an “estimated average requirement” of a hundred grams of carbohydrates a day for adults, so that the brain can run exclusively on glucose, “without having to rely on a partial replacement of glucose by [ketone bodies].” It then sets the “recommended dietary allowance” at 130 grams to allow margin for error. But the IOM report also acknowledges that the brain will be fine without these carbohydrates, because it runs perfectly well on ketone bodies, glycerol, and the protein-derived glucose.)”[45]

Let’s take a look at the IOM report:

“The lower limit of dietary carbohydrate compatible with life apparently is zero, provided that adequate amounts of protein and fat are consumed. However, the amount of dietary carbohydrate that provides for optimal health in humans is unknown. There are traditional populations that ingested a high fat, high protein diet containing only a minimal amount of carbohydrate for extended periods of time (Masai), and in some cases for a lifetime after infancy (Alaska and Greenland Natives, Inuits, and Pampas indigenous people) (Du Bois, 1928; Heinbecker, 1928). There was no apparent effect on health or longevity. Caucasians eating an essentially carbohydrate-free diet, resembling that of Greenland natives, for a year tolerated the diet quite well (Du Bois, 1928). However, a detailed modern comparison with populations ingesting the majority of food energy as carbohydrate has never been done.

It has been shown that rats and chickens grow and mature successfully on a carbohydrate-free diet (Brito et al., 1992; Renner and Elcombe, 1964), but only if adequate protein and glycerol from triacylglycerols are provided in the diet as substrates for gluconeogenesis. It has also been shown that rats grow and thrive on a 70 percent protein, carbohydrate-free diet (Gannon et al., 1985). Azar and Bloom (1963) also reported that nitrogen balance in adults ingesting a carbohydrate-free diet required the ingestion of 100 to 150 g of protein daily. This, plus the glycerol obtained from triacylglycerol in the diet, presumably supplied adequate substrate for gluconeogenesis and thus provided at least a minimal amount of completely oxidizable glucose.

The ability of humans to starve for weeks after endogenous glycogen supplies are essentially exhausted is also indicative of the ability of humans to survive without an exogenous supply of glucose or monosaccharides convertible to glucose in the liver (fructose and galactose). However, adaptation to a fat and protein fuel requires considerable metabolic adjustments.

The only cells that have an absolute requirement for glucose as an oxidizable fuel are those in the central nervous system (i.e., brain) and those cells that depend upon anaerobic glycolysis (i.e., the partial oxidation of glucose to produce lactate and alanine as a source of energy), such as red blood cells, white blood cells, and medulla of the kidney. The central nervous system can adapt to a dietary fat-derived fuel, at least in part (Cahill, 1970; Sokoloff, 1973). Also, the glycolyzing cells can obtain their complete energy needs from the indirect oxidation of fatty acids through the lactate and alanine-glucose cycles.

In the absence of dietary carbohydrate, de novo synthesis of glucose requires amino acids derived from the hydrolysis of endogenous or dietary protein or glycerol derived from fat. Therefore, the marginal amount of carbohydrate required in the diet in an energy-balanced state is conditional and dependent upon the remaining composition of the diet. Nevertheless, there may be subtle and unrecognized, untoward effects of a very low carbohydrate diet that may only be apparent when populations not genetically or traditionally adapted to this diet adopt it. This remains to be determined but is a reasonable expectation.

Of particular concern in a Western, urbanized society is the long-term consequences of a diet sufficiently low in carbohydrate such that it creates a chronically increased production of β-hydroxybutyric and acetoacetic acids (i.e., keto acids). The concern is that such a diet, deficient in water-soluble vitamins and some minerals, may result in bone mineral loss, may cause hypercholesterolemia, may increase the risk of urolithiasis (Vining, 1999), and may affect the development and function of the centra1 nervous system. It also may adversely affect an individual’s general sense of well being (Bloom and Azar, 1963), although in men starved for an extended period of time, encephalographic tracings remained unchanged and psychometric testing showed no deficits (Owen et al., 1967). It also may not provide for adequate stores of glycogen. The latter is required for hypoglycemic emergencies and for maximal short-term power production by muscles (Hultman et al., 1999).

EVIDENCE CONSIDERED FOR ESTIMATING THE AVERAGE REQUIREMENT FOR CARBOHYDRATE

The endogenous glucose production rate, and thus the utilization rate, depends on the duration of starvation. Glucose production has been determined in a number of laboratories using isotopically labeled glucose (Amiel et al., 1991; Arslanian and Kalhan, 1992; Bier et al., 1977; Denne and Kalhan, 1986; Kalhan et al., 1986; King et al., 1982; Patel and Kalhan, 1992). In overnight fasted adults (i.e., postabsorptive state), glucose production is approximately 2 to 2.5 mg/kg/min, or approximately 2.8 to 3.6 g/kg/d. In a 70-kg man, this represents approximately 210 to 270 g/d. In the postabsorptive state, approximately 50 percent of glucose production comes from glycogenolysis in liver and 50 percent from gluconeogenesis in the liver (Chandramouli et al., 1997; Landau et al., 1996).

The minimal amount of carbohydrate required, either from endogenous or exogenous sources, is determined by the brain’s requirement for glucose. The brain is the only true carbohydrate-dependent organ in that it oxidizes glucose completely to carbon dioxide and water. Normally, the brain uses glucose almost exclusively for its energy needs. The endogenous glucose production rate in a postabsorptive state correlates very well with the estimated size of the brain from birth to adult life. However, not all of the glucose produced is utilized by the brain (Bier et al., 1977; Felig, 1973). The requirement for glucose has been reported to be approximately 110 to 140 g/d in adults (Cahill et al., 1968).

Nevertheless, even the brain can adapt to a carbohydrate-free, energy-sufficient diet, or to starvation, by utilizing ketoacids for part of its fuel requirements. When glucose production or availability decreases below that required for the complete energy requirements for the brain, there is a rise in ketoacid production in the liver in order to provide the brain with an alternative fuel. This has been referred to as “ketosis.” Generally, this occurs in a starving person only after glycogen stores in the liver are reduced to a low concentration and the contribution of hepatic glycogenolysis is greatly reduced or absent (Cahill et al., 1968). It is associated with approximately a 20 to 50 percent decrease in circulating glucose and insulin concentration (Carlson et al., 1994; Owen et al., 1998; Streja et al., 1977). These are signals for adipose cells to increase lipolysis and release nonesterified fatty acids and glycerol into the circulation. The signal also is reinforced by an increase in circulating epinephrine, norepinephrine, glucagon, and growth hormone concentration (Carlson et al., 1994). The nonesterified fatty acids are removed by the liver and converted into ketoacids, which then diffuse out of the liver into the circulation. The increase in nonesterified fatty acids results in a concentration-dependent exponential increase in ketoacids (Hanson et al., 1965); glucagon facilitates this process (Mackrell and Sokal, 1969).

In an overnight fasted person, the circulating ketoacid concentration is very low, but with prolonged starvation the concentration increases dramatically and may exceed the molar concentration of glucose (Cahill, 1970; Streja et al., 1977). In individuals fully adapted to starvation, ketoacid oxidation can account for approximately 80 percent of the brain’s energy requirements (Cahill et al., 1973). Thus, only 22 to 28 g/d of glucose are required to fuel the brain. This is similar to the total glucose oxidation rate integrated over 24 hours determined by isotope-dilution studies in these starving individuals (Carlson et al., 1994; Owen et al., 1998).

Overall, the key to the metabolic adaptation to extended starvation is the rise in circulating nonesterified fatty acid concentrations and the large increase in ketoacid production. The glycerol released from the hydrolysis of triacylglycerols stored in fat cells becomes a significant source of substrate for gluconeogenesis, but the conversion of amino acids derived from protein catabolism into glucose is also an important source. Interestingly, in people who consumed a protein-free diet, total nitrogen excretion was reported to be in the range of 2.5 to 3.5 g/d (35 to 50 mg/kg), or the equivalent of 16 to 22 g of catabolized protein in a 70-kg man (Raguso et al., 1999). Thus, it is similar to that in starving individuals (3.7 g/d) (Owen et al., 1998). Overall, this represents the minimal amount of protein oxidized through gluconeogenic pathways (Du Bois, 1928). This amount of protein is considerably less than the Recommended Dietary Allowance (RDA) of 0.8 g/kg/d for adults with a normal body mass index (Chapter 10). For a 70-kg lean male, this equals 56 g/d of protein, which is greater than the estimated obligate daily loss in body protein from the shedding of cells, secretions, and other miscellaneous functions (approximately 6 to 8 g/d for a 70-kg man; see Chapter 10) and has been assumed to be due to inefficient utilization of amino acids for synthesis of replacement proteins and other amino acid-derived products (Gannon and Nuttall, 1999). In part, it also may represent the technical difficulty in determining a minimal daily protein requirement (see Chapter 10).

If 56 g/d of dietary protein is required for protein homeostasis, but the actual daily loss of protein is only approximately 7 g, then presumably the remaining difference (49 g) is metabolized and may be utilized for new glucose production. It has been determined that for ingested animal protein, approximately 0.56 g of glucose can be derived from every 1 g of protein ingested (Janney, 1915). Thus, from the 49 g of protein not directly utilized to replace loss of endogenous protein or not used for other synthetic processes, approximately 27 g (0.56 × 49) of glucose may be produced. In people on a protein-free diet or who are starving, the 16 to 22 g of catabolized protein could provide 10 to 14 g of glucose.

If the starving individual’s energy requirement is 1,800 kcal/d and 95 percent is supplied by fat oxidation either directly or indirectly through oxidation of ketoacids (Cahill et al., 1973), then fat oxidation represents 1,710 kcal/d, or 190 g based upon approximately 9 kcal/g fat. The glycerol content of a typical triacylglycerol is 10 percent by weight, or in this case 19 g of glycerol, which is equivalent to approximately 19 g of glucose. This, plus the amount of glucose potentially derived from protein, gives a total of approximately 30 to 34 g ([10 to 14] + 19). Thus, a combination of protein and fat utilization is required to supply the small amount of glucose still required by the brain in a person fully adapted to starvation. Presumably this also would be the obligatory glucose requirement in people adapted to a carbohydrate-free diet. Thus, the normal metabolic adaptation to a lack of dietary protein, as occurs in a starving person in whom the protein metabolized is in excess of that lost daily, is to provide the glucose required by the brain. Nevertheless, utilization of this amount of glucose by the brain is vitally important. Without it, function deteriorates dramatically, at least in the brain of rats (Sokoloff, 1973).

The required amount of glucose could be derived easily from ingested protein alone if the individual was ingesting a carbohydrate-free, but energy-adequate diet containing protein sufficient for nitrogen balance. However, ingested amounts of protein greater than 30 to 34 g/d would likely stimulate insulin secretion unless ingested in small amounts throughout a 24-hour period. For example, ingestion of 25 to 50 g of protein at a single time stimulates insulin secretion (Krezowski et al., 1986; Westphal et al., 1990), despite a lack of carbohydrate intake. This rise in insulin would result in a diminution in the release of fatty acids from adipose cells and as a consequence, reduce ketoacid formation and fatty acid oxidation. The ultimate effect would be to increase the requirement for glucose of the brain and other organs. Thus, the minimal amount of glucose irreversibly oxidized to carbon dioxide and water requires utilization of a finely balanced ratio of dietary fat and protein.

Azar and Bloom (1963) reported that 100 to 150 g/d of protein was necessary for maintenance of nitrogen balance. This amount of protein could typically provide amino acid substrate sufficient for the production of 56 to 84 g of glucose daily. However, daily infusion of 90 g of an amino acid mixture over 6 days to both postoperative and nonsurgical starving adults has been reported to reduce urinary nitrogen loss without a significant change in glucose or insulin concentration, but with a dramatic increase in ketoacids (Hoover et al., 1975). Thus, the issue becomes complex in nonstarving people.”[46]

Let me repeat the words of Gary Taubes: “What the brain uses and what it requires are two different things. Without carbohydrates in the diet, the brain and central nervous system will run on ketone bodies, converted from dietary fat and from the fatty acids released by the adipose tissue; on glycerol, also released from the fat tissue with the breakdown of triglycerides into free fatty acids; and on glucose, converted from the protein in the diet. Since a carbohydrate-restricted diet, unrestricted in calories, will, by definition, include considerable fat and protein, there will be no shortage of fuel for the brain.”[47]

There is no essential need for carbohydrates. Thus, any individual, group, or organization espousing the need for carbohydrates must be advancing their own agenda, or advancing the agenda of a third party, whether they know it—and benefit from it—or not. We’ll delve into that subject a little more later; for now, let’s complete the metaphors.

In a similar way, then, though created within a much shorter time span, the treatment—the galaxy—of diabetes has evolved around and upon the singularity of the DCCT, yes, our supermassive black hole.

We see the DCCT cited in nearly every reference book that advocates a specific diet available at the Santa Clara City Library. If I ever survey those 3,359 diabetes books at the Library of Congress, and publish my findings, I will be sure to include a section on reference books published after the DCCT concluded, at which time I will be able to say with certainty how many and what percentage cite the DCCT. My best guess from the evidence gathered to date—my hypothesis if you will—is that the number of reference books with specific sections detailing diabetes mellitus, advocating a low-fat diet, that cite the DCCT, approaches 100%.

The oldest reference book, with a section devoted to diabetes mellitus, in the reference section at Santa Clara City Library, which included a citation of the DCCT, was Family Medicine Principles & Practice, Fifth Edition (1998). That reference book states:

“One study showed, however, that early poor control despite later good control results in diabetes complications. The Diabetes Control and Complications Trial (DCCT) proved the profound impact of intensive therapy on reducing the risk of microvasular complications. Decades of questions about the glucose hypothesis are therefore finally answered, with the obvious recommendation that most individuals with type 1 diabetes mellitus be treated with intensive therapy.”[48]

According to Rudolph's Pediatrics 21st Edition (2003):

“The goals of treatment of children with type 1 diabetes mellitus are as follows: 1. Stabilize blood level of glucose within a target range; 2. Avoid metabolic decompensation (diabetic ketoacidosis, severe hypoglycemia); 3. Ensure normal growth and development at both a physical and emotional level; 4. Prevent long-term complication of both hyperglycemia and hypoglycemia. The best means to achieve these goals have been established through several long-term studies involving adolescents and adults, most notably the Diabetes Control and Complications Trial (DCCT). This 9-year prospective multicenter trial compared outcomes among patients who underwent intensive treatment in an attempt to maintain euglycemia with outcomes among those treated in the conventional manner, in which the goal was clinical well-being. Patients in the intensive therapy group received three or more insulin injections per day or used an insulin pump; measured blood glucose several times a day; had monthly clinic visits with the health-care team and weekly follow-up telephone calls; and were encouraged to use a dynamic regimen with adjustments for variation in daily food intake and activities. Those in the conventional treatment group received one to two insulin injections per day, were seen in the clinic every several months, and followed a static daily insulin regimen. The study showed definitively that tighter glucose control reduces the risk of long-term complications of type 1 diabetes mellitus, decreases risk of development of microvascular complications, and slows progression of preexisting lesions 35 to 75%. The DCCT showed that any improvement in glucose control lowers the risk of long-term complications. Every 10% decrease in HbA1c is associated with a 40 to 45% lower risk of progression of retinopathy. Therefore, even if the stated target range is not achieved, any incremental decrease in blood glucose value decreases the risk of future microvascular disease.”[49]

In Cecil Textbook of Medicine 22^nd Edition (2004):

“The benefits achieved by intensive control in the DCCT were not without risk. Weight gain was more common, and most importantly, the frequency of severe hyperglycemia (including episodes in some patients) was three-fold higher in the intensive care group. In many cases, such episodes occurred without classic warning symptoms, often while the patient was asleep. Thus, in some patients, the risks of intensive therapy may outweigh the benefits; possibly included are patients with advanced complications, young children, and patients who are unable or unwilling to participate in their management (e.g., self-monitoring of blood glucose). Such individuals are likely to benefit from less aggressive therapy designed to moderately lower glucose levels without the risk of hypoglycemia. It is noteworthy that despite the higher rate of hypoglycemia, intensive therapy in the DCCT had no detectable long-term effects on cognitive function.”[50]

In Harrison’s Principles of Internal Medicine, 17^th Edition (2008):

“The DCCT demonstrated that improvement of glycemic control reduced nonproliferative and proliferative retinopathy (47% reduction), microalbuminuria (39% reduction), clinical nephropathy (54% reduction), and neuropathy (60% reduction). Improved glycemic control also slowed the progression of early diabetic complications.”[51]

In Williams Textbook of Endocrinology, Tenth Edition (2003):

“On the basis of these results, the authors of the study [the DCCT] recommended that most patients with type 1 diabetes be treated with an intensive treatment regimen under the close supervision of a health-care team consisting of a physician, nurses, nutritionist, and behavioral and exercise specialists as needed.”[52]

Additionally, according to the International Textbook of Diabetes Mellitus (2004):

“It was not until 1993 that definitive proof for the value of good glycemic control was established. The landmark Diabetes Control and Complications Trial (DCCT) study showed that the microvascular complications of diabetes could be delayed or avoided by good glycemic control, which required intensive insulin therapy.”[53]

This idea is again validated in Joslin’s Diabetes Mellitus (2005):

“Joslin and his early associates became identified with the conservative viewpoint that “good” control delayed or prevented microvascular complications, particularly in type 1 diabetes. This position inaugurated an intense nationwide 30-year debate that only ended in 1993 with the publication of the results of the Diabetes Control and Complications Trial, which clearly supported Joslin’s claim.”[54]

In the most recent reference book, Lange 2009 Current Medical Diagnosis & Treatment (2009), after summarizing the DCCT, the writers conclude:

“The general consensus of the ADA is that intensive insulin therapy associated with comprehensive self-management training should become standard therapy in patients with type 1 diabetes mellitus after the age of puberty. Exceptions include those with advanced renal disease and the elderly, since in those groups the detrimental risks of hypoglycemia outweigh the benefits of tight glycemic control.”[55]

The far-reaching influence of the DCCT puts it at the center of the diabetes treatment galaxy. Let’s now take a closer look at the study and its design.

The Diabetes Control and Complications Trial was launched by the National Institute of Diabetes, Digestive and Kidney Diseases (NIDDK) in 1981 when requests for proposals were issued for clinical centers and a central Data Coordinating Center. In early 1982 the Biostatistics Center of the George Washington University was awarded the contract to serve as the Coordinating Center. In addition, 29 clinical centers in the United States and Canada, and 8 central laboratories and units participated in the trial. The Coordinating Center contract spanned the period 1982-1998. The complete study group is listed in the Appendix to the principal publication of study results in the New England Journal of Medicine.[56]

Since the discovery of insulin in 1921, the medical community debated the glucose hypothesis that the marked elevation of blood glucose, hyperglycemia, associated with diabetes mellitus, was responsible for the development and progression of the microvascular complications of type 1 diabetes: retinopathy leading to blindness, nephropathy leading to end-stage kidney disease, and neuropathy leading to loss of sensation, ulceration and amputation. The DCCT was designed to definitively answer whether a program of intensive therapy aimed at near normal levels of glycemia, when compared to conventional therapy aimed at maintenance of clinical well being, would affect the risk of onset and progression of these complications.[57]

During the period 1983-1989, 1441 subjects were enrolled in the study, half the subjects assigned at random to intensive therapy and half to conventional therapy. All subjects were scheduled to be followed until the fall of 1993. However, the dramatic beneficial results of the trial lead to its termination one year early. The results were presented at the June, 1993, meeting of the American Diabetes Association and the initial principal results paper appeared in the New England Journal of Medicine in September of that year.[58] The risks of the microvascular complications over the average of 6.5 years of follow-up were reduced by 26-63% with intensive versus conventional therapy. Intensive therapy, however, was associated with an excess weight gain of about 1 kg per year greater than that with conventional therapy, and a 3-fold greater risk of episodes of hypoglycemia where patients experience seizures and/or loss of consciousness, compared to conventional therapy.[59]

Subsequent extensive statistical epidemiologic investigations showed that the risk of development of microvascular complications was principally determined by the lifetime exposure to hyperglycemia.[60] However, the risk of hypoglycemia was weakly related to the level of glycemia, and more strongly related to intensive versus conventional therapy.[61] All totaled, 57 papers have been published that present the various methods and results of the DCCT. The complete DCCT bibliography has been included in Appendix D.

The Harvard Health Letter named the DCCT the number one advance in medicine during 1993. In 1994, the DCCT Research Group was awarded the Charles H. Best Medal for distinguished service in the cause for diabetes, named for the co-founder of insulin, given by the American Diabetes Association. The DCCT has been used to set standards of care for diabetes mellitus worldwide.[62]

After the close of the DCCT, the NIDDK launched the study of the Epidemiology of Diabetes Interventions and Complications (EDIC), for which the Biostatistics Center also serves as the Data Coordinating Center. Under the EDIC, the original DCCT cohort is being followed to assess the development of significant microvascular disease and the development of cardiovascular and other macrovascular diseases.[63]

A more detailed examination of the DCCT shows that the improvements in the intensive therapy group were found with only a modest reduction in hemoglobin A1c. The mean hemoglobin A1c for the intensive therapy group was 7.1%, corresponding to a mean serum glucose level of 155 mg/dL. The DCCT intensive therapy protocol included a daily carbohydrate intake of 230 grams, self-monitoring of glucose levels at least four times daily, four daily insulin injections, monthly clinical visits, and a diet and exercise plan. Despite the extensive monitoring effort, the intensive therapy cohort had a threefold increase of severe hypoglycemic events compared with the standard therapy cohort. Accordingly, subjects following the intensive therapy had a reduction in long-term complications, but this benefit was tempered by an increased risk of severe hypoglycemic reactions.[64]

In the minds of those that led, supported, financed, and judged the DCCT, not to mention those that decided to include it as the basis for treatment in fixed reference media, the DCCT proved that an intensive treatment of insulin is the best way to treat type 1 diabetes. Case closed.

But isn’t there one important question left to consider? I think you can see where this is going.

What was the diet used in both the conventional and intensive treatments?

To answer that question, as we surely must, we have to take a look at a document explaining how the trial was designed. Such a document exists. We can answer the question of what diets were used by reading through “The Diabetes Control and Complications Trial (DCCT) Design and Methodologic Considerations for the Feasibility Phase,” first published in Diabetes, in 1986.

Here is the diet fed to those participants of the standard (also known as the conventional) treatment group:

“A balanced diet containing sufficient calories and other nutrients to maintain weight at 90-120% of ideal and normal growth and development in adolescents. The diet consists of approximately 45-55% of the calories as carbohydrate, no more than 30% as fat, cholesterol content of <600 mg/day, and a P/S ratio of approximately 1.0 [P/S ratio is the ratio between polyunsaturated and saturated fatty acids]. An individual meal plan is provided for each subject that includes daily snacks and emphasizes consistency and regularity of caloric and carbohydrate intake.”[65]

And here is the diet fed to those participants of the experimental (also known as the intensive) treatment:

“A balanced diet as in the standard treatment group.”[66]

Stop to think about that for a moment. The same diet of approximately 45-55% of the calories as carbohydrates were fed to both the control group and the intensively treated group. True, keeping diets similar to test the effects of an independent variable—in this case insulin—is an indicator of a closely controlled study; but, the conclusion reached—that is, complications and risk are reduced by intensive insulin treatment—assumes you’re eating carbohydrates as a major potion of your diet. This study does not provide us with any new, actionable information, as we’ve known through observation for more than a century that diabetes is the relative inability of the body to effectively oxidize carbohydrates, albeit words such as “oxidize,” and “carbohydrate,” weren’t always used. And that we need to normalize our glucose levels if we want to reduce the risk of complications and shortened lifespan. This study really reminds type 1s that if prescribed bolus insulin, due to their consumption of carbohydrates, they should take enough—follow their prescription—to keep their blood sugar within normal range. And this enlightenment came at the expense of mostly tax-payer dollars, at a price of about $169 million.[67]

Let me add an analogy here for clarification. Remember the old “Off!” TV commercials? “Off!” is a name-brand mosquito repellent, and in the TV commercial, they showed two bare arms, each connected to a live human, of course, being placed consecutively into a long, glass container full of hungry mosquitoes. The first arm, which can be thought of as the experimental arm, is sprayed with a generous amount of “Off!,” and the second, which can be thought of as the control arm, has not been sprayed with anything. Not surprisingly, the first arm, the one sprayed with “Off!,” suffered fewer, if any, mosquito bites than that of the bare arm. This analogy can be related to diabetes in that the mosquito bites represent the complications, and the “Off!” represents the insulin. Carbohydrates are equivalent to the actual sticking of the arm into the mosquito-filled glass container.

I’m sure you’re ahead of my discussion here; clearly it would be ideal to simply not be sticking your arm into a container full of hungry mosquitoes. This solution seems even more obvious than extricating a truck from an overpass by deflating its tires. Yes, “Off!” would come in handy if you’re hiking in the woods; an activity to be enjoyed while on vacation or a pretty weekend day, but it’s not something done often. Similarly, doesn’t it make sense to, at a minimum, reduce your intake of carbohydrates?

So, this study’s result is simply a monumental example of inherent bias.[68] The study itself was done well, the statistics are correct, there was no bias during the literature review of the study question, during selection of the study sample, during measurement of exposure or outcome, during analysis of the data, during the interpretation of the analysis, or even during the publication of the analysis. There was no selection bias, information bias, or confounding bias.

Further, there was no bandwagon effect, base rate fallacy, bias blind spot, choice-supportive bias, confirmation bias, congruence bias, conservatism bias, contrast effect, distinction bias, endowment effect, expectation bias, extreme aversion, focusing effect, framing, hyperbolic discounting, illusion of control, impact bias, irrational escalation, loss aversion, mere exposure effect, moral credential effect, need for closure, neglect of probability, omission bias, outcome bias, planning fallacy, post-purchase rationalization, pseudocertainty effect, reactance, selective perception, Von Restorff effect, wishful thinking, or zero-risk bias. There were no biases in probability and belief, social biases or memory errors.[69]

No, what we have here is just good, old fashioned, simple bias. The study was set up to not include a group that didn’t raise their blood sugar to begin with by not eating carbohydrates.*

The bias to not add a group of test subjects that simply didn’t eat carbohydrates could be thought of as a strain of “not invented here,” a sociological phenomenon manifested as an unwillingness to adopt an idea because it originates from another culture, i.e., the practice of natural medicine. Sociologically, it could also stem from a status-quo bias, the tendency for people to like things to stay relatively the same.

Again, it only makes sense to, at a minimum, reduce your intake of carbohydrates. And a growing number of physicians would agree, including Daniel F. O’Neill, Eric C. Westman, M.D., M.H.S., and Richard K. Bernstein, M.D. In “The Effects of a Low-Carbohydrate Regimen on Glycemic Control and Serum Lipids in Diabetes Mellitus,” (2003), the above authors state:

“These DCCT findings suggest that normal glycemic control (hemoglobin A1c of 4.0-6.0%) is not possible even with intensive treatment, unless there is some other way to improve glycemic control without increasing the risk of hypoglycemia. Recent preliminary studies have suggested that reduction of daily carbohydrate intake leads to improved glycemic control. One study over a 19-month period found that diabetics who increased their daily carbohydrate consumption from 38% (206.3 g/day) carbohydrate to 45.4% (241.4 g/day) carbohydrate had an increase in mean hemoglobin A1c from 9.4% to 11.2%.[70] Another study with a cross-over design involving 28 type II diabetics found an increase in hemoglobin A1c from 7.8% to 9.2% after increasing dietary carbohydrate from 25% to 55% of the daily intake.[71] A third clinical series including type II diabetics who reduced their daily carbohydrate consumption to 100 g/day obtained a mean hemoglobin A1c of 6.9%.[72] Therefore a growing number of studies suggest that carbohydrate restriction can lead to better glycemic control.”[73]

Interestingly, the authors of the above study also noted that prior to the discovery of insulin, Elliot P. Joslin recommended a low-carbohydrate diet as a treatment for diabetes mellitus.[74]

In “Dietary Carbohydrate Restriction in Type 2 Diabetes Mellitus and Metabolic Syndrome: Time for a Critical Appraisal,” (2008), written by a host of renowned doctors, researchers and diabetologists including Anthony Accurso, Richard K. Bernstein, Annika Dahlqvist, Boris Draznin, Richard D. Feinman, Eugene J. Fine, Amy Gleed, David B. Jacobs, Gabriel Larson, Robert H. Lustig, Anssi H. Manninen, Samy I. McFarlane, Katharine Morrison, Jørgen Vesti Nielsen, Uffe Ravnskov, Karl S. Roth, Ricardo Silvestre, James R. Sowers, Ralf Sundberg, Jeff S. Volek, Eric C. Westman, Richard J. Wood, Jay Wortman, and Mary C. Vernon, the authors state:

“Current nutritional approaches to metabolic syndrome and type 2 diabetes generally rely on reductions in dietary fat. The success of such approaches has been limited and therapy more generally relies on pharmacology. The argument is made that a re-evaluation of the role of carbohydrate restriction, the historical and intuitive approach to the problem, may provide an alternative and possibly superior dietary strategy. The rationale is that carbohydrate restriction improves glycemic control and reduces insulin fluctuations which are primary targets. Experiments are summarized showing that carbohydrate-restricted diets are at least as effective for weight loss as low-fat diets and that substitution of fat for carbohydrate is generally beneficial for risk of cardiovascular disease. These beneficial effects of carbohydrate restriction do not require weight loss. Finally, the point is reiterated that carbohydrate restriction improves all of the features of metabolic syndrome.”[75]

In the same article, the authors amplify their position:

“The epidemic of diabetes continues unabated, and impassioned calls for better treatment and prevention strategies are common features of scientific conferences. While it is generally acknowledged that total dietary carbohydrate is the major factor in glycemic control, strategies based on reduction of dietary carbohydrate have received little support. The American Diabetes Association, for example, has traditionally recommend against low carbohydrate diets (less than 130 g/day); while the most recent guidelines admit such diets as an alternative approach to weight loss, they continue to emphasize concerns and downplay benefits. Similarly, the Diabetes and Nutrition Study Group of the European Association for the Study of Diabetes reported “no justification for the recommendation of very low carbohydrate diets in persons with diabetes.” We feel, however, that there is ample evidence to warrant an alternative perspective and that diets based on carbohydrate restriction should be re-evaluated in light of current understanding of the underlying biochemistry and available clinical data.”[76]

If you’re scratching your head at this point, you’re not alone. At some point in nearly every type 1 diabetic’s life, this thought—“Hmmm, I’m eating carbohydrates and taking bolus insulin, what would happen if I didn’t eat carbohydrates? Could I stop taking insulin?”—permeates the brain. It did for me early in my treatment. So, why not just stop eating carbohydrates, and, more importantly, why is it that the DCCT is so influential, resulting in treatments throughout the globe based upon carbohydrates and insulin?

To answer these two important questions, we might start by trying to figure out who is most negatively affected by restricting carbohydrates in a diabetic’s diet. Not the diabetic, ironically. No, if we stop eating carbohydrates, and thus reduce our intake of exogenous insulin, it is the pharmaceutical companies that will sell less insulin, diminishing demand for all the complimentary insulin goods such as insulin delivery devices (syringes, pumps & pens), lancets, test strips, blood sugar meters, batteries, test kit carrying cases, glucose tabs, ketone test strips, alcohol wipes, et al. And, of course, we’ll visit our health-care providers less often. The myriad carbohydrate manufacturers and marketers will find reduced demand for their products too, though, they can manufacture and market something else in a capital driven economy.

