Specifically, this book was … written for the reader who needs to learn more about critically evaluating my (or any other) interpretation of historical events.� As a college professor, I have found that many students passively accept historical interpretations without demanding supporting evidence and without critically evaluating the quality of the evidence before them.� Many of my students seem stunned to learn that history books sometimes contain interpretations that are not fully accurate, or even just plain false.� This may be because most historical accounts are solely focused on providing historical information (i.e., facts and interpretations).� This focus assumes that readers already understand both the process of recreating the past and the need to critically evaluate such historical recreations.

My book does not make this assumption, but instead tries to teach readers about the critical evaluation of historical interpretation.� Thus, another primary focus of this book is to teach the process of history and provide the reader with the tools to critically evaluate historical interpretations.� Students should leave a history course with a clear understanding that historical interpretations should not be confused with historical facts, and I have provided many examples that reinforce this important lesson.

The book is a� fun and interesting read. It’s written by a friend of mine who teaches critical thinking at the college level. And it’s FREE! Through today, Sunday, April 21. Grab a copy.

Also, if you want another great read by the same friend, grab a copy of When Good Thinking Goes Bad. It truly is a primer on critical thinking. It’s a great companion book to another of my favorites Mistakes Were Made. Dr. Riniolo’s book differs in that it walks you through several critical thinking exercises. I will review it more extensively in a later post, but wanted to at least mention it now while I’m recommending his free Kindle book on Freud. Unfortunately, When Good Thinking Goes Bad is not free, but it’s well worth the small price. It is one of the very few books I like enough that I purchased both the paperback and Kindle versions. This was before Dr. Riniolo and I became friends, so I truly did purchase both versions. If you do grab a copy of this book, you’ll see early in the introduction why I had to overcome my own cognitive dissonance and confirmation bias to keep on reading. And why I contacted Dr. Riniolo to start a dialogue.

The post Free book on critical thinking appeared first on The Blog of Michael R. Eades, M.D..

I briefly contemplated doing an in-depth review of this book replete with multiple quotes and my digressions, but since I don’t know how long the book is going to remain free on Kindle, I figured it would be best if I just got the post up quickly.� In short, the book discusses how small intestine bacterial overgrowth (SIBO) causes most cases of heartburn. SIBO can be successfully treated in most cases with a low-carbohydrate diet. Dr. Robillard’s book discusses treatment, including some not-so-low-carb options. In lieu of my review, here is Dr. Robillard’s website, which provides more info.� I highly recommend this book to anyone with heartburn.

Grab a copy now.

Disclosure: Dr. Robillard is a friend of mine. We had a few discussions during his writing of the book, and I am mentioned in the acknowledgements.

Note: Just heard from Dr. Robillard.� The book will be free through Jan 1, 2013.� So don’t dilly dally.� Get your copy now.

And Happy New Year everyone!

The post Free book on heartburn appeared first on The Blog of Michael R. Eades, M.D..

Many years ago, I was taking questions after giving a presentation to a large group of both doctors and laymen.� A lady stood up and told me she always lost weight whenever she went on a low-carbohydrate diet, but she also always gained it back more quickly after going off such a diet than she did when she regained weight she had lost on a low-fat diet.� As I listened to her question, my brain was busily formatting a smart-assed answer along the lines of, Well, that�s God�s way of telling you not to go off of your low-carb diet.� But, looking out over the audience, I noticed a lot of heads nodding in agreement.� I realized I needed a reasonable answer.

The truth was, I didn�t really think there was anything to it.� I figured it was all in her imagination.� I had heard such reports before, and I didn�t think much of them.� But as I saw heads nodding throughout the auditorium, it reminded me of the old maxim that one report is anecdotal, but many similar anecdotes become data.

So, I thought about it quickly and concocted and answer on the spot.� Most public speakers know the surest way to embarrassment is to engage in original thinking while in a public forum.� Though I was in peril, I think in this case I came out okay.

I�ll go through my thought processes, as I remember them well.

My bias was/is that carbohydrates are vastly more fattening than the same number of fat or protein calories, so let�s assume that at the start.

A low-carb diet restricts carbohydrates, and so restricts the most fattening of the three macronutrients.� If my assumption is true, then people on low-carb diets should lose more weight faster, which the majority of studies shows to be the case.

A low-fat diet restricts fat and secondarily protein, because most forms of high-quality protein contain fat.� Both fat and protein are less fattening per kcal than carbohydrate.� If this assumption is true, then people on low-fat diets that restrict fat and/or protein should lose less weight and lose it more slowly, which a majority of studies shows to be the case.

How does one cheat or go off a low-fat diet? By eating more fat and/or protein.

How does one cheat or go off a low-carb diet? By eating more carbohydrate.

Since – in my view – carbs are more fattening than fat and/or protein, it makes sense that adding the more fattening carbs to a low-carb diet would cause more weight gain than adding the less-fattening fat/protein to a low-fat diet.

Ergo, in going off of a low-carb diet one would pack on pounds more quickly as compared to going off a low-fat diet.

Seemed to make sense to me at the time, and it made sense to the audience.

I�ve thought about it a lot since then and have concluded that my on-the-spot thinking was probably correct.� And I�ve used it since whenever asked the question.

But unlike the numerous studies showing the low-carb diet to be quicker and more effective for weight loss, there have been no studies (at least not that I�ve seen) showing that people who go off of low-carb diets regain faster.

Until now.

A recent paper in the NEJM looked at what happens over the four years after subjects go off of different kinds of diets.

Subjects were studied on one of three diets over a two-year period.� One group went low-carb, another low-fat and a third group followed a Mediterranean diet.� The original two-year study, published in 2008, clearly showed the obvious advantage of a low-carb diet.� But, at the time, the media kept misrepresenting what the study really showed, so I corrected the record here and here.

After completion of the study, the researchers kept in touch with 95 percent of the subjects and were able to gather data from them four years after the end of the original two-year study.

What the researchers found is what you would expect if carbs really are more fattening.� The low-carb dieters gained more weight after going off their low-carb diets than did the low-fat dieters after going off theirs.

You can see from the charts below (click to enlarge) the outcome of several parameters.

First, in Chart A, you can see that the low-carbers both lost the most weight in the first study then regained the most, which provides some evidence in support of the notion that carbs are more fattening than fat and/or protein.

The study gets really interesting when you start looking at what happens to lipid levels when people go off of either low-fat or a low-carb diets.

Chart B looks at the LDL cholesterol to HDL cholesterol ratio.� Low fat diets lower LDL cholesterol but they also lower HDL cholesterol levels, and, consequently, end up not driving a lot of change in this ratio.� The LDL/HDL ratio typically improves slightly with low-fat dieting because there is generally a greater drop in the LDL cholesterol level than there is in the HDL level, driving the ratio down a bit. (Lower is better.)

Low-carb diets tend to keep the LDL levels the same or elevate them slightly (in some cases, though, low-carb diets can also lower LDL levels as well).� And low-carb diets typically raise HDL levels.�� So when the LDL stays the same or goes up a little (or even falls) while the HDL goes up, the LDL/HDL ratio goes down.

As you can see in Chart B, both the low-carb diet and the low-fat diet brought about positive changes in the LDL/HDL ratio (the low-carb was slightly better), but look what happened after the subjects went off their respective diets.� Those on the low-fat diet saw LDL/HDL ratios going the wrong way.� They experienced a substantial increase in their LDL/HDL ratio.� The low-carb dieters, on the other hand, found their LDL/HDL ratios refusing to budge much despite adding more carb to their diets.

Why did this happen?� As far as I know, no one knows.� But it would seem that two years on a low-carb diet appears to confer some protection against increases in the LDL/HDL ratio despite the increase in carb intake.� And this protection lasts at least four years.

Looking at Chart C, we find some interesting corroborating data.� It is well known that carbs tend to raise triglyceride levels while restricting carbs lowers them.� Chart C shows that those on the low-fat diet didn�t experience much change in their triglyceride levels, which would be expected. Those on the low-carb diet saw substantial reductions.� After the two year study period the original low-carbers shot their triglycerides up when they went back to eating carbs, which confirms the message that chowing down on carbs increases triglyceride levels.

And Chart D shows that reductions in total cholesterol brought about by low-carb dieting seem to be maintained despite the increase in carb intake after the end of the two year study.� Once again, it appears that restricting carbs for a couple of years provides some protection for at least the next four.

So what does it all mean?

Well, I think one of the take home messages from this study is that following a low-carb diet for a couple of years brings about improvements in lipids that last for a least four more years – even if you go off the low-carb diet. Which, to my way of thinking at least, would be reason enough for following a low-carb diet instead of a low-fat one.