Too, if we stop eating carbohydrates, reducing our intake of exogenous insulin, we may even live a little longer.

So why does the DCCT continue to influence health-care providers on a near-global basis?

One explanation is termed “déformation professionnelle,” a French phrase, meaning a tendency to look at things from the point of view of one's own profession, forgetting the broader perspective. It is a pun on the expression “formation professionnelle,” meaning “professional training.” The implication is that all, or most, professional training results to some extent in a distortion of the way the professional views the world.

A better explanation is what Richard Dawkins terms a “meme.”[77] “Dawkins himself used the analogy to illustrate how natural selection pertains to anything that can replicate, not just DNA,” as Steven Pinker describes in How the Mind Works.[78] According to Dawkins:

“I think that a new kind of replicator has recently emerged on this very planet. It is staring us in the face. It is still in its infancy, still drifting clumsily about in its primeval soup, but already it is achieving evolutionary change at a rate that leaves the old gene panting far behind.

The new soup is the soup of human culture. We need a name for the new replicator, a noun that conveys the idea of a unit of cultural transmission, or a unit of imitation. ‘Mimeme’ comes from a suitable Greek root, but I want a monosyllable that sounds a bit like ‛gene’. I hope my classicist friends will forgive me if I abbreviate mimeme to meme. If it is any consolation, it could alternatively be thought of as being related to ‛memory’, or to the French word même. It should be pronounced to rhyme with ‛cream’.

Examples of memes are tunes, ideas, catch-phrases, clothes fashions, ways of making pots or of building arches. Just as genes propagate themselves in the gene pool by leaping from body to body via sperm or eggs, so memes propagate themselves in the meme pool by leaping from brain to brain via a process which, in the broad sense, can be called imitation. If a scientist hears, or reads about, a good idea, he passes it on to his colleagues and students. He mentions it in his articles and his lectures. If the idea catches on, it can be said to propagate itself, spreading from brain to brain. As my colleague N. K. Humphrey neatly summed up an earlier draft of this chapter: ‛…memes should be regarded as living structures, not just metaphorically but technically. When you plant a fertile meme in my mind you literally parasitize my brain, turning it into a vehicle for the meme’s propagation in just the way that a virus may parasitize the genetic mechanism of a host cell. And this isn’t just a way of talking—the meme for, say, “belief in life after death” is actually realized physically, millions of times over, as a structure in the nervous systems of individual men the world over.’”[79]

Commenting on Dawkins and memes, Steven Pinker said:

“Richard Dawkins has drawn the clearest analogy between the selection of genes and the selection of bits of culture, which he dubbed memes. Memes such as tunes, ideas, and stories spread from brain to brain and sometimes mutate in the transmission. New features of a meme that make its recipients more likely to retain and disseminate it, such as being catchy, seductive, funny, or irrefutable, will lead to the meme’s becoming more common in the meme pool. In subsequent rounds of retelling, the most spreadworthy memes will spread the most and will eventually take over the population. Ideas will therefore evolve to become better adapted to spreading themselves. Note that we are talking about ideas evolving to become more spreadable, not people evolving to become more knowledgeable.”[80]

So we see carbohydrates, fiber, the DCCT, black holes, supermassive black holes, wearing a baseball cap backward, et al., ad infinitum, all in a new light. These are all memes, all replicators, each fighting for their own permanence, through replication, in an otherwise impermanent universe. Viruses, bacterium, animals, plants, fungi, names, forms, ideas, melodies, processes, fashion, games, methods, madness: memes all.

Now, whether some of them are good, bad, or indifferent, who knows, depending, of course, on who or what is the protagonist. Well, pardon my speciesism, and kingdomism for that matter, but I do believe we are not here to serve the interests of carbohydrates, or those whose interests include carbohydrates. While we are not the center of the universe, it is in our own best interest to, well, work in our own best interest.

How we deal with some of these competing memes may pose a bit of a dilemma, something we will solve by book’s end. For now, though, having learned how we came to be where we are, let’s develop and implement our optimal solution…

* Since its launch on July 23, 1999, the Chandra X-ray Observatory has been NASA’s flagship mission for X-ray astronomy, taking its place in the fleet of “Great Observatories.” NASA’s premier X-ray observatory was named the Chandra X-ray Observatory in honor of the late Indian-American Nobel laureate, Subrahmanyan Chandrasekhar. Known to the world as Chandra, which means “moon” or “luminous” in Sanskrit, born October 19, 1910 in Lahore, died August 21, 1995, in Chicago, was widely regarded as one of the foremost astrophysicists of the twentieth century. Chandra was an Indian born American astrophysicist, a Nobel laureate in physics along with William Alfred Fowler for their work in the theoretical structure and evolution of stars, and nephew of Indian Nobel Laureate Sir C. V. Raman. Chandrasekhar served on the University of Chicago faculty from 1937 until his death. He became a naturalized citizen of the United States in 1953. Abridged biography courtesy of Wikipedia, available online at: http://en.wikipedia.org/wiki/Subrahmanyan_Chandrasekhar. Retrieved on 2/22/09.

* In statistical hypothesis testing, the p-value is the probability of obtaining a result at least as extreme as the one that was actually observed, assuming chance alone. In this case, P<0.001 means that the odds of the results happening by chance alone are 0.1%.

* In addition to refraining from carbohydrate consumption, type 1s should inject an optimal amount of basal insulin, also known as long-acting insulin, once or twice in a 24 hour period, to keep blood sugar stable throughout the day and offset the inevitable rise in BG caused by the dawn phenomenon.

[1] See http://chandra.harvard.edu/xray_sources/blackholes_stellar.html. Retrieved on 1/19/09.

[2] See Ibid.

[3] See Ibid.

[4] See Ibid.

[5] See Ibid.

[6] See Ibid.

[7] See Ibid.

[8] See Ibid.

[9] See Ibid.

[10] See Ibid.

[11] Ferguson, Kitty. Prisons of light: Black Holes. NY: Cambridge University Press, 1996, page 15.

[12] See http://chandra.harvard.edu/xray_sources/blackholes_sm.html. Retrieved on 1/19/09.

[13] See Ibid.

[14] See Ibid.

[15] For a good, authorized biography of Stephen Hawking, see Stephen Hawking: Quest for a Theory of the Universe, by Kitty Ferguson (New York: Franklin Watts, 1991). Kitty Ferguson is a remarkable person, receiving both a bachelor’s and master’s from the Julliard School. For many years she was a successful professional musician, conducting and performing oratorio, early music and chamber music, before renewing her lifelong interest in physics and cosmology by auditing graduate lectures and seminars at the Department of Applied Mathematics and Theoretical Physics at Cambridge University.

[16] See “General Treatment of Diabetes,” D. A. Pyke, Br Med J. 1970 Aug 1;3(5717):269. Available online at http://www.ncbi.nlm.nih.gov/pubmed/5448803. Retrieved on 3/7/09.

[17] Singh, Inder. “Low-Fat Diet and Therapeutic Doses of Insulin in Diabetes Mellitus.” Lancet, 1955, Feb 26; 268(6861): p. 422.

[18] Ibid, p. 423.

[19] Kinsell, L.W. “The Diabetic Diet.” In: Diabetes Mellitus: Diagnosis and Treatment, edited by G.J. Hamwi and T.S. Danowski. New York, American Diabetic Association, 1967, vol. II, pp. 97-99. See also Pyke, D.A. General Treatment of Diabetes. Brit. Med. J. 3: 268, 1970.

[20] Bierman, E.L., M.J. Albrink, R.A. Arky, W.E. Conner, et al. “Special Report. Principles of Nutrition and Dietary Recommendations for Patients with Diabetes Mellitus.” Diabetes. 20: 633, 1971.

[21] Singh, Inder. “Low-Fat Diet and Therapeutic Doses of Insulin in Diabetes Mellitus.” Lancet. 1955, Feb 26; 268(6861): p. 422. Anderson, J.W. “Influence of High Carbohydrate Diets on Glucose Tolerance of Normal and Diabetic Men.” Proc. Int. Sugar Res. Symposium. Washington, D.C., March, 1974. Kempner, W., R.L. Peschel and C. Schlayer. “Effect of Rice Diet on Diabetes Mellitus Associated with Vascular Disease.” Postgrad. Med. 24: 359, 1958. Brunzell. J.D., R.L. Lerner, W.R. Hazzard, D. Porte, Jr., et al. “Improved Glucose Tolerance with High Carbohydrate Feeding in Mild Diabetes.” N. Engl. J. Med. 284: 521, 1971. Brunzell, J.D., R.L. Lerner, D. Porte, Jr., and E.L. Bierman. “Effect of a Fat Free, High Carbohydrate Diet on Diabetic Subjects with Fasting hyperglycemia. Diabetes. 23: 138, 1974.

[22] Tae G. Kiehm, M.D., James W. Anderson, M.D., and Kyleen Ward, R.D. “Beneficial Effects of a High Carbohydrate, High Fiber Diet on Hyperglycemic Diabetic Men,” Am. J. Clin. Nutr. 29: 1976, p. 895.

[23] Ibid.

[24] See “High-carbohydrate diets and insulin-dependent diabetics,” by R W Simpson, J I Mann, J Eaton, R D Carter, and T D Hockaday, Br Med J. 1979 September 1; 2(6189): 523–525. Available online at http://www.pubmedcentral.nih.gov/pagerender.fcgi?artid=1596170&pageindex=1#page. Retrieved on 5/3/09.

[25] In a randomised cross-over study 18 nondependent (NIDDM) and 9 insulin-dependent (IDDM) diabetics were put on to a high carbohydrate diet containing leguminous fibre (HL) for 6 weeks, and also a standard low carbohydrate diet (LC) for 6 weeks. During two identical 24 hour metabolic profiles mean preprandial and mean 2 hour postprandial blood glucoses were significantly lower on HL in both groups, as were also several overall measures of diabetic control, including the degree of glycosuria. Total cholesterol was reduced significantly on HL in both groups, and the HDL/LDL cholesterol ratio increased significantly on HL in the NIDDM group.

See “A high carbohydrate leguminous fibre diet improves all aspects of diabetic control,” by Simpson HC, Simpson RW, Lousley S, Carter RD, Geekie M, Hockaday TD, and Mann JI. Lancet. 1981 Jan 3;1(8210):1-5. Available online at http://www.ncbi.nlm.nih.gov/pubmed/6109047. Retrieved on 5/3/09.

[26] This study investigated the possible beneficial effects of the digestible carbohydrate component. A diet rich in carbohydrate was compared with a traditional low carbohydrate diet in 10 Type 2 (non-insulin-dependent) diabetic patients, using a crossover design; both diets contained < 20 g dietary fibre/day. During 24-h metabolic profiles carried out after 4 weeks on each diet, the mean basal plasma glucose (mean of 03.00, 05.00 and 07.00 h values) was 5.3 mmol/l on the high carbohydrate diet and 5.9 mmol/l on the low carbohydrate diet (p < 0.05), despite the 2-h postprandial glucose (mean of three main meals) being higher on the high carbohydrate diet than on the low carbohydrate diet (8.7 versus 7.3 mmol/1, p < 0.01). Overall diabetic control was the same throughout the study, as judged by a mean 24-h plasma glucose of 6.7 mmol/1 on the high carbohydrate and 6.6 mmol/1 on the low carbohydrate diet, and haemoglobin Alc percentage of 8.3 on both diets. Mean cholesterol was 4.55 mmol/1 on both diets and fasting plasma triglyceride was 2.83 mmol/l on the high carbohydrate and 2.55 mmol/1 on the low carbohydrate diet (p = NS).

See “Digestible Carbohydrate—an Independent Effect on Diabetic Control in Type 2 (Non-Insulin-Dependent) Diabetic Patients?” by H. C. R. Simpson, R. D. Carter, S. Lousley, and J. I. Mann. Diabetologia (1982) 23:235-239. Available online at http://www.springerlink.com/content/x272687026872634/fulltext.pdf. Retrieved on 5/3/09.

[27] “What carbohydrate foods should diabetics eat?” by J I Mann. Br Med J (Clin Res Ed). 1984 April 7; 288(6423): 1025. Available online at http://www.pubmedcentral.nih.gov/pagerender.fcgi?artid=1442616&pageindex=1#page. Retrieved on 5/3/09.

[28] Ibid.

[29] Ibid.

[30] See Ravnskov, Uffe. Fat and Cholesterol are Good for You! What Really Causes Heart Disease, Sweden: GB Publishing, 2009, page 76.

[31] Taubes, Gary. Good Calories, Bad Calories. First Anchor Books Edition. New York: Anchor Books, 2008, page 395.

[32] Ibid, pages 395-396.

[33] This tale is adapted from the Wikipedia article entitled “Thrifty Gene hypothesis,” available online at http://en.wikipedia.org/wiki/Thrifty_gene_hypothesis. Retrieved on 3/8/09.

[34] Neel JV (1962). “Diabetes mellitus: a “thrifty” genotype rendered detrimental by “progress”?” Am. J. Hum. Genet. 14: 360. PMID 13937884. Available online at http://www.ncbi.nlm.nih.gov/pubmed/13937884. Retrieved on 3/8/09.

[35] Ibid, p.359

[36] Ibid, p.355

[37] Ibid, p.353

[38] Neel, J.V. 1982. “The Thrifty Genotype Revisited.” In: The Genetics of Diabetes Mellitus, ed. J. Kobberling and R. Tattersall. New York: Academic Press, 293-93.

[39] Speilman, R.S., S.S. Fajans, J.V. Neel, S. Pek, J.C. Floyd, and W.J. Oliver. 1982. “Glucose Tolerance in Two Unacculturated Indian Tribes of Brazil.” Diabetologia. Aug.;23(2):90-93.

[40] Neel, J.V. 1989. “Update to ‘The Study of Natural Selection in Primitive and Civilized Human Populations.’” Human Biology. Oct.-Dec.;61(5-6):811-23.

[41] Neel, J.V. 1999. “The ‘Thrifty Genotype’ in 1998.” Nutrition Reviews May; 57(5, pt.2):S2-9.

[42] Speakman JR (2007). “A nonadaptive scenario explaining the genetic predisposition to obesity: the “predation release” hypothesis.” Cell Metab. 6 (1): 5–12; doi: 10.1016/j.cmet.2007.06.004. PMID 17618852. Available online at http://www.ncbi.nlm.nih.gov/pubmed/17618852. Retrieved on 3/8/09.

[43] Baschetti R (1998). “Diabetes epidemic in newly westernized populations: is it due to thrifty genes or to genetically unknown foods?” J R Soc Med. 91 (12): 622–625. See also Lee, R.B. 1968. “What Hunters Do for a Living, or, How to Make Out on Scarce Resources.” In: Lee and Devores, eds. 1968.

[44] Speakman JR (2007). “A nonadaptive scenario explaining the genetic predisposition to obesity: the “predation release” hypothesis.” Cell Metab. 6 (1): 5–12; doi: 10.1016/j.cmet.2007.06.004. PMID 17618852. Available online at http://www.ncbi.nlm.nih.gov/pubmed/17618852. Retrieved on 3/8/09.

[45] Taubes, Gary. Good Calories, Bad Calories. First Anchor Books Edition. New York: Anchor Books, 2008, page 456.

[46] Reprinted with permission from the National Academies Press, Copyright 2005, National Academy of Sciences, “Dietary Carbohydrates: Sugars and Starches,” in Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients) (2005). Food and Nutrition Board, 2005, pages 275-279. License number 2241560984249. Available online at http://www.nap.edu/catalog.php?record_id=10490. Retrieved on 3/7/09. Established in 1970 under the charter of the National Academy of Sciences, the Institute of Medicine (http://www.iom.edu/) provides independent, objective, evidence-based advice to policymakers, health professionals, the private sector, and the public. The mission of the Institute of Medicine embraces the health of people everywhere.

[47] Taubes, Gary. Good Calories, Bad Calories. First Anchor Books Edition. New York: Anchor Books, 2008, page 456.

[48] Family Medicine Principles & Practice, Fifth Edition. Editor: Robert B. Taylor. Springer-Verlag, 1998, page 1067.

[49] Rudolph's Pediatrics 21st Edition. Edited by Colin D. Rudolph, Abraham M. Rudolph, Margaret K. Hostetter, George Lister, Norman J. Siegel. McGraw-Hill, Medical Publishing Division, 2003, page 2123.

[50] Cecil Textbook of Medicine 22^nd Edition. Edited by Lee Goldman, MD, and Dennis Ausiello, MD. Saunders, an imprint of Elsevier, 2004, pages 1432-1433.

[51] Harrison’s Principles of Internal Medicine, 17^th Edition. Edited by Anthony S. Fauci, MD, et al. McGraw-Hill Medical, 2008, page 2286.

[52] Williams Textbook of Endocrinology, Tenth Edition. P. Reed Larsen, MD, FACP, FRCP, Henry M. Kronenber, MD, Shlomo Melmed, MD, and Kenneth S. Polansky, MD. Saunders, an imprint of Elsevier, 2003, page 1496.

[53] International Textbook of Diabetes Mellitus. Editors-in-chief: R.A. Defronzo, E. Ferrannini, H. Keen, and P. Zimmet. John Wiley & Sons, Ltd., 2004, page 1067.

[54] Joslin’s Diabetes Mellitus. Edited by C. Ronald Kahn, Gordon C. Weir, George L. King, Alan M. Jacobson, Alan C. Moses, Robert J. Smith. Lippincott Williams & Wilkin & The Joslin Diabetes Center. Page 2.

[55] Lange 2009 Current Medical Diagnosis & Treatment. Edited by Stephen J. McPhee, MD, Maxine A. Papadakis, MD, and Lawrence M. Tierney, Jr., MD, Senior Editor. McGraw-Hill Medical, 2009, pages 1059-1060.

[56] See the Biostatistics Center of the George Washington University website, available online at http://www.bsc.gwu.edu/bsc/studies/dcct.html. Retrieved on 1/19/09.

[57] See Ibid.

[58] The DCCT Research Group (1993). The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. The New England Journal of Medicine329: 977-986.

[59] The DCCT Research Group (1995). Adverse events and their association with treatment regimens in the Diabetes Control and Complications Trial. Diabetes Care18: 1415-1427.

[60] The DCCT Research Group (1995). The relationship of glycemic exposure (HbA1c) to the risk of development and progression of retinopathy in the Diabetes Control and Complications Trial. Diabetes44: 968-983. See also The DCCT Research Group (1996). The absence of a glycemic threshold for the development of long-term complication: the perspective of the Diabetes Control and Complications Trial. Diabetes45: 1289-1298.

[61] The DCCT Research Group (1997). Hypoglycemia in the Diabetes Control and Complications Trial. Diabetes45: 271-286.

[62] See the Biostatistics Center of the George Washington University website, available online at http://www.bsc.gwu.edu/bsc/studies/dcct.html. Retrieved on 1/19/09.

[63] See Ibid.

[64] Diabetes Control and Complications Trial (DCCT). N Engl J Med 1993;329:977-986.

[65] “The Diabetes Control and Complications Trial (DCCT) Design and Methodologic Considerations for the Feasibility Phase,” Diabetes 1986; 35:534.

[66] Ibid.

[67] The DCCT was supported under cooperative agreements and a research contract with the Division of Diabetes, Endocrinology, and Metabolic Diseases of the National Institute of Diabetes and Digestive and Kidney Diseases and by the National Heart, Lung, and Blood Institute, the National Eye Institute, the National Center for Research Resources, and various corporate sponsors listed in Diabetes Care 1987;10:1-19). In addition, the Epidemiology of Diabetes Intervention and Complications (EDIC) ongoing funding was $58 million. See the National Institutes of Health Fact Sheet online at http://www.aimbe.org/assets/84_nihresearchintowhatworksb.pdf. Retrieved on 4/11/09.

[68] For a particularly enlightening article explaining how claimed research findings may often be simply accurate measures of the prevailing bias, see Ioannidis JPA (2005) Why Most Published Research Findings Are False. PLoS Med 2(8): e124; doi: 10.1371/journal.pmed.0020124. Available online at http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0020124. Retrieved on 3/24/09.

[69] For a good discussion of all the different types of cognitive bias, see the Wikipedia article “List of Cognitive Biases” online at http://en.wikipedia.org/wiki/List_of_cognitive_biases. Retrieved on 3/22/09.

[70] McCullough DK, Mitchell RD, Ambler J, et al. A prospective comparison of “conventional” and high-carbohydrate/high-fibre/low-fat diets in adults with type 1 diabetes. Diabetologia 1985;28:208-212.

[71] Gutierrez M, Akhavan M, et al. Utility of a short-term 25% carbohydrate diet on improving glycemic control in type II diabetes mellitus. J Am Coll Nutr 1998;17:595-600.

[72] Hays JH, et al. Abstract presented at the 81^st Annual Meeting of the Endocrine Society, 1999.

[73] O’Neill DF, Westman EC, Bernstein RK. The effects of a low-carbohydrate regimen on glycemic control and serum lipids in diabetes mellitus. Metabolic Syndrome and Related Disorders. Volume 1, number 4, 2003, p. 291-298.

[74] See Osler W, McCrae T. The Principle and Practice of Medicine. New York: D. Appleton and Company, 1923. Op Cit. O’Neill (2003).

[75] See “Dietary carbohydrate restriction in type 2 diabetes mellitus and metabolic syndrome: time for a critical appraisal,” by Anthony Accurso, Richard K Bernstein, Annika Dahlqvist, Boris Draznin, Richard D Feinman, Eugene J Fine, Amy Gleed, David B Jacobs, Gabriel Larson, Robert H Lustig, Anssi H Manninen, Samy I McFarlane, Katharine Morrison, Jørgen Vesti Nielsen, Uffe Ravnskov, Karl S Roth, Ricardo Silvestre, James R Sowers, Ralf Sundberg,, Jeff S Volek, Eric C Westman, Richard J Wood, Jay Wortman, and Mary C Vernon. Nutrition & Metabolism 2008, 5:9; doi: 10.1186/1743-7075-5-9. Available online at http://www.nutritionandmetabolism.com/content/5/1/9#B29. Retrieved on 5/8/09.

For another good review of low-carbohydrate diets in the treatment of diabetes, as reprinted in my previous book Thrive With Diabetes, see Surender K Arora and Samy I McFarlane. “The Case for Low Carbohydrate Diets in Diabetes Management.” Nutr Metab (Lond). 2005; 2: 16. Published online July 14, 2005; doi: 10.1186/1743-7075-2-16. Available online at http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1188071. Retrieved on 3/14/08.

[76] See “Dietary carbohydrate restriction in type 2 diabetes mellitus and metabolic syndrome: time for a critical appraisal,” by Anthony Accurso, Richard K Bernstein, Annika Dahlqvist, Boris Draznin, Richard D Feinman, Eugene J Fine, Amy Gleed, David B Jacobs, Gabriel Larson, Robert H Lustig, Anssi H Manninen, Samy I McFarlane, Katharine Morrison, Jørgen Vesti Nielsen, Uffe Ravnskov, Karl S Roth, Ricardo Silvestre, James R Sowers, Ralf Sundberg, Jeff S Volek, Eric C Westman, Richard J Wood, Jay Wortman, and Mary C Vernon. Nutrition & Metabolism 2008, 5:9; doi: 10.1186/1743-7075-5-9. Available online at http://www.nutritionandmetabolism.com/content/5/1/9#B29. Retrieved on 5/8/09.

[77] For a good, brief history detailing three other possible attributions of the word “meme” see “A Note on the Origin of ‘Memes’/’Mnemes,’” by John Laurent, School of Science, Griffith University, available online at http://cfpm.org/jom-emit/1999/vol3/laurent_j.html. Retrieved on 4/9/09.

For a comprehensive list of Mimetics publications on the web including those of Susan Blackmore, Richard Dawkins, Daniel Dennett, Liane Gabora, Derek Gatherer, Francis Heylighen, Aaron Lynch, and Paul Marsden, et al., compiled by Dave Gross, see http://users.lycaeum.org/~sputnik/Memetics/. Retrieved on 4/9/09.

For a compelling short video replete with written transcript, see “Dan Dennett on Dangerous Memes,” on TED.com, recorded February, 2002, in Monterey, CA, (video duration: 15:39), online at http://blog.ted.com/2007/07/dan_dennett_on_2.php. Retrieved on 4/9/09.

See also Dennett, Daniel C. Darwin’s Dangerous Idea: Evolution and the Meanings of Life. New York: Simon & Schuster Paperbacks, 1995,

For further resources, see also the Wikipedia article “Meme” online at http://en.wikipedia.org/wiki/Meme. Retrieved on 4/9/09.

[78] Pinker, Steven. How the Mind Works. New York: W.W. Norton & Company, 1997, page 208.

[79] Dawkins, Richard. The Selfish Gene. New York: Oxford University Press, 30^th Anniversary Edition, 2006, page 192.

[80] Pinker, Steven. How the Mind Works. New York: W.W. Norton & Company, 1997, page 208.

At The Library

2014-05-26T11:14:00.000-07:00

AT THE LIBRARY

“I think the health of our civilization, the depth of our awareness about the underpinnings of our culture and our concern for the future can all be tested by how well we support our libraries.”

CARL SAGAN, Cosmos, 1980

“Libraries are brothels for the mind. Which means that librarians are the madams, greeting punters, understanding their strange tastes and needs, and pimping their books. That’s rubbish, of course, but it does wonders for the image of librarians.”

GUY BROWNING, The Guardian, October 18, 2003

Finding credible information, let alone an optimal treatment, for diabetes shouldn’t be a terribly difficult task. The options of said optimal treatment, however, permutations of direct or indirect influencers of blood sugar are finite but vast. So how does one find then categorize the differing options, narrowing the field to such optimal solution, in spite of credible, though oftentimes divergent information? Well, there really are only a few places that house and disseminate such information: a doctor, the internet, a friend, other health-providers such as a nurse or dietician, a bookstore, a national library[1] such as the US Library of Congress, a private library, or a regional, state, city, university, or local library.

There certainly must be good information about diabetes somewhere on the internet,[2] and it does provide the added benefit of being accessible by anyone on the globe with a connection and an interface. Trouble is, navigating to all the relevant sites, documenting, cataloging, then analyzing and drawing conclusions about a best practice from the internet, unless you have a specific site in mind already, is a near-impossible task, as we shall see.

Searching the term “diabetes” on five well-known search engines in early 2009, I found the following number of relevant pages: 82,000,000 on GOOGLE, 395,000,000 on YAHOO, 49,000,000 on MSN, 12,769,380 on LYCOS, and 11,380,000 on ASK. Working alone, and assuming that I’m able to successfully navigate to each site, spending no more than ten minutes total reading through each site, documenting my findings, and navigating to the next site, for eight hours each day, including weekends, it would take 4,703 years to work through the GOOGLE search results, 22,546 years to catalogue YAHOO’s, 2,842 years for MSN, 729 years to get through the results from LYCOS, and 650 for ASK. I’ll leave this problem to a more ambitious researcher with substantially more resources at hand to solve.

Before I move on, however, it is important to remember that we have put ourselves in the shoes of a recently diagnosed person with diabetes, and thus are tying to find the optimal solution to our disease. But the search results, if that task is ever completed, from the internet will not be presented to us categorized as “good” or “bad,” “effective” or “ineffective,” “true” or “not true.” It is up to the searcher to make that determination. This concept is best summarized by Hal Abelson, Ken Ledeen, and Harry Lewis, in their book Blown to Bits: Your Life, Liberty, and Happiness After the Digital Explosion (2008):

“The web is no longer a library. It is a chaotic marketplace of the billions of ideas and facts cast up by the bits explosion. Information consumers and information producers constantly seek out each other and morph into each other’s roles. In this shadowy bits bazaar, with all its whispers and its couriers running to and fro, search engines are brokers. Their job is not to supply the undisputed truth, nor even to judge the accuracy of material that others provide. Search engines connect willing producers of information to willing consumers. They succeed or fail not on the quality of the information they provide, because they do not produce content at all. They only make connections. Search engines succeed or fail depending on whether we are happy with the connections they make, and nothing more. In the bazaar, it is not always the knowledgeable broker who makes the most deals. To stay in business, a broker just has to give most people what they want, consistently over time.”[3]

Skipping doctors, friends, family, relatives, other health-care providers, periodicals, and bookstores as sources of objective information for the moment, let’s take a look at a national library. My apologies in advance for being US-centric; take heart, however, as there is most likely a national library in your country, though, perhaps with a different classification system.[4]

First visiting http://www.loc.gov/index.html, the Library of Congress home page, then navigating to the catalogue page at http://catalog.loc.gov/, one can search by keyword, title, author, or subject. The most general search would be by subject, at which one finds 3,359 matches for the keyword “diabetes.”

On closer inspection of the search results, eight of our 3,359 books are from the 18^th century, 1762-1798, to be exact, under the subclass RC, internal medicine, and five of those rare books, all dissertations entitled Dissertatio Medica Inauguralis, De Diabete, are written in Latin. The authors and their books’ published dates, are, respectively, William Stevenson (1762), George Jessop (1771), William Boyd, M.D. (1773), Joseph Hart Myers (1779), and James Vernon, M.D. (1796). Tentamen Medicum Inaugurale, De Diabete, by Alexander Marcet (1797), is the sixth book, leaving two books by John Rollo to complete the century. One of his books is simply entitled Cases of the Diabetes Mellitus (1797), and the other, also published in 1797, has the enormous title:

An account of two cases of the diabetes mellitus, with remarks, as they arose during the progress of the cure: to which are added, a general view of the nature of the disease and its appropriate treatment, including observations on some diseases depending on stomach affection, and a detail of the communications received on the subject since the dispersion of the notes on the first case / by John Rollo; with the results of the trials of various acids and other substances in the treatment of the lues venerea, and some observations on the nature of sugar, &c., [etc.] by William Cruickshank.

This book is particularly important, as Dr. John Rollo (d. 1809), a Scots physician and Surgeon General of the Royal Artillery, pioneered the systematic treatment of the disease by a restricted diet. Using a urine glucose test devised by Dobson, he came up with the first effective treatment for diabetes: a diet high in what he called “animal food” (fat and meat) and low in “vegetable matter” (grains and breads). This diet prolonged life for many diabetics, those with what we now call type 2, and with modifications, was the only treatment for diabetes until the 1920s.[5]

Moving on to the 19^th century, there were 27 books listed in the Library of Congress search database, with publishing dates in the 1802 to 1897 timeframe.

So let’s now return to the books from the Library of Congress dating to the 19^th century. There were 27 books listed in the LOC search database, with publishing dates in the 1802-1897 timeframe. They are listed here. And, yes, some of these can be found and read online.

Title: An essay on the disease commonly called diabetes

Author: Washington, William

Year: 1802

Title: Medical reports of cases and experiments, with observations, chiefly derived from hospital practice: to which are added, an enquiry into the origin of canine madness; and thoughts on a plan for its extirpation from the British isles

Author: Bardsley, Samuel Argent

Year: 1807

Title: Cases of diabetes, consumption, &c., with observations on the history and treatment of disease in general

Author: Watt, Robert

Year: 1808

Title: English olive-tree, or, A treatise on the use of oil and the air bath: with miscellaneous remarks on the prevention and cure of various diseases, gout, rheumatism, diabetes, &c.