And it�s pretty clear that going off the low-carb diet will result in more weight gain than going off of a low-fat diet.� Which would have to at least imply that carbohydrates are more fattening than are fat and protein.� We can see from the length of this second follow-up – four years – we�re not talking about the immediate water gain that comes from going off a low-carb diet for just a few days, but the long-term weight gain.

I have to issue my standard caveat here.� This is a single study.� I don�t know of any others like it.� So, repeat after me, we can�t draw certain conclusions from a single study like this.� Other studies may come along and show differing results.

But having said that, this study along with the enormous mass of anecdotal data seems to indicate that weight gain is more rapid after bolting from a low-carb diet as compared to straying from a low-fat diet.� If this proves to be true, then it really is indicative that carbohydrates are more fattening than fat or protein.

I would love to learn of your experiences in going off various kinds of diets.� Did you gain more after a low-carb diet or after a low-fat diet?� Let me hear from you in the comments.

The post Are carbohydrates fattening? appeared first on The Blog of Michael R. Eades, M.D..

Humans should adapt to foods they have consumed for a great part of their time on earth, and these same foods should pose fewer problems than consumption of similar but newer (in an evolutionary sense) foods.� A nice paper from the British Journal of Nutrition I�ve had lying around for a couple of years awaiting this post looks at the inflammatory changes in people eating an old food versus a newer food and finds the newer food to be more inflammatory.

Bad news and good news re this paper.� Bad news is that I haven�t posted on it in two years – good news is that it�s been so long the full text version of it is now available free.

Before we get into the paper, which studies the consumption of kangaroo, just to get us all in the mood, I�m going to put up a quote from The Protein Power LifePlan.� I had to fight our editor tooth and nail to keep these few paragraphs in the book.� She thought they were too gross for the average reader.� The quote comes from the records of an 1948 expedition to Arnhem Land, a remote part of of the Northern Territory of Australia set aside for the �use and benefit of the aboriginal inhabitants of northern Australia.�� It�s about how the indigenous Australians cook and eat a wallaby.

A large fire was made in a depression in the sand, and stones and shells were heated.� Small green branches were placed on top of the stones and the wallaby was flung on these.� After 5-10 minutes it was taken off the fire, placed on a layer of green leaves, and the singed fur was removed with a tomahawk. [Just the fur, not the skin.] Although the women sometimes did this preliminary treatment, a man always did the subsequent cutting up, which was done with a metal spear blade.

The first cut was made horizontally on the ventral [belly] surface at the level of the anus, and next on the dorsal [back] surface along both sides to sever the leg muscles.� Another cut was then made from the anus to the neck.� The viscera were pulled out; and the kidneys, liver, heart and lungs, and the omental and mesenteric fat [the fat surrounding the intestines] were separated from the rest, and cooked on the hot stones and coals for 5 minutes.� The cooked lungs were used to soak up the blood inside the carcass and then eaten.� The offal was regarded as a delicacy by everybody and a certain amount of squabbling always followed its distribution.

The tail was cut off, and during the cooking was put on or alongside the body.� The carcass was laid flat, dorsal side downwards, on the hot stones and ashes and the body cavity was filled with hot stones. Sheets of paperbark formed a cover over the animal, and sand was scooped out to make an oven.� Wallabies weighing 15-20 pounds were cooked for 25-35 minutes.� Everything edible was eaten except the stomach and intestines.� The skull was cracked open to get the brain, and the bones were broken to extract the marrow.

I�m reasonable certain this method of wallaby preparation has been in use since man first occupied Australia.� It is probably a pretty fair description of how all game animals were cooked in ancient times.� And it leads us into our discussion of the a paper on old foods vs new foods.� But first, let�s talk a little about food and inflammation.

We require both food and oxygen to sustain life, yet, in a bizarre twist of fate, both of these necessities slowly kill us.

Slings and arrows in the form of free radicals accrued from a lifetime of breathing gradually dent and ding our mitochondria to the point that more and more of of them give up their ghosts until we, deprived of enough functioning cellular furnaces, follow suit.

Same thing happens with food albeit via a different mechanism.

As I contemplated one early morning in Rome a few years ago, food is inflammatory.� And too much food weighs a body down with not only adiposity but with excess inflammation as well.

I would like to be able to say that carbohydrates are the only drivers of inflammation, but, sadly, that would not be true.� All food intake stimulates inflammation. Although the weight of the research evidence seems to tip the scales in favor of carbs promoting more than non-carbs, all food is guilty.

It�s difficult to limit the amount of free radical damage as a consequence of breathing by trying to breathe less. We can�t go on an intermittent breathing regimen as we can an intermittent fast, so we�re pretty much stuck with breathing about 20 times per minute.� But we can change our food.

The question then becomes, What kind of a diet generates the least inflammation?

To answer that question, we need to know how food provokes inflammation.

For the most part, the proteins in food are the culprits.� Carbohydrates are not proteins, they stimulate inflammation differently.� Carbohydrates in the diet end up as glucose in the blood.� Glucose in the blood is kind of like oxygen – it�s a requirement for life, but we don�t want too much.� Even a normal level of blood sugar is a little corrosive, but when levels are high for sustained periods, much more damage ensues.

Almost everything that gets our immune systems fired up is a foreign protein.� The body is always on the lookout for foreign proteins, and when it encounters one, the immune system rallies and mounts an effort to get rid of it.

What�s a foreign protein? Any protein the body doesn�t recognize as self.� Other than in cases of autoimmune diseases in which the body�s immune system turns on one or more of its own proteins, the body pretty much recognizes itself as non-foreign.� But, proteins coming in from outside the body are foreign.� Proteins in food are definitely foreign.

But there are degrees of foreign.� Less-foreign proteins stimulate less of an immune response than do more-foreign proteins.� What makes a protein more or less foreign?� In general, our immune systems� familiarity with it.� Foods we have consumed for millennia are more familiar.� People who had problems with those foods tended to die out, while the ones who didn�t have problems tended to flourish and reproduce more.� In the end, those of us here now are the beneficiaries of the forces of natural selection and should have fewer inflammatory problems with food proteins that have been in the diet since prehistoric times.� At least that�s an hypothesis. (It�s the hypothesis of Dr. William Davis, author of Wheat Belly (my review here), who believes that the new dwarf wheat, which has only been around for about 50 years, causes vastly more problems than the older versions of wheat that humans have consumed since Biblical times.� The proteins in the new wheat are different than those in the old.)

Problem is, how do we test this hypothesis?

One way would be to take a genetically homogeneous group of people, present them with a food they�ve eaten forever, measure the inflammatory response and compare it to that provoked by a modern version of the same food.

This is how the researchers did it in this paper.� Here is how the authors� start out with a pretty good description of the notion of newer vs older foods as inflammation inducers.

The researchers recruited ten healthy native Australian subjects (six male, four female), all with normal body weights and no history of any metabolic disorders or prescription drug use.� These subjects were divided into two groups and fed a diet composed of loin steak (100g) from either kangaroo or wagyu beef, baked potato (75g) and green peas (50g).� (Kangaroo has been a part of the traditional Aboriginal diet in Australia, while wagyu beef is a breed of newly hybridized domestic beef.)� This study was a cross-over study so that all the subjects ended up being their own controls.� The feeding schedule is shown below:

The subjects provided blood samples just prior to each meal and hourly for two hours after each meal.� The samples were tested for serum triglyceride levels and for levels of the inflammation indicators TNF-α, IL-6 and C-reactive protein.

What was the outcome?

Blood from the subjects consuming the meal with kangaroo showed a significant increase in the levels of TNF-α and IL-6, a non-significant rise in C-reactive protein and a drop in triglycerides.� This isn�t surprising because, as I mentioned earlier, all food is inflammatory.

The subjects who ate the wagyu beef experienced a greater increase in TNF-α and IL-6 along with a significant increase in C-reactive protein and triglyceride not seen in those consuming the kangaroo.

As the authors concluded

Our findings show that a �newly� introduced form of beef (wagyu) has a significantly greater postprandial [after eating] inflammatory effect than a traditional kind of meat (kangaroo).

Here is the abstract of the paper:

This is only one paper, with a small sample size, and is the only paper like this I�ve seen.��� I would like to see more work done in this area.� It would be nice to know, for example, how long this inflammation lasts past the two hour window.� It would be of great interest to see what happens if these meals are followed for a couple of days of meals instead of just one meal.� And it would be nice to see what would happen if the two meals were isocaloric, i.e., contained the same number of calories.� These meals both contained 100 g (about 3.5 ounces) of meat, but the wagyu beef has a much, much higher fat content (25%-30% fat) as compared to the kangaroo (~4% fat).� Since the wagyu meat is so much higher in fat content, 100 g of it will provide way more calories than 100 g of kangaroo.� For all anyone knows, it was the extra calories causing the uptick in the inflammatory markers and not the difference in new vs old food.� We just don�t know from this study.

This isn�t a perfect study, but it is a start.� It is, after all, called a preliminary study in the title.� What it does provide is a nice foundation for this research group or another to do a more in-depth evaluation.

The post How to reduce inflammation with food appeared first on The Blog of Michael R. Eades, M.D..

As I am sure is true of most people, I have a multi-faceted life with many and varied interests.� I remembered books that had a profound effect on my political and philosophical thinking.� Others about business, technology, and relationships.� And yet others about engineering and science, especially physics.� But this blog is mainly about nutrition and medicine, so I decided to share the short list of books that provoked substantive shifts in my nutritional and medical paradigms.� This won’t be a list of every book that influenced my thinking on these subjects – in fact, it is far from it – but it catalogs the books that steered me down specific pathways I follow to this day.� Some of these books are not the best on the subject; they are simply the first ones I read, the ones that inspired my interest and drove me to dig deeper.� For instance, I wouldn’t particularly recommend the book I’m writing about in this post because much more information has become available since. It’s not an earth-shattering book – it was simply the catalyst for me.

Napoleon’s Glands was the first book to really send me off down a rabbit hole of discovery.� Via a single sentence, this book tripped me to a line of inquiry that threatened to take over the writing of Protein Power.� Because of the momentous changes it caused, I’m going to devote this first post to this book alone.

A little history. In the late 1980s I wrote Thin So Fast, a book on how to do a Medifast/Optifast type diet at home.� It’s hard to believe now, but at that time, people undertook these protein-sparing, modified fasts (PSMF) only under physician supervision.� I was treating obese patients with low-carb diets, and many were clamoring to go on one of these fasting programs.� I relented and ended up successfully treating countless patients with my own low-carb version of a PSMF program.� After watching my first hundred or so patients closely, I realized that this program was one that dieters could easily do at home on their own, if they but had a way to do so.

In the late 1980s, there were almost no commercially available protein supplements.� It’s difficult to imagine now when they are everywhere you look, but then protein powders were not common.� There were a couple, but they were hard to find, usually sold only at health food stores (which, at that time, were also thin on the ground), tasted wretched, and were used mainly for supplementing other foods, not as a meal replacements.� People then had no ready access to meal replacement protein powders – Medifast, Optifast and a handful of others were distributed only through physicians.� I realized it was kind of a racket, so I decided to write a book explaining how a PSMF could be safely done at home.

The first problem, though, was in coming up with a recipe for a suitable protein shake that could put together from available ingredients.� I had MD help me fiddle around with it until we (mainly she) came up with something palatable and effective.� Thus, my first book.

In order to flesh out Thin So Fast, I wrote sections on all kinds of diet-related material. One of the chapters, The Insulin Connection, was about all the things insulin did besides drive sugar into the cells. I suspected insulin was a primary driver of obesity, elevated cholesterol, high blood pressure, and a host of other disorders, so I speculated on some of the mechanisms involved, most of which have since proven to be correct.� A few years after the publication of Thin So Fast, I had read everything I could get my hands on about the effects of insulin and wanted to write about it, so I submitted a proposal for a new book called The Insulin Connection.� The book publisher loved the idea but hated the title; he figured it would appeal only to people who were diabetic. They changed the title to Protein Power, which I hated at the time and am still not too crazy about, though it has grown on me.

Between the writing of Thin So Fast and Protein Power, I had been in discussion with the publisher about writing what he called a medical narrative.� I have always been interested in the history of medicine and the impact of specific diseases on the course of history.� Some authors had written such books, but no one I knew of had written a book describing the actual diseases in a way laymen could understand.� Most people know about syphilis, tuberculosis, plague, malaria, yellow fever, rabies, etc., but they don’t really understand what happens physiologically and pathologically when one of these diseases sets in.� I was going to write a book explaining it all for the layman. But Protein Power came along, and the medical narrative was back-burnered, where it still simmers to this day.

While doing the research for this medical narrative, I came across the book that would profoundly change my thinking. Napoleon’s Glands and Other Ventures in Biohistory, by science writer Arno Karlen, is a series of essays on intriguing episodes in the history of medicine.� Though hard at work on Protein Power, I continued my habit of omnivorous reading, and, still with the idea of the medical narrative in mind, decided to dip into Napoleon’s Glands at bedtime one night.� At this point, Protein Power was going to be my argument as to why the untoward effects of excess insulin validated the low-carb diet as the preferred way of eating for most people. But then I came to the chapter in Napoleon’s Glands titled “Mummy Powder, Mummy Blood, Toward a Biohistory of Peoples.”

“Mummy Powder, Mummy Blood” was about early paleopathologists, who autopsied ancient Egyptian mummies, and about their modern counterparts who were continuing those studies with much more sophisticated equipment, including X-ray and CT studies and, believe it or not, even labwork.� These mummy autopsies revealed that ancient Egyptians were crawling with parasites, had dental caries and even a fair amount of arthritis.� In reading through the roll call of these disorders, the following sentence leaped out at me:

Blood-vessel disease was common, contrary to assumptions that it rises from urban stress and a modern high-fat diet.

Say what?!

As I recall, I was starting to get a little sleepy, but I bolted alert when I read then reread this sentence.� I remembered reading somewhere that the ancient Egyptian diet was heavy in carbohydrates, and I started wondering…

Wide awake, I raced through the rest of the chapter and on to the next� – “Dry Bones, the Unwritten Past” – about the diagnosis of ancient disease through skeletal remains.� I was hooked.� I flipped to the back of the book where, to my absolute delight, I discovered a bibliography listing a host of sources and journals that theretofore had been completely unknown to me.� I was unable to sleep, so I got up, went down to our library and rummaged through all our books I could find on Ancient Egypt.� There were a few, and all seemed to confirm that the early Egyptian people, the ones whose mummies I had just been reading about, did indeed subsist on a diet heavy in carbohydrate, primarily wheat.

I made a copy of the bibliographic pages in the book, took them to bed and began marking them up so that I could track them down more easily when I went to the medical library the next day.� As I turned to those pages again today while preparing to write this post, just the memory of the excitement I felt when I first encountered them started to get me a little fired up.� Not quite the Chris Matthews’ thrill up the leg, but almost.� (I don’t have my original marked up biblio so I scanned these pages from my copy of the book and converted them to pdf.� Here they are so you can see what kind of stuff really gets me worked up. Napoleon’s Glands Ch 4 & 5 Biblio� I guess I need to get out more.� Pretty pitiful.)

The next day, as soon as I had seen my last patient, I made my way to the medical library and began pulling all the references.� Reminiscing about this makes me realize what huge strides have been made over the past 18 years in the ability to do this kind of research.� Today I would sit down in front of my computer and start going to the journal websites and accessing the papers.� Back then – which was in the early 1990s – I had to go to the medical library and start wandering through the stacks of bound journals.� They were all stacked alphabetically, which was how I marked up my copies of the bibliography pages so that I could start at the As and go from there.� I would remove the bound journals – which were often the size of large phone books – and stack them on a cart I pushed along with me.� I roamed through the stacks, piling the journals on the cart, and ended up in the copy room.� I would then have to copy each paper page by page.� Today, in the same time it took me just to drive to the medical library, I can grab more papers from the web than I gathered all that afternoon.� And they wouldn’t cost me ten cents per page to copy as they did then.� Ain’t technology grand?!

As I read these papers at home in my study, I checked citations and gathered a list of yet more papers to get.� It was off to the medical library the next day to get those papers. Then read them, made another list, and repeated.� Until I had pretty much all the papers I could track down that had anything to do with paleopathology and diet.

Many of these references were books, so I had to track those down, too.� A number of the references cited Paleopathology at the Origins of Agriculture.� Because I couldn’t get my hands on it any other way, I ended up forking over $140 or so for this book (it’s now about $300), but it was well worth it, because through it I got on the track of Claire Cassidy, Ph.D., whom I wrote about in Protein Power, and who wrote the paper I wrote about here.

I joined the Paleopathology Association and immediately purchased all back issues of the Paleopathology Newsletter.� I dragooned MD into going to Paleopathology Association meetings, which I loved, and which are still my favorite medical meetings. There we could converse, confab and otherwise hobnob with all the nabobs of academic paleopathology, all of whom have written books at some point, and all of whose books I now own.

After attending these meetings and poring over my ever-growing mountain of paleopathology and anthropology literature, it became more and more apparent to me that although the agricultural revolution was a good thing for mankind it was a bad thing for individual men.� I learned that the health devolution that took place due to dietary changes incurred as a result of man’s turn to agriculture were so substantive that at a glance an anthropologist could identify skeletal remains as being those of a agriculturalist or a pre-agriculturalist.� How? Because as compared to agriculturalists, pre-agriculturalists had greater stature, stronger bones, better teeth, fewer signs of infection, less evidence of malnutrition and/or vitamin deficiencies – all signs visible to the trained eye.� And not only were the pre-agriculturalists more robust, studies on groups of their remains showed they even experienced greater longevity than their agricultural progeny.