Author: Trinder, William Martin

Year: 1812

Title: De diabete mellito

Author: Bennewitz, Heinrich Gottlob

Year: 1824

Title: An inquiry into the nature and treatment of diabetes, calculus, and other affections of the urinary organs: with remarks on the importance of attending to the state of the urine in organic diseases of the kidney and bladder: and some practical rules for determining the nature of the disease from the sensible and chemical properties of that secretion

Author: Prout, William

Year: 1825

Title: An inquiry into the nature and treatment of diabetes, calculus, and other affections of the urinary organs; with remarks on the importance of attending to the state of the urine in organic diseases of the kidney and bladder: and some practical rules for determining the nature of the disease from the sensible and chemical properties of that secretion. From the 2d London ed., rev. and much enl.: with notes and additions by S. Colhoun.

Author: Prout, William

Year: 1826

Title: Hospital facts and observations: illustrative of the efficacy of the new remedies, strychnia, brucia, acetate of morphia, veratria, iodine, &c. in several morbid conditions of the system: with a comparative view of the treatment of chorea, and some cases of diabetes: a report on the efficacy of sulphureous fumigations in diseases of the skin, chronic rheumatism, &c.

Author: Bardsley, James Lomax

Year: 1830

Title: Du diabète sucré

Author: Chaloin, Louis Ernest

Year: 1853

Title: Diabetes mellitus

Author: Clapp, Sylvanus

Year: 1854

Title: Case of diabetes mellitus

Author: Jones, Joseph

Year: 1858

Title: On diabetes, and its successful treatment

Author: Camplin, John Mussendine

Year: 1858

Title: On diabetes, and its successful treatment. From the 2d London ed.

Author: Camplin, John Mussendine

Year: 1861

Title: Zur lehre vom diabetes mellitus

Author: Engmann, Wilhelm

Year: 1869

Title: On the origin of diabetes, with some new experiments regarding the glycogenic function of the liver

Author: Lusk, William Thompson

Year: 1870

Title: Ueber diabetes mellitus

Author: Wünnenberg, Ludwig

Year: 1870

Title: De la glycosurie, ou, Diabète sucré: son traitement hygiénique: avec notes et documents sur la nature et le traitement de la goutte, la gravelle urique, sur l'oligurie, le diabète insipide avec excès d'urée, l'hippurie, la pimélorrhée, etc.

Author: Bouchardat, Apollinaire

Year: 1875

Title: Considerations sur la pathogénie et sur le traitement du diabète

Author: Dumoulin, Auguste

Year: 1877

Title: A treatise on Bright's disease and diabetes

Author: Tyson, James

Year: 1881

Title: De la gymnastique de l'hydrothérapie

Author: Hoffmann, Louis

Year: 1882

Title: Does the present state of knowledge justify a clinical and pathological correlation of rheumatism, gout, diabetes, and chronic Bright's disease?

Author: Tyson, James

Year: 1886

Title: Diabetes. Mellitus and insipidus

Author: Smith, Andrew Heermance

Year: 1889

Title: Diabetes: its causes, symptoms, and treatment

Author: Purdy, Charles Wesley

Year: 1890

Title: Cookery for the diabetic

Author: Poole, W.H.

Year: 1891

Title: Ueber coma diabeticumm im anschluss an die narcose

Author: Müller, Wilhelm

Year: 1894

Title: Die Zuckerkrankheit und ihre Behandlung

Author: von Noorden, Carl

Year: 1895

Title: Kliniske undersøgelser over kvælstofudskilningens forhold til den diætetiske behandling ved diabetes mellitus

Author: Lauritzen, Marius

Year: 1897

One such book, Diabetes: Its Causes, Symptoms, and Treatment, by Charles Wesley Purdy, is available on the internet. And it should come as no surprise, that more than a century ago, in 1890, Charles Purdy wrote:

“Prophylactic [preventive] measures are advisable for people of diabetic parentage, or for those whose families present marked tendencies to the disease. In such cases it is wise to adopt a system of diet which limits the use of starchy and saccharine foods to the most moderate proportions. Occupations should be selected which entail the least possible mental pressure and excitement; and, if practicable, a residence should be chosen as near the sea-level as possible, with a mean temperature range of about 70 F. The observance of the above conditions will insure the individual the best chances of avoiding the disease.

Until future investigation shall have revealed some agency through which we are able to check the excessive formation of sugar in the liver, our chief resource against the disease must consist in withholding from the system that which it is capable of converting into sugar, and in supplying that which it is capable of assimilating as nourishment. The accomplishment of this object is the essential aim of the dietetic treatment of diabetes.

Physiological chemistry as well as experience have shown us that the chief source of sugar-production in the system is the carbohydrate foods, more especially starches and sugar. In nearly all mild cases of diabetes, and in most cases of recent origin, the avoidance of these foods arrests the excretion of sugar, as well as the more prominent symptoms of the disease. The sugar-forming powers of the organism in diabetes are feeblest in their operation upon nitrogenous materials, and therefore animal foods are the least susceptible of conversion into sugar. Next in order rank the green parts of certain vegetables, which quite strongly resist sugar transformation. Finally, the starchy and saccharine members of the carbohydrate group are the most easily transformed into sugar of all, and are therefore the most dangerous for use. Practically, then, the more completely we are able to eliminate the starchy and saccharine foods from the diet, the more completely we are able to hold the disease under control. At first sight this might seem to be a very simple matter; but when we come to furnish a diet-list that strictly conforms to the above principle, it will be found a most difficult problem to solve, owing to the very wide diffusion of starch and sugar throughout the organic world.

Of the other foods derivable from the vegetable kingdom, the cereals and seme of the tubers are the most dangerous. Potatoes, beets, parsnips, carrots, among the latter; and, of the former, rice, sago, oatmeal, cornmeal, buckwheat, rye, barley, peas, and beans, should be prohibited without compromise in most, if not in all, cases. In the strict form of dieting we are obliged to avoid the whole list. In cases of moderate severity we may, however, draw upon one class of vegetables greens. Green vegetables consist mostly of cellulose, and contain little, sometimes almost no, starch. They are rendered still less objectionable if boiled before being eaten, as the hot water dissolves out much of the remaining starch and sugar. The starch and sugar contents of vegetables vary considerably, according to the degree of cultivation and the nature of the soil and climate in which they are grown. As a rule, a high degree of domestic cultivation favors an increase of the starch and sugar, while high temperature and sunny skies have an opposite tendency. Among the least objectionable vegetables may be mentioned lettuce, cucumbers, olives, mushrooms, Brussels-sprouts, cabbage, spinach, and water-cresses.

Most nuts except chestnuts may be permitted, the list including almonds, walnuts, Brazil nuts, filberts, butternuts, and cocoanuts.

Great differences prevail in practice with regard to the use of fruits in diabetic conditions, some authorities allowing them freely, while others curtail them. Some fruits, such as apples and strawberries, really contain very little sugar, and in the case of apples the sugar is in such form that it is often well assimilated by diabetics.

The truth is that it is more difficult to make a rule which will apply universally with regard to the use of fruits than with any other class of foods in these cases; and therefore it must to some extent be a matter of experiment in each individual case. It may be stated, however, in a general way, that mild cases will bear a moderate use of such fruits as apples, tomatoes, and strawberries; but in severe cases it is best to prohibit their use without exception.”[6]

Purdy’s treatment is particularly salient even today, but I will hold off on my comments for the moment, as surveying books is the primary task at hand.

The interesting observation to bring up here is that although the Library of Congress holds the most books in the world, it does not contain every book. While searching for an electronic version of William Washington’s book An Essay of the Disease Commonly Called Diabetes online, which I did not find, I fortuitously found the book entitled Diabetes Mellitus and Its Treatment, by Richard Thomas Williamson, M.D., M.R.C.P., published in 1898. Interestingly, this book is not in the collection of the Library of Congress, however, it is an important book.

In the chapter “General Principles of Treatment,” Dr. Williamson writes:

“Potatoes should be excluded from the diet first, then bread, and gradually all carbohydrates should be cut off. In the place of bread, the aleuronat and cocoa-nut cakes mentioned on p. 357 may be given.”[7]

He states that the chief object to be aimed at in the treatment is to diminish the amount of sugar in the urine and blood, and to diminish the amount of urine, and to relieve thirst. And that object may be attained by removal of the carbohydrates from the diet. Reflecting on the work of John Rollo, Dr. Williamson writes:

“Ever since Rollo published his book on diabetes in 1797, and pointed out the value of restriction of the carbohydrates in the food, it has been acknowledged that of all forms and methods of treatment this dietetic one is the most important.”[8]

He also writes:

“All authors agree as to the great value of fat in the severe forms of diabetes; and, in addition to fatty food, cod-liver oil, lipanin [an artificial cod-liver oil substitute], and other fats may be given.”[9]

“Most articles of food from the animal kingdom may be taken freely by diabetic patients. Butchers’ meat and flesh meat of various kinds, poultry, game, and fish, may be taken in any form. But in the cooking thereof flour or bread crumbs should not be used, if a very strict diet is indicated; aleuronat may be used in place of flour, however, and butter and fats may be freely employed.

The following articles may also be allowed freely: tongue, ham, bacon, potted beef, and chicken, preserved meats of various kinds, sardines, tinned and preserved fish, beef extracts, beef-tea, meat juices, broth, soups, and jellies (when prepared without the addition of any saccharine or starchy materials).

Eggs in various forms are most useful articles of diet. An egg weighing about 600 grs. contains about 90 grs. of albumin and 75 grs. of fatty material. When hard boiled they can be taken with comparatively large quantities of butter. The “buttered” egg or omelet is a useful form…Honey, of course, ought never to be taken. Butter, cheese, and cream may be allowed in large quantities.”[10]

“Fats, both animal and vegetable, are the most valuable articles of diet for diabetic patients, especially for those who suffer from the severe forms of the disease, and may be allowed in large quantities.

The more important articles of diet, containing a large quantity of fat, are butter, cream, bacon, cheese, eggs, suet.”[11]

“Cocoa-nuts contain a small quantity of sugar, but this may be removed easily, and cocoa-nut flour may be used for the preparation of biscuits.”[12]

Dr. Williamson concludes his discussion on “cocoa-nuts” with recipes consisting of water, “cocoa-nut,” eggs, and cream for “excellent” cakes, biscuits and buns made without sugar or carbohydrates that a diabetic can tolerate quite well, prepare inexpensively at home, and prefer more, i.e., they taste better, than most diabetic cakes offered at the time.

In the Appendix, Richard Thomas Williamson presents the following list of articles of diet and beverages, arranged in tabular form, which ought to be sanctioned or forbidden, when for diagnostic or therapeutical purposes a very strict diet is desirable:[13]

Sanctioned

Butchers' meat of all kinds (except liver); potted and preserved meats.

Ham, tongue, bacon.

Poultry, game.

Fish (Fresh, dried, and preserved; sardines, shrimps.

Broths, animal soups, and jellies (prepared without the addition of saccharine or starchy materials).

Eggs, cheese, cream.
Butter, suet, oils, and fats.
Custard (without sugar).
Reliable bread substitutes (gluten bread, almond and aleuronat cakes).
Green vegetables--mustard and cress, watercress, endive, lettuce, spinach, turnip-tops, cabbage, broccoli, Brussels sprouts, spring onions.
Nuts (walnuts, almonds, filberts, hazel nuts, Brazil nuts), but not chestnuts.
Water, soda-water, and mineral waters.
Tea, coffee.
Dry Sherry, claret, Burgundy, hock, Moselle, Ahr wines, most Rhine wines, Austrian and Hungarian table wines (all in moderate quantities, however).
Brandy in small quantities.

Forbidden

Sugar, saccharine and farinaceous articles of food.

Pastry and farinaceous puddings.

Rice, sago, arrowroot, tapioca, macaroni, vermicelli, semolina.

Potatoes.

Wheaten bread and biscuits.

Carrots, turnips, parsnips, beetroot, beans, peas, large onions.

Liver.

Oysters, cockles, mussels, the "puddings" of crabs and lobsters.

Honey.

All sweet fruit and dried fruits.

Port, Tokay, champagne, and sweet wines.

Must, fruit juices and syrups.

Sweet lemonade.

Liqueurs.

Beer, ale, porter, and stout.

Rum and sweetened gin.

Cocoa and chocolate.

Milk in large quantities.

Now, let’s conclude our discussion of the LOC book search.

From the 18^th century’s eight books on diabetes, at least from the perspective of the Library of Congress, the 19^th century’s growth rate of 237.5%—there are now an additional 27 books on the shelf—pales in comparison with the next century. Between the beginning and end of the 20^th century, there are now an additional 1,930 books published and stocked on the shelves. That represents a century-to-century growth rate of slightly more than 7,048%. Instead of keeping you in suspense, let me mention here that, although we’re far from the end of the 21^st century, the Library of Congress already holds an additional 1,367 from this century. Add to that the 27 books in the LOC diabetes search results that are undated, and we have the grand total of 3,359 books that we originally found in the database. Books from the 20^th century make up a majority 57%, and those of the 21^st century, not a decade old—10% young at the time of this writing—make up 41% of the collection.

Let me surprise you, and, perhaps, quell your fears, by noting that I won’t be listing or going through any of the afore-mentioned 1,930 20^th, or 1,367 21^st century books here. True, I am not the same caliber investigator as a Gary Taubes, Barry Groves, or host of other past- and present-day saints. But we know what truly separates these books from those of the prior centuries. Those writers in the 20^th century, to borrow and alter Charles Purdy’s words, were the future investigators that revealed the agency through which we are able to check the excessive formation of sugar in the liver. Moreover, the identification of beta cells—those little heaps of cells—within the islets of Langerhans in the pancreas as the center of insulin production, tied inexorably to the diabetes condition, and leading to the purification and dissemination of analog insulin for patient self-management, is the primary driver of the burgeoning—scientific, dietetic, therapeutic, historical, and otherwise informational—diabetes book growth in the 20^th century.

3,359 sources are considerably less than the millions found online, but still pose some practical problems. First, unless you’re an elected official, you cannot “check-out” any books from the Library of Congress; that’s a perk reserved for any voracious reader winning office. Yes, you can read any of them—while you’re there—but, you cannot bring any books out of the library for any period of time. And, of course, you have to be in Washington, DC. I’ve toyed with the idea of taking a sabbatical there, finding a relatively inexpensive hotel, and reading through the list of 3,359 books. Assuming three hours per book, which would include documenting my findings, at eight hours a day, seven days a week, my sabbatical would have to be almost three-and-a-half years. Sounds more like retirement. Even if I skim each book for an hour, I would still need more than a year to complete the task. And that wouldn’t include sight-seeing. A two to three year’s sabbatical, however, is an intriguing thought.

So, like me, the average diabetic looking for information is relegated to visiting something more local to learn the totality of the world of diabetes. And so it is here that we really begin our journey.

What type of information is available about diabetes at the local library? I hypothesized that most books contain good information about the disease, i.e., etiology, physiology, impact on society, history, A_1c tutorials, nutritional options, etc., and that there would also be some books advocating a specific diet. So to test that hypothesis, I decided to visit my local library.

As of 2008, there were 30,022[14] total United States Libraries, categorized as armed forces, college and university, electronic, government, community college, law, medical, public and state, religious, and special, including industry and company libraries as well as libraries serving associations, clubs, foundations, institutes, and societies. Add to those 30,022 the 80 total libraries administered by the United Stated in its territories, and the 3,685 total Canadian libraries, and we have a grand total of 33,787 libraries listed in the American Library Directory.[15]

During the last week of 2008, and into the first few weeks of 2009, I visited the Santa Clara City Library, 2635 Homestead Road, in Santa Clara, California. Not an average library as it turns out, but a very good library with 354,579 book titles and 724 periodical subscriptions[xix] in its collection, giving it a 2008 HAPLR score of 897, putting it in the 99^th percentile of all libraries.[16]

Peering at the shelf of books contained within the 616.4 classification, I found 75 books published from 1997 to 2008.[xxi] An additional 19 reference books—not surprisingly in the reference section—published from 1998 to 2008, that included significant articles on diabetes, were also found. General diet or other health books neither on the shelf in section 616.4, nor in the reference section, were disregarded. Reading through the books off the shelf, I was surprised to find that, with but one exception, each and every book advocated a specific diet. Of the 75 books off the shelf, only 10 advocated a low-carbohydrate diet to treat the disease. One book, The First Year: Type 2 Diabetes. An Essential Guide for the Newly Diagnosed (2001), contained only objective information, and all the rest—64—an astounding 85% of the books off the shelf, advocated a low-fat, high-carbohydrate diet to treat a disease manifested by impaired carbohydrate metabolism. I’ve included the entire list of both “books off the shelf,” which I’ve simply labeled as “Books on Diabetes,” and “Reference Books” in, respectively, Appendices A & B, complete with the evidence; that is, the specific references in those books that determine whether it advocates a low-fat or a low-carbohydrate diet.

By the way, general agreement about what it means to have a low-fat, low-carbohydrate, or even a low-protein diet has never really been attained, so let’s try to bring some clarity. From a purely mathematical standpoint, if you have three parameters—in our case the three parameters are carbohydrate, protein, and fat—and, additionally, three levels—low, medium, and high—the first question to ask is how many combinations are there? The answer is 3x3x3, of course, which is 27 total combinations. But we then have to define what it means to have a low, medium, or high level. Again, there isn’t any general agreement in the literature of those distinctions. To help with our discussion, let’s define “low” as a range of 0%-30%, medium as a range of 30%-40%, and high as a range of 40%-100% of total calories. With only three variables, 50% of any one variable would be a plurality, and slightly over 50% would be a majority; therefore by definition any percentage greater than 50% has to be high. We could consider anything in the 40%-50% range to be either in the “high-medium” area or the “low-high,” but I’ve chosen that range to simply be within the “high” amount.

We can now see from Table 1 those 27 total combinations of low, medium, and high for the three different parameters of carbohydrate, protein and fat. But notice that there are only 22 total real possibilities given the above definitions. Note that the ranges given above (low = 0%-30%, medium = 30%-40%, high = 40%-100%) do not work for any specific percentage in number 1 (low carbohydrate, low protein, low fat); that is, since the low range is 0%-30%, even at the far end of that range—30%—if the three parameters of carbohydrate, protein and fat were each 30%, the total is only 90%, not 100%, so we are forced to drop that as a valid option. The same holds true for numbers 18 (medium carbohydrate, high protein, high fat), 24 (high carbohydrate, medium protein, high fat), 26 (high carbohydrate, high protein, medium fat), and 27 (high carbohydrate, high protein, high fat). These numbers, then, the five discounted options, have all been highlighted. Thus the total amount of real possibilities of combinations of low, medium, and high portions of carbohydrate, protein, and fat is 22.

	Carbohydrate	Protein	Fat
1	Low	Low	Low
2	Low	Low	Medium
3	Low	Low	High
4	Low	Medium	Low
5	Low	Medium	Medium
6	Low	Medium	High
7	Low	High	Low
8	Low	High	Medium
9	Low	High	High
10	Medium	Low	Low
11	Medium	Low	Medium
12	Medium	Low	High
13	Medium	Medium	Low
14	Medium	Medium	Medium
15	Medium	Medium	High
16	Medium	High	Low
17	Medium	High	Medium
18	Medium	High	High
19	High	Low	Low
20	High	Low	Medium
21	High	Low	High
22	High	Medium	Low
23	High	Medium	Medium
24	High	Medium	High
25	High	High	Low
26	High	High	Medium
27	High	High	High

Table 1 The 27 total combinations of low, medium, and high for the three different parameters of carbohydrate, protein and fat. The five discounted options, numbers 1, 18, 24, 26, & 27 have been highlighted gray.

Back to our discussion. We found that 64 books—85% of the books off the shelf, advocated a low-fat, high-carbohydrate diet to treat a disease manifested by impaired carbohydrate metabolism. None described high protein intake, so we are safe to conclude that these books all refer to either medium or low protein, which is not particularly relevant to our discussion.

And the reference books, those written and commented on exclusively by doctors, faired much, much worse. With but one tenuous exception—the diabetes section in Childhood Diseases and Disorders Sourcebook (2003) didn’t advocate a diet per se, it stated that “…A child or teen needs to follow a meal plan developed by a physician, diabetes educator, or a registered dietician,” but, of course, in 2003, a physician, diabetes educator, or a registered dietician would most likely have advocated a low-fat diet—18 out of the 19 reference books advocated, not simply informed about, but advocated a low-fat, and by definition, a high-carbohydrate diet to best treat a disease characterized by, at best, impaired, and, at worst, non-existent carbohydrate metabolism.

Kind of makes me wonder that if there were a section written devoted to cigarette, alcohol, or drug abuse, would these same reference books tout cigarettes, alcohol, and drugs as the basis for treatment?

Granted, our results are just from one library, and not from a random sample of, say, 30 from the population of 30,000+ libraries. Nonetheless, the odds that I found the one library with a large majority of shelved books, or all reference books, written advocating a high-carbohydrate diet, out of all the libraries out there is rather small. Yes, it would be interesting to survey a random sample of this nation’s libraries, perhaps even others around the globe, to find the true mean and variance of the numbers of diabetes books on the shelves that advocate low- or high-carbohydrate diets, and then the mean and variance of the reference books, but I have neither the time nor resources necessary to devote to that task.

The more relevant question anyway is why do nearly all the reference books, those credible, driving forces behind replication by also-rans, why is it that they advocate a high-carbohydrate, low-fat diet?

AT THE LIBRARY

[1] A national library is a library specifically established by the government of a nation to serve as the preeminent repository of information for that country. Unlike public libraries, these rarely allow citizens to borrow books. Often, they include numerous rare, valuable, or significant works; such as the Library of Congress’ Gutenberg Bible. National libraries are usually notable for their size, compared to that of other libraries in the same country. Some national libraries may be thematic or specialized in some specific domains, beside or in replacement of the 'main' national library. For a comprehensive list of national libraries and further resources, see the Wikipedia article “List of National Libraries,” online at http://en.wikipedia.org/wiki/List_of_national_libraries. Retrieved on 4/5/09.

[2] In “We knew the web was big...” posted by Jesse Alpert & Nissan Hajaj, Software Engineers, Web Search Infrastructure Team, GOOGLE (July 25, 2008), on the blog http://googleblog.blogspot.com/2008/07/we-knew-web-was-big.html, the authors were surprised to find that content hit a milestone: 1 trillion (as in 1,000,000,000,000) unique URLs on the web at once. Retrieved on 3/31/09.

[3] See Abelson, Hal, Ledeen, Ken, and Lewis, Harry. Blown to Bits: Your Life, Liberty, and Happiness After the Digital Explosion. Upper Saddle River, NJ: Addison-Wesley, 2008, page 112.

[4] A library classification is a system of coding and organizing library materials (books, serials, audiovisual materials, computer files, maps, manuscripts, realia) according to their subject and allocating a call number to that information resource. Similar to classification systems used in biology, bibliographic classification systems group entities that are similar together typically arranged in a hierarchical tree structure. A different kind of classification system, called a faceted classification system, is also widely used which allows the assignment of multiple classifications to an object, enabling the classifications to be ordered in multiple ways.

Library classification of a piece of work consists of two steps. Firstly the ‘aboutness’ of the material is ascertained. Next, a call number, (essentially a book's address), based on the classification system in use at the particular library will be assigned to the work using the notation of the system.

It is important to note that unlike subject heading or Thesauri where multiple terms can be assigned to the same work, in library classification systems, each work can only be placed in one class. This is due to shelving purposes: a book can have only one physical place. However, in classified catalogs one may have main entries as well as added entries. Most classification systems like DDC and Library of Congress classification, also add a cutter number to each work which adds a code for the author of the work.

Classification systems in libraries generally play two roles. Firstly they facilitate subject access by allowing the user to find out what works or documents the library has on a certain subject. Secondly, they provide a known location for the information source to be located (e.g., where it is shelved).

Until the 20th century, most libraries had closed stacks, so the library classification only served to organize the subject catalog. In the 20th century, libraries opened their stacks to the public and started to shelve the library material itself according to some library classification to simplify subject browsing.

Some classification systems are more suitable for aiding subject access, rather than for shelf location. For example, UDC which uses a complicated notation including plus, colons are more difficult to use for the purpose of shelf arrangement but are more expressive compared to DDC in terms of showing relationships between subjects. Similarly faceted classification schemes are more difficult to use for shelf arrangement, unless the user has knowledge of the citation order.

Depending on the size of the library collection, some libraries might use classification systems solely for one purpose or the other. In extreme cases a public library with a small collection might just use a classification system for location of resources but might not use a complicated subject classification system. Instead all resources might just be put into a couple of wide classes (Travel, Crime, Magazines etc). This is known as a “mark and park” classification method, more formally called reader interest classification.

There are many standard system of library classification in use, and many more have been proposed over the years. However in general, classification systems can be divided into three types depending on how they are used: (1) Universal schemes covering all subjects. Examples include Dewey Decimal Classification, Universal Decimal Classification and Library of Congress Classification. (2) Specific classification schemes. Examples include Iconclass, British classification of Music, and Dickinson classification. (3) National schemes specially created for certain countries. An example is the Swedish library classification system, SAB (Sveriges Allmänna Biblioteksförening).

In terms of functionality, classification systems are often described as (1) enumerative: produce an alphabetical list of subject headings, assign numbers to each heading in alphabetical order, (2) hierarchical: divides subjects hierarchically, from most general to most specific, (3) faceted or analytico-synthetic: divides subjects into mutually exclusive orthogonal facets.

There are few completely enumerative systems or faceted systems, most systems are a blend but favoring one type or the other. The most common classification systems, LCC and DDC, are essentially enumerative, though with some hierarchical and faceted elements (more so for DDC), especially at the broadest and most general level. The first true faceted system was the Colon classification of S. R. Ranganathan.

Universal classification systems used in English-speaking world: Bliss bibliographic classification (BC), Dewey Decimal Classification (DDC), Library of Congress Classification (LCC), EnglishHarvard-Yenching Classification - An English classification system for Chinese language materials.

Universal classification systems in other languages: A System of Book Classification for Chinese Libraries (Liu's Classification), Nippon Decimal Classification (NDC), Chinese Library Classification (CLC), Korean Decimal Classification (KDC), Library-Bibliographic Classification (BBK) from Russia.

Universal classification systems that rely on synthesis (faceted systems): Bliss bibliographic classification, Colon classification, Cutter Expansive Classification, Universal Decimal Classification, Brinkler classification.

Newer classification systems tend to use the principle of synthesis (combining codes from different lists to represent the different attributes of a work) heavily, which is comparatively lacking in LC or DDC. Abridged from the Wikipedia article “Library Classification,” online at http://en.wikipedia.org/wiki/Library_classification. Retrieved on 4/5/09.

[5] Not listed in the Library of Congress search database, Matthew Dobson (1731-1784) wrote Experiments and Observations on the Urine in Diabetes (Medical Observations and Inquiries), published in London, in 1776. Matthew Dobson from Yorkshire graduated MD at Edinburgh in 1756. By evaporating the urine of a diabetic patient, Dobson was the first to prove the presence of sugar in urine. He also made the crucial observation of the excess of sugar in blood, and demonstrated that diabetes is a systemic disorder rather than, as had been previously thought, a primary disease of the kidneys. See the Royal College of Physicians of Edinburgh webpage online at http://www.rcpe.ac.uk/library/exhibitions/diabetes/diabetes.php. Retrieved on 4/30/09.

[6 Purdy, Charles Wesley. Diabetes: Its Causes, Symptoms, and Treatment. Philadelphia and London: F.A. Davis Publisher, 1890, pages 80-87. Entire book available online at http://www.archive.org/stream/diabetesitscause00purduoft/diabetesitscause00purduoft_djvu.txt Retrieved on 5/1/09.

[7] Williamson, M.D., M.R.C.P., R.T. Diabetes Mellitus and Its Treatment. Edinburgh & London: Young J. Pentland; New York: The Macmillan Company, 1898, pages 322-323. Available through GOOGLE Book Search online at http://books.google.com/books?id=QrsnAAAAYAAJ&pg=PR3&lpg=PR3&dq=Williamson,+M.D.,+M.R.C.P.,+R.T.++Diabetes+Mellitus+and+Its+Treatment.&source=bl&ots=0Gr_k5umq7&sig=IN_EaRtR9e0eQCcuLTfqI_fecDc&hl=en&ei=q438SeiiCKP4tAOMg7HoAQ&sa=X&oi=book_result&ct=result&resnum=1

[8] Ibid, page 325.

[9] Ibid, page 330.

[10] Ibid, pages 330-331.

[11] Ibid, page 337.

[12] Ibid, page 343.

[13] “The diabetic dietaries recommended by most authors agree generally with that just given, but the following are minor points of difference: Sir William Roberts adds “torrified” bread and celery to the articles sanctioned.

Pavy sanctions also turnips, French beans, cauliflower, asparagus, and vegetable marrow, but only in moderate quantity, and when boiled in a large amount of water; also radishes and celery.

Seegen allows the following in moderate quantities: Cauliflower, carrots, turnips, white cabbage, green peas, berries (such as strawberries, raspberries, currants); also oranges and almonds. But he forbids other fruits, such as grapes, cherries, peaches, apricots, plums, and all kinds of dried fruits.

In addition to the articles mentioned, v. Noorden sanctions mussels, oysters, lobster, cauliflower, spinach, onions, leeks, asparagus, sorrel, French beans. He also allows the following (amongst other articles), but only in very limited quantities: Celery, green peas, beans, carrots, mushrooms, radishes, two medium-sized tomatoes, a thin slice of cocoanut, a thin slice of melon, one small acid apple, one or one and a half peach, one tablespoon of wild raspberries or strawberries, four spoonfuls of currants, six greengages[xvi], twelve cherries, half a medium-sized pear.

Cantini prescribes a very rigid diet of nitrogenous and fatty foods only. He allows: Bouillon of various kinds. Beef, tongue, veal, mutton (but liver is forbidden), duck, goose, chicken, pigeon, and game of all kinds. Fish, crustacea, lobster, crabs.

In the cooking and preparation of the above he forbids the use of flour, sugar, wine, butter, vinegar, and lemon juice; but he sanctions the use of olive oil and fats, and recommends dilute acetic acid in place of inegar [sic.], and citric acid in place of lemon juice.

Cantini allows 500 to 600 grms. of nitrogenous food daily. In order to improve the digestion, and to increase the strength of emaciated patients, he recommends 60 to 200 grms. of pancreatic fat. The fresh pancreas of a cow, calf, or lamb is cut into small pieces, and mixed with pig’s suet. After three hours it is lightly roasted.” See Ibid, Appendix, pages 406-408.

[14] This number is significantly lower than the total of 116,393 libraries as stated by The Whole Library Handbook 4, because it doesn’t include “school library media centers” which in 2004 totaled 93,861. See The Whole Library Handbook 4, edited by George M. Eberhart, American Library Association, 2006, page 3.

[15] American Library Directory, 61^st Edition. Medford, New Jersey: Information Today, Inc., 2008, page xiii.