Agriculturalists replaced their previous diet of primarily fat and protein with high-starch plant foods and paid for it with their health.� It didn’t take a rocket scientist to realize that modern man was treading the same path.� And with the same results.

Problem was, that the nutritional ‘experts’ of the late 20th Century had deemed the diet man evolved over multiple millennia to thrive upon – one of primarily protein and fat – as extremely unhealthful.� And to make matters worse, modern nutritional dogma glorified as optimal the self-same grain-based, meat-poor, low-fat diet that had cratered the health of our post-agricultural ancestors .

I was gearing up to write a book showing how low-carb dieting would treat not just excess body fat, but most of the diseases common to modern man. My plan was to develop the hypothesis that the insulin to glucagon ratio was the metabolic underpinning for both the development of –� and thus the treatment of — obesity, high blood pressure, elevated blood sugar, heart disease and hyperlipidemia (which at that time I still thought was a disease).� I was going to marshal the evidence from all the studies I could find (there weren’t a lot at that time) to explain the results I was seeing in myself and in my patients.

And then, thanks to that one sentence about coronary artery disease being a common finding in Egyptian mummies, this mountain of paleopathological data I was unaware of dropped into my lap.

The realization that a major argument on behalf of the low-carb diet lurked in the literature of Paleolithic disease led me to the orgy of study mentioned above and threatened to take over the book I was writing.� This anthropological material so fascinated me that I didn’t want to read anything else.� I missed my deadline because I kept finding just one other thing to add, and, ultimately, my editor left (not because of my delay, but because she went to work for another publisher) leaving me with an orphaned book.� My agent said I needed to find another publisher, so I went to New York to do yet another dog and pony show for a handful of book companies.� An editor from Bantam Books finally decided to buy my contract from my former publisher.� MD went with me to the presentations, and the Bantam group liked the idea of the two of us being co-authors, so that’s how our publishing collaboration began.� I had written This So Fast by myself, and MD had by then written four or five books on her own.� Since that time, we’ve co-written every book.

Our new editor indulged me in the chapter on anthropology and diet I called “Curse of the Mummies,” but, alas, when it came time for the paperback our editor had left Bantam (an occupational hazard of mainstream publishing), and the new editor assigned to us did not like the Paleo stuff, so she militated to have it removed.� As you might imagine, I went berserk.� It was my favorite part of the book and the one I felt most strongly argued the notion that we were genetically programmed to thrive on low-carb diets.� She disagreed.� She had her own ideas as to what a diet book should be, and a chapter on the anthropology of diet didn’t fit her script.� Out of frustration, I let her browbeat me into moving the chapter to the back of the book.� So, if you have a hardback of Protein Power,� you’ll find “Curse of the Mummies” as Chapter Two, right up front where it belongs.� If you have the paperback, it will be way in the back in an epilogue right in front of the appendix.� And it will be titled “Overcoming the Curse of the Mummies.”� It wasn’t until I just now went back to look at it in the paperback that I realized that not only had this editor moved the chapter to the back of the book, she changed the title as well. What a troll!

(Thanks to the success of Protein Power, we had vastly more pull with our next publisher, so we wrote The Protein Power LifePlan as a total evolutionary-based, Paleo kind of book.� Maybe our former editor was right because the PPLP never sold as well as Protein Power.)

Another benefit of reading that one little sentence in Napoleon’s Glands and acting on it was a great and lasting friendship.� Upon publication of Protein Power, Loren Cordain, whom I had never met, contacted me, introduced himself and asked me to speak at the Colorado State University in Ft. Collins, CO.� I accepted. Loren and I became friends, and when he wanted to write his book on the Paleo diet, I lent him my agent, who has been his agent since.� Through Loren I met Rob Wolf,� Staffan Lindeberg and a host of other writers and researchers the world over.� Which would doubtless have never happened had we just written a typical diet book.

After receiving all the feedback on the Paleo stuff in our book, I began to think Protein Power was the first book for the layman using the Paleolithic diet to argue for low-carb eating.

I knew the Paleolithic Prescription was out there, but it was written in an attempt to shoehorn the real Paleo diet into a low-fat framework. Which was bizarre because the authors of the book wrote a groundbreaking paper on the Paleo diet in the New England Journal of Medicine that got them much notoriety along with a book contract.� From what I’ve since heard, their editor strong-armed them into making their diet low-fat, because that was what ‘everyone’ believed in then.

I then remembered Neanderthin, a book that came out while Protein Power was going through the publication process.� It originally was a little, self-published paperback I happened upon in a Borders (RIP) in Dallas.� And it probably would have escaped my notice had I not been so attuned to dietary anthropology.� I tracked down the main author, Ray Audette, who lived in Dallas.� MD and I had dinner with him and his wife a time or two, and after his little paperback had sold enough copies, he got a mainstream contract, and I agreed to write the forward to his mainstream-published book.

I’ve since found two more books published before Protein Power that based their diets on Paleolithic principles.

(Actually four if you count books by Vihljalmur Stefansson and Wolfgang Lutz.� Stefansson wrote Not By Bread Alone in 1946 and it’s expansion and sequel The Fat of the Land in 1956.� These were not really diet books but were more descriptions of the diets followed by the early peoples who populated North America.� Lutz wrote Dismantling a Myth: The Role of Fats and Carbohydrates in Our Diet, which was an actual textbook and a follow up to his book in German, Life Without Bread.� Dismantling a Myth, published in 1987, contains a chapter titled “Evolution as an Argument,” which is his argument that anthropology shows man to be designed to consume a diet of primarily protein and fat.� I wish I had had this book when I wrote the relevant material in Protein Power, but I didn’t know of it’s existence until the early 2000s.� It is almost impossible to find — I was not able to get my own copy until just a few years ago.)

The two low-carb low-carb, Paleo diet books were written by two physicians on opposite sides of the country.� In 1961, Blake F. Donaldson, M.D. wrote� Strong Medicine, a book describing his methods of treating pretty much anything that ailed his patients.� His book contains one of my all time favorite lines that I quote often.

During the millions of years that our ancestors lived by hunting, every weakling who could not maintain perfect health on fresh fat meat and water was bred out.

Dr. Donaldson was having trouble getting his overweight patients in his practice in New York to drop the pounds.� He had heard of Stefansson’s experiment in which he and another explored went a year under supervision at Bellevue Hospital on a meat-only diet and emerged from the experience lighter and in better health.� Donaldson invited Stefansson to dinner and picked his brain.� As a result, Donaldson began treating his own obese patients on basically an all-meat diet.� (His actual diet was a half pound of meat, one small boiled potato, and a half cup of black coffee or tea at each meal – and nothing else throughout the day.) He had such success that he began treating just about every health problem presenting to his clinic with his almost all-meat diet. Unlike with Dismantling a Myth, you can find copies of Donaldson’s Strong Medicine pretty easily.� It makes an interesting read.� But beware.� It will show you how much times have changed since 1961.� By today’s standards, it is sexist and racist to the max.

The Stone Age Diet, written in 1975 by Seattle gastroenterologist Walter Voegtlin, M.D., is the second book I’ve found using a Paleolithic rationale for the low-carb diet.� Dr. Voegtlin was a GI doc and a comparative anatomist.� He noticed the similarities in the GI tracts of carnivores and humans and concluded that the human GI tract was essentially that of a carnivore.� He then reasoned that maybe a fair number of the GI problems he was seeing in his practice arose as a consequence of the high amount of carbohydrate in the typical diet, an amount no carnivore would eat.� He tried treating some of his patients with GI disorders with all-meat diets and saw them experience dramatic improvement.� He, like Donaldson, began treating most of his patients with such diets and found that not only did their GI symptoms improve, but they lost weight, too.� Dr. Voegtlin couldn’t interest a publisher in his book, so he self published.� Consequently, his book is almost impossible to find.� I had to search for years before finding a copy and ended up dropping $200 for it. It’s a shame this book didn’t have wider distribution because it is elegantly written and a delight to read. Dr. Voegtlin must have spent a lot of time thinking about these dietary issues because his book is full of insights I’ve never read anywhere else.� If enough people ask, via the comments, I’ll take the time to transcribe his chapter on the difference between the digestive tracts of carnivores and herbivores and make it available. It is illuminating.

These are the only books I’m aware of that pre-date our own using paleopathology to argue for low-carb. If anyone knows of any other books published prior to Protein Power (1996) using the Paleo diet or an evolutionary/natural selection basis as the rationale for a low-carb diet, I would love to hear about them.� I will seek them out to add to my collection and mention them in an addendum to this post.

I promise my next post/posts on books that changed my life will not be this lengthy.� I will try to put them in a single post with a paragraph about each one and a brief description of why and how each affected me.� I planned to do that with this one, but the change was so momentous that I decided to take it and run with it.� I hope you enjoyed reading about the odyssey as much as I enjoyed reliving it.

ADDENDUM: A hat tip to commenter Ash Simmonds who posted a link to the complete version of The Stone Age Diet.� If you want to read the parts about the comparative anatomy of carnivores, herbivores and humans take a look at chapters 4, 5 and 6.

And a hat tip to commenter Monkeyman, who found a full-text, online version of Stefansson’s The Fat of the Land. (Clicking the link will download the entire book in pdf.)

The post Books That Changed My Life appeared first on The Blog of Michael R. Eades, M.D..

A paper recently appeared in the scientific literature demonstrating an enormous and previously unknown benefit of low-carbohydrate dieting. (1) I haven’t seen this study mentioned anywhere, so, important though it is, it seems to have flown under the radar of all the low-carb experts and the press. It is a study about how restricting carbohydrates – even in the face of overfeeding – drives profound signaling protein changes. This is an exciting study, but before we get to the specifics, I want to digress a bit.

First, a story about my own peripheral involvement in a similar study many years ago.

At a scientific meeting in the late 1980s I found myself in a hotel bar with a couple of young anti-aging researchers, who were affiliated with a major government nutritional research facility. The brunt of their research focused on the enzymatic changes in lab animals undergoing caloric restriction. In the course of their work, they found that calorically-restricted rodents exhibited the same changes as did primates and, they assumed, humans. But they had no human data to confirm. They, along with everyone else in caloric-restriction research, knew that reducing the calories fed to rodents improved their health and extended their lives. And at that time, it was looking as if the primate research would show the same thing. (It ultimately did.) What these guys wondered about, though, were humans. Did humans undergoing caloric restriction display the same enzymatic changes?

No one knew because at that time there were no human caloric-restriction studies.

During the course of our conversation, I told these researchers about my practice and about the success I was having with patients on low-carb diets. I explained how my patients lost weight fairly easily and experienced significant and rapid changes in blood pressure, lipids, fasting insulin and blood sugar levels. They became intrigued since these changes pretty much mirrored those seen over time in caloric-restriction studies on lab animals. It set them to wondering whether humans following low-carb diets would manifest the same enzymatic changes as calorically-restricted animals. They proposed an experiment.

Before we plunge ahead, though, let’s take a minute to review enzymes. Enzymes are such an integral part of everything that makes life possible that I often forget that they are not really common knowledge. This was brought home to me with great clarity when I was having a conversation a couple of weeks ago with someone who, though not a doctor or a scientists, has a pretty firm grasp of the overall workings of the metabolic system. I was rambling on about the phenomenal results of the study we’ll soon be delving into and mentioned enzymes. My friend fixed me with a quizzical look and asked, “What is an enzyme?”� I figure if this guy didn’t know, there are many people out there in the same boat. If you know all about enzymes, feel free to skip on down to where I pick up on happy hour.

What are enzymes? Where do enzymes come from and what do they do?

Enzymes give us life. If it were not for enzymes catalyzing the unimaginable number of reactions required for us to live, we would all be giant lumps of fairly inert chemicals instead of the moving, breathing creatures we are. Every impulse we have, every beat of the heart and blink of the eye, every breath we take is the end result of a series of chemical reactions, none of which would take place without enzymes driving them. Every time you see a chemical reaction that takes place in the body, each step is catalyzed by a specific enzyme. Take a look at the partial pathway of glycolysis from Wikibooks. Each of the steps shown is catalyzed by a specific enzyme.

Below right is another well known biochemical pathway, the synthesis pathway for cholesterol. The most important enzyme in this pathway, hydroxyl-methylglutaryl coenzyme A reductase (HMG CoA reductase), is the rate-limiting enzyme in the cholesterol synthesis pathway. And it is the enzyme that statin drugs inhibit. Inhibiting HMG CoA reductase decreases the body’s production of cholesterol. Unfortunately, there are some downstream effects of this inhibition that the statin folks don’t like to talk about. The next molecule in the pathway, mevalonic acid, is catalyzed by yet another enzyme into farnesyl phosphate, which is the precursor to Coenzyme Q10, an important substance found throughout the body. So inhibiting HMG CoA reductase in an effort to reduce cholesterol often ends up also depleting the body of Coenzyme Q10. Graphic came� from this paper on statins and Coenzyme Q10.

Enzymes are large proteins coded for in the DNA and transcribed from an RNA template. Enzymes have varying degrees of activity, typically controlled by other enzymes upstream in the reaction cascade. The synthesis of new enzymes takes a while (which is why there is an adaption period when switching to low-carb dieting) but the activation of existing enzymes can take place almost instantly. Activation typically involves adding or removing a chemical group from one of the amino acid chains of the inactive enzyme.

Some enzymes catalyze only one reaction, while others catalyze many. A few are master regulator enzymes in that they catalyze many reactions and activate or deactivate multiple other enzymes and enzyme pathways. These enzymes, often called signaling proteins, drive and/or inhibit multiple systems. It is these enzymes that scientist measure the activity levels of to determine what effect various drug treatments or nutritional therapies bring about.

So, back to my happy hour conversation.

The two researchers proposed an experiment in which I saved a little blood from the regular labwork that I did on all my new patients. They wanted me to then send them a bit of blood from these same patients when they came in for their regular six-week blood tests. (I drew blood on all patients during their initial visit and again at six week intervals to monitor progress.) They sent me special collection vials and a coding system so that patients would remain anonymous. I asked the patients if they minded, and no one did, so the experiment started.

I dutifully collected the blood and sent if off. After enough patients had cycled through their first six weeks, I got an enthusiastic call from the researchers. And enthusiastic is a mild word for their state of mind. They were practically gibbering with excitement, because they had found the same enzymatic changes in the blood from the patients who weren’t trying to restrict calories but were simply following a low-carb diet. They told me they were going to report their preliminary data to their boss to see if they could pursue funding to continue research with my patients.

When they called me back their enthusiasm was gone. In its place was an overwhelming glumness. They presented the data to their boss, who was the head of the research institute at which they worked, and the response was not what they expected. He told them that they had not followed academic protocol, they hadn’t gone through an institutional review board, and had no business doing an off the books experiment using the institute’s equipment. They got the lecture about how they put the institution at risk and how they could be fired if and on and on. He told them to wash their hands of the whole thing. Which they did.

They didn’t share their data with me, so I never learned what changes had taken place. I did figure, however, that the changes must have been pretty good given the degree of excitement they generated. At that time, I was simply a clinician taking care of patients and hadn’t started my deep dive into the scientific literature, so I really had no idea what the enzymes they looked at were.

Which brings us 25 years later back to the paper just published online ahead of print in Hormone and Metabolic Research. This paper discusses the activity level of adenosine monophosphate-activated protein kinase (AMPK) as a function of carbohydrates in the diet. AMPK is an enzyme with all manner of downstream effects and can be considered as the Queen Mother of all enzymes, a powerful signaling protein that drives multiple metabolic pathways. You can see a photo of a 3D model of AMPK at the top right of this post from Wikipedia.

The ‘K’ in AMPK stands for kinase, which means that it adds a high-energy phosphate group to other downstream compounds. AMPK is itself activated by an upstream kinase called, appropriately enough, an AMP kinase kinase.

AMPK: what does it do?

AMPK basically monitors the energy levels inside the cells, and when it finds them low, it kicks off several chains of reactions directed toward energy repletion.(2)

As most of you know, ATP is the body’s energy currency. It is made from its precursors ADP and AMP. The food we eat ends up as high-energy electrons that drive the process designed to keep the cells filled with their high-octane energy molecules ATP. You can think of how a battery works. When it is charged, it is at the ready to discharge current to run an iPad, flashlight, cellular phone, whatever. After a time the battery needs recharging or it ceases to provide current. Human cells operate much the same way, but they have an advantage over an iPhone. Human cells have the ability to constantly recharge as their supplies of ATP are consumed. The ratio of the ATP precursors ADP and AMP to ATP signals whether the body should be in the energy discharging or energy storing state.

The signaling protein AMPK monitors this cellular ‘battery’ and sends the appropriate signals to ramp up the forces required to restore the ATP balance to the fully charged state.(3)

If we eat less or don’t eat, we discharge our cellular batteries, because we continue to use ATP but aren’t providing the energy via food to make more. If we exercise, we discharge our batteries, because we are consuming large amounts of ATP quickly, and unless we’re eating on the run – literally – we are not getting the food energy needed to replace our depleted ATP. So when we eat less and/or exercise, we put ourselves in a cellular battery discharge state.