[16] Nationwide public library statistics are collected and disseminated annually through the Federal-State Cooperative System for public library data (FSCS). Statistics are collected from nearly 9,000 public libraries. The FSCS web site is at: http://nces.ed.gov/pubsearch/getpubcats.asp?sid=041#052. The HAPLR Index includes 15 factors. The focus is on circulation, staffing, materials, reference service, and funding levels. The Index does not include data on audio and video collections, or interlibrary loan, among other items that could have been calculated from the FSCS data. Perhaps most prominently absent from the data are any measures of electronic use or Internet service. While such measures would have been desirable, the FSCS data simply are simply not sufficient for such comparisons at this time. Internet, electronic services and audiovisual services are excluded because there is simply not enough data reported by enough libraries to make comparisons meaningful. What remains are fairly traditional data for print services, book checkouts, reference service, funding and staffing. It is likely that in the future, additional measures can be added to the FSCS data to begin to evaluate such other library services as internet use, electronic services, and non-print services. The FSCS data have only been collected on a consistent national basis since 1981. Since then the data have been refined to be more consistent and to include more information. That trend is likely to accelerate, making the additional comparisons possible soon. See Hennen's American Public Library Ratings, available online at http://www.haplr-index.com/index.html. Retrieved on 1/24/09.

Note: When starting a collection, libraries frequently consult the Public Library Catalog, a list of recommended reference and nonfiction books for adults, classified by subject. There are seven books on diabetes within the 616.4 classification listed for inclusion in any collection, of which three were on the shelf. The seven books listed are: (1) American Diabetes Association Complete Guide to Diabetes; The Ultimate Home Reference from the Diabetes Experts. 3^rd edition, completely rev. American Diabetes Assn., 2002, 517 pages, (2) The Joslin Guide to Diabetes; A Program for Managing Your Treatment; [by] Richard S. Beaser, with Joan C.V. Hill and the Joslin Education Committee. Simon & Schuster, 1995, 351 pages, (3) Diabetes Sourcebook; edited by Dawn D. Matthews. 3^rd edition. Omnigraphics, 2003, 621 pages, (4) The Thyroid Guide; [by] Beth Ann Ditkoff and Paul loGerfo. HarperPerennial, 2000, 171 pages, (5) Mayo Clinic on Managing Diabetes; Maria Collazo-Clavell, editor in chief. Mayo Clinic; [distributed by] Mason Crest, 2002, 194 pages, (6) Women & Diabetes: Staying healthy in Body, Mind, and Spirit; by Laurinda M. Poirier and Katharine M. Coburn. 2^nd edition. American diabetes Assn., 2000, 230 pages, and (7) The John Hopkins Guide to Diabetes: for Today and Tomorrow; [by] Christopher D. Saudek, Richard R. Rubin, and Cynthia S. Shump. John Hopkins Univ. Press. 1997, 422 pages. See Public Library Catalog 12th Edition: Guide to Reference Books and Adult Nonfiction. Edited by Juliette Yaakov. The H.W. Wison Company. 2004.

On the Relationship Between Diabetes Mellitus and Cancer

2013-08-06T14:59:00.003-07:00

Author's note: the following article first appeared as the chapter entitled "Epilogue" in my second book Essential Diabetes Leadership (2010).

“The known is finite, the unknown infinite; intellectually we stand on an islet in the midst of an illimitable ocean of inexplicability. Our business in every generation is to reclaim a little more land, to add something to the extent and the solidity of our possessions. And even a cursory glance at the history of the biological sciences during the last quarter of a century is sufficient to justify the assertion, that the most potent instrument for the extension of the realm of natural knowledge which has come into men’s hands, since the publication of Newton’s Principia, is Darwin’s Origin of Species.” [1]

PROFESSOR T.H. HUXLEY, 1887

Diabetes is the relative inability of the body to naturally and effectively process carbohydrates due to an insulin function disturbance; either our bodies are resistant to our own insulin and perhaps we produce too much, or, in the case of type 1s, we do not produce enough, or any. We can buy different types of analog insulin—with a prescription—and take basal plus bolus insulin, consume a balanced diet including 45%-55% carbohydrates, and live with the ever-present chance of hyper- and hypo-glycemia. Or we can forgo the bolus insulin and carbohydrates, and eat just fat and protein. The logical question to then ask is: “Are carbohydrates essential to human life?” If yes, then our hypothesis—forgo the bolus insulin and carbohydrates, and eat just fat and protein to live a healthy, long life—falls on its face. If no, then the simple solution, the trivial solution, the optimal solution, the solution left unharmed sitting atop Occam’s razor is basal insulin, fat and protein, sans bolus insulin and carbohydrates. The ample evidence presented points to the latter.

If carbohydrates are not essential, then, and our diet is based upon fat—and saturated fat at that—will our arteries clog and our destiny manifest itself in heart disease? If yes, then, once again, our hypothesis is moot. If no, then basal plus bolus insulin plus carbohydrates descends down Ocamm’s razor and basal insulin, fat, and protein remain safely perched on top. The overwhelming evidence presented by authors such as Dr. Uffe Ravnskov, Dr. Barry Groves, Dr. Malcolm Kendrick, Dr. Kilmer S. McCully, Gary Taubes, et al., points again to the latter.

And what about a cure? Can type 2’s go under anesthesia and a knife to have a gastric bypass? Yes. Is there a day in the not too distant future when type 1s can have stem cells effectively and efficiently grown to replace our atrophied beta cells? The answer, again, is yes.

And those two treatments simply scratch the surface. There are many other interventions being investigated from metabolic control, i.e., developing an artificial pancreas, to regenerating insulin producing cells, to replacing beta cells with functioning ones from a donor, to artificial preventative treatments, i.e., stopping or reversing the immune system response that causes diabetes.

But, especially in type 1s, then what? Eat normal, balanced meals, burn out the replacement beta cells, and then go in for a refill? Does anyone think that, for example, stem cells implanted in a recipient’s pancreas will somehow not be subjected to the same influencers in the environment that originally triggered the condition, and, overtime, fail too?

I do not know why some people stay slim and healthy throughout life and others develop a deranged metabolism given the same carbohydrate load. When doctors don’t understand a metabolic process, they call it “genetics,” when ethologists can’t pinpoint a reason for an animal’s behavior, they call it “instinct.” You too probably know a slim, healthy person that eats far more than their fair share of cereal with milk in the morning, sandwiches on white bread with potato chips for lunch, ice cream for dessert, and a thousand more calories for dinner made up of those same carbohydrates and a variety more, plus acidic, caffeinated, carbonated, sugar water, and still manage to look good at the beach. Although I must say that I’m happy for them—yes, it all sounds so delicious—it is a disappointment.

But far more disappointing are the health-professionals, health-based organizations, figureheads, and speakers, whether knowledgeable on the subject of diabetes or not, that recommend, prescribe or otherwise espouse the role of carbohydrates as the basis of our diet and treatment. My disappointment culminated when a former favorite author of mine, and, through his books, mentor, Stephen R. Covey, partnered with the American Association of Diabetes Educators, and Bayer Diabetes Care, to write for and distribute free of charge a pamphlet entitled The 7 Habits of Highly Effective People with Diabetes in 2007. Discussing his second habit, “Begin with the end in mind,” he wrote to “Choose one behavior and set a small goal,” and here is one proposed goal:

“For Healthy Eating, I will switch from whole milk to skim milk [my italics].” [2]

Milk—whole, 2%, 1%, low-fat, skimmed, or skim—contains a considerable amount of the simple sugar lactose and will rapidly raise blood sugar once consumed. Skim milk contains the most lactose per ounce. By his suggestion, Dr. Covey displays support for the “fat antagonizes diabetes” dogma—a diabetic should reduce their consumption of fat, and, instead, increase the amount of carbohydrate. He espouses a dogma on the same par as that of health benefits to lungs from five to ten minute sessions of repeatedly inhaling and exhaling the smoke of burning, rolled-up, dried tobacco particulate.

Recall that memes propagate themselves in the meme pool by leaping from brain to brain via a process which, in the broad sense, can be called imitation. When a credible, respected member of human society helps to spread an idea, from the idea’s perspective it is the idea evolving to become better adapted at spreading itself. So another way to look at it is that Dr. Covey’s well intended but misguided effort is the result of being infected with an evolved strain of the “fat antagonizes diabetes” virus, which may be better stated as the “eat carbohydrates” virus. He too spreads it, but as you read these words now, and those of the preceding chapters, be hopeful that it can be countered by the “don’t eat carbohydrates” meme, of which I am a proud and purposeful carrier.

And there are other noble meme’s to spread.

The Millennium Development Goals [3] (MDGs) are eight goals commissioned by the UN Secretary General and supported by the UN Development Group to be achieved by 2015, that respond to the world's main development challenges. The MDGs are drawn from the actions and targets contained in the Millennium Declaration [4] that was adopted by 189 nations-and signed by 147 heads of state and governments during the UN Millennium Summit in September, 2000. Here are the eight goals:

Eradicate extreme poverty and hunger. [5]
Achieve universal primary education.
Promote gender equality and empower women.
Reduce child mortality.
Improve maternal health.
Combat HIV/AIDS, malaria and other diseases.
Ensure environmental sustainability. Integrate the principles of sustainable development into country policies and programs and reverse the loss of environmental resources.
Develop a Global Partnership for Development. Develop further an open, rule-based, predictable, nondiscriminatory trading and financial system, which includes a commitment to good governance, development, and poverty reduction, both nationally and internationally.

Complementing these eight Millennium Development Goals are the 14 Grand Challenges for Engineering in the 21st Century, sponsored by the National Science Foundation. [6] Here are the 14 Grand Challenges for Engineering in the 21st Century:

Make solar energy affordable
Provide energy from fusion
Develop carbon sequestration methods [7]
Manage the nitrogen cycle
Provide access to clean water
Restore and improve urban infrastructure
Advance health informatics
Engineer better medicines
Reverse-engineer the brain
Prevent nuclear terror
Secure cyberspace
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I never could find answers to life’s questions—nor an optimal solution to our diabetes dilemma, which I had wanted to find first—at, or working my way to, the bottom of a bottle, glass, or can of beer. Although, yes, I have tried. In seeking an optimal solution via paradigms in physics, astronomy, mathematics, cosmology, medicine, ethology, geology, or simple trial and error, I’ve found that the best lens to view the problem comes from Charles Darwin. [8] As it has been said, nothing in biology makes sense except in the light of evolution.

“Nothing in Biology Makes Sense Except in the Light of Evolution” [9] is a 1973 essay by the evolutionary biologist and Russian Orthodox Christian Theodosius Dobzhansky, [10] criticizing anti-evolution creationism and espousing theistic evolution. The essay was first published in the American Biology Teacher. [11]

Dobzhansky first published the title statement, in a slight variation, in a 1964 article in American Zoologist, “Biology, Molecular and Organismic,” to assert the importance of organismic biology in response to the challenge of the rising field of molecular biology. The term “light of evolution”—or sub specie evolutionis—had been used earlier by biologist Julian Huxley.

Dobzhansky starts with a reductio ad absurdum of the alleged geocentrism of an Arab cleric (identical to or namesake of Shaikh Abdulaziz bin Baz, later the Grand Mufti of Saudi Arabia) who believes the Sun revolves around the Earth because of scripture. Dobzhansky asserts his own belief that scripture and science do not contradict each other. He criticizes creationists for implying that God is deceitful and asserts that this is blasphemous.

Dobzhansky then goes on to describe the diversity of life on Earth, and that the diversity of species cannot be best explained by a creation myth because of the ecological interactions between them. He uses examples of evidence for evolution: the genetic sequence of cytochrome C to show evidence for common descent (citing the work of Emanuel Margoliash & Walter M. Fitch); embryology; and his own work on fruit flies in Hawaii. Dobzhansky concludes that scripture and science are two different things: “It is a blunder to mistake the Holy Scriptures for elementary textbooks of astronomy, geology, biology, and anthropology.”

The central issue of the essay is the need to teach biological evolution in the context of debate about creation and evolution in public education in the United States. The fact that evolution occurs explains the interrelatedness of the various facts of biology, and so makes biology make sense. The concept has become firmly established as a unifying idea in biology education.

The notion of the “light of evolution” came originally from the Jesuit priest Pierre Teilhard de Chardin, whom Dobzhansky much admired. In the last paragraph of the article, de Chardin is quoted as having written the following:

“(Evolution) is a general postulate to which all theories, all hypotheses, all systems must henceforward bow and which they must satisfy in order to be thinkable and true. Evolution is a light which illuminates all facts, a trajectory which all lines of thought must follow—this is what evolution is.”

The phrase “nothing in biology makes sense except in the light of evolution” has come into common use by those opposing creationism or its variant called intelligent design. While the essay argues that Christianity and evolutionary biology are compatible, a position described as evolutionary creationism or theistic evolution, the phrase is also used by those who consider that “in biology” includes anthropology, and those who consider a creator to be unnecessary, such as Richard Dawkins who published The Selfish Gene just three years later. [12]

And it is Richard Dawkins, one of my favorite authors, that provides answer upon answer to some of life’s greatest questions, e.g., “why are people?” [13] It is only after understanding the answer to that question that we can begin to grasp the answer to “why is diabetes?”

All his books are seminal in their own right, but most remarkable is The Ancestor’s Tale: A Pilgrimage to the Dawn of Evolution (New York: Houghton Mifflin Company, 2005). In this treatise, Richard Dawkins creatively, eloquently utilizes backward chronology to search out ancestors to “sensibly aim towards a single distant target.” On opposite ends of a small log, he serves as gentle, factual storyteller, bringing us “back to the universal progenitor of all surviving organisms, probably resembling some kind of bacterium.” His lexicon includes “rendezvous,” “confluence,” and, most notably, “concestor.”

“In a backward chronology, the ancestors of any set of species must eventually meet at a particular geological moment. Their point of rendezvous is the last common ancestor that they all share, what I shall call their ‘Concestor’: the focal rodent or the focal mammal or the focal vertebrate, say. The oldest concestor is the grand ancestor of all surviving life.” [14]

And the oldest concestor, according to Dawkins, before animals and plants, before multicellularity, is the single cell progenitor bacteria.

“The analogy of insect colony to human body is often made, and it is not a bad one. The majority of our cells subjugate their individuality, devoting themselves to assisting the reproduction of the minority that are capable of it: ‘germ-line’ cells in the testes or ovaries, whose genes are destined to travel, via sperm or eggs, into the distant future. But genetic relatedness is not the only basis for subjugation of individuality in fruitful division of labor. Any sort of mutual assistance, where each side corrects a deficiency in the other, can be favored by natural selection on both.” [15]

In answering our diabetes conundrum, it makes sense to see what, if anything, benefits from diabetes. I’m sure that sounds strange, after all, how could anything benefit from our decline? Well, our environment consists of living things that are themselves adapted to profit at our expense. Although all the evidence isn’t in just yet, it seems that cancer is one example of a beneficiary.

In “Diabetes and Cancer. Epidemiological Evidence and Molecular Links,” (2008), the authors highlighted the following findings:

“…cancer cells growing under hyperglycemic conditions with elevated levels of insulin and other glucose-regulating hormones do have an advantage compared to healthy cells and even over the same cancer cells in a non-diabetic setting.” [16]

“Numerous studies revealed a direct link between hyperglycemia, high insulin levels and high concentrations of insulin-like growth factor (IGF) and an increased risk of various types of cancer.” [17]

“Many studies revealed that dietary patterns that accelerate insulin resistance or secretion, including high consumption of sucrose, various sources of starch, a high glycemic index and high saturated fatty acid intake [sic], are associated with a higher risk of colon cancer.” [18]

“…we discovered that most cancer cell lines display enhanced features of tumor progression when cultured under diabetic conditions. Not only the established stimulus for cell proliferation—insulin—increased the activity of tumor cells, but also hyperglycemic glucose concentrations per se enhanced proliferation and migratory activity of tumor cells.” [19]

In “The Relationship Between Diabetes and Cancer,” authors Dion Smyth and Theresa Smyth point out the following:

Insulin and insulin-like growth factor-1 (IGF-1) have been shown to act as growth-promoting hormones that foster cell proliferation and inhibit apoptosis. [20]
High circulating levels of IGF-1 increase the risk of breast cancer in premenopausal women. [21]
High levels of IGF-1 are also associated with an increased risk of prostate cancer. [22]
Various studies have shown that adults with impaired glucose tolerance have a greater risk of cancer mortality. [23]
Type 2 diabetes is a risk factor for endometrial cancer. [24]
Data from the long-running US Nurses Health Study suggest a slight but significant increased risk of breast cancer in post-menopausal women with type 2 diabetes. [25]
Recent reports have suggested that diabetes and high blood glucose levels appear to increase the risk of cancer independent of obesity. [26]
A prospective cohort study of almost 1.3 million Koreans, who are typically leaner than their Western counterparts, found that increased levels of fasting serum glucose were strongly linked with an increased risk of pancreatic cancer and significantly associated with an increased risk of cancers of the gullet, liver and colorectum in men and the cervix and liver in women. [27]
The Khaw, et al. (2004), study suggested that high blood glucose levels—even levels below those diagnostic of diabetes—could be linked to bowel cancer and people with diabetes could be up to 3 times more likely to get colorectal cancer. [28]
The role of medication such as exogenous insulin (that is, the use of therapeutic insulin injections) in the development of cancer has been reported on. The US National Cancer Institute (NCI) highlighted research presented at the most recent American Association for Cancer Research Annual Meeting that men who had diabetes and took medication are at 4 times the risk of developing liver cancer and 2.5 times the risk of developing pancreatic cancer of men who did not have diabetes. [29]
Continuous use of insulin for a period of more than 3 years was associated with a significant risk of developing colorectal cancer. [30]

Validated from another source, patients diagnosed with cancer who have preexisting diabetes are at increased risk for long-term, all-cause mortality compared with those without diabetes. [31]

In “Abnormal Glucose Tolerance and the Risk of Cancer Death in the United States,” by Saydah SH, Loria CM, Eberhardt MS, and Brancati FL, the authors first stated that “…Although abnormal glucose tolerance is a well-established risk factor for cardiovascular disease, its relation to cancer risk is less certain.” After performing their study, they concluded that “…in the United States, impaired glucose tolerance is an independent predictor for cancer mortality.” [32]

In “Diabetes Mellitus as a Predictor of Cancer Mortality in a Large Cohort of US Adults,” by S. Coughlin, E. Calle, L. Teras, J. Petrelli, and M. Thun, one of the largest prospective studies worldwide, enrolling 467,922 men and 588,321 women who had no reported history of cancer at the time of enrollment, revealed after 16 years of follow up that:

“…diabetes was significantly associated with fatal colon cancer in men and women, and with prostate cancer in men, and significantly associated with liver cancer and bladder cancer. In addition, diabetes was significantly associated with breast cancer in women. These findings strongly suggest that diabetes is an independent predictor of mortality from these cancer entities.” [33]

The Västerbotten Intervention Project is a subcohort of the Northern Sweden Health and Disease Cohort, and, in brief, all residents in the county of Västerbotten in northern Sweden were invited to a health survey, in the years in which they became 40, 50, or 60 years old since 1985. The results are detailed in “Prospective Study of Hyperglycemia and Cancer Risk,” (2007), where the authors stated:

“In conclusion, our finding of a statistically significant association of hyperglycemia with overall cancer risk in women and an increase in risk of cancer at many sites in women and men is essentially in accordance with the observations in some other large cohort studies, suggesting that abnormal glucose metabolism is a general risk factor for cancer development. Although the proportion of subjects with hyperglycemia was highest among obese subjects, the absolute numbers of subjects with hyperglycemia were larger among women and men who were overweight or had normal body weight, and plasma glucose levels remained associated with cancer risk after adjustment for BMI. This observation may have considerable implications for public health strategies, as key determinants of hyperglycemia are known and modifiable. A lifestyle that decreases plasma glucose levels may reduce overall cancer risk not only among overweight or obese subjects but most likely also among subjects with normal body weight. At the same time, current evidence suggests that such a strategy also would contribute to the prevention of diabetes and cardiovascular disease.” [34]

Cancer, according to the National Cancer Institute, US National Institutes of Health (www.cancer.gov), is a term used for diseases in which abnormal cells divide without control and are able to invade other tissues. Cancer cells can spread to other parts of the body through the blood and lymph systems. [35] Cancer is a class of diseases in which a group of cells display uncontrolled growth (division beyond the normal limits), invasion (intrusion on and destruction of adjacent tissues), and sometimes metastasis (spread to other locations in the body via lymph or blood). These three malignant properties of cancers differentiate them from benign tumors, which are self-limited, and do not invade or metastasize. Most cancers form a tumor but some, like leukemia, do not. Leukemia is a cancer of the blood or bone marrow and is characterized by an abnormal proliferation of blood cells, usually white blood cells (leukocytes). [36]

In short, cancer is the abnormal proliferation of cells.

With our above discussion on diabetes, cancer and that specific definition of cancer in mind, then, at best, diabetes enables cancer. If we relax the above definition, however, from “abnormal proliferation of cells,” to “abnormal proliferation of cells or substances, e.g., hormones,” and we recall the essence of untreated diabetes, that it is:

the abnormal proliferation of insulin (type 2)
the abnormal proliferation of glucose
the abnormal proliferation of glycosylated hemoglobin
the abnormal proliferation of triglycerides
the abnormal proliferation of complications

then we see that, at worst, diabetes is cancer. Sans any tumor(s).

Just as Copernicus showed that the universe does not revolve around the earth, Darwin showed that the natural world does not revolve around humans; we are no more unique than any other species. In his own words:

“I view all beings not as special creations, but as the lineal descendants of some few beings which lived long before the first bed of the Silurian system was deposited, they seem to me to become ennobled.” [37]

And all species—all memes—struggle to survive, reproductively, at the level of the individual. [38]

Nothing is alone in the universe. The possibilities for organisms, cells, organelles, proteins, etc., to interact in the universe, include, and are on a continuum of, altruism to exploitation, antagonism to synergism, attraction to repulsion, catabolism to anabolism, catalyst to anti-catalyst, stimulator to repressor, and mutualism through commensalism to parasitism; with specific roles, whether one to one, one to many, or many to many, such as brother to sister, cell wall to environment, enzyme to reactant, friend to friend, husband to wife, manipulator to submitter, master to slave, parasite to host, parent to child, predator to prey, signaler to receiver, et al. And in the rivalrous, predator-prey and parasite-host relationships, arms races explain the relative increasing strength of sides in the struggle for fitness. [39]

Cancer does not appreciate any of our discoveries or advancements, whether we can travel to or populate distant stars and ocean depths, or whether our deep thinking scientists are working to tie—let alone succeed in tying—the forces of gravity, weak, strong, and electromagnetic into a theory of everything. It does not care about our civilization, our cultures, our libraries, languages, Betts or Cassavetti Stradivarii. It does not sit in awe listening to Dufay, Palestrina, de Prez, Gesualdo, Monteverdi, Bach, Albinoni, Handel, Haydn, Mozart, Beethoven, Paganini, Schubert, Berlioz, Mendelssohn, Chopin, Schumann, Liszt, Verdi, Wagner, Bruckner, Brahms, Saint-Saëns, Bizet, Mussorgsky, Tchaikovsky, Dvořák, Grieg, Rimsky-Korsakov, Puccini, Mahler, Debussy, Strauss, Sibelius, Rachmaninoff, Schoenberg, Ravel, Bartók, Stravinsky, Webern, Berg, Villa-Lobos, Prokofiev, Orff, Gershwin, Copland, Khachaturian, Shostakovich, Messiaen, Barber, Cage, Britten, Bernstein, Xenakis, Ligeti, Penderecki, Glass, and many, many more. It, better stated, they, are content siphoning our blood, glucose, and, eventually, our lives. [40]

Once cancer manifests itself in daughter cells that further divide, it may not even care about itself. It certainly doesn’t care about its host. Cancer works toward its own end, an unintended yet deeply troubling double entendre, emphasizing the difficulty we humans have placing it in the universal schema. And killing it before it kills us is the central problem in cancer treatment:

“The mutations that benefit the survival and reproduction of cells in a tumor are the things that drive it towards malignancy. Evolution is also driving therapeutic resistance. When you apply chemotherapy to a population of tumor cells, you're quite likely to have a resistant mutant somewhere in that population of billions or even trillions of cells. This is the central problem in oncology. The reason we haven't been able to cure cancer is that we're selecting for resistant tumor cells. When we spray a field with pesticide, we select for resistant pests. It's the same idea.” [41]

Returning to the question that started this discussion, why is diabetes? Well, having lived with it for so many years, I can answer that question first by saying that it is certainly not here to benefit us, unless a prompt leading to self-development and enlightenment can be thought of as a benefit. Yes, diabetes is related to stress—stress from injury, surgery, infection, pregnancy, mental anguish and the like—or it could be a natural consequence of aging. It may simply be attributed to metabolic error or miscommunication between cells, imposed on a random selection of unlucky individuals in the human population, though that doesn’t explain why some populations have a higher incidence than others. [42] Nor does it explain why other substances or cells are able to thrive in its environment. Obesity, inflammation, and immunosuppression can lead to a myriad of complications, not the least of which is diabetes; but, we’re left wondering why some with the former conditions do not develop the latter. [43]

Diabetes may exist due to faulty genes, though that doesn’t explain why some with the “genes for diabetes” don’t express the disease and some do. [44] It may exist for the benefit of health-providers, though that is hopefully a tenuous explanation for a disease that has been around longer than a profession. It could be that its purpose is to benefit itself, i.e., that diabetes is its own meme, and that it too is struggling for lineage-based reproductive survival against the odds of a solitary, poor, nasty, brutish, and short existence. [45] The Coxsackie B4 virus is strongly associated with the development of insulin dependent diabetes mellitus. [46] Conversely, it appears that bacterial phyla normally present in the human gut may provide protection against developing diabetes. [47]

There are cases of chemicals, environmental toxicants and drugs causing temporary or permanent type 1 or type 2 diabetes documented in the medical literature. High serum selenium concentrations are associated with higher prevalence of diabetes. [48] The atypical antipsychotic drugs clozapine, olanzapin, risperidone, quetiapine and ziprasidone are known to induce insulin resistance, hyperglycemia, and even diabetic ketoacidosis (DKA). [49] The biologic plausibility of a diabetogenic effect of exposure to persistent organic pollutants, e.g., dioxins, polychlorinated biphenyls, and organophosphate insecticides, e.g., chlordane, is supported by numerous studies. [50] Alloxan, synthesized by the oxidation of uric acid by nitric acid, and the antibiotic streptozocin, produced by the soil bacterium Streptomyces achromogenes, are two of the best known toxins capable of damaging the pancreatic beta cells. [51] Vacor, a rat poison derived from the waste product urea, also has been reported to cause insulin dependent diabetes in humans who survived the exposure. [52]

The existence of naturally occurring toxins produced by many species of fungi capable of causing diabetes is also deeply troubling. Fungi are living things in our environment adapted to profit at our expense, though other microorganisms are probably the “intended” victims. [53] According to A.V. Costantini, M.D., Head (retired) of the World Health Organization Collaborating Center For Mycotoxins In Food:

“Fungi are masters at producing a wide array of biologically active substances which serve the producing fungus extremely well. These biological metabolites are anti-predatory, i.e., territory-protective, and exist to ensure that the fungus will survive as long as possible in this quite hostile world. These metabolites are anti-viral, anti-bacterial, anti-protozoan, anti-insect, anti-animal and, of course, anti-human. These metabolites are referred to as mycotoxins. The term is derived from the Greek mykes, meaning fungus, and toxicum, meaning toxin or poison. Fungi and mycotoxins are present in variable amounts in the food products of Western civilization such as the stored grains, particularly corn, fat-ladened meat of stored grain-fed animals, yeast-fermented beer, wine, bread, cheeses, coffee, and cured (fermented) meats and tobacco leaf.” [54]

Others too, such as Doug Hoffman and David Holland, M.D., [55] and Laurens Maas, [56] each extensively drawing from Dr. Costantini’s works, emphasize, perhaps better stated as reiterate, that the link between diabetes and fungi is not entirely from the “utterly rotten fabric of guess and speculation.” [57] Although I agree that it is disconcerting to think that we are mere fodder for some other form, these authors do make a strong case.

What I do know with much certainty is that eliminating carbohydrates from the diet halts the abnormal proliferation of all five of the aforementioned items: insulin, glucose, glycosylated hemoglobin, triglycerides, and complications. If the relaxed definition makes sense to you, and you prefer to collectively call those five items cancer, then carbohydrate consumption is the proximate cause and ingesting near-zero of the same is the cure. [58]

Diabetes manifests itself in the body as ineffective carbohydrate processing; the corollary is that diabetes is a disease of insulin derangement. Too much insulin ought to be treated with too few carbohydrates. Not enough, or any, insulin ought to be treated similarly, with the addition of just enough exogenous, long-acting, basal insulin. Fat and protein only, as diet for both.

No, it’s not easy; nothing worthwhile ever is. But it is simple. And it works without enabling ischemic heart disease, cancer, or any other parasitoid, from any biota or mineralia, more, from any category—kingdom, chemical, compound, name, form, or idea—providing the great escape from our prisoner’s dilemma.

[1] Huxley, Professor T.H., “On the Reception of the Origin of Species,” 1887. In Darwin, Francis. The life and letters of Charles Darwin, including an autobiographical chapter. London: John Murray. Volume 2, ed. 1887. Available online at http://darwin-online.org.uk/converted/published/1887_Letters_F1452/1887_Letters_F1452.2.html.

“If T.H. Huxley (May 4, 1825 to June 29, 1895) is known at all, it is as “Darwin’s bulldog.” This self-imposed nickname recognizes the collegiate defense and enthusiastic offense—he undertook in support of the theory of evolution. In November of 1859, after reading the newly-published Origin of Species, he warned Charles Darwin that there would be mischief from anti-evolutionists, and that he himself, T.H. Huxley, was sharpening up his claws preparing to annihilate these creationist critics. He devoted himself for most of his career defending Darwinism and related notorious subversive subjects.” See The Huxley File online at http://aleph0.clarku.edu/huxley/.

[2] See Covey, Stephen R. The 7 Habits of Highly Effective People with Diabetes. Tarrytown, NY: Bayer Healthcare, LLC Diabetes Care, 2007, Habit No 2.

[3] For more information about the UN’s Millennium Development Goals, see http://www.unmillenniumproject.org/goals/index.htm.

[4] To see the online Resolution adopted by the General Assembly, [without reference to a Main Committee (A/55/L.2)], 55/2, United Nations Millennium Declaration, see http://www.un.org/millennium/declaration/ares552e.htm.

[5] A common, often altruistic, theme amongst many is to be able to solve world hunger via some method that may produce more food. However, often missed is the relationship between poverty and hunger. Hunger is an effect of poverty and poverty is largely a political issue (While manifesting itself as an economic issue, conditions causing poverty are political and end up being economic.). People are hungry not due to lack of availability of food, but because people do not have the ability to purchase food and because distribution of food is not equitable. In addition, there is also a lot of politics influencing how food is produced, who it is produced by (and who benefits), and for what purposes the food is produced (such as exporting rather than for the hungry, feedstuff, etc.). See, for example, http://www.globalissues.org/TradeRelated/Poverty/Hunger/Solutions.asp. Of particular interest to a diabetic, is how to get the right food, i.e., less emphasis on carbohydrates, and more on essential proteins and fats, to the right people.