Numerous studies have shown health and longevity benefits from eating less and exercising, though these prescriptions are tough to stick with for the long haul. If this is true, and I believe it is, then the body is better off health-wise to be in a battery-draining state more of the time than in a battery-charging state.

Just for clarity’s sake, a distinction should be made so that confusion doesn’t set in. By cellular battery, I’m referring to the ratio of ATP to ADP and AMP in the cells. I’m not talking about stored fat and sugar. In this model, stored fat and stored sugar would be considered the wall charger or power company where the power comes from to charge the batteries in our devices.

Whether the body is exercising or resting, eating or fasting, the cells need to have their ATP levels pretty much constant. But caloric restriction and/or exercise deplete ATP quickly, so this ATP needs to be restored just about as quickly as it is being depleted.(4) The new ATP needed to top off the tank comes from high energy electrons thrown off from burning fat and/or glucose. If there is no fat or glucose coming in via the mouth, it must come from stores socked away in the body. From glycogen (stored glucose) and body fat.(5)

When ATP levels fall as the batteries discharge, signals go out to the parts of the metabolic system that are responsible for harvesting the energy from stored sugar and fat to create the high energy electrons required to make more ATP.

AMPK is one of the primary signaling proteins that monitors the ATP levels in the cells and signals for more energy when levels drop. When AMPK is activated indicating our cellular energy tanks are depleted, all kinds of good things happen. Here is a short list of metabolic efforts all kicked into action by activated AMPK and why they’re important. (adapted from ref #6)

• Increases glucose uptake: We want to get glucose out of the blood and into the cells to burn.
• Increases glycolysis: We need to break down glycogen (stored sugar) to get the glucose to burn.
• Increases fatty acid oxidation: An obvious one. We want to start burning fat to replenish the depleted energy stores.
• Increases mitochondrial biogenesis: we want to make more mitochondria to burn fat and generate as much ATP as possible.
• Inhibits gluconeogenesis: We don’t want to spend energy making more sugar – we want to burn it.
• Inhibits glycogen synthesis: Same thing – we don’t want to store sugar, we want to burn it.
• Inhibits fatty acid and cholesterol synthesis: We don’t want to spend energy making fat and cholesterol.
• Inhibits insulin secretion: We want insulin to be low, so that we can move stored fat and sugar to where it needs to be burned.

When our ATP tanks are filled to the bursting, as when we eat and are stuffed with food (especially carbohydrates) and/or we don’t exercise, all the above pathways go in the opposite direction. If we chronically overeat the wrong foods, our metabolic systems end up sending all the above pathways in the opposite direction most of the time.

When viewed from this perspective, it’s pretty easy to see why AMPK activated by a calorically-restricted diet and/or exercise brings about many healthful changes. It also might make one wonder why drugs haven’t been developed to increase the activity of AMPK to provide these same benefits to people who suffer from obesity, high blood sugar, diabetes and all the other disorders caused by overnutrition. A drug designed to activate AMPK would be diet and exercise in a pill. Who wouldn’t want that?

Well, there are several such drugs. Most have probably heard of one of them: metformin (trade name Glucophage.) Metformin, derived from an ancient herbal remedy, is used by doctors to treat diabetes and insulin resistance and works by activating AMPK. In 2010, physicians wrote some 100 million prescriptions for metformin to treat type 2 diabetes.(5) Some use it to treat obesity, and many folks who can get access to it, take metformin in hopes of increasing longevity.

Drugs that increase the activity of AMPK, when used over time, along with all the effects mentioned above tend also to increase the number of mitochondria, which increases the capacity to burn fat and turn it into ATP. More mitochondria leads to improved endurance, and, consequently, many of these drugs have been placed on the banned list of the World Anti-Doping Agency, the regulating body that deals with drug abuse in sports.(7)

Up to this point in this post, your take away message should be that activated AMPK is a very good thing. If your AMPK is activated much of the time, it would indicate you are eating less, exercising more and making mitochondria. All to be desired. Plus, though it has no bearing on the study we’re about to discuss, it looks like AMPK activation modulates the immune response in a positive way (8) and may even prevent some kinds of cancer.(9) More good things.

At last, to the paper at hand.

Now that I’ve set the stage, lets get to the exciting study that kicked off this blog post.

The researchers knew that AMPK was activated with calorically-restricted diets. They wanted to test whether or not macronutrient composition had an effect on AMPK activity.

These folks from the medical school at the University of Colorado presented two different studies in this paper. I’m going to discuss them in reverse order.

Study #2

In the second study, eighteen obese subjects (8 men – 10 women; avg age 32.4 years and avg wt 227.3 lbs) went on a eucaloric (enough calories to match energy output) diet of 30% fat, 50% carbohydrate and 20% protein for five days to establish a baseline. After the five days, the subjects were randomized to receive either five days of a low-fat, high-carb diet (20% fat, 60% carb, 20% protein) or five days of a high-fat, low-carb diet (50% fat, 30% carb, 20% protein). Both of these diets were restricted to 30% of the calories in the baseline diet. On the night of the fifth day of the study, patients were hospitalized and after an overnight fast, the researchers performed insulin clamp studies and muscle biopsies.

What did study #2 show?

After five days on the calorically-restricted diet, obese subjects in both groups experienced modest weight loss. There were no significant changes in the subjects in either group in any parameters of insulin sensitivity. In both groups, as would be expected on a calorically-restricted diet, fasting insulin levels fell.

Since both diets were calorically restricted, it was expected that the activity levels of AMPK would be increased. And in the low-carb/high-fat diet, AMPK levels were significantly increased. The big surprise, however, was that the activation of AMPK in those subjects on the low-fat/high-carb diet was basically unchanged.

As the study authors put it, this change as a function of carb restriction

suggest[ed] that high carbohydrate intake prevents activation of AMPK… in skeletal muscle that otherwise would have been induced by caloric deprivation.

In other words, these subjects were rowing one way by reducing calories while rowing in the other direction by increasing carbs. Maybe this is the explanation of why it’s so difficult to lose weight and improve health parameters on a low-calorie, high-carbohydrate diet.

Study #1

In the first study – which I think is the much more interesting – the researchers recruited 21 lean (11 men, 10 women; avg age 27.8 yrs; avg wt 147.4 lbs), healthy, non-diabetic subjects, all of whom were started on the same five-day eucaloric baseline diet as the subjects in the other study (30% fat, 50% carb, 20% prot). The subjects were then randomized into two different groups, both of which consumed 40% more calories as compared to baseline. These five-day overfeeding diets were either low-carb (50% fat, 30% carb, 20% prot) or low-fat (20% fat, 60% carb, 20% prot). As before, on the fifth day of the overfeeding study, subjects were hospitalized so that insulin clamp studies and muscle biopsies could be done the next morning. Then, unlike with the other study, this same group of subjects came back a month later and went through the process again except in a cross-over fashion so that each subject could act as his/her own control.

What did study #1 show?

Interestingly, despite the 40% caloric overfeeding, no significant changes in body weight occurred in either diet. And there were no changes in insulin sensitivity, glucose, lipids or other parameters measured. What was truly amazing, however, was what happened to AMPK activation. Low-fat/high-carb overfeeding did not produce any effect of AMPK activity as compared to baseline. But low-carb/high-fat overfeeding produced a significantly increased activation of AMPK.

In referring to these two studies, the researchers noted:

We observed that caloric restriction with [a low-fat/high-carb] diet did not alter the AMPK [activation], suggesting that increased dietary carbohydrate content even in the face of caloric restriction prevented activation of AMPK… in skeletal muscle of obese individuals. In contrast, overfeeding with [a low-carb/high-fat] diet increased the activity of this pathway [AMPK] indicating that low carbohydrate content may be sufficient for its activation.

And in summary, they commented:

Our data indicate that a relative deficiency in carbohydrate intake or, albeit less likely, a relative excess of fat intake even in the absence of caloric deprivation is sufficient to activate this network and increase fat oxidation.

These studies may provide an answer as to why most weight-loss studies comparing low-fat/high-carb diets to low-carb/high-fat diets almost always find the low-carb diet to bring about the greatest loss.

And this activation of AMPK even in the face of overfeeding may explain why it is difficult for most people to gain weight on a true low-carbohydrate diet. Even one with a large dollop of extra calories.

This paper is exciting because, at least in this case, researchers are looking at what macronutrient differences do to signaling proteins, even in the face of overfeeding. Up until now, most researchers have written if off to a caloric-restriction phenomenon. It’s nice to see that this group has tried to tease out what is really doing the heavy lifting in terms of AMPK activation. It appears to be the carb restriction.

If these findings hold up in other studies, then it would seem that, in a manner of speaking, you could have your cake and eat it, too. Wouldn’t it be nice to be able to go on a diet that truly allowed you to eat all you wanted and have that diet not only not put excess avoirdupois on you but even make your body think it had been exercising?