[6] A diverse committee of experts from around the world, convened at the request of the National Science Foundation (NSF), and announced 14 grand challenges for engineering in the 21st century that, if met, would improve how we live.

“Tremendous advances in quality of life have come from improved technology in areas such as farming and manufacturing,” said committee member and GOOGLE co-founder Larry Page. “If we focus our effort on the important grand challenges of our age, we can hugely improve the future.”

The panel, some of the most accomplished engineers and scientists of their generation, was established in 2006 and met several times to discuss and develop the list of challenges. Through an interactive Web site, the effort received worldwide input from prominent engineers and scientists, as well as from the general public, over a one-year period. The panel's conclusions were reviewed by more than 50 subject-matter experts.

The final choices fall into four themes that are essential for humanity to flourish: sustainability, health, reducing vulnerability and increasing joy of living. The committee did not attempt to include every important challenge, nor did it endorse particular approaches to meeting those selected. Rather than focusing on predictions or gee-whiz gadgets, the goal was to identify what needs to be done to help people and the planet thrive.

“We chose engineering challenges that we feel can, through creativity and commitment, be realistically met, most of them early in this century,” said committee chair and former U.S. Secretary of Defense William J. Perry. “Some can be, and should be, achieved as soon as possible.”

The National Science Foundation (NSF) is an independent federal agency that supports fundamental research and education across all fields of science and engineering, with an annual budget of $5.92 billion. NSF funds reach all 50 states through grants to over 1,700 universities and institutions. Each year, NSF receives about 42,000 competitive requests for funding, and makes over 10,000 new funding awards. The NSF also awards over $400 million in professional and service contracts yearly. The NSF website is http://www.nsf.gov/index.jsp.

The National Academy of Engineering website is located at: http://www.nae.edu/nae/naehome.nsf. Retrieved on 3/4/08. The Grand Challenges site features a five-minute video overview of the project along with committee member interview excerpts.

[7] Although this meme is highly visible in nearly every industrialized nation, this challenge may be the least important of the 14 grand challenges.

“Claimed human-caused warming of the Earth to dangerous and unprecedented levels by human-related emissions of carbon dioxide is contradicted by a non-correlation of carbon dioxide levels with warming.

The Anthropogenic Global Warming Hypothesis states that sunlight radiation warms the Earth by being absorbed at its surface. Then some of the absorbed heat is reradiated into the atmosphere. Some gases in the atmosphere, called “greenhouse gases,” absorb much of this heat, and then reradiate it, some toward the surface of the Earth, making the Earth warmer than it would be without a heat-absorbing atmosphere. The primary “greenhouse gases” by far is said to be carbon dioxide, with some hints about methane, ozone, and traces of halocarbons.

Many serious scientists cite evidence that it’s the variations in solar output, solar distance and number of sunspots that are primarily responsible for temperature changes on Earth. This makes up the Solar Output Variation Hypothesis.

The predominant greenhouse gas is water vapor, not carbon dioxide. More water vapor also limits the day/night temperature range. This should not be construed as condoning wasteful use of hydrocarbon fuels. For the obvious economic reasons, not an unthreatening global warming, hydrocarbon fuels should be conserved or substituted when possible.”

See “Climate Change Reexamined,” by Joel M. Kauffman, Emeritus, Department of Chemistry & Biochemistry, University of the Sciences in Philadelphia, PA. Available online at http://www.scribd.com/doc/14299932/Climate-change-reexamined-joel-m.

[8] Perhaps no one has influenced our knowledge of life on Earth as much as the English naturalist Charles Robert Darwin (1809-1882). His theory of evolution by natural selection, now the unifying theory of the life sciences, explained where all of the astonishingly diverse kinds of living things came from and how they became exquisitely adapted to their particular environments. His theory reconciled a host of diverse kinds of evidence such as the succession of fossil forms in the geological record, the geographical distribution of species, recapitulative appearances in embryology, homologous structures, vestigial organs and nesting taxonomic relationships. No other explanation before or since has made sense of these facts.
In further works Darwin demonstrated that the difference between humans and other animals is one of degree not kind. In geology, zoology, taxonomy, botany, paleontology, philosophy, anthropology, psychology, literature and theology Darwin's writings produced profound reactions, many of which are still ongoing. Yet even without his evolutionary works, Darwin's accomplishments would be difficult to match. His brilliantly original work in geology, botany, biogeography, invertebrate zoology, psychology and scientific travel writing would still make him one of the most original and influential workers in the history of science. Darwin's writings are consequently of interest to an extremely wide variety of readers.

For more on Darwin, see The Complete Work of Charles Darwin Online (or Darwin Online) at http://darwin-online.org.uk/. The site contains over 79,000 pages of searchable text and 190,000 electronic images.

[9] To read the article “Nothing in Biology Makes Sense Except in the Light of Evolution,” see http://www.pbs.org/wgbh/evolution/library/10/2/text_pop/l_102_01.html.

[10] Theodosius Grygorovych Dobzhansky, also known as T. G. Dobzhansky, and sometimes Anglicized to Theodore Dobzhansky (Ukrainian—January 24, 1900 - December 18, 1975) was a noted geneticist and evolutionary biologist, and a central figure in the field of evolutionary biology for his work in shaping the unifying modern evolutionary synthesis. Dobzhansky was born in Ukraine (then part of Imperial Russia) and emigrated to the United States in 1927.

Dobzhansky was born on January 24, 1900 in Nemyriv, Ukraine (then in the Russian Empire). An only child, his father Grigory Dobzhansky was a mathematics teacher, and his mother was Sophia Voinarsky. In 1910 the family moved to Kiev, Ukraine. At high school, Dobzhansky collected butterflies and decided to become a biologist. In 1915, he met Victor Luchnik who convinced him to specialize in beetles instead. Dobzhansky attended the University of Kiev between 1917 and 1921, where he then studied until 1924. He then moved to Leningrad, Russia, to study under Yuri Filipchenko, where a Drosophila melanogaster lab had been established.

In 1937 he published one of the major works of the modern evolutionary synthesis, the synthesis of evolutionary biology with genetics, entitled Genetics and the Origin of Species, which amongst other things defined evolution as “a change in the frequency of an allele within a gene pool.” Dobzhansky's work was instrumental in spreading the idea that it is through mutations in genes that natural selection takes place. Also in 1937, he became a naturalized citizen of the United States. During this time he had a very public falling out with one of his Drosophila collaborators, Alfred Sturtevant, based primarily in professional competition.

Dobzhansky returned to Columbia University from 1940 to 1962. He was one of the signatories of the 1950 UNESCO statement The Race Question. He then moved to the Rockefeller Institute (shortly to become Rockefeller University) until his retirement in 1971.

On June 1, 1968 it was discovered that Dobzhansky was suffering from lymphocytic leukemia, a chronic form of leukemia, and given a few months to a few years to live. Natasha died of coronary thrombosis on February 22, 1969. In 1971 he retired but continued working as an emeritus professor, moving to the University of California, Davis where his student Francisco Jose Ayala was made assistant professor.

Meanwhile, he continued working and published a famous essay “Nothing in Biology Makes Sense Except in the Light of Evolution.” A loyal defender of Darwinian evolution, Dobzhansky, according to Francisco J. Ayala “was a religious man.” Dobzhansky himself spoke of God as creating through evolution, and considered himself a communicant of the Eastern Orthodox Church.

His leukemia became more serious in the summer of 1975; on November 11 he made a trip to San Jacinto, California where he died of heart failure on December 18. He was cremated and his ashes were scattered in the Californian wilderness.

Abridged biography courtesy of the Wikipedia article entitled “Theodosius Dobzhansky.” Available online at http://en.wikipedia.org/wiki/Theodosius_Dobzhansky.

[11] American Biology Teacher, volume 35, pages 125-129.

[12] Abridged description courtesy of the Wikipedia article entitled “Nothing in Biology Makes Sense Except in the Light of Evolution.” Available online at http://en.wikipedia.org/wiki/Nothing_in_Biology_Makes_Sense_Except_in_the_Light_of_Evolution.

[13] “Why Are People?” is the title of the first chapter of Richard Dawkin’s book The Selfish Gene (New York: Oxford University Press, 30^th Anniversary edition, 2006).

[14] Dawkins, Richard. The Ancestor’s Tale: A Pilgrimage to the Dawn of Evolution. New York: Houghton Mifflin Company, 2005, page 7.

[15] Ibid, page 530.

[16] Ibid.

[17] Masur K, Thévenod F, Zänker KS (eds): Diabetes and Cancer. Epidemiological Evidence and Molecular Links. Frontiers in Diabetes. Basel; Karger, 2008, Vol 19, page 50.

[18] Ibid, page 51.

[19] Ibid, page 44.

[20] Calle EE, Kaaks R (2004) Overweight, obesity and cancer: epidemiological evidence and proposed mechanisms. Nature Reviews: Cancer 4(8): 579-91. Op cit. Smyth D, and Smyth T., “The Relationship Between Diabetes and Cancer,” Journal of Diabetes Nursing, July-August, 2005. Available online at http://findarticles.com/p/articles/mi_m0MDR/is_7_9/ai_n15727529/?tag=content;col1.

[21] Shi R, Yu H, McLarty, J, Glass J (2004) IGF-I and breast cancer: a meta-analysis. International Journal of Cancer 111(3): 418-23. Op cit. Smyth D, and Smyth T. (2005).

[22] Stattin P, Rinaldi S, Biessy C, Stenman UH, Hallmans G, Kaaks R (2004) High levels of circulating insulin-like growth factor-1 increase prostate cancer risk: a prospective study in a population-based nonscreened cohort. Journal of Clinical Oncology 22(15): 3104-12. Op cit. Smyth D, and Smyth T. (2005).

[23] Richardson LC, Pollack LA (2005) Therapy Insight: influence of type 2 diabetes on the development, treatment and outcomes of cancer. Nature Clinical Practice Oncology 2(1): 48-53. Op cit. Smyth D, and Smyth T. (2005).

[24] Anderson KE, Anderson E, Mink PJ, Hong CP, Kushi LH, Sellers TA et al (2001) Diabetes and endometrial cancer in the lowa women's health study. Cancer Epidemiology, Biomarkers & Prevention 10(6): 611-6. Op cit. Smyth D, and Smyth T. (2005).

[25] Michels KB, Solomon CG, Hu FB, Rosner BA, Hankinson SE, Colditz GA et al (2003) Type 2 diabetes and subsequent incidence of breast cancer in the Nurses' Health Study. Diabetes Care 26(6): 1752-8. Op cit. Smyth D, and Smyth T. (2005).

[26] Khaw KT, Wareham N, Bingham S, Luben R, Welch A, Day N (2004) Preliminary communication: glycated hemoglobin, diabetes, and incident colorectal cancer in men and women: a prospective analysis from the European prospective investigation into cancer-Norfolk study. Cancer Epidemiology, Biomarkers & Prevention 13(6): 915-9. See also Jee SH, Ohrr H, Sull JW, Yun JE, Ji M, Samet JM (2005) Fasting serum glucose level and cancer risk in Korean men and women. Journal of the American Medical Association 293(2): 194-202. Op cit. Smyth D, and Smyth T. (2005).

[27] Jee SH, Ohrr H, Sull JW, Yun JE, Ji M, Samet JM (2005) Fasting serum glucose level and cancer risk in Korean men and women. Journal of the American Medical Association 293(2): 194-202. Op cit. Smyth D, and Smyth T. (2005).

[28] Khaw KT, Wareham N, Bingham S, Luben R, Welch A, Day N (2004) Preliminary communication: glycated hemoglobin, diabetes, and incident colorectal cancer in men and women: a prospective analysis from the European prospective investigation into cancer-Norfolk study. Cancer Epidemiology, Biomarkers & Prevention 13(6): 915-9. Op cit. Smyth D, and Smyth T. (2005).

[29] National Cancer Institute: Diabetes increases men's risk of liver, pancreatic cancer, study finds. NCI Cancer Bulletin. NCI, Bethesda, MD. Available online at http://www.cancer.gov/NCICancerBulletin/NCI_Cancer_Bulletin_102604/page4. Retrieved on 5/20/09. Op cit. Smyth D, and Smyth T. (2005).

[30] Yang YX, Hennessy S, Lewis JD (2004) Insulin therapy and colorectal cancer risk among type 2 diabetes mellitus patients. Gastroenterology 127(4): 1044-50. Op cit. Smyth D, and Smyth T. (2005).

[31] Having diabetes when given a cancer diagnosis increases the risk of death by 41%, researchers here said. That finding comes from the first systematic assessment of long-term, all-cause mortality in newly diagnosed cancer patients with or without diabetes, according to Frederick Brancati, M.D., and colleagues at Johns Hopkins University.

All told, they found 48 articles that evaluated the effect of pre-existing diabetes on cancer outcome, including 23 that could be combined in a meta-analysis.

Possible explanations include interactions between the two disease types, treatment effects, poorer response to therapy, and sub-optimal cancer screening that leads diabetic patients to be diagnosed later, the researchers said.

It's even possible that the observed increase in risk of death is just a result of the effect of diabetes on cardiovascular health and has nothing to do with cancer at all, Dr. Brancati and colleagues said.

See the online article “Diabetes Increases Cancer Death Risk,” By Michael Smith, North American Correspondent, MedPage Today, Published: December 16, 2008. Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston. Available online at http://www.medpagetoday.com/Endocrinology/Diabetes/12177.

The above source comments on the original article by Barone BB, et al., “Long-term all-cause mortality in cancer patients with preexisting diabetes mellitus: a systematic review and meta-analysis,” JAMA 2008; 300(23): 2754-2764. Available online at http://jama.ama-assn.org/cgi/content/short/300/23/2754.

[32] The authors performed a prospective cohort study using data from the Second National Health and Nutrition Examination Survey and the Second National Health and Nutrition Examination Survey Mortality Study to determine this relation.

This analysis focused upon a nationally representative sample of 3,054 adults aged 30-74 years who underwent an oral glucose tolerance test at baseline (1976-1980). Deaths were identified by searching national mortality files through 1992. Adults were classified as having either previously diagnosed diabetes (n = 247), undiagnosed diabetes (n = 180), impaired glucose tolerance (n = 477), or normal glucose tolerance (n = 2250). There were 195 cancer deaths during 40,024 person-years of follow-up. Compared with those having normal glucose tolerance, adults with impaired glucose tolerance had the greatest adjusted relative hazard of cancer mortality (relative hazard = 1.87, 95% confidence interval (CI): 1.06, 3.31), followed by those with undiagnosed diabetes (relative hazard = 1.31, 95% CI: 0.48, 3.56) and diabetes (relative hazard = 1.13, 95% CI: 0.49, 2.62).

See “Abnormal glucose tolerance and the risk of cancer death in the United States,” by Saydah SH, Loria CM, Eberhardt MS, Brancati FL. Am J Epidemiol. 2003 Jun 15;157(12):1092-100. Available online at http://www.ncbi.nlm.nih.gov/pubmed/12796045?ordinalpos=87&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum.

[33] Coughlin SS, Calle EE, Teras LR, Petrelli J, Thun M, “Diabetes Mellitus as a Predictor of Cancer Mortality in a Large Cohort of US Adults,” Am J Epidemiol, 2004;159:1160-1167. Available online at http://aje.oxfordjournals.org/cgi/content/full/159/12/1160.

[34] See “Prospective Study of Hyperglycemia and Cancer Risk,” by Pär Stattin, MD, PHD, Ove Björ, BSC, Pietro Ferrari, BSC, Annekatrin Lukanova, MD, PHD, Per Lenner, MD, PHD, Bernt Lindahl, MD, PHD, Göran Hallmans, MD, PHD and Rudolf Kaaks, PHD. Diabetes Care, March, 2007, vol. 30, no. 3, 561-567. doi: 10.2337/dc06-0922. Available online at http://care.diabetesjournals.org/content/30/3/561.full.

[35] See http://www.cancer.gov/cancertopics/what-is-cancer.

[36] Abridged from the Wikipedia article entitled “Cancer,” available online at http://en.wikipedia.org/wiki/Cancer.

[37] Darwin, Charles. On the Origin of Species by Means of Natural Selection, or The Preservation of Favoured Races in the Struggle for Life. London: John Murray, Albemarle Street, 1859. In Darwin: The Indelible Stamp. Four Essential Volumes in One. Edited, with commentary, by James D. Watson. Philadelphia: Running Press, 2005, page 600. Please note that this is not a first edition quote, as preferred by more scholarly writers, but the gist of the message is just as clear in any edition.

[38] I had originally written “…at a level much higher than the individual,” however, after further reading, most notably, Richard Dawkins’s Unweaving the Rainbow, I came to realize that evolution, whether through domestication, sexual selection, or natural selection, unfolds gradually from the level of the individual. Being American, most of my knowledge was shaped by the American-based writer Stephen Jay Gould. “Ironically, Gould is one of the few Darwinians who still think of natural selection as working at levels higher than the individual organism.” See Dawkins, Richard. Unweaving the Rainbow. Boston & New York: A Mariner Book, Houghton Mifflin Company, 1998, p. 199.

For two great, recent overviews of the fact of evolution, see Dawkins, Richard. The Greatest Show on Earth: The Evidence for Evolution. New York: Free Press, 2009; and Coyne, Jerry A. Why Evolution is True. New York: Viking, the Penguin Group, 2009. According to Coyne, “Life on Earth evolved gradually beginning with one primitive species—perhaps a self-replicating molecule—that lived more than 3.5 billions years ago; it then branched out over time, throwing off many new and diverse species; and the mechanism for most (but not all) of evolutionary change is natural selection.” (Page 3)

[39] For a good discussion of arms races, manipulation, and descriptions of the five different types of fitness, see the chapters entitled “Arms Races and Manipulation,” and “An Agony in Five Fits,” in Dawkins, Richard. The Extended Phenotype: The Long Reach of the Gene. New York: Oxford University Press, 2008.

Note that all these concepts, namely, parasitism, symbiosis, conflict, cooperation, and co-evolution—which were developed with reference to whole organisms—are relevant to genes within an organism. See Ibid, page 178.

[40] For a fascinating article detailing how cancer is not an “it” but a “they,” see “Evolution of Cooperation Among Tumor Cells,” by Robert Axelrod, David E. Axelrod, and Kenneth J. Pienta. Published online before print August 28, 2006, doi: 10.1073/pnas.0606053103. Proceedings of the National Academy of Sciences of the United States of America (PNAS), September 5, 2006 vol. 103 no. 36 13474-13479. Available online at http://www.pnas.org/content/103/36/13474.full#sec-3.

“…We marshal evidence that tumor cells overcome certain host defenses by means of diffusible products. Our original contribution is to raise the possibility that two nearby cells can protect each other from a set of host defenses that neither could survive alone. Cooperation can evolve as by-product mutualism among genetically diverse tumor cells. Our hypothesis supplements, but does not supplant, the traditional view of carcinogenesis in which one clonal population of cells develops all of the necessary genetic traits independently to form a tumor. Cooperation through the sharing of diffusible products raises new questions about tumorigenesis and has implications for understanding observed phenomena, designing new experiments, and developing new therapeutic approaches.”

[41] See The Wistar Institute (2006, November 17). Does Natural Selection Drive The Evolution Of Cancer? ScienceDaily. Available online at http://www.sciencedaily.com/releases/2006/11/061117114616.htm.

[42] For percentage breakdown by geography, see the Disease Control Priorities Project online at http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=dcp2.table.4313.

For actual numbers of diabetics worldwide, see the World Health Organization’s diabetes pages online at http://www.who.int/diabetes/facts/world_figures/en/index.html.

“The reasons for the uneven worldwide distribution of Type 1 diabetes mellitus have yet to be fully explained. Epidemiological studies have shown a higher prevalence of Type 1 diabetes in northern Europe, particularly in Scandinavian countries, and Sardinia. Recent animal research has uncovered the importance of the generation of elevated levels of glucose, glycerol and other sugar derivatives as a physiological means for cold adaptation. High concentrations of these substances depress the freezing point of body fluids and prevent the formation of ice crystals in cells through supercooling, thus acting as a cryoprotectant or antifreeze for vital organs as well as in their muscle tissue. In this paper, we hypothesize that factors predisposing to elevated levels of glucose, glycerol and other sugar derivatives may have been selected for, in part, as adaptive measures in exceedingly cold climates.”

See “The sweet thing about Type 1 diabetes: a cryoprotective evolutionary adaptation,” by Moalem S, Storey KB, Percy ME, Peros MC, Perl DP. Med Hypotheses, 2005;65(1):8-16. Available online at http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15893109.

[43] Over the last decade, an abundance of evidence has emerged demonstrating a close link between metabolism and immunity. It is now clear that obesity is associated with a state of chronic low-level inflammation. In the below cited article, the authors discuss the molecular and cellular underpinnings of obesity-induced inflammation and the signaling pathways at the intersection of metabolism and inflammation that contribute to diabetes. They also consider mechanisms through which the inflammatory response may be initiated and discuss the reasons for the inflammatory response in obesity. The authors put forth for consideration some hypotheses regarding important unanswered questions in the field and suggest a model for the integration of inflammatory and metabolic pathways in metabolic disease.”

See “Inflammation, stress, and diabetes,” by Kathryn E. Wellen and Gökhan S. Hotamisligil. J. Clin. Invest. 115(5): 1111-1119 (2005). doi: 10.1172/JCI25102. Available online at http://www.jci.org/articles/view/25102/version/1.

[44] “…genes are named after the conditions and abnormalities that led to their discovery. This, inevitably, means that their name commemorates what happens when they don’t work. The gene that triggers the development of eyes in fruit flies—discovered in 1915—is called ‘eyeless’.” See Ings, Simon. A Natural History of Seeing: The Art and Science of Vision. New York: W.W. Norton & Company, 2008, p. 83.

Researchers have found nearly 20 different genes that can affect one’s risk for developing diabetes. See GeneticHealth online at http://www.genetichealth.com/dbts_genetics_of_type_1_diabetes.shtml.

There are hundreds, more, thousands of articles in the medical literature pertaining to the genetic associations with diabetes. Here I’ll provide just two such recent articles that you may find interesting:

Regarding type 2 diabetes, see for example “Genetic Basis of Beta-Cell Dysfunction in Man,” by Groop L and Lyssenko V. Diabetes Obes Metab 2009 Nov;11 Suppl 4():149-58. “Although the genetic causes of monogenic disorders have been successfully identified in the past, the success in dissecting the genetics of complex polygenic diseases has until now been limited. With the introduction of whole genome wide association studies (WGAS) in 2007, the picture has been dramatically changed. Today we know of about 20 genetic variants increasing the risk of type 2 diabetes (T2D). Most of them seem to influence the capacity of beta-cells to increase insulin secretion to meet the demands imposed by an increase in body weight and insulin resistance. This probably represents only the tip of the iceberg, and over the next few years refined tools will provide a more complete picture of the genetic complexity of T2D. This will not only include the current dissection of common variants increasing the susceptibility of the disease but also rare variants with stronger effects, copy number variations and epigenetic effects like DNA methylation and histone acetylation. For the first time, we can anticipate with some confidence that the genetics of a complex disease like T2D really can be dissected.” Available online at http://www.ncbi.nlm.nih.gov/pubmed/19817797?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=3. PMID: 19817797; doi: 10.1111/j.1463-1326.2009.01117.x.

Regarding type 1 diabetes, see for example “Genetic Basis of Type 1 Diabetes: Similarities and Differences between East and West,” by Ikegami H, Noso S, Babaya N, Hiromine Y, and Kawabata Y. Rev Diabet Stud 2008 Summer;5(2):64-72. “Type 1 diabetes is a multifactorial disease caused by a complex interaction of genetic and environmental factors. The genetic factors involved consist of multiple susceptibility genes, at least five of which, HLA, INS, CTLA4, PTPN22 and IL2RA/CD25, have been shown to be associated with type 1 diabetes in Caucasian (Western) populations, as has recently been confirmed by genome-wide association studies. It has been proposed, however, that the contribution of these genes to type 1 diabetes susceptibility may be different in Asian (Eastern) populations.” Available online at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2556443/?tool=docline. PMID: 18795209; doi: 10.1900/RDS.2008.5.64.

[45] The famous quotation describing life in the state of war of every man against every man: “…the life of man, solitary, poor, nasty, brutish, and short,” is from Chapter XIII “Of the Natural Condition of Mankind, as concerning their Felicity, and Misery,” from Leviathan, The Matter, Forme and Power of a Common Wealth Ecclesiasticall and Civil, commonly called Leviathan, a book written by Thomas Hobbes which was published in 1651. It is titled after the biblical Leviathan. The book concerns the structure of society and legitimate government, and is regarded as one of the earliest and most influential examples of social contract theory. Adapted from the Wikipedia article entitled “Leviathan (book),” available online at http://en.wikipedia.org/wiki/Leviathan_(book).

[46] See “Diabetes induced by Coxsackie virus: Initiation by bystander damage and not molecular mimicry,” by Horwitz, et al. Nature Medicine 4, 781 - 785 (1998), doi: 10.1038/nm0798-781. Available online at http://www.nature.com/nm/journal/v4/n7/abs/nm0798-781.html. Retrieved on 6/13/09. For the first prospective study, see “A prospective study of the role of coxsackie B and other enterovirus infections in the pathogenesis of IDDM. Childhood Diabetes in Finland (DiMe) Study Group,” by Hyöty, et al. Diabetes June, 1995, vol. 44, no. 6, 652-657. doi: 10.2337/diabetes.44.6.652. Available online at http://diabetes.diabetesjournals.org/content/44/6/652.abstract.

[47] See “Innate immunity and intestinal microbiota in the development of Type 1 diabetes,” by Li Wen, et al. Nature. 2008, October 23; 455(7216): 1109–1113. Published online 2008, September 21. doi: 10.1038/nature07336. PMCID: PMC2574766; NIHMSID: NIHMS67288. Available online at http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2574766.

“Humans consist of about a trillion cells, but there are some 10 trillion bacterial cells on or in us at any given time. Bacteria digest our food, make our vitamins, educate our immune system to keep harmful antigens out. But there are also notorius and harmful bacteria.” See http://www.ted.com/talks/bonnie_bassler_on_how_bacteria_communicate.html.

Bonnie Bassler discovered that bacteria “talk” to each other, using a chemical language that lets them coordinate defense and mount attacks. The find has stunning implications for medicine and industry. See http://www.molbio.princeton.edu/index.php?option=content&task=view&id=27.

For more on quorum sensing see the Wikipedia article entitled “Quorum Sensing,” online at http://en.wikipedia.org/wiki/Quorum_sensing.

[48] In summary, high serum selenium concentrations were associated with higher prevalence of diabetes in a representative survey of US adults conducted in 2003-2004. These findings are consistent with an earlier National Health and Nutrition Examination Survey (NHANES) survey conducted in 1988-1994. See “Serum Selenium Concentrations and Diabetes in US Adults: National Health and Nutrition Examination Survey (NHANES) 2003-2004,” by Martin Laclaustra, Ana Navas-Acien, Saverio Stranges, Jose M Ordovas, and Eliseo Guallar. Environmental Health Perspectives, doi: 10.1289/ehp.0900704. Aavailable online at http://ehp.niehs.nih.gov/docs/2009/0900704/abstract.html.

[49] American Diabetes Association; American Psychiatric Association; American Association of Clinical Endocrinologists; North American Association for the Study of Obesity (February 2004). “Consensus development conference on antipsychotic drugs and obesity and diabetes.” Diabetes Care 27 (2): 596–601. doi: 10.2337/diacare.27.2.596. PMID 14747245. Available online at http://care.diabetesjournals.org/cgi/content/full/27/2/596.

[50] See “Incident Diabetes and Pesticide Exposure among Licensed Pesticide Applicators: Agricultural Health Study, 1993–2003,” by M. P. Montgomery, F. Kamel, T. M. Saldana, M. C. R. Alavanja, and D. P. Sandler. American Journal of Epidemiology, March 14, 2008. doi: 10.1093/aje/kwn028. Available online at http://www.toxfree.net/chlordane/Education/Healthrisk/Applicators.pdf.

“The authors’ aim was to investigate the relation between lifetime exposure to specific agricultural pesticides and diabetes incidence among pesticide applicators. The study included 33,457 licensed applicators, predominantly non-Hispanic White males, enrolled in the Agricultural Health Study. Incident diabetes was self-reported in a 5-year follow-up interview (1999–2003), giving 1,176 diabetics and 30,611 nondiabetics for analysis. Lifetime exposure to pesticides and covariate information were reported by participants at enrollment (1993–1997). Using logistic regression, the authors considered two primary measures of pesticide exposure: ever use and cumulative lifetime days of use. They found seven specific pesticides (aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor, and cyanazine) for which the odds of diabetes incidence increased with both ever use and cumulative days of use. Applicators who had used the organochlorine insecticides aldrin, chlordane, and heptachlor more than 100 lifetime days had 51%, 63%, and 94% increased odds of diabetes, respectively. The observed association of organochlorine and organophosphate insecticides with diabetes is consistent with results from previous human and animal studies. Long-term exposure from handling certain pesticides, in particular, organochlorine and organophosphate insecticides, may be associated with increased risk of diabetes.

This study is to our knowledge the largest study to evaluate the potential effects of pesticides on diabetes incidence in adults. The prospective design of the study ensures that exposures were reported prior to the diagnosis of diabetes and reduces the potential for recall bias. Of the 50 pesticides evaluated, seven displayed evidence suggesting an association with diabetes incidence in both ever-use and cumulative days-of-use models: aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor, and cyanazine. It is noteworthy that all of these pesticides are chlorinated compounds, while only half of the pesticides investigated were chlorinated. Few studies, if any, have considered the potential diabetogenic effects of alachlor and cyanazine, which both showed a dose-response association with diabetes in the present study. However, the biologic plausibility of a diabetogenic effect of exposure to persistent organic pollutants (e.g., dioxins, polychlorinated biphenyls, and organochlorine insecticides) and organophosphate insecticides is supported by numerous studies.”

See also “Treatment of Homes for Termites Decades Ago May Cause Diabetes Today,” by Dr. Richard Cassidy, DiabetesHealth, Mar 13, 2009. Available online at http://www.diabeteshealth.com/read/2009/03/12/6117/treatment-of-homes-for-termites-decades-ago-may-cause-diabetes-today/.

“Recently, the Centers for Disease Control mapped the incidence of diabetes by state. There is a striking correlation between the incidence of diabetes and the use of chlordane for termite control in these states. Southern states with the highest temperatures and humidity have not only the highest rates of termite infestations and chlordane use, but also the highest rate of diabetes. States from the midsection of the United States, with moderate temperatures and humidity and lower chlordane applications, have lower rates of diabetes. In northern states such as Minnesota, where chlordane was rarely used, the incidence of diabetes is less than 50 percent that of southern states.”

Because of concern about damage to the environment and harm to human health, the United States Environmental Protection Agency (EPA) banned all uses of chlordane in 1983 except termite control. The EPA banned all uses of chlordane in 1988.

[51] See, for example, “Blood levels of alloxan in children with insulin-dependent diabetes mellitus,” by A. Mrozikiewicz, D. Kielstrokczewska-Mrozikiewicz, Z. Lstrokowicki, E. Chmara, K. Korzeniowska and P. M. Mrozikiewicz. Acta Diabetologica, Volume 31, Number 4, December, 1994, pages 236-237. doi: 10.1007/BF00571958. Available online at http://www.springerlink.com/content/r001211h96j18266/.

The mechanisms underlying alloxan and streptozotocin diabetes are a major research topic of the Institute of Clinical Biochemistry of Hannover Medical School. For the full list of publications addressing this topic, which can all be downloaded via PubMed, see http://www.mh-hannover.de/8750.html.

[52] See “Diabetes mellitus and orthostatic hypotension resulting from ingestion of Vacor rat poison: endocrine and autonomic function studies,” by K S Peters, T G Tong, K Kutz, and N L Benowitz. West J Med. 1981 January; 134(1): 65–68. Available online at http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1272465.

[53] According to Nicholas P. Money, in Mr. Bloomfield’s Orchard, “In England in 1960, 100,000 turkeys died following loss of appetite, lethargy, and liver failure. It was discovered that they had been fed aflatoxin-contaminated peanut meal, and the name turkey X-disease was coined for their plague…It is unlikely that turkeys, or any other animals, are the targets for aflatoxins in an evolutionary sense. It has been suggested that animals compete with fungi for the same food—harvested grain, for example—and that aflatoxins would reduce the number of these rivals. But I’m not convinced; other microorganisms are probably the “intended” victims. While fungi produce mycotoxins in minute quantities in the soil and in plant tissues, local concentrations may be high enough in the immediate vicinity of the growing hyphae to clear the territory for the mold.” See Money, Nicholas P. Mr. Bloomfield’s Orchard: The Mysterious World of Mushrooms, Molds, and Mycologists. New York: Oxford University Press, 2002, Page 162.

Regarding another mycotoxin, amatoxin, Dr. Money writes: “Insects and fungi have interacted with one another for 400 million years or more, an expanse of time that has offered ample opportunity for the evolution of defense and counter-defense mechanisms in both groups of organisms. If insect larvae are the real targets of amatoxins, then human casualties were “unintended” by evolution. In every sense, then, mushrooms couldn’t care less about Homo sapiens.” See page 156.

Interestingly, in this book he wrote about Curtis Gates Lloyd, one of Cincinnati’s most eligible bachelors, and a millionaire obsessed with fungi. Mr. Lloyd became a self-taught expert in fungal identification and had undertaken the publication of his own mycological work. “Mr. Lloyd had suffered from diabetes for many years, and with little in the contemporary pharmacopia to prolong his life, he died of complications from the disease in 1926.” See page 102.

See also Money, Nicholas P. Carpet Monsters and Killer Spores: A Natural history of Toxic Mold. New York: Oxford University Press, 2004.

“Fungi never intended to inflame or poison humans. After all, black molds spent hundreds of millions of years rotting dead plants before the evolution of wheezing authors and bleeding babies. Their spores were designed for drifting in air, not for swimming in lung mucous, so problems with molds are rooted in our insistence on breathing rather than any microbial malevolence.” See page 58.

“Fungi produce hundreds of different kinds of toxins, a few of proven harm to humans, most of dubious significance. Everyone is familiar with poisonous mushrooms. A single fruiting body of a death cap or a destroying angel contains a few thousandths of a gram of amatoxins, which is adequate to kill an adult. Amatoxins are peptides that block protein synthesis in cells. The reason that the mushroom accumulates these poisonous molecules is unclear, but the most satisfying answer is that they defend the fruiting body against insect grubs.” See page 59.

[54] See The Garden of Eden Longevity Diet Antifungal/Antimycotoxin,Anti-Cancer, Anti-Atherosclerosis; see also The Fungal/Mycotoxin Etiology of Breast Cancer Foods That Cause & Foods that Prevent; see also The Fungal/Mycotoxin Etiology of Prostate Cancer Foods That Cause & Foods That Prevent; and The Fungal/Mycotoxin Etiology of Atherosclerosis Foods That Cause & Foods that Prevent all written by A.V. Costantini, M.D., H. Wieland, M.D., and Lars Qvick, M.D. For excerpts, see http://www.fungalbionicbookseries.com/index.htm.

In describing the strength of mycotoxins, the above authors wrote the following:

“As many as 1,000 compounds, classifiable as mycotoxins, were studied by the pharmacology industry as potential antibiotics in the 1930s and 1940s only to be discarded as being too toxic for higher life forms to be of value in treating bacterial diseases in humans. Little, if any of the discarded data was published. Yet what these toxicity studies actually documented was the existence of a large number of fungal-derived toxins which caused serious target organ injury in various animal models. Obviously, in retrospect, what was being seen was the pathology produced by the mycotoxins. In order to understand this toxicity, one only has to look at what some of these mycotoxins, used as medications, causes in humans: The mycotoxin cyclosporin used for transplantation causes cancer and atherosclerosis, complete with hyperlipidemia, in ALL humans who have received it. Many others develop gout and other diseases.”

Prof. Dr. A.V. Costantini, MD was the keynote speaker at the 1993 conference of the American Academy of Environmental Medicine held in Reno, Nevada, where he stated the following:

“Auto-immune diseases are characterized by the finding of so-called auto-antibodies. It is a most popular concept but biologically fatally defective in that no species of life can make an antibody against itself; particularly causing fatal disease such as scleroderma. Scleroderma is considered to prove the validity of the auto-immune concept with the presence of auto-antibodies. However these are now documented to be antibodies against ubiquitin which is present in many species including fungi. Scleroderma responds well to the antifungal agent griseofulvin. Against whose ubiquitin is the host raising antibodies to, its own, or fungal-derived, in a disease state which responds to an antifungal drug? The auto-immune diseases appearing to have a fungal and mycotoxin origin are: scleroderma, diabetes mellitus, HLA-related disease, rheumatoid arthritis, Sjogren’s syndrome, psoriasis & systemic lupus erythematosus. All of the drugs effective in the treatment of these diseases possess antifungal or anti-mycotoxin activity. This includes all NSAIDs [Non-Steroidal Anti-Inflammatory Drugs].”

From the Chesser-Naugle International Lectureship Grant: The Fungal/Mycotoxin Connections: Autoimmune Diseases, Malignancies, Atherosclerosis, Hyperllpldemias, and Gout, October 11, 1993. Twenty-eighth annual meeting entitled “New horizons in Chemical Sensitivities: State of the Art Diagnosis and Treatment. Available online at http://www.arthritistrust.org/Articles/Fungal-Mycotoxin%20Connection/index.htm.

[55] See Kaufmann, Doug and Holland, David. The Fungus Link to Diabetes: A Cutting-Edge Approach to Stopping One of America’s Fastest Growing Epidemics in Its Tracks. Rockwall, Texas: MediaTrition, Inc., 2003.

[56] See Maas, Laurens. The Hidden Cure: The Five Laws of Perfect Health. Wheatmark: Tuscan, Arizona, 2009.

[57] The most outraged and formidable opponent of Charles Darwin was Richard Owen, Hunterian Professor at the Royal College of Surgeons, who examined the fossil bones Darwin had had brought back from South America. Owen acted largely behind the scenes, and was the one who provided material for Bishop Wilberforce’s scathing review in the Quarterly Review, where Wilberforce referred to Darwin’s ideas as “his utterly rotten fabric of guess and speculation.” See “Commentary: On the Origin of Species,” in Darwin: The Indelible Stamp. Four Essential Volumes in One. Edited, with commentary, by James D. Watson. Philadelphia: Running Press, 2005, page 342.

The four volumes include: The Voyage of the Beagle (no publication information given); On the Origin of Species by Means of Natural Selection (London: John Murray, Albemarle Street, 1859); The Descent of Man, and Selection in Relation to Sex (Second Edition, London: John Murray, Albemarle Street, 1882); and The Expression of the Emotions in Man and Animals (London: John Murray, Albemarle Street, 1872).

The Voyage of the Beagle is a title commonly given to the book written by Charles Darwin published in 1839 as his Journal and Remarks, which brought him considerable fame and respect. The title refers to the second survey expedition of the ship HMS Beagle, which set sail from Plymouth Sound on December 27, 1831, under the command of captain Robert FitzRoy.

[58] Appendix C of the book ESSENTIAL DIABETES LEADERSHIP (2010) contains scores of low-carbohydrate, ketogenic diet articles, including several on point to ketogenic diet and cancer. See for example:

· Implementing a ketogenic diet based on medium-chain triglyceride oil in pediatric patients with cancer. Nebeling LC, Lerner E., J Am Diet Assoc. 1995 Jun;95(6):693-7. Available online at http://www.ncbi.nlm.nih.gov/pubmed/7759747.

· Effects of a ketogenic diet on tumor metabolism and nutritional status in pediatric oncology patients: two case reports. Nebeling LC, Miraldi F, Shurin SB, Lerner E., J Am Coll Nutr. 1995 Apr;14(2):202-8. Available online at http://www.ncbi.nlm.nih.gov/pubmed/7790697.

· The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer. Weihua Zhou,Purna Mukherjee,Michael A Kiebish,William T Markis,John G Mantis,and Thomas N Seyfried, Nutr Metab (Lond). 2007; 4: 5. Published online 2007 February 21. doi: 10.1186/1743-7075-4-5. Available online at http://www.ncbi.nlm.nih.gov/pubmed/17313687.

· The Effects of Varying Dietary Carbohydrate and Fat Content on Survival in a Murine LNCaP Prostate Cancer Xenograft Model. Mavropoulos JC, Buschemeyer WC 3rd, Tewari AK, Rokhfeld D, Pollak M, Zhao Y, Febbo PG, Cohen P, Hwang D, Devi G, Demark-Wahnefried W, Westman EC, Peterson BL, Pizzo SV, Freedland SJ, Cancer Prev Res (Phila Pa). 2009 May 26. Available online at http://www.ncbi.nlm.nih.gov/pubmed/19470786.

· Targeting energy metabolism in brain cancer with calorically restricted ketogenic diets. Seyfried TN, Kiebish M, Mukherjee P, Marsh J, Epilepsia. 2008 Nov;49 Suppl 8:114-6. Available online at http://www.ncbi.nlm.nih.gov/pubmed/19049606.

The ketogenic diet has also been used successfully in the treatment of epilepsy.

The biggest modern study with an intent-to-treat prospective design was published in 1998. As with most studies of the ketogenic diet, there was no control group, which would be patients who were denied the treatment. A team from the Johns Hopkins Hospital studied 150 children for at least 12 months. By three months, 25 patients had dropped out, 26% had a good reduction in seizures (50–90% reduction), 31% had an excellent reduction (90–99% reduction) and 3% became seizure free. By twelve months, 67 patients had dropped out, 23% had a good reduction, 20% had an excellent reduction and 7% were seizure free. See Freeman JM, Vining EP, Pillas DJ, Pyzik PL, Casey JC, Kelly LM. The efficacy of the ketogenic diet–1998: a prospective evaluation of intervention in 150 children. Pediatrics. 1998 Dec;102(6):1358–63. PMID 9832569. Available online at http://www.ncbi.nlm.nih.gov/pubmed/9832569.

In the same year, a multi-center study of 51 children showed similar efficacy, and proved that the results could be repeated by other institutions. See Vining EP, Freeman JM, Ballaban-Gil K, Camfield CS, Camfield PR, Holmes GL, et al. A multicenter study of the efficacy of the ketogenic diet. Arch Neurol. 1998 Nov;55(11):1433–7. PMID 9823827. Available online at http://www.ncbi.nlm.nih.gov/pubmed/9823827. Retrieved on 5/28/09. See also Hartman AL, Vining EP. Clinical aspects of the ketogenic diet. Epilepsia. 2007 Jan;48(1):31–42. PMID 17241206. doi: 10.1111/j.1528-1167.2007.00914.x. Available online at http://www.ncbi.nlm.nih.gov/pubmed/17241206.

The first randomised controlled trial was published in 2008, which had an intent-to-treat prospective design, but no blinding. It studied 145 children, half of whom were randomly selected to start the ketogenic diet immediately, and half to start after a three-month delay. The children who were delayed treatment acted as a control, which is particularly important for medical conditions where patients may get better or worse regardless of treatment. Of the children in the diet group, 38% had at least a 50% reduction in seizure frequency, 7% had at least a 90% reduction; one child became seizure-free. Only 6% of the control group saw a greater than 50% reduction in seizure frequency and no children had a 90% reduction. The mean seizure frequency of the diet group fell by a third; the control group's mean seizure frequency actually got worse. See Neal EG, Chaffe H, Schwartz RH, Lawson MS, Edwards N, Fitzsimmons G, et al. The ketogenic diet for the treatment of childhood epilepsy: a randomised controlled trial. Lancet Neurol. 2008 Jun;7(6):500–6. PMID 18456557. doi: 10.1016/S1474-4422(08)70092-9. Available online at http://www.ncbi.nlm.nih.gov/pubmed/18456557.

Abridged from the Wikipedia article entitled “Ketogenic Diet,” available online at http://en.wikipedia.org/wiki/Ketogenic_diet.

DILEMMAS

2012-11-04T17:53:00.000-08:00

DILEMMAS

“No one in this world, so far as I know, has ever lost money by underestimating the intelligence of the great masses of the plain people.” H.L. MENCKEN, Chicago Tribune, September 19, 1926

The following article was originally a chapter in my second book, ESSENTIAL DIABETES LEADERSHIP (2010). I still wonder whether or not I am making a mountain out of a molehill of it and whether the reaction to my definitely inelegant tables would be: “True; but, of course, all fairly obvious.” As to the making of the mountain, if such it is, I am utterly tired of it and prefer to write novels. Nonetheless, my increasing confidence in the basic application of low-, very low-, or near-zero-carbohydrate diets as a template for health—so many people are healthier for it—decided me that I’m probably not a crank.

It is hard even to feel and harder still to write in a way that runs counter to a current world view, especially a moral one, and it is all the harder when the way is re-shaping a plane of perfection to which all civilized cultures are thought to be striving. A scientist or philosopher with a program of such heresy has to be tough if he or she is to communicate it and, while doing so and for long after, must endure the tortures of Orestes.

I do so love repurposing the elegant words of those I hold in high esteem and if you now think “kinship selection” and “evolution” instead of “low-carbohydrate diet” you will recognize that the above words were written by W.D. Hamilton and were sourced from several articles comprising NARROW ROADS OF GENE LAND. They convey my feelings well, and, with them, I introduce you to my “Dilemmas.” Best wishes… - lc

This book [ESSENTIAL DIABETES LEADERSHIP] was written in the conviction that an optimal solution to diabetes once presented a great mystery, but that it is a mystery no longer because it is solved.[1] Dr. Richard Bernstein solved the problem by experimenting with his diet, notably by reducing his consumption of carbohydrates. In so doing, Dr. Bernstein validated the work done nearly a century before him by Richard Thomas Williamson, Charles Purdy, and many others, who, of course, validated John Rollo’s solution recommended 100 years before them. We have added, and shall continue to add, footnotes to the optimal solution, such as developing the insulins glargine & detemir that enable us type 1s to achieve a normal, stable blood sugar level in our sleep, upon awakening, and throughout the day.

Too, I wrote this book because I continue to be surprised and dismayed that so many people seem not only unaware of the elegant and beautiful dietary solution to our problem; but, incredibly, actually many are unaware what the problem is in the first place!

There are two problems, really. First, diabetes mellitus manifests itself in our bodies as ineffective carbohydrate processing due to an insulin function disturbance; we produce too much, too little, or none at all. And second, the optimal solution espoused by would-be health-providers may be optimal for their needs, not ours. Humbly, though passionately, I hope that my books—and the citations therein—have removed all sane doubt as to the veracity of the first problem and its solution. Explaining, proving then solving the second problem is the focus of this chapter.

So to present this material, let me briefly introduce an effective framework for understanding relationships between people with opposing interests, the basis of all dilemmas. We will then apply this device to a couple of real-world scenarios. “Game theory” is thus our topic, William Poundstone our teacher, PRISONER’S DILEMMA our textbook, and the decision strategy of a couple of imprisoned gang members our subject.

Two members of a criminal gang are arrested and imprisoned. Each prisoner is in solitary confinement with no means of speaking to or exchanging messages with the other. The police admit they don’t have enough evidence to convict the pair on the principal charge. They plan to sentence both to a year in prison on a lesser charge. Simultaneously, the police offer each prisoner a Faustian bargain. If he testifies against his partner, he will go free while the partner will get three years in prison on the main charge. Oh, yes, there is a catch. If both prisoners testify against each other, both will be sentenced to two years in jail.[2]

The prisoners are given little time to think this over, but in no case may either learn what the other has decided until he has irrevocably made his decision. Each is informed that the other prisoner is being offered the very same deal. Each prisoner is concerned only with his own welfare—with minimizing his own prison sentence. The below 2x2 matrix graphically depicts the scenario. Note that the first number in each cell is the payoff in terms of jail time for the row player, “A,” and the second number in each cell is the payoff in terms of jail time for the column player, “B.”

The prisoners can reason as follows: “Suppose I testify and the other prisoner doesn’t. Then I get off scot-free, rather than spending a year in jail. Suppose I testify and the other prisoner does too. Then I get two years, rather than three. Either way I’m better off turning state’s evidence. Testifying takes a year off my sentence, no matter what the other guy does.”

The trouble is, the other prisoner can and will come to the very same conclusion. If both parties are rational, both will testify and both will get two years in jail. If only they had both refused to testify, they would have got just a year each!

And so ends this short but prophetic tale. For a great primer on game theory, you are encouraged to read William Poundstone’s classic book PRISONER’S DILEMMA: JOHN VON NEUMANN, GAME THEORY, AND THE PUZZLE OF THE BOMB (New York: Doubleday, 1992). Here we will move from theoretical games to the actual challenge, for that is where we—fellow members of the club—find ourselves.

You go to your health-provider(s) with the classical triad of symptoms of polyuria, polydipsia, and polyphagia—respectively, frequent urination, increased thirst and consequent increased fluid intake, and increased appetite—with the hope that they are more knowledgeable than you and will help you find an optimal solution. But therein lies the dilemma: your health-provider(s) may not be fully vested in your interests alone.

Much has been written on the subject. In “Conflict of Interest in Clinical Practice,” (2007), first published in Chest, the author Mark R. Tonelli, M.D., M.A., FCCP, provides some background:

“The inherent tension built into remuneration for the healing arts has been recognized as far back as Plato, who devoted a small part of The Republic[3] to the issue.[4] In a classic fee-for-service arrangement, physicians benefit financially from the provision of more interventions, with patients and the market poorly positioned to make judgments regarding the necessity of these services.[5] Historically, a physician’s service largely equated with the physician’s presence, but systemic conflicts of interest could still arise, such as agreements for fee splitting from referrals or commissions from pharmacies. As the number and kinds of medical services have exploded over the last half-century, so has the potential for clinicians to profit from the profligate use of these services. The practice of medicine now provides the entrepreneurial physician with ample opportunities to develop ancillary business interests, such as owning radiology and other diagnostic or therapeutic centers or equipment, even entire hospitals.[6] Clearly, the attendant financial gain in “self-referring” a patient for testing or intervention under such circumstances creates a conflict of interest as, logically, only a subset of patients will be likely to benefit from the additional procedures, whereas all patients (at least all those with the ability to pay) sent for testing or intervention would financially benefit the physician-owner. Empiric evidence amply demonstrates that such circumstances lead not simply to a perceived conflict of interest, but to a marked increase in utilization of services when compared to financially disinterested clinicians.[7],[8]

We’re primarily concerned with the ongoing treatment of diabetes, so, admittedly, there’s little to worry that your general practitioner will recommend visiting a radiologist in exchange for a small referral fee when presented with your potential blood sugar surges. There are, however, other ancillary service providers in the supply chain that would be happy to pay a small referral fee for a new customer, e.g., an endocrinologist, dietician, exercise trainer, laboratory technician. The predominant source of referrals, better stated, gifts, as the authors of the article suggest, are the pharmaceutical and medical device providers.

“Over the last several years, particular professional and public attention has been focused on conflicts of interest that arise from various relationships between the pharmaceutical and medical device industries and clinicians.[9] Businesses that happen to make drugs or medical devices have interests that are no different than those of other businesses: maximizing shareholder value, generally by increasing sales.[10] The profession of medicine, in general, and individual practitioners, in particular, continue to embrace a primary goal of improving and maintaining the health and well-being of individual patients. A conflict of interest develops when interactions with industry create circumstances in which the individual physician’s interest coincides with that of business, not patients. Beyond appearances, such conflicts have demonstrated the potential to alter physician practice in a manner that favors the pharmaceutical industry at the expense of the patient. Multiple specific interactions between industry and clinicians, including gift giving, consultancy arrangements, support of CME and guideline development, create conflicts of interest that vary in terms of effect, but each acts to bias the clinician away from patients and toward the interests of industry.”[11],[12]

And, in case you wondering about the percentage of doctors receiving these gifts, there was a study performed recently that provides that information. In “A National Survey of Physician-Industry Relationship,” (2007), the authors surveyed physicians to collect information about their financial associations with industry and the factors that predict those associations. They conducted a national survey of 3,167 physicians in six specialties (anesthesiology, cardiology, family practice, general surgery, internal medicine, and pediatrics) in late 2003 and early 2004. The raw response rate for this probability sample was 52%. Here are the results:

“Most physicians (94%) reported some type of relationship with the pharmaceutical industry, and most of these relationships involved receiving food in the workplace (83%) or receiving drug samples (78%). More than one third of the respondents (35%) received reimbursement for costs associated with professional meetings or continuing medical education, and more than one quarter (28%) received payments for consulting, giving lectures, or enrolling patients in trials. Cardiologists were more than twice as likely as family practitioners to receive payments. Family practitioners met more frequently with industry representatives than did physicians in other specialties, and physicians in solo, two-person, or group practices met more frequently with industry representatives than did physicians practicing in hospitals and clinics.”[13]

The results of this national survey indicate that relationships between physicians and industry are common and underscore the variation among such relationships according to specialty, practice type, and professional activities.

And as you delve deeper into the literature, specifically on the results of medical practice, the information can leave you feeling quite pessimistic. According to Dr. Joseph Mercola, in his popular natural health website:

“The traditional medical paradigm contains fatal flaws that have led to this startling statistic: doctors are the third leading cause of death in this country killing a quarter million people a year. Cancer and heart disease are the only two causes that have killed more people. Drugs, surgeries and hospitals are rarely the answer to chronic health problems. Diet, exercise, and lifestyle are the key components to staying healthy.”[14]

Hard to believe; but, if there was nothing to the theory of good doctors doing what they were trained to do with poor results, then surely if there were periods in recent memory without available doctors, we would see sickness and/or death rates increasing. Alas, the evidence points in the opposite direction. According to Barry Groves in TRICK AND TREAT: HOW ‘HEALTHY EATING’ IS MAKING US ILL, Israel, Canada, the US, and Columbia share a common occurrence:

“Doctors don’t often go on strike, but it has happened sufficiently often for a disturbing trend to be noticed. During the rare times that they have gone on strike—in several countries—the death rate has always gone down.”[15]

Once again, you’re probably a step ahead of this writing, so, yes, a read of DO WE STILL NEED DOCTORS by John D. Lantos, MD, may be indicated here.[16] Although it is an interesting book, the issues involved in the disintermediation of an entire channel from the marketplace are a bit overwhelming, so I won’t discuss here whether or not we need doctors other than to say that more likely than not—outside of acute emergency medical situations, and to prescribe basal insulin and delivery devices—as we will see, they probably need you more. The plain and simple fact is: we will see a doctor.

Whatever it is that doctors do—primarily consult with patients—potential customers have the perception that doctors may provide hope; they know or can at least access information and products that patients do not know or cannot access without the aid and support of, yes, doctors. We call this phenomenon “information asymmetry,” and sufficient demand for doctors is all the driving force necessary to incentivize a supply for them in the marketplace. Vice-versa, a supply of doctors in the marketplace will induce demand. When tastes, preferences, and population are held constant, the only true, measurable variables are the price paid for by patients, received by doctors, based upon the quantity of services exchanged between them. Service quality may be an assumption by those on the demand side, but aside from government- and industry-mandated requirements, not much else enters into the equation.

So let us now return to discuss this specific, real-life diabetic’s dilemma. There are two cases here: 1) you are not prepared with any information, or 2) you have done your homework. Let’s take a look first at those that are not prepared and, instead, will rely on their doctor to give the optimal treatment with the intent on following it.

The above table shows the asymmetrical relationship. Note that the real power comes from the health-provider’s strategy, as they ultimately decide which treatment the diabetic will follow, and, subsequently, the payoffs. Although the payoffs noted in the table are assertions, those assertions are based upon the evidence presented in the previous chapter. Recall that the first number is the payoff for the row player, the health-provider, and the second number is the payoff for the column player, the diabetic. The numbers themselves are somewhat arbitrary, however, they are used here for illustrative purposes; namely, that a low-fat diet, with corresponding necessity for a high consumption of carbohydrates, will lead to an increase in free radicals and oxidative stress in the body, and, if bolus insulin is taken, the risk of hypoglycemia is ever-present. When the health-provider recommends, and the diabetic follows, the low-fat diet, utilizing both basal and bolus insulin, and perhaps other drugs too, the diabetic’s payoff is -20.

“Health-provider” is a deliberately general title, as it may include all those influencers noted in the previous chapter and more, including pharmaceutical companies, pharmacists, researchers, doctors, endocrinologists, nutritionists, educators, the American Diabetes Association, the World Health Organization, medical schools, nurses, reference media such as the Physician’s Desk Reference, food manufacturers, food marketers, popular internet sites, print media, the news, friends, family, co-workers & acquaintances.

Moreover, the payoff at this point for the diabetic is -20 because the diabetic now returns again and again for checkups, providing a fee to the clinic each time; some of the stated health-providers, doctors especially, are in the business of patient management. This system keeps the dutiful patient coming back for regular doctor appointments, while at the same time keeping the pharmacist busy refilling prescriptions. And medical insurance coverage becomes an absolute necessity. Of course, the health-provider’s payoff is +20, because they’re the ones being paid. They espouse party-line mis-information due to the constraints of their clinical practice guidelines; and, given the perceived information asymmetry, most patients will believe them. The final irony is the report that physicians frequently choose low-carbohydrate diets for themselves while recommending low-fat for their patients.[17]

Now let’s imagine the case of a symmetrical relationship between health-providers and diabetics. In the next table, we’ll enable the diabetic with power of his/her own: the ability to make an informed choice regarding their treatment, based upon the insight imparted by cited authors.

In PRISONER’S DILEMMA, William Poundstone described how Dr. John Nash[18] proved that every two-person finite game has at least one equilibrium point, but that there are a few catches. These equilibrium points can have “strange and undesirable properties.” In fact, sometimes Nash equilibriums appear to be distinctly irrational.

The best solution for our diabetic is to always “insist on a low-carbohydrate diet.” This strategy earns, on average, 20 “points,” whereas, acquiescing to the health-provider earns, on average, zero. But contrast that to the health-provider’s strategies. On average, they receive 5 “points” for doing the right thing, whereas, if they always preach party-line, that is, advocate a low-fat diet with basal and bolus insulin, and perhaps other drugs, they will earn on average 12.5 “points.”

Is that not a strange and undesirable property? The client-health-provider relationship is now on its head. The payoff “incentivizes” all health-providers to advocate the deleterious diet plus ample meds. We—the patients—are now responsible for teaching and training them. And we pay the health-providers for the opportunity to do so.

Whether or not they can be trained is another matter entirely. We’ve seen that it is in their best interest to always choose the “advocate low-fat diet” strategy, and this is the diet based upon certain standards of care. Those standards of care, at least in North American and European societies, are called Clinical Practice Guidelines (CPGs), and they are intended to present a synthesis of current evidence and recommendations preformed by expert clinicians and may affect the practice of large numbers of physicians. As a result, any influence that the authors of CPGs experience from their interactions with pharmaceutical companies may be transmitted many times over to the readers of CPGs. Consequently, if individual authors have relationships that pose a potential conflict of interest, readers of these CPGs may wish to know about them to evaluate the merit of those guidelines.

In 2002, Niteesh K. Choudhry, M.D., Henry Thomas Stelfox, M.D., and Allan S. Detsky, M.D., Ph.D., surveyed authors of CPGs throughout North America and Europe to find out the extent to which the authors of CPGs interact with the pharmaceutical industry. They were seeking to provide empirical evidence concerning this issue to improve the process of CPG development in the future. Here are the conclusions from that study:

“Eighty-seven percent of authors had some form of interaction with the pharmaceutical industry. Fifty-eight percent had received financial support to perform research and 38% had served as employees or consultants for a pharmaceutical company. On average, CPG authors interacted with 10.5 different companies. Overall, an average of 81% (95% confidence interval, 70%-92%) of authors per CPG had interactions. Similarly, all of the CPGs for 7 of the 10 diseases included in our study had at least 1 author who had some interaction. Fifty-nine percent had relationships with companies whose drugs were considered in the guideline they authored, and of these authors, 96% had relationships that predated the guideline creation process. Fifty-five percent of respondents indicated that the guideline process with which they were involved had no formal process for declaring these relationships. In published versions of the CPGs, specific declarations regarding the personal financial interactions of individual authors with the pharmaceutical industry were made in only 2 cases. Seven percent thought that their own relationships with the pharmaceutical industry influenced the recommendations and 19% thought that their coauthors’ recommendations were influenced by their relationships.”[19]

Although the survey’s response rate was low,[20] there appears to be considerable interaction between CPG authors and the pharmaceutical industry.

The most interesting, and perhaps regrettable, part of the discussion on clinical practice guidelines, is that there isn’t one, universally accepted guideline for diabetes. There is one universally established way of looking at gravitation & gravity—gravitation is a general term describing the phenomenon by which bodies with mass are attracted to one another, while gravity refers specifically to the net force exerted by the Earth on objects in its vicinity as well as by other factors, such as the Earth’s rotation—but, like politics, there are many diabetes treatment paradigms.

There are guidelines written for type 1 and 2 diabetes from the American Association of Clinical Endocrinologists, the American Academy of Family Physicians, the American Geriatrics Society, the Canadian Diabetes Association, the Institute for Clinical Systems Improvement, the National Institute for Health and Clinical Excellence, the Scottish Intercollegiate Guidelines Network, and the Veterans Health Administration. In fact, each independent health-provider, or health-providing group may have their own clinical practice guidelines. Utilizing GOOGLE for a quick internet search of “Clinical Practice Guidelines Diabetes” returned 1,500,000 hits, where I found the 2009 Clinical Practice Guidelines for Malaysia, which, by the way, and, of course, encouraged a balanced diet consisting of 50-60% energy from carbohydrate, 15-20% energy from protein and 25-30% energy from fats, not to mention a high fibre diet.[21]

But one organization, the American Diabetes Association, provides the most commonly cited and adopted guidelines in the US, and, perhaps, throughout the world.