Before I get too carried away here, there are a few questions this study raises.

First, as anyone who looked at the different diets critically would notice, the low-carb arm of the diet wasn’t really all that low-carb. Reducing carbs to 30 percent of calories is a semi-sort-of low-carb diet. Most people following true low-carb diets get their carbs down to anywhere from 5-15% of total calories. If would be nice to know if these findings held with subjects following a really low-carb diet and not the minimal restriction studied. I would bet the findings would be even better. I base this on the enthusiasm of the researchers years ago who studied the blood of my own patients on very-low-carb diets. But that kind of data won’t feed the whippet, so we’ll have to wait until further studies are done with lower carb restriction to know for sure.

Second, these studies were of only five days duration. We don’t know if AMPK activity runs up and hits a max at five days only to begin to decline thereafter and end up lower on a low-carb diet after two weeks or a month or six months. We simply don’t know based on the data from this study.

Third, there weren’t a huge number of subjects in these studies, so, once again, though the data looks tantalizing, it might not hold if several hundred subjects were evaluated.

Given my bias, installed by several decades of using low-carb diets to treat all kinds of problems, I suspect the data will hold up and get even better with more carb restriction and longer study periods. But we’ll have to wait and see until we know for sure.

Such an exciting study as this one should drive a fair amount of research in this direction quickly. If you do a PubMed search for AMPK, you will find there is plenty of interest. I hope we don’t have to wait long. But until new research comes along definitively overriding this paper, I’m going to continue my own regimen of restricted carb dieting and recommend you to do the same.

Citations

1. Draznin B, et al. Effect of Dietary Macronutrient Composition on AMPK and SIRT1 Expression and Activity in Human Skeletal Muscle. Horm Metab Res. 2012 Aug;44(9):650-5.
2. Hardie DG, et al. Management of cellular energy by the AMP-activated protein kinase system. FEBS Lett. 2003 Jul 3;546(1):113-20.
3. Kahn BB, et al. AMP-activated protein kinase: ancient energy gauge provides clues to modern understanding of metabolism. Cell Metab. 2005 Jan;1(1):15-25.
4. Hardie DG, et al. AMPK: a nutrient and energy sensor that maintains energy homeostasis.
Nat Rev Mol Cell Biol. 2012 Mar 22;13(4):251-62.
5. Hardie DG. Organismal carbohydrate and lipid homeostasis. Cold Spring Harb Perspect Biol.
2012 May 1;4(5).
6. Hasenour, C.M., et al. Emerging role of AMP-activated protein kinase in endocrine control of metabolism in the liver. Molecular and Cellular Endocrinology 2012, Epub ahead of print. http://dx.doi.org/10.1016/j.mce.2012.06.0185.
7. Hardie DG. AMP-activated protein kinase: an energy sensor that regulates all aspects of cell function. Genes Dev. 2011 Sep 15;25(18):1895-908.
8. Lui TF, et al. Fueling the flame: bioenergy couples metabolism and inflammation. J Leukoc Biol. 2012 May 9. [Epub ahead of print]
9. Fogarty S & Hardie DG. Development of protein kinase activators: AMPK as a target in metabolic disorders and cancer. Biochim Biophys Acta. 2010 Mar;1804(3):581-91.

The post Can your food make you fit? appeared first on The Blog of Michael R. Eades, M.D..

The two videos below pretty much tell the whole sad tale of doctors and nutrition.� Taken together, they confirm the widespread notion that doctors, in general, know very little about nutrition and seem to be proud to keep it that way.

This first video has made the rounds on the internet.� I�ve had it sent to me or recommended to me a dozen times, but I had never watched it until just a few days ago.� I was put off because of its length, which, at a little over 17 minutes, seems like an eternity in internet viewing time.� But I hope anyone reading this post doesn�t make the mistake I did and avoid watching because of the length.� It is a spectacular talk given by Dr. Terry Wahls, a female physician who was struck down by a relentlessly progressive neurodegenerative disorder.� She describes how she was able to restore her health by revamping her diet in in a way designed to properly feed her mitochondria.*� The transformation is almost unbelievable, especially considering the disease she was battling.� If you haven�t already seen this video – watch it.� I guarantee you�ll be glad you did.� And while you watch, pay careful attention to what her diet doesn�t contain much of.

Click here to view the embedded video.

After you�ve seen the above video, take a look at the one below.� It is a little over 2 minutes long and was developed to give doctors – who, for the most part, don�t give a flip about diet – advice they can pass along to their obese or overweight patients.� Watching the longer video above first will give you more context to better appreciate the one below and show you just how lame mainstream medicine can be.

This video came from Medscape, a subscription service for doctors to keep them abreast of all the latest and greatest news and updates from the world of mainstream medicine.

Click here to view the embedded video.

Pitiful, isn�t it?

Links:

The Medscape article containing this video.� (Although Medscape is a free subscription service for physicians, non-physicians can sign up as well.� For free.� Register if you would like to see the article, which is nothing more than a transcript of the video above.)� It is amazing to me that an online newsletter designed for physicians would regurgitate dietary information from a newsweekly and pass it off as serious medical information.� Especially in such a condescending and patronizing way.� The whole thing is infuriating.

The list of the 22 nutritional �experts� who came up with the dietary rankings mentioned.

The US News and World Report article that inspired the video.

Power, Sex and Suicide� A pretty thorough book on mitochondrial function that is accessible to the non-scientist.� I read this book 6 or 8 years ago and learned a fair amount about mitochondrial DNA.� I had been interested in the issue of mitochondrial rehab for a while, and this book filled in some, but not all, of the blanks.� A good place to start if your interested.

Why Are Cells Powered by Proton Gradients?� Full text of a paper written by Nick Lane, the author of the above book, discussing how mitochondria work by creating an energy gradient across the inner membrane.� Accessible to non scientists.

Source of photo of mitochondria at top of post.

* Mitochondria are the little sausage-shaped organelles inside the cells that convert the energy stored in food to ATP, the energy currency of the body. I think the idea of correctly feeding mitochondria is an important one.� If your mitochondria don�t work well, you don�t work well.� I�ve got a couple of posts in the works on this subject of just what does keep the mitochondria fit and what happens when they become unfit.� And what it takes to rehab them if broken.� Based on my own pretty extensive review of the scientific literature over the past few years coupled with my clinical experience, I have a few minor quibbles with Dr. Wahls� notions of what constitutes a perfect diet for the mitochondria, but I�ve got to say that her results speak for themselves.� I just think her diet could be even better with a little judicious tweaking.

The post Mitochondria rejuvenating diet the nutritional ‘experts’ bash appeared first on The Blog of Michael R. Eades, M.D..

These were observational studies and, as such, can’t be used to determine causality.� But they are interesting nonetheless because according to one of the authors there have been other clinical trials showing the same thing.� One of the authors of the study, Dr. JoAnn Manson, Professor of Medicine and Harvard Medical School commented on the findings of this study and what they mean to doctors who put patients on statins.� Dr. Manson’s commentary was provided by Medscape, a site for physicians to go to learn about the latest in medical wizardry.� The site requires registration, but if you are interested, you are allowed to register even if you aren’t a physician.

I decided that instead of commenting on Dr. Manson’s video after the fact, I would do it in real time right on the video.� This is my first effort at anything like this, so you can let me know what you think of it.� If you find it enjoyable and/or helpful, please drop a note in the comments, and I may be inspired to try it again.

You’ll notice my repeated assertions that statins don’t provide any benefits.� What I’m talking about is the fact that statins have never been shown to decrease all-cause mortality. (See the first sentence in the Lipitor product insert above.) � In other words, if you take a statin, you gain no increase in life expectancy.� If I, myself, am evaluating a drug that I might have to take, I would certainly want to make sure it didn’t simply replace one risk factor for another.

Click here to view the embedded video.

Note: The comments on this video made by me are my opinions based on my reading of the medical literature.� They are no substitute for consultation with your own physician, and should in no way be construed as medical advice.� The decision to start, continue or discontinue any drug regimen is a serious one and should be a decision made after careful discussion with your own physician.

As I mentioned in the video above, I just read a book by a cardiologist practicing the California who has dived deeply into the scientific evidence and feels the same way about the lipid hypothesis as I do.� And about statin drugs.� And this a real cardiologist.� Ernest N. Curtis, M.D. has written The Cholesterol Delusion, a book that takes a different approach to dismantling the lipid hypothesis than The Great Cholesterol Con, but is just as effective.� If you’re still in the camp that worries about cholesterol, you may take solace from the information in this terrific book.� If you need to persuade a friend or loved one, this is the book.

If you enjoy the way I sometimes dissect studies on this blog, you will love Dr. Curtis’s book because that’s what he does.� He dismembers the studies that the lipophobes rely on to maintain their fantasy that cholesterol really does cause heart disease.