According to their website:

“The Association funds research to prevent, cure and manage diabetes; delivers services to hundreds of communities; provides objective and credible information; and gives voice to those denied their rights because of diabetes. Founded in 1940, our mission is to prevent and cure diabetes and to improve the lives of all people affected by diabetes.”[22]

Quite a noble mission. In fact, they do allocate millions of dollars per year toward research; in 2008, it was approximately $43 million.[23] But our focus here is not the relative good that they do in the world, for surely a person with type 1 diabetes that eats carbohydrates and undergoes an intensive insulin regimen is far better off than one that solely eats carbohydrates at will, given that their body’s cells lack an effective glucose uptake mechanism. Rather, it is the inherent conflict between the ADA’s conclusions promulgated through guidelines, and who supports that platform, that is of particular concern.

Cutting to the chase, the ADA works in its own best interest as evidenced by the following, taken directly from their conflict of interest policy:

“The American Diabetes Association and its subsidiaries (collectively, the Association) requires all members of the Board of Directors, members of Board-appointed committees and staff to act solely in the best interest of the Association without regard to their personal or business interests.”[24]

The ADA isn’t as altruistic as one would like to believe. They don’t act primarily in the interest of diabetics; but, instead, in their own best interest, and, at least in appearance, based upon their guidelines—as we will shortly see—in the interest of their main stakeholders. But just who are their main stakeholders? According to the ADA’s strategic plan, the folks that have the deepest pockets from which the ADA will base their growth upon are the corporate and pharmaceutical organizations, for whom the following strategy applies:

“Maximize corporate, pharmaceutical and foundation contributions to achieve revenue of $42 million, which reflects an annual compound growth rate of 9.1%.”[25]

Nothing at first can appear more difficult to believe than that the American Diabetes Association, a credible, long-standing institution in the community, does not necessarily act in the best interest of those most negatively affected by the complications of diabetes. The truth of the following assertion, however, cannot be disputed: the only way to get pharmaceutical companies to contribute at that level, i.e., $42,000,000 per year, and at that growth rate, i.e., 9.1%, is to serve their interests; the only way to effect that is to directly or indirectly support the use of their products, which, of course, are the many insulins and their compliments. And the only way to support that endeavor is to espouse carbohydrates as an essential source of energy. A source of energy; yes, exogenous carbohydrates are that. An essential source of energy? No. Homo sapiens can manufacture their own glucose in the liver after the ingestion and digestion of exogenous fat and protein.[26]

So let’s now look a little more closely at the ADA’s Guidelines. I’ll call this story “The Tale of the Tell.”

As late as 2006 and 2007, the ADA’s position, promulgated sedulously through their guidelines, was that “Low-carbohydrate diets (restricting total carbohydrate to <130 g/day) are not recommended in the management of diabetes,” and that “Saturated fat intake should be <7% of total calories.”[27] The ADA in 2006 wrote:

“Low-carbohydrate diets are not recommended in the management of diabetes. Although dietary carbohydrate is the major contributor to postprandial glucose concentration, it is an important source of energy, water-soluble vitamins and minerals, and fiber. Thus, in agreement with the National Academy of Sciences-Food and Nutrition Board, a recommended range of carbohydrate intake is 45–65% of total calories. In addition, because the brain and central nervous system have an absolute requirement for glucose as an energy source, restricting total carbohydrate to <130 g/day is not recommended.”[28]

They went on to state:

“Similar to the general population, people with diabetes are encouraged to choose a variety of fiber-containing foods, such as legumes, fiber-rich cereals (≥5 g fiber/serving), as well as fruits, vegetables, and whole-grain products because they provide vitamins, minerals, fiber, and other substances important for good health.”[29]

And, of course, the Guidelines were based upon the DCCT:

“The DCCT clearly showed that intensive insulin therapy (three or more injections per day of insulin or continuous subcutaneous insulin infusion (CSII, or insulin pump therapy) was a key part of improved glycemia and better outcomes. At the time of the study, therapy was carried out with short- and intermediate-acting human insulins. Despite better microvascular outcomes, intensive insulin therapy was associated with a marked increase in severe hypoglycemia (62 episodes per 100 patient-years of therapy). Since the time of the DCCT, a number of rapid-acting and long-acting insulin analogs have been developed. These analogs were designed to be more “physiological” in their pharmacokinetics and pharmacodynamics and are associated with less hypoglycemia with equal A1C lowering in type 1 diabetes.

Therefore, recommended therapy for type 1 diabetes consists of the following components: 1) use of multiple dose insulin injections (3–4 injections per day of basal and prandial insulin) or CSII therapy; 2) matching of prandial insulin to carbohydrate intake, premeal blood glucose, and anticipated activity; and 3) for many patients (especially if hypoglycemia is a problem), use of insulin analogs. There are excellent reviews available that guide the initiation and management of insulin therapy to achieve desired glycemic goals.”[30]

And in 2007, not much had changed:

“Low-carbohydrate diets (restricting total carbohydrate to <130 g/day) are not recommended in the treatment of overweight/obesity [or in diabetes]. The long-term effects of these diets are unknown, and although such diets produce short-term weight loss, maintenance of weight loss is similar to that from low-fat diets and the impact on CVD risk profile is uncertain.”[31]

But then in 2008, what seems like a sea-change occurred in the ADA’s Guidelines. For the first time, the ADA added the following:

“For weight loss, either low-carbohydrate or low-fat calorie-restricted diets may be effective in the short term (up to 1 year).”[32]

Though a subtle caveat was placed on the low-carbohydrate diet:

“For patients on low-carbohydrate diets, monitor lipid profiles, renal function, and protein intake (in those with nephropathy), and adjust hypoglycemic therapy as needed.”[33]

And although I have been able to find hundreds of studies concluding then espousing the efficacy of low-carbohydrate diets, the ADA justified their position with only three:

“The optimal macronutrient distribution of weight loss diets has not been established. Although low-fat diets have traditionally been promoted for weight loss, several randomized controlled trials found that subjects on low-carbohydrate diets (<130 g/day of carbohydrate) lost more weight at 6 months than subjects on low-fat diets; however, at 1 year, the difference in weight loss between the low-carbohydrate and low-fat diets was not significant and weight loss was modest with both diets. Another study of overweight women randomized to one of four diets showed significantly more weight loss at 12 months with the Atkins low-carbohydrate diet than with higher-carbohydrate diets. Changes in serum triglyceride and HDL cholesterol were more favorable with the low-carbohydrate diets. In one study, those subjects with type 2 diabetes demonstrated a greater decrease in A1C with a low-carbohydrate diet than with a low-fat diet. A recent meta-analysis showed that at 6 months, low-carbohydrate diets were associated with greater improvements in triglyceride and HDL cholesterol concentrations than low-fat diets; however, LDL cholesterol was significantly higher on the low-carbohydrate diets.”[34]

Still, the ADA, in 2008, remained firmly planted in making sure folks ingest their 130 grams of carbohydrates per day:

“The recommended dietary allowance (RDA) for digestible carbohydrate is 130 g/day and is based on providing adequate glucose as the required fuel for the central nervous system without reliance on glucose production from ingested protein or fat. Although brain fuel needs can be met on lower-carbohydrate diets, long-term metabolic effects of very-low-carbohydrate diets are unclear, and such diets eliminate many foods that are important sources of energy, fiber, vitamins, and minerals and are important in dietary palatability.”[35]

And the DCCT continued to be cited as the holy grail:

“Glycemic control is fundamental to the management of diabetes. The DCCT, a prospective, randomized, controlled trial of intensive versus standard glycemic control in type 1 diabetes, showed definitively that improved glycemic control is associated with sustained decreased rates of microvascular (retinopathy and nephropathy) as well as neuropathic complications. Follow up of the DCCT cohorts in the Epidemiology of Diabetes Interventions and Complications (EDIC) study has shown persistence of this effect in previously intensively treated subjects, even though their glycemic control has been equivalent to that of previous standard arm subjects during follow-up. In addition, EDIC has shown a significant reduction of the rate of cardiovascular outcomes in the previous intensive arm.

The DCCT clearly showed that intensive insulin therapy (three or more injections per day of insulin or continuous subcutaneous insulin infusion [CSII, or insulin pump therapy]) was a key part of improved glycemia and better outcomes. At the time of the study, therapy was carried out with short- and intermediate-acting human insulins. Despite better microvascular outcomes, intensive insulin therapy was associated with a marked increase in severe hypoglycemia (62 episodes per 100 patient-years of therapy). Since the time of the DCCT, a number of rapid-acting and long-acting insulin analogs have been developed. These analogs were designed to be more “physiological” in their pharmacokinetics and pharmacodynamics, and are associated with less hypoglycemia with equal A1C lowering in type 1 diabetes.

The 2009 ADA Guidelines are replicated from those of 2008. The DCCT continues to serve as the foundation of their Guidelines—the foundation to a house of cards—as it “clearly showed that intensive insulin therapy was a key part of improved glycemia and better outcomes.” Yet I, and countless others, who simply don’t eat many carbohydrates, and therefore haven’t a need for an intensive insulin treatment, able to keep our glucose levels within a normal range, simply, effectively, and efficiently, wonder not who holds the extreme, unsupported view.

William Poundstone stated at the end of his book that “The only satisfying solution to the prisoner’s dilemma is to avoid prisoner’s dilemmas.”[37] Options in applying that to our situation are rather limited. Clearly, not getting diabetes is the ideal. Not sure how to accomplish that with any level of confidence, so let’s move on to something a little more promising. A vaccine—two such vaccines in the works are GAD-alum and BCMA—might be a little late for type 1s without any remaining beta function, but if they can save the beta cells of anyone, then I’m all for it.[38]

One could simply live in a state of denial, eating carbohydrates at will, not checking their BG, too, not seeing any health providers. Yes, it is a simple option, though, not very effective or efficient.

We’re really left with one simple, inexpensive, non-time consuming, effective, efficient option. It is both the way to solve and the way to avoid the prisoner’s dilemma. And we’ve known about it, sans the basal insulin, for centuries.

[1] The statements “This book is written…” and “shall continue to add footnotes…” and “I wrote this book…” are all from the first paragraph of the Preface to Dawkins, Richard. The Blind Watchmaker: Why the Evidence of Evolution Reveals a Universe Without Design. New York: W.W. Norton & Company, page XV. Of course, he was referring to “our own existence” and not an optimal solution to diabetes, however, the constructs fit so well in this book’s context that I just had to use them.

[2] See Poundstone, William. Prisoner’s Dilemma; John Von Neumann, Game Theory, and the Puzzle of the Bomb. New York: Doubleday, 1992, pages 117-119.

[3] For a particularly good discussion of Plato’s The Republic and the role of doctors, see Terence Irwin’s Plato’s Ethics (Oxford University Press, 1995, pages 351-352). “Does Plato expect anything more from people with wisdom than he would expect from them if they simply had correct belief? In some striking and important passages of the Laws, Plato makes it clear that he expects them to display one distinguishing feature of knowledge in contrast to belief. They must understand why the things they are told are right and good really are right and good; they must not simply take other people’s word for it. To explain this demand, Plato introduces a comparison with doctors. On the one hand, the slave doctor, who also gives treatment to slaves, just gives instructions without giving any reason for them. The free doctor, on the other hand, who treats free people, explains why the treatment prescribed is the best one for the patients. Instead of simply giving orders, the free doctor discusses the patients’ conditions with them and tells them enough to persuade them that the treatment being prescribed is the best one for them (719e7-720e5 in The Republic). This discussion involves communicating some theortetical understanding to the patient...”

[4] Stell, L Two cheers for physicians’ conflicts of interest. Mt Sinai J Med 2004;71,236-242. Available online at http://www.ncbi.nlm.nih.gov/pubmed/15365589?dopt=Abstract. Retrieved on 3/14/09.

[5] McDowell, TJ Physician self referral arrangements: legitimate business or unethical “entrepreneurialism.” Am J Law Med 1989;15,61-109. Available online at http://www.ncbi.nlm.nih.gov/pubmed/2764015?dopt=Abstract. Retrieved on 3/14/09.

[6] Moore, N Entrepreneurial doctors and lawyers: regulating business activity in the medical and legal professions. Spece, R Shimm, D Buchanan, A eds. Conflicts of interest in clinical practice and research 1996,171-196, New York, NY: Oxford University Press.

[7] Kouri, B, Parsons, R, Alpert, H Physician self-referral for diagnostic imaging: review of the empiric literature. AJR Am J Roentgenol 2002;179,843-850. Available online at http://www.ajronline.org/cgi/content/full/179/4/843?ijkey=9700ac1ab1459c8a27e2b9a0084d5137b80d8ec2&keytype2=tf_ipsecsha. Retrieved on 3/14/09. See also Mitchell, J, Sass, T Physician ownership of ancillary services: indirect demand inducement or quality assurance? J Health Econ 1995;14,263-289. Available online at http://www.ncbi.nlm.nih.gov/pubmed/10145136?dopt=Abstract. Retrieved on 3/14/09. See also Nallamothu, B, Rogers, M, Chernew, M, et al Opening of specialty cardiac hospitals and use of coronary revascularization in Medicare beneficiaries. JAMA 2007;297,962-968. Available online at http://jama.ama-assn.org/cgi/content/abstract/297/9/962?ijkey=bfc824f70f476933c2c4d63f1fa858999211ce44&keytype2=tf_ipsecsha. Retrieved on 3/14/09.

[8] See Tonelli, M.D., M.A., FCCP, Mark R. “Conflict of Interest in Clinical Practice,” Chest August, 2007, vol. 132, no. 2, 664-670. doi: 10.1378/chest.07-0315. Available online at http://www.chestjournal.org/content/132/2/664.full#ref-21. Retrieved on 3/14/09.

[9] Angell, M The Truth About Drug Companies. 2004 Random House. New York, NY. See also Kassirer, J On the Take: How Medicine’s Complicity with Big Business Can Endanger Your Health. 2004 Oxford University Press. New York, NY. See also Blumenthal, D Doctors and drug companies. N Engl J Med 2004;351,1885-1890. Available online at http://content.nejm.org/cgi/content/full/351/18/1885?ijkey=0423b68ab05b7d39ec9e9bbd72d1f905e82f10da&keytype2=tf_ipsecsha. Retrieved on 3/14/09. “Interactions between drug companies and doctors are pervasive. Relationships begin in medical school, continue during residency training, and persist throughout physicians’ careers. The pervasiveness of these interactions results in part from a huge investment by the pharmaceutical industry in marketing. In 2002, the industry expended 33 percent of its revenues on "selling and administration.” In 2001, one company, Novartis, reported spending 36 percent of its revenues on marketing alone. The marketing expenditures of the drug industry have been estimated variously at $12 billion to $15 billion yearly, or $8,000 to $15,000 per physician. In 2001, the industry's sales force of drug detailers, whose job is to meet individually with physicians and promote company products, numbered nearly 90,000 in the United States—1 salesperson for every 4.7 office-based physicians.”

[10] Kassirer, J. On the Take: How Medicine’s Complicity with Big Business Can Endanger Your Health. New York: Oxford University Press, 2004.

[11] Moynihan, R Who pays for the pizza? Redefining the relationships between doctors and drug companies: 1. Entanglement. BMJ 2003;326,1189-1192. Available online at http://www.bmj.com/cgi/content/full/326/7400/1189?ijkey=1d0ba84bbe6c5e26d9cc59d1ab5e10bef47b6921&keytype2=tf_ipsecsha. Retrieved on 3/14/09.

[12] See Tonelli, M.D., M.A., FCCP, Mark R. “Conflict of Interest in Clinical Practice,” Chest August, 2007, vol. 132, no. 2, 664-670. doi: 10.1378/chest.07-0315. Available online at http://www.chestjournal.org/content/132/2/664.full#ref-21. Retrieved on 3/14/09.

[13] See “A National Survey of Physician-Industry Relationship,” Campbell EG, Gruen RL, Mountford J, Miller LG, Cleary PD, Blumenthal D. N Engl J Med. 2007 Apr 26;356(17):1742-50. Available online at http://content.nejm.org/cgi/content/full/356/17/1742. Retrieved on 3/14/09.

[14] See “Why do Doctors Use Treatments That Don't Work?” online at http://articles.mercola.com/sites/articles/archive/2004/03/13/doctor-treatments.aspx. Retrieved on 4/18/08. There are many more articles available on Dr. Mercola’s website on point. See, for example, “Medical Research or Drug Company Secrets?” online at http://articles.mercola.com/sites/articles/archive/2002/11/20/drug-companies-part-nine.aspx; “The Doors Of Perception: Why Americans Will Believe Almost Anything,” at http://articles.mercola.com/sites/articles/archive/2001/08/15/perception.aspx; “Drugs and Doctors May be the Leading Cause of Death in U.S.” at http://articles.mercola.com/sites/articles/archive/2003/01/15/doctors-drugs-part-two.aspx; “Doctors Are The Third Leading Cause of Death in the US, Causing 250,000 Deaths Every Year,” at http://articles.mercola.com/sites/articles/archive/2000/07/30/doctors-death-part-one.aspx; “Why Doctors Are 9,000 Times More Likely to Accidentally Kill You Than Gun Owners,” at http://articles.mercola.com/sites/articles/archive/2000/05/14/doctor-accidents.aspx; and “Shame: A Major Reason Why Most Medical Doctors Don't Change Their Views,” at http://articles.mercola.com/sites/articles/archive/2002/03/30/doctors-shame.aspx. All online articles retrieved on 4/18/09.

[15] See Groves, Barry. Trick and Treat: How ‘Healthy Eating’ is Making us Ill. London, UK: Hammersmith Press Limited, 2008, pages 30-31. Used by permission

[16] For a compeling discussion from the point of view of a practicing medical doctor and ethicist, see Lantos, John D. Do We Still Need Doctors: A Physician’s Personal Account of Practicing Medicine Today. New York: Routledge, 1997.

[17] See La Puma J, Szapary P, Maki KC. Physicians recommendations for and personal use of low-fat and low-carbohydrate diets. Int J Obes Relat Metab Disord. 2005;29:251–253. doi: 10.1038/sj.ijo.0802840. Available online at http://www.ncbi.nlm.nih.gov/pubmed/15534615. Retrieved on 7/29/09.

I am grateful to the authors Surender K Arora and Samy I McFarlane, as the quote comes from their article entitled: “The Case for Low Carbohydrate Diets in Diabetes Management,” Nutr Metab (Lond). 2005; 2: 16. Published online 2005 July 14. doi: 10.1186/1743-7075-2-16. PMCID: PMC1188071. Available online at http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1188071. Retrieved on 7/29/09.

[18] The subject of the film A Beautiful Mind was John Forbes Nash, Jr. Dr. Nash did not have diabetes, but he was the most notable of the schizophrenic patients treated in the Insulin Coma Unit at Trenton Psychiatric Hospital (TPH) in West Trenton, New Jersey, in 1961. An American mathematician and economist whose works in game theory, differential geometry, and partial differential equations provided insight into the forces that govern chance and events inside complex systems in daily life, his theories are still used today in market economics, computing, accounting and military theory. Serving as a Senior Research Mathematician at Princeton University during the later part of his life, he shared the 1994 Nobel Memorial Prize in Economic Sciences with game theorists Reinhard Selten and John Harsanyi.

In 1961, John was committed by Alicia and his sisters to Trenton State Hospital in New Jersey. There, he was subjected to insulin-coma therapy, which involved injecting the patient with large amounts of insulin to put them into a coma, often causing seizures. His colleagues in mathematics were outraged and wrote a letter to the hospital, urging the doctors to protect his mind for the good of humanity. He was discharged after six months of the insulin treatment and looked absolutely terrible to his family members.

Dr. Manfred Sakel, a Viennese psychiatrist, developed the technique of Insulin Coma Therapy (ICT) in 1928 and introduced it to the United States in 1936. Nondiabetic patients with schizophrenia and major depression were treated with ICT 5 days a week for 6 weeks.

The insulin unit at TPH treated 24 males and 24 females daily in separate wards. The initial dose of regular insulin was 10–20 units administered intramuscularly at 7:00 a.m. in the unit; the dose was increased by about 10 units per day to about 90–100 units until hypoglycemic coma developed. A team of trained nurses and physicians supervised the care of the patients, who rested on litters. In some patients, more than 100 units of insulin were needed to produce coma.

After 30–60 minutes of hypoglycemic coma, nurses reversed the condition by intragastric glucose solution or Karo syrup. Patients were carefully observed until cognitive, returned to their room, and then provided meals and snacks.

In her book A Beautiful Mind, Sylvia Nasar reports that Dr. Nash first showed the overt signs of schizophrenia in 1959 when he began to see encrypted messages in newspaper stories. He was teaching at the Massachusetts Institute of Technology and after a poorly presented lecture in March, he was involuntarily committed to the McLean Hospital, a private hospital for wealthy patients affiliated with the Harvard Medical School in Boston.

He received injections of chlorpromazine but the principal treatments offered were psychotherapy, group therapy, and counseling. After a stay of 50 days, he was released. In May, his wife gave birth to a son. He was not able to return to work, and for the next two years, in the grip of a persistent psychosis, he roamed Europe.

He underwent 6 weeks of insulin coma treatment. When he was released from the hospital, he was much improved. His thoughts were under control and he was able to once again work on a scientific paper. From July of 1961 to August 1962, he worked at Princeton.

His illness recurred and sadly, further treatment was refused. He spent the next decades as a shadowy figure on the Princeton University campus.

Why was Dr. Nash treated with ICT? In 1961, the options available for patients with schizophrenia were antipsychotic drugs, Electroconvulsive Therapy (ECT), insulin coma, and lobotomy. The optimal treatment was believed to be chlorpromazine, although many psychiatrists still looked to ECT for its benefits. When chlorpromazine failed, ECT was the realistic option. While most psychiatric hospitals had abandoned ICT, it had persisted at Trenton State Hospital, and it was a logical offering when these other treatments were refused. (Lobotomy was no longer a realistic option, having been replaced by antipsychotic drugs.)

For biographical information see the Wikipedia article entitled “John Forbes Nash, Jr.” online at http://en.wikipedia.org/wiki/John_Forbes_Nash; see also http://nobelprize.org/nobel_prizes/economics/laureates/1994/nash-autobio.html. Both retrieved on 3/14/09. See also http://www.pbs.org/wgbh/amex/nash/filmmore/ps_ict.html. Retrieved on 3/1/09.

For information about IST, see Sakel M: The Pharmacological Shock Treatment of Schizophrenia. New York, Nervous and Mental Diseases Publishing Co., 1938. See also Sakel M: The Insulin Treatment of Schizophrenia. In An Introduction to Physical Methods of Treatment in Psychiatry. 1st edition. Sargent W, Slater E, Eds. Edinburgh, U.K., E. & S. Livingstone, 1944. See also Fink, M., Shaw, R., Gross, G., and F. S. Coleman. “Comparative study of chlorpromazine and insulin coma in the therapy of psychosis.” Journal of the American Medical Association. 1958; 166:1846-50. See also Rinkel, M., and H. E. Himwich. Insulin Treatment in Psychiatry. New York: Philosophical Library, 1959.

See also Arthur Krosnick, MD, FACP, CDE, “Five Decades of Diabetes Patient Care: The Time of My Life,” Clinical Diabetes 20:173-178, 2002.

And see Nasar S. A Beautiful Mind. New York: Simon & Schuster, 1961, pages 288-294.

[19] See “Guidelines and the Pharmaceutical Industry Relationships Between Authors of Clinical Practice,” by Niteesh K. Choudhry, Henry Thomas Stelfox, and Allan S. Detsky. JAMA. 2002;287(5):612-617; doi: 10.1001/jama.287.5.612. Available online at http://jama.ama-assn.org/cgi/reprint/287/5/612.pdf. Retrieved on 6/13/09.

[20] “One hundred twenty CPGs were identified by our search strategy, of which 35 were excluded because a major North American or European society did not endorse the CPG and 38 were excluded because they were editorials about CPGs or comparisons of different CPGs. Therefore, 47 CPGs were initially included. Subsequently, 1 CPG was excluded because the authors could not be identified and 2 CPGs were excluded after the authors had been surveyed since these were evaluations of CPGs rather than actual CPGs. Therefore, 44 CPGs with 192 authors were included in the study.

Current addresses of 13 authors could not be located and 3 authors had died, resulting in a total of 176 potentially contactable authors. Of these, 107 authors (61%) responded representing 37 of the 44 CPGs included in our study. Therefore, 7 guidelines were not represented in our final sample. Despite this, all of the disease states that were initially included in our study protocol were still represented by at least 2 CPGs, with the exception of depression, for which there was only 1 CPG included in the sample and for which we received a response. Seven respondents refused to participate, all of whom were involved with different guidelines. Three of these 7 authors were from Europe, 2 were from the United States, and 2 were from Canada. This left 100 completed surveys, which form the basis of our results. Overall, the response rate was 57% of potentially contactable authors and 52% of all authors initially included in our sample. The distribution of sex and disease to which the guidelines pertained was similar for respondents and nonrespondents; however, the distribution of current country of residence was not. Sixty-three percent of authors currently residing in the United States did not respond whereas 29% of authors living in Canada did not respond (P=.001). Twenty-eight (26%) of 107 authors responded with a letter attached to their survey. These letters could be interpreted as being supportive (21%), neutral (57%), or critical (21%) of our study. Of the 100 authors who completed the first survey, 1 had died and 1 had moved and was unreachable, leaving 98 potentially contactable authors for the second survey. Of these, 82 (83%) responded. One of these authors refused to participate and 1 could not recall the nature of the disclosure process and, therefore, left the survey blank. Consequently, the response rate for the second survey was 82%.” See Ibid.

[21] See “Clinical Practice Guidelines. Management of Type 2 Diabetes Mellitus (4th Edition),” May, 2009. Malaysian Endocrine & Metabolic Society, Ministry of Health Malaysia, Academy of Medicine Malaysia, and Persatuan Diabetes Malaysia. Available online at http://www.diabetes.org.my/article.php?aid=590. Retrieved on 7/27/09.

[22] Available online at http://www.diabetes.org/aboutus.jsp?WTLPromo=HEADER_aboutus&vms=302103524165. Retrieved on 7/28/09.

[23] See the ADA 2008 Consolidated Financials online at http://www.diabetes.org/uedocuments/2008_ADA_ConsolidatedFinancialsFS_Final.pdf. Retrieved on 7/38/09.

[24] See the American Diabetes Association “About Us” page online at http://www.diabetes.org/aboutus.jsp?WTLPromo=HEADER_aboutus&vms=302103523106. Retrieved on 7/28/09.

[25] American Diabetes Association 2008-2011 Strategic Plan. Available online at http://www.diabetes.org/uedocuments/2008-2011ADAStrategicPlan.pdf. Retrieved on 7/28/09.

[26] What limits the liver’s capacity to convert amino acids to glucose? “Conversion of amino acids to glucose involves several metabolic processes; deamination or transamination, conversion of the released NH4+ to urea and finally synthesis of glucose from amino acid residues. The key to understanding the physiological limitation of glucose formation from amino acids lies in the large amount of energy required to fuel these processes. Energy in the sense used here means the hydrolysis of adenosinetriphosphate (ATP) to either AMP + PPi or ADP + Pi. Four ATP molecules are used to convert two NH4+ to urea and six more are required to convert the carbon skeletons of these amino acids to glucose. One ATP is also required to add a glucosyl group to a glycogen molecule so, you see, a lot of energy is used in this process. All cells and tissues are built up such that ATP levels are relatively stable. This is a basic prerequisite for life. Under gluconeogenesis the liver must rely upon aerobic metabolism to replace the ATP that is consumed. By definition this is an oxygen-dependent process. The “catch” is that the liver obtains most of its oxygen from the portal vein where the partial pressure of oxygen is rather low. This limits uptake of oxygen, limits ATP production and, therefore, the synthesis of glucose from amino acids. We have data about the total amount of oxygen supplied to the human liver. Calculations based on this (and assuming that all of this oxygen goes to support conversion of amino acids to glucose) suggest that the maximum capacity of hepatic glucose synthesis from amino acids lies around 400 grams/day. This is the equivalent of approximately 1600 kcal...” See “Rabbit Starvation: High Protein and High Fat Diets,” by Professor Emeritus Robert S. Horn. Available online at http://www.medbio.info/Horn/PDF%20files/rabbit%20starvation.pdf. Retrieved on 12/16.09.

[27] See “Standards of Medical Care in Diabetes—2006,” Diabetes Care, January, 2006, vol. 29, no. suppl 1 s4-s42. Available online at http://care.diabetesjournals.org/content/29/suppl_1/s4.full. Retrieved on 7/27/09.

[28] Ibid.

[29] Ibid.

[30] Ibid.

[31] See “Standards of Medical Care in Diabetes—2007,”doi: 10.2337/dc07-S004. Diabetes Care, January, 2007, vol. 30, no. suppl 1 S4-S41. Available online at http://care.diabetesjournals.org/content/30/suppl_1/S4.full. Retrieved on 7/28/09.

[32] See “Standards of Medical Care in Diabetes—2008,” doi: 10.2337/dc08-S012. Diabetes Care, January, 2008, vol. 31, no. Supplement 1 S12-S54. Available online at http://care.diabetesjournals.org/content/31/Supplement_1/S12.full. Retrieved on 7/28/09.

[33] Ibid.

[34] Ibid.

[35] Ibid.

[36] Ibid.

[37] Poundstone, William. Prisoner’s Dilemma: John Von Neumann, Game Theory, and the Puzzle of the Bomb. New York: Doubleday, 1992, page 278.

[38] See “GAD Treatment and Insulin Secretion in Recent-Onset Type 1 Diabetes,” by Johnny Ludvigsson, M.D., Ph.D., Maria Faresjö, Ph.D., Maria Hjorth, M.Sc., Stina Axelsson, M.Sc., Mikael Chéramy, M.Sc., Mikael Pihl, M.Sc., Outi Vaarala, M.D., Ph.D., Gun Forsander, M.D., Ph.D., Sten Ivarsson, M.D., Ph.D., Calle Johansson, M.D., Agne Lindh, M.D., Nils-Östen Nilsson, M.D., Jan Åman, M.D., Ph.D., Eva Örtqvist, M.D., Ph.D., Peter Zerhouni, M.Sc., and Rosaura Casas, Ph.D. The New England Journal of Medicine, Volume 359:1909-1920, October 30, 2008, Number 18. Available online at http://content.nejm.org/cgi/content/full/359/18/1909. Retrieved on 5/30/09. See also http://www.dvdc.org.au/. Retrieved on 5/30/09. See also http://www.jdrf.org.au/news/view/research-breakthrough-type-1-diabetes-vaccine-a-step-closer. Retrieved on 5/30/09.

Transcend Diabetes

2012-07-21T13:52:00.000-07:00

Most of our lives we are caught up in the moment. Let’s now take a moment to look at diabetes from 10,000 feet up, where we can see clear patterns and insight emerge from the fog of hypoglycemia, and its opposite, hyperglycemia. If we plot carbohydrate consumption from low to high on the y-axis, and injected, fast acting (bolus) insulin from low to high on the x-axis, we can see all possible combinations of expected results on the following matrix:

When injected bolus insulin is low or zero, and carbohydrate consumption is high, we are presented with the classical triad of diabetes symptoms: polyuria, polydipsia, and polyphagia: respectively, frequent urination, increased thirst and consequent increased fluid intake, and increased appetite. Other manifestations will include weight loss (despite normal or increased eating), irreducible fatigue, and changes in the shape of the lenses of the eyes, resulting in vision changes.

When the glucose concentration in the blood is raised beyond the renal threshold, reabsorption of glucose in the proximal renal tubuli is incomplete, and part of the glucose remains in the urine, which is called glycosuria.

Surrounding this cell on the matrix is hyperglycemia, both to the right, when carbohydrates consumed are high and injected insulin is moderate, but not enough to cover the load, and below, when a decrease in carbohydrates is consumed, but still not offset enough by injected insulin.

In the middle of the chart, where one eats a moderate amount of carbohydrates and injects a moderate amount of bolus insulin, lies the typical diabetes treatment. “Eat a balanced diet and learn to adjust your insulin accordingly” is the principal treatment that is followed here. It is possible to attain near-normal A1c levels with this approach, however, normal levels of cholesterol, weight, and blood pressure may prove unreachable.

Furthermore, this area of the table is fraught with negative consequences at nearly all adjacent and opposite borders. Not enough insulin puts one in hyperglycemia territory both to the left and above. Not enough carbohydrates, and one finds themselves hypoglycemic to the right and below.

Too, if carbohydrates and insulin injected are high, the result is a hyper-hypo-glycemic swing—a rollercoaster ride if you will—of great magnitude, where the patient is constantly adjusting carbohydrate and insulin loads to offset their blood sugar.

But look what happens when both carbohydrates consumed and insulin injected are as low as possible. At the far lower-left cell of the matrix, one doesn’t eat a great many carbohydrates, and, subsequently, does not need to inject much insulin as a result. In this case, one can achieve a stable and normal blood sugar concentration, and enjoy the benefits of a normal life: lower VLDLs, higher HDLs, stable or decreasing weight, and less anxiety not having to think about whether one has injected the right amount of insulin. And testing can be reduced to once a day, in the morning, to validate your successful Insulin Glargine dosing, i.e., whether or not your morning BG is in the 70-110 mg/dL range. This home base is where thriving begins.

At the zero bolus-insulin and near-zero carbohydrate home, you may thrive for a long, long time. There are three major centenarian studies going on around the world, the New England Centenarian Study, the Georgia Centenarian Study and the Okinawa Centenarian Study. According to Dr. Ron Rosedale:

They are trying to find the variable that would confer longevity among this group of people who live to be 100 years old. Why do centenarians become centenarians? Why are they so lucky? Is it because they have low cholesterol, exercise a lot and live a healthy, clean life?

What researchers are finding from these major centenarian studies is that there is hardly anything in common among these people. They have high cholesterol and low cholesterol, some exercise and some don't, some smoke, some don't. Some are nasty as can be, some nice and calm and some are ornery. But, they all have relatively low sugar for their age, and they all have low triglycerides for their age. And, they all have relatively low insulin…The way to treat virtually all of the so-called chronic diseases of aging is to treat insulin itself” (“Insulin and its Metabolic Effects,” Ron Rosedale, Signs for Health Institute’s BoulderFest, August, 1999).

Although the use of exogenous bolus insulin as a treatment to mitigate the effects of carbohydrate consumption was innovative, exciting, and promising nearly a century ago, its use has become—save on the acutely serious hyperglycemic—obsolete with the introduction of Insulin Glargine, and the knowledge that carbohydrates are non-essential.

A remarkable picture develops when you take those three highlighted cells from the previous figure and place them on two different axes, one a continuum of complexity from low to high, and the other, a continuum of knowledge, skill, efficiency, and effectiveness, again, from low to high.

The y-axis, complexity, relates to the treatment—medication & nutrition—and lifestyle a person implements or recommends. Regarding the x-axis, knowledge, skill, efficiency, and effectiveness, it could be looked at from two perspectives; one, from a diabetic’s perspective, where the focus is on their knowledge & skill as it relates to implementing advice from a third-party or self-directed behavior, and another, from the perspective of a third-party’s knowledge & skill, be it friend, relative, caregiver, nutritionist, nurse, or doctor. Treatment efficiency and effectiveness in either case is also measured.

The lowest complexity matched with the lowest skill & knowledge, will result in a diabetic on the brink. It is quite easy for them to eat carbohydrates at will and develop the hyperglycemic symptoms of full-blown diabetes: polyuria, glycosuria, polydipsia, polyphagia, ketoacidosis, weight loss, etc., culminating in shortened life span. Knowledge for the patient about diabetes may be non-existent, and they will likely seek out medical attention for help, though, unfortunately, some don’t or for many reasons even if they do, helpful advice is not available. Acquaintances will also most likely notice the change in persona or appearance, and they too will make it a point to tell the person that something is wrong.

“Diabetes Managed” represents a diabetic trying to follow the instructions and advice of his or her general practitioner, though both are influenced by a wide variety of stakeholders with oftentimes divergent self-interests. A majority of the influencers in the medical advice providing supply chain include:

· Pharmaceutical companies

· Researchers

· Doctors

· Endocrinologists

· Nutritionists

· Educators

· American Diabetes Association

· World Health Organization

· Medical schools

· Nurses

· Reference media such as the Physician’s Desk Reference

· Food manufacturers

· Food marketers

· Popular internet sites, print media & the news

· Friends, family, co-workers & acquaintances

By default, advocates of each group act in their own perceived best interest, based upon their knowledge and skill, which may in turn be based upon the state of information available at their time of training or education. Many of the above stakeholders, with the exception of the end users themselves—the people with diabetes—have significant power. In fact, some have a near-absolute advantage in the marketplace—the ability to influence behavior without question or pause—leaving the buyer of an optimal diabetes treatment treating their diabetes sub-optimally, i.e., carbohydrate & bolus-insulin intensive.

And the results? Perhaps an HbA_1c at or below 7%, weight gain, increasing VLDL levels, increasing blood pressure, too much time spent counting carbohydrates and measuring insulin doses, anxiety caused by constantly wondering whether or not too much or too little carbohydrates were eaten or insulin dosed, the ever present chance of hypo- or hyper-glycemia, constant blood sugar testing, and the list goes on. “Diabetes Managed” may not achieve optimal results for the end user, but, for the other stakeholders, it brings and keeps customers longer.

Although the science behind the drugs that either limit the amount of glycogen released from the liver or that bind and carry glucose from the blood to the receptors that transport it across cell membranes is remarkable, it is based upon two assumptions: (I) that carbohydrates are an essential majority part of the diet, and/or (II) that through education, a patient cannot, will not, or should not keep from consuming them. Remove those key assumptions, and the house of cards from which that remarkable science is based comes toppling down.

As knowledge about diabetes increases, trusted advisers and patients alike will choose a less-complex method, one that transcends diabetes by avoiding the root cause of symptoms and complications—carbohydrates—and replacing those carbohydrates in the diet with fat, resulting in benefits such as healthy weight loss, lowered VLDL levels, increasing HDL levels, reduced mTOR activity, normal blood pressure, etc.; in short, leading to a longer, happier, healthier life.

Terrestrial Cause for Obesity, Overweight and Related Chronic, Non-Contagious Diseases (CNCDs)

2012-07-15T10:42:00.001-07:00

Author: Laurence D. Chalem, Independent Researcher

Conflict of Interest: Nothing to declare

Abstract: Exogenous, digestible carbohydrates—sugar (sucrose), starch (amylose & amylopectin) and their constituents—have long been considered addictive, obesogenic, diabetogenic and atherogenic. The mechanism leading to deranged metabolism—perturbation of the insulin-glucose system—has been known for decades. Little, if any, research, however, has been undertaken to understand why. This article presents a hypothesis for further study.

Keywords: Adaptation, Addiction, Carbohydrates, Diabetes Mellitus, Glycosis, Maladaptation, Obesity, Overweight, Sugar

Introduction

The two independent variables most commonly associated with obesity, eating too much food and sloth, have recently been dismissed.[1], [2], [3], [4]

Additional associations recently proffered include: sleep debt, pollution, air conditioning, decreased smoking, medicine, population age, ethnicity, older moms, ancestors’ environment, obesity linked to fertility, unions of obese spouses, and others, including a fat-inducing virus, increases in childhood depression, less consumption of dairy products and hormones used in agriculture.[5]

Francois Magendie

In 1816, Francois Magendie set out to observe the effects of a restricted diet. He was interested in what role nitrogen played in digestion. The answer he got, after ten years of painstaking work was none at all. “As so often in research,” Magendie wrote, “unexpected results had contradicted every reasonable expectation.” But in the pursuit of this knowledge, Magendie had stumbled upon a striking, if unpleasant discovery: he had found that he was able to starve his experimental dogs to death on diets that should, on the face of it, have given them all the energy they needed for life.

By his own account, Magendie “placed a small dog about three years old upon a diet exclusively of pure refined sugar with distilled water for drink; he had both ad libitum.” By the third week the animal, already weakened, lost its appetite, and developed small ulcers in the centre of each cornea. The ulcers spread, and then the corneas liquefied. Shortly afterwards, the dog died.

Magendie tried other nutritious foods. “Everyone knows that dogs can live very well on bread alone,” he asserted; but, when he put this to the test, he found that “a dog does not live above fifty days.” The most calorific foods in Magendie’s pantry—wheat gluten, starches, sugar, olive oil—were not enough for life. This was totally unexpected. There was something missing—something available only as part of a varied diet—but what?[6]

No Thrifty Gene

Diabetes confers a significant reproductive disadvantage; yet, populations that James Neel studied had diabetes in such high frequencies that a genetic predisposition to develop diabetes seemed plausible.[7]

The most significant problem for the “thrifty gene” idea is that it predicts that modern hunter gatherers should get fat in the periods between famines. Yet data on the body mass index of hunter-gatherer and subsistence agriculturalists clearly show that between famines they do not deposit large fat stores.

Neel wrote that modern, very-high levels of obesity and diabetes among formerly native populations were a recent phenomenon most likely caused by dietary changes. Given that some populations, e.g., the Inuit, experienced a rise in obesity and diabetes in conjunction with a reduction of the proportion of fat and protein in their diets, Neel concluded that the dietary causes of obesity and diabetes lay in carbohydrate consumption.[8]

Emotional States as Addiction

Group identity established by emotional mechanisms requires both a long-lasting negative component and a less stable positive component, the basic elements of an addiction module.[9] Eating starch- and sugar-based snacks in a social setting entails both positive and negative emotional states. Positive emotions would include those of pleasure, joy, happiness and contentment. The stable negative component may not be apparent until after this initial acquisition, when feelings of guilt or unhappiness result from the finding of fat accumulation. Negative emotional states then might include anxiety, depression and anger.

Although not everyone that consumes sugar is addicted, sugar is implicated in obesity,[10], [11] asthma,[12] and every one of the abnormalities seen in coronary heart disease and in diabetes can be produced by the inclusion of sugar in the diet.[13]

That low carbohydrate diets work best in the treatment of both type 1 and type 2 diabetes,[14], [15], [16], [17], [18], [19], [20], [21], [22] reducing pharmaceutical dependencies, and in weight loss,[23], [24], [25], [26], [27], [28], [29], [30], [31] is the prima fascia case that carbohydrates are the keystone of the obesity, overweight and related CNCDs arch.

Obesity Today

2.7% of UK men and women were obese in 1972. Fewer than three decades later, in 1999, 22.6% of men and 25.8% of women were obese.[32] Two-thirds of UK citizens are now overweight or obese.

70% of Americans are currently overweight or obese. Animals inhabiting human influenced environments haven’t fared much better.[33]

Figure 1. US Overweight & Obesity. Centers for Disease Control and Prevention, 2006.

Evidence accumulated since 1917 has indicated that eat less, do more does not work;[34], [35] in fact, those that implement the advice fail 98% of the time.[36] Calorie restriction results in a disproportionate reduction in energy expenditure and metabolic activity.[37], [38]

Carbohydrates

Carbohydrates are defined by two criteria. First, they usually contain only of carbon, hydrogen, and oxygen, although a few carbohydrates contain nitrogen or sulphur. Second, the ratio of hydrogen to oxygen is close to 2:1, the same ratio as in water; the generalized chemical formula is (CH₂O)_n.[39]

Carbohydrates are divided into four groupings. Oligosaccharides and polysaccharides, commonly referred to as complex carbohydrates, can further be classified either as non-structural carbohydrates (NSCs) or structural carbohydrates. Amylose and amylopectin—starch—are polysaccharide NSCs. Cellulose, hemicellulose and lignin (wood), are structural polysaccharides.[40], [41]

Polysaccharide NSCs—complex carbohydrates—reduce to simple carbohydrates during human digestion. But humans can’t digest structural polysaccharides; we don’t produce cellulase, the necessary enzyme for breaking them down. Wood-rotting fungi and bacteria have cellulose-degrading enzymes, but even termites, cockroaches and cattle can live on cellulose only because their digestive tracts contain microorganisms with the proper enzymes that then convert it to short-chain fatty acids for energy.[42], [43]

Monosaccharides and disaccharides are referred to as simple sugars, of which all are NSCs. Blood sugar is the monosaccharide glucose and table sugar is the disaccharide sucrose, consisting of glucose and fructose.

Starch serves as a long-term storage chemical for energy. Although sugars are excellent for storing energy because they are not very reactive, cells cannot store large amounts of sugars. Sugars absorb and hold water, causing cells to swell; starch does not.[44]

Figure 2. US Dept. of Commerce reports and the USDA: continuous yearly sweetener sales from 1822 to 2005. Stephan Guyenet, Ph.D. & Jeremy Landen, 2012.

Figure 2 presents added sweeteners such as cane sugar, high-fructose corn syrup and maple syrup, but not naturally occurring sugars in fruit and vegetables. It’s a remarkably straight line, increasing steadily from 6.3 pounds per person per year in 1822 to a maximum of 107.7 lb/person/year in 1999. In 1822, we ate the amount of added sugar in one 12 ounce can of soda every five days; today, every seven hours.

Figure 3 presents the consumption of the three macronutrients from 1971 to 2000.

Figure 3. Percent kilocalories from macronutrient intake among men aged 20-74 years (NHANES).

Ancestor’s Diet

The best benchmark to use is what we ate before the agricultural revolution. But it is difficult to accurately determine the nature of past hominid diets because survival of organic materials is very rare. The morphological changes—based on analogies with living primates—increasing gracilization of the mandible and increasing brain size, have been interpreted as the move from plants to higher-quality, more digestible, animal meat, although this explanation is debated. Artefacts, such as stone tools which are likely to be used for hunting, and animal bones with evidence of human processing and butchering, do indicate that hunting did occur at many times in the past; but, it is impossible to judge the frequency. Direct evidence from bone chemistry, such as the measurement of the stable isotopes of carbon and nitrogen, provide direct evidence of past diet and indicates the importance of animal protein in diets. There is a rapid increase in population associated with domestication of plants, and in many cases a general decline in health and stature and the appearance of new nutritional disorders.[45]

Present-day hunter-gatherer societies, on average, consume a diet of 65% animal food and 35% plant food.[46] Contrast that with the fact that 72% of the total daily energy consumed by people in the United States is made up of dairy products, cereals, refined sugars, refined vegetable oils, and alcohol, all items that didn’t exist until about ten-thousand years ago.[47] According to Dr. Loren Cordain, the word for the difference between what we evolved to eat and what we currently eat is “discordance,” and is due to the fact that our cultural evolution has paced faster than our biological evolution. Our biology has not caught up with the nutritional, cultural, and activity patterns of contemporary western populations, and thus, many of the so-called diseases of civilization have emerged.[48]

Most of those diseases are related to the glycemic load of our diets. Within the past two decades, substantial information has accumulated showing that long-term consumption of high glycemic load carbohydrates can adversely affect metabolism and health. Specifically, chronic hyperglycemia and hyperinsulinemia, induced by high glycemic load carbohydrates may elicit a number of hormonal and physiological changes that promote insulin resistance. Diseases of insulin resistance include obesity, coronary heart disease, type two diabetes, hypertension, acne, gout, some cancers, and many others. Diseases of insulin resistance are rare or absent in hunter-gatherer and other less-westernized societies living and eating in their traditional manner.[49]

Strategies

The sugar first formed as a result of photosynthesis was discovered in the early 20th century to be glucose; part of it was then converted into fructose. Condensation converts both into sucrose, and it is as sucrose that translocation takes place to the bulbs.[50]

Plant organs that provide resources to other tissues in the same plant are termed sources, and those that receive the resource are called sinks. Sucrose from a source cell is loaded into the phloem for long-distance transport. Then, the sucrose is unloaded from the phloem at a sink, such as a root, where it is used for storage, growth or respiration. When plants are defoliated, storage organs become sources and the growing shoots are sinks.[51]

Among many strategies, plants produce fruit or nectar to entice animals to disperse their seeds or pollen. In seed dispersal known as endozoochory, an animal eats the fruit and the seeds inside it; the seeds survive the digestive process of the animal, and, later, are deposited when the animal defecates. When an animal feeds on nectar, however, plants deposit their pollen—mobile, single-use sperm production and delivery devices—on them. On its quest for more nectar, the animal moves pollen from male anthers of one flower to female stigma of another.

Although sucrose is the main sugar found in nectar, other carbohydrates, including arabinose, galactose, mannose, gentiobiose, lactose, maltose, melibiose, trehelose, melezitose, raffinose, and stachyose have been identified in nectars of some flowers.[52] The various types of nectars can be ordered into three groups according to sugar content: sucrose prevalent, glucose and fructose prevalent, and equal amounts of sucrose, glucose, and fructose.[53]

Some animals remove nectar without contacting anthers or stigma. These nectar robbers include a small number of species of ants, bees, birds, bats and others. But, contrary to the pure sucrose humans obtain from sugar cane, all twenty of the amino acids found in protein have been identified in various nectars, with alanine, arginine, serine, proline, glycine, isoleucine, threonine, and valine, most prevalent.[54]

H. sapiens does not obtain sugar via pollination or nectar robbery; but, through two operations separated in space time. We methodically depredate croplands then cultivate them back again.

There are other depredating species. The Asian giant hornet Vespa mandarinia is especially adapted to raid bee hives. A single giant hornet can kill tens of bees a minute and only a few can decimate an entire bee colony of 30,000 in just a few hours. The hornets depredate bees to satiate the hunger of their demanding young. Swarm-raiding army ants Eciton burchelli devastate the arthropod fauna on the ground and low vegetation over which they conduct their daily forays.[55]

Leafcutter ants consume far more vegetation than any other group of animals of comparable taxonomic diversity. The amount of vegetation cut from tropical forests by Atta alone has been calculated to lie between 12%-17% of leaf production. Because of the catholicity of the diets of the fungus that they eat, leafcutters have an extraordinary diverse impact on agriculture; loss to human interests is estimated in the billions of dollars.[56]

Members of the myrmicine tribe Attini share with macrotermitine termites and certain wood-boring beetles the sophisticated habit of culturing and eating fungi.[57] But no other animal depredates-cultivates palatable, non-essential food. Although it’s true that humans manipulate the plants, the opposite is equally true. We increase their fecundity; they, in turn, reduce our fitness.

“They” refer to a number of plants containing accessible NSCs. Included is sugar cane (Saccharum spp.) and corn (Zea mays)—grasses—and beet sugar (Beta vulgaris), a tuber. Corn is an annual; that is, it germinates, flowers and dies in one year or season. So too are the grasses wheat (Triticum spp.) and rice (Zizania spp. & Oryza spp.). Beet sugar is biennial, taking two years to complete its lifecycle, and the sugar canes are all perennial, living for years.

Unlike an angiosperm that uses sweetness to entice an animal to pollinate it or disperse its seeds, sugar cane attracts humans to raid its stem, for it is there that phloem contain significant, translocating sucrose. H. sapiens has diverged into consumers and producers, members of the latter doing much more work than any bat, bee, butterfly, hummingbird or moth.

Think how much of these organisms we depredate-cultivate each year. Worldwide, Homo sapiens—referred to by some as Homo ludens, yet by others as H. stultus—produce two-billion metric tons of sugar cane, a billion metric tons of corn and about a half-billion metric tons of beet sugar to meet demand.[58]

Beet sugar and sugar cane have a high water content, about 75% of the total weight of the plants. The sugar content of sugar cane ranges from 10%-15% of the total weight, while that of beet sugar is between 13%-18%. Assuming seven billion people worldwide, that’s more than a quarter-pound of sugar produced per day per person, not including the high fructose corn syrup which is now nearly equal to sugar consumption. Add in the billion metric tons of corn—a large portion goes to produce ethanol—and a billion metric tons each of wheat and rice, and we have well over a pound of edible, non-essential carbohydrate production per person per day. Although rice and wheat provide some protein—the mysterious, life-sustaining component of food that Magendie the dog killer would eventually find—the protein and fat content of sugar is zero.

Some that try to eat just a little sugar are surprised and discouraged when they crave more. It’s no coincidence that sugar is sweet; sweetness is a powerful bribe. Once ensnared in the taste, humans demand more, driving further cultivation and depredation. We wind up favoring the plant’s interests at the expense of our own because we have uncoupled food intake from functional needs. Animals that must flap their wings fifty times a second in order to feed have a hard time staying fat and do not develop diabetes, at least as we know it.[59]

Still, why can some people eat all the NSCs they want and remain fit? Richard Lenski provides a prescient template.

Richard E. Lenski

Michigan State University biologist Richard Lenski, his colleagues and students started off with a single bacteria of E. coli; after it divided a few times into identical clones, he started twelve colonies, each in its own flask. Each day he and his colleagues provided the bacteria with a little glucose, which the bacteria ate by the afternoon. The next morning, the scientists took a small sample from each flask and put it in a new one with fresh glucose. They did this for more than twenty years and it’s still running today.[60]

Lenski expected that the bacteria would experience natural selection in their new environment. In each generation, some of the microbes would mutate. Most of the mutations would be harmful, killing the bacteria or making them grow more slowly. Others would be beneficial allowing them to breed faster in their new environment. They would gradually dominate the population, only to be replaced when a new mutation arose to produce an even fitter sort of microbe.

Over the generations, the bacteria did indeed evolve into faster breeders. The bacteria in the flasks today breed seventy-five percent faster on average than their original ancestor. Lenski and his colleagues have pinpointed some of the genes that have evolved along the way; in some cases, for example, the same gene has changed in almost every line, but it has mutated in a different spot in each case. Lenski and his colleagues have also shown how natural selection has demanded trade-offs from the bacteria; while they grow faster on a meager diet of glucose, they’ve gotten worse at feeding on some other kinds of sugars.

But that’s not all. In addition to becoming faster breeders, they also became larger.[61] And then the bacteria had abandoned their glucose-only diet and had evolved a new way to eat.[62]

After 33,127 generations, Lenski and his students noticed something strange in one of the colonies. The flask started to turn cloudy. This happens sometimes when contaminating bacteria slip into a flask and start feeding on a compound in the broth known as citrate. Citrate is made up of carbon, hydrogen, and oxygen; our own cells produce citrate in the long chain of chemical reactions that lets us draw energy from food. Many species of bacteria can eat citrate, but in an oxygen-rich environment like Lenski’s lab, E. coli can’t. The problem is that the bacteria can’t pull the molecule in through their membranes. In fact, their failure has long been one of the defining hallmarks of E. coli.

If citrate-eating bacteria invade the flasks, however, they can feast on the citrate, and their exploding population turns the flask cloudy. This has only happened rarely in Lenski’s experiment, and when it does, he and his colleagues throw out the flask and start the line again from its most recently frozen ancestors.

So in one remarkable case, they discovered that a flask had turned cloudy without contamination. It was E. coli thriving on the citrate. The researchers found that when they put the bacteria in pure citrate, the microbes could use it as their sole source of nutrition and energy.

What was going on? What was it that suddenly happened to that one tribe? If a mutant could discover how to deal with citrate, a bonanza would open up for it. This is exactly what happened with that one tribe. This tribe, and this tribe alone, suddenly acquired the ability to eat citrate as well as glucose, rather than just glucose. The amount of available food in each successive flask in the lineage therefore shot up. The only explanation was that this one line of E. coli had evolved the ability to eat citrate on its own.[63]

Glycosis (glī-kō’sĭs)

Why are there some people who consume quite a lot of sugar but are not overweight? John Yudkin in Pure, White and Deadly (1988) proposed that some lucky people have the facility of burning off surplus calories.[64] That may or may not be true; but, why should some be luckier than others? In all likelihood it is because they are better adapted to that fare than others.

Adaptedness is the morphological, physiological, and behavioural equipment of a species or of a member of a species that permits it to compete successfully with other members of its own species or with individuals of other species and that permits it to tolerate the extant physical environment. Adaptation, as measured by evolutionary success, consists of a greater ecological-physiological efficiency of an individual than is achieved by most other members of the population or at least by the average. Adaptation is achieved by the greater survival or higher reproductive success of certain individuals owing to the fact that they possess ecological-physiological traits not, or only partially, shared by other individuals of their population, traits that are useful in the struggle for existence.[65]

Surely every fish is adapted for its life in water and yet in the history of the vertebrates, ten thousands of species of fish have become extinct, either because they were not sufficiently well-adapted to some component of the environment or because they lost in the competition with some “better adapted” other species. The same is true for individuals within a species. All have the same species-specific adaptations and yet only a small minority will survive into the next generation. Thus, it is evident that we have “adapted” and “better adapted.” This is precisely the process of natural selection, which, on average, favors those that are “better adapted.”[66]

Proposed is a word to indicate relative maladaptedness to carbohydrates: glycosis. It is defined as the quantifiable maladaptation to one or more specific carbohydrates in a given species. For example, if a species that uses glucose as its sole food source is fed a different carbohydrate, the survival rate would serve as the measure of adaptation or maladaptation to that carbohydrate, depending on whether the value was high or low. If a hundred percent of the population survives, then there is no adaptational benefit to any select few and the species as a whole is adapted. If they all die out, then they are completely maladapted.

Quantifying adaptation in humans is complex because carbohydrates are not essential macronutrients. Homo sapiens need exogenous amino acids, DHA and EPA fatty acids, energy, water, vitamins, electrolytes and minerals; but, we never need to eat carbohydrates.[67] Although we get all the glucose we need endogenously from our livers, adaptation to carbohydrates as an energy source can theoretically be calculated.

Population glycosis could be depicted as the percent of people suffering from CNCDs related to NSC consumption such as obesity, overweight, diabetes mellitus, some types of heart disease, some cancers, gout, etc. Diseases related to the use of tobacco (Nicotiana spp.) and alcohol—ethanol, the product of carbohydrate fermentation—could be included. Thus, the higher the consumption of NSCs, the higher the prevalence of CNCDs, the higher the maladaptation to those NSCs, the higher the glycosis.

Although there may be a lag between NSC consumption levels and CNCD presentation, that 63% of the global population expire as a result of CNCDs[68] implies that the current limit of glycosis in Homo sapiens is the same, given current NSC consumption. In sub-populations with known overweight rates of two-thirds or more, that’s an underestimation.

Like psychosis—abnormal condition of the mind—the word glycosis at the individual level could be defined as the abnormal condition of glucose in the blood. People with diabetes mellitus of any type are most demonstrably glycotic.

An analogy might be helpful. In an old TV commercial for “Off!,” a name-brand mosquito repellent, two bare arms, each connected to a live human, were placed consecutively into a glass tube full of hungry mosquitoes. The first arm, which can be thought of as the experimental arm, was sprayed with a generous amount of “Off!,” and the second arm, the control, wasn’t sprayed with anything. Not surprisingly, the first arm, the one sprayed with “Off!,” suffered fewer, if any, mosquito bites than that of the bare arm. This commercial is analogous to diabetes mellitus if you imagine that the mosquito bites represent complications and the “Off!” represents insulin. Carbohydrates are equivalent to the actual placing of an arm into the mosquito-filled glass container.

Ideally, one probably shouldn’t be placing their arm into a container full of hungry mosquitoes. Similarly, for the obese and overweight too—because insulin is the main hormone that stores fat and carbohydrates are the most significant secretagogue of insulin—doesn’t it make sense to reduce carbohydrate intake? That would be congruent with recent research indicating that anything enabling the reproduction and growth of microbial parasites—carbohydrates, nicotine, mental stress, and low vitamin B, C and D levels, are primary risk factors for cardiovascular disease.[69]

A New Found Path

Once deranged metabolism manifests, the simple way to proceed is to eat natural foods made up of mostly fat and protein. Without carbohydrates in the diet, the brain and central nervous system will run on ketone bodies, converted from dietary fat and from the fatty acids released by the adipose tissue; on glycerol, also released from the fat tissue with the breakdown of triglycerides into free fatty acids; and on glucose, converted from the protein in the diet. Since a carbohydrate-restricted diet, unrestricted in calories, will, by definition, include considerable fat and protein, there will be no shortage of fuel for the brain.[70]

Every fat is part saturated, part mono-unsaturated and part polyunsaturated.[71] All “saturated” means is that every carbon has a hydrogen attached to it; intake of saturated fat is associated with reduced progression of coronary atherosclerosis. Greater NSC intake is linked to increased progression.[72], [73]

Of the many vertebrate protein sources available, one necessitates clarity. “Grass-fed beef” is a peculiar expression because cattle naturally eat grass; they’re graminivores. The problem becomes clear after considering three arguments: (1) grass stems are higher in NSCs than leaves; but, (2) lush grass is much lower in NSCs than dry grass or fruit, and, (3) the content of NSCs is higher when sampled closer to the ground. Cattle and their bacteria are best adapted to eat structural carbohydrates.[74]

For grass, high levels of NSCs enable them to be more persistent under drought conditions. Moreover, the distribution of NSCs being higher the lower they are in the stem is an adaptive advantage. It allows plants to maintain reserves for re-growth after the tops have been consumed by grazing animals.[75] Hence, feeding cattle corn—which although is fruit from a grass, it contains a higher proportion of NSCs than their natural diet of lush grass tops—is the bane of some cattle, not to mention in some people that eat their beef.

While ruminant livestock enterprises benefit from higher levels of NSCs in grass, various forms of carbohydrate intolerance are recognized in horses. Obesity, laminitis, insulin resistance, developmental orthopedic disease, polysaccharide storage myopathy, all involve excess dietary NSC in their etiology.[76]

In those with diabetes, obesity, overweight, etc., or the propensity to become so, risk may be mitigated by avoiding carbohydrate intake. No, it’s not easy; but, it is simple. For those free of CNCDs, it’s also good policy. As there used to be only one way to distinguish between edible and poisonous mushrooms, so too might learning of one’s own maladaptedness to carbohydrates: it will be in retrospect of having become less fit.

And that fits nicely into nature’s scheme. Stephan Jay Gould eloquently stated it at the conclusion of Wonderful Life: “We are the offspring of history, and must establish our own paths in this diverse world, one indifferent to our own suffering, and therefore offering us maximal freedom to thrive, or to fail, in our own chosen way.”[77]

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Acknowledgements

The section "Obesity Today" was adapted from the work of Zoe Harcombe and many of the cited articles were made available by Lt. Col., Dr. Luca Mascitelli. The author is grateful to both.

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Figure 1. US Overweight & Obesity. Centers for Disease Control and Prevention, 2006.

Figure 2. US Dept. of Commerce reports and the USDA: continuous yearly sweetener sales from 1822 to 2005. Stephan Guyenet, Ph.D. & Jeremy Landen, 2012. http://wholehealthsource.blogspot.com/2012/02/by-2606-us-diet-will-be-100-percent.html

Figure 3. Percent kilocalories from macronutrient intake among men aged 20-74 years. (NHANES).