Take for example the Lipid Research Clinics Coronary Primary Prevention Trial (LRCCPPT), the authors of which made the oft repeated claim that each 1 percent reduction in cholesterol gives a 2 percent reduction in cardiac risk.� Dr. Curtis eviscerates this study and describes how the authors dishonestly spun their experiment’s end result, which was essentially meaningless, in such a way that it has become one of the mainstays in the argument for cholesterol lowering.

During the study, 7 percent of the subjects on a cholesterol-lowering drug died while 8.6 percent of those on placebo died.� Dr. Curtis describes how this minuscule difference can be converted into a relative risk difference of 19 percent, which is what the authors were crowing about.� But that number isn’t nearly as important as the absolute risk, which is the difference between the 8.6 and 7, or 1.6 percent.� So those subjects on the drug (which is not without side effects and costs if the subjects had been paying for it themselves) ended up with a 1.6 percent lower absolute risk than those who didn’t take the drug.

But that’s not the end of the story.� Was the 1.6 percent difference even statistically significant?� Here’s where things get interesting.

How significant is the difference between 7.0% and 8.6%? Common sense tells us that this difference is of no practical significance.� But what about the more esoteric criterion of statistical significance?� According to the pretrial protocol, which called for a level of certainty with p<0.01, it didn’t even come close.� If one applies the more lenient criterion of p<0.05, it still fails the test when the typical two-tailed test is employed.

If one applies the p<0.05 criterion and uses the less rigorous one-tailed test, however, this difference barely qualifies as statistically significant.� This is, in fact, what the investigators did.� In one of the most flagrantly dishonest acts ever seen in a major medical study, the authors apparently changed the criteria for significance after reviewing the data.

The is absolutely shameful behavior way beyond the pale.� When researchers design a study, they set on the front end the statistical parameters by which the outcome of their experiment is to be measured.� They do this at the start so there can be no fudging at the end when the results are in.� Everyone agrees to the standards and off they go to do the study, and the outcome either reaches the level of statistical significance by the predetermined measure or not.� In this case, the standards were set, but when they weren’t reached, the standards were reduced once and then again before the results barely were able to claim statistical significance.� Shameful indeed.� And this is one of the major studies, quoted daily, showing that a reduction in cholesterol brings about a reduction in heart disease.� Jesus wept.

Why didn’t other scientists say anything about this.� One did and wrote� a withering critique in the Journal of the American Medical Association, but the journal kept it under wraps for a year before publishing.� By that time, the LRCCPPT had gotten so much coverage and the cholesterol-lowering-prevents-heart-disease mantra had swept the nation, so everyone pretty much ignored the grousing of a scientist who saw the emperor without any clothes. (You can’t tell much from the abstract I linked to, but Dr. Curtis reprints some of the juicier parts.)

This study isn’t the only one with warts all over it nor the only one routinely misinterpreted.�� But it’s not surprising given the vast amount of money at stake in the business of reducing cholesterol by drug therapy whether that cholesterol reduction is important or not.

After you read Dr. Curtis’s book you will become as big a skeptic as I am of medical studies and regard them all with a jaundiced eye.

The post Statins and diabetes appeared first on The Blog of Michael R. Eades, M.D..

I get feedback on the posts I write from three sources.� First, MD looks at them and tones them down if I�ve gone off on some sort of political tangent or if I�ve scattered in a bit of too colorful language.� After she gives me the go, I put the posts up and wait to see what the commenters have to say.� The third source for feedback is my friends, some MDs and/or PhDs and some not, who pick up the phone and call me.

MD okayed what I wrote. The readers who commented seemed to realize what I was trying to say.� But the phone calls were a different story.

One friend called to say she had been low-carbing since Jan 1, and when she read my post she became so depressed she almost quit.� �How can you tell people it�s hard,� she said.� �It�s the easiest thing I�ve ever done. I can eat till I�m full.� I�m losing weight; I�m losing the water I�ve been retaining; I feel great.� What a downer that post was.�

I heard different versions of that rant from three other people.� They all wanted to know why I would be idiotic enough to put up such a post right at the time everyone was trying to commit or recommit to losing weight.� Depressing was a word everyone used.

I guess I got off easy with the written comments on the blog.

I didn�t really mean for the post to be a downer.� Really.� I wanted to tell people who might be struggling to lose that MD and I fall prey to all the same problems.� We gained weight over the holidays.� We are back on the straight and narrow.� I was trying to say that we were right in there with everyone else working away to reestablish our own thinner selves.� (In fact, we�ve made great progress in the week or so we�ve been on the plan.)� I just wanted people to be aware that long-term weight loss requires effort and constant vigilance.� And to view the process as a life change and not a quick one-time fix. My goal was to get people to recommit seriously, not to depress them.

Obesity is a medical problem caused by a damaged metabolism, which is why one person, without the damage, can eat the same foods without gaining weight that pack the pounds on someone else.� Once you realize you have the underlying problem that leads to obesity, you simply have to recognize that you have to deal with it for the long term.

Let�s look at it in terms of another medical problem: high blood pressure.� For argument�s sake, let�s ignore the fact that about 80 percent of cases of high blood pressure can be reversed with a low-carb diet, and let�s just assume that the case we�re talking about is responsive only to high blood pressure medication.� If you were the patient with the high blood pressure, and I gave you a pill that brought your blood pressure down to normal, you would consider the medication effective.� Would you then say, Hey, my blood pressure is normal, yippee! now I can quit taking the medicine?�� I doubt it.� You would say, Great, the medicine is working.� Furthermore, if you quit taking the medicine and your blood pressure went back up to what it was before you started taking the medicine, would you say the medicine didn�t work?

Of course not.� Your high blood pressure was kept in check with the medicine, and your BP, not surprisingly, went back up when you quit taking the medicine.� The medicine itself was effective.

Same thing with dieting.� If you have an obesity problem that responds to a low-carb diet and you lose to your target weight, then go back to your old way of eating and gain your weight back, it isn�t the low-carb diet�s fault.� You have a problem that responds to a low-carb diet, and you pretty much have to stick with a low-carb diet (although not in nearly as extreme a structure as when you are trying to lose) for the long haul.

Having said all that, I can tell you that in my experience there is nothing that helps people lose weight more quickly and with less deprivation than a good quality, whole food low-carbohydrate diet.� You don�t have to be hungry.� You can eat rich, delicious foods, you�ll get rid of heartburn, drop your blood pressure, ditch excess fluid, and feel remarkably better.� You�ve just got to hang in there until you lose what you need to lose (which process you can speed along if desired with a little Metabosol), then you can loosen up and start adding some of the foods you�ve been foregoing.� And continue to eat them in moderation on maintenance.

Virtually all the studies in the medical literature show that at worst the low-carbohydrate diet equals the low-fat diet in all parameters and at best completely leaves it in the dust.� As far as I�m concerned, there is no faster, safer, more delicious way to lose weight. Hell, a study was just presented recently showing that women who did low-carb just two days a week lost almost twice as much weight as women following a calorically-restricted Mediterranean diet daily.� So, to be clear: Is weight loss tough?� Sure.� Is it easier when you cut the carbs? Absolutely! Low carb rocks!

Which brings me to the book that started this post.� In my opinion, The Art and Science of Low Carbohydrate Living is simply the best how-to book on low-carb dieting ever written.� As I wrote above, it is the book I wish MD and I had written.

The reason we didn�t write it is because a) some of this information wasn�t available when we last wrote a book (much of it is now available thanks to the work of Drs. Volek and Phinney), and b) no mainstream publisher would pay an author for this book.� If a mainstream publisher would buy it, the editor would force the authors to change it.� What do I mean by that?

All books fall into different genres, as they�re called in publishing.� One genre is diet/nutrition books.� So if you come to a publisher offering a diet/nutrition book, it gets pigeonholed into that genre and has to conform structurally to that genre�s standardized format.� Editors of mainstream publishing houses believe that the great mass of readers of nutritional books are not very bright and so have to be served real scientific information in small, small bites and not very many of them at that.� So the genre formula for a diet book is to have the actual diet regimen way up front because these editors don�t believe the readers of these books are smart enough or patient enough to wade through the explanations of why a particular diet works in order to get to the plan.� They want the plan up front within the first couple of chapters so people can get started without really having to read the book.� They also want a ton of recipes and meal plans to fill up the last half of the book.� Squeezed in between the plan and the recipe section is where they want to meat of book cubbyholed, and, in their view, with as little science as possible.

MD and I fought this structure tooth and toenail with Protein Power and ended up beating our editor down by agreeing to write a summary of each chapter called The Bottom Line that explained what each chapter said in non-scientific terms.� (Fortunately, we’ve been able to use this strategy in most of our books.) We worked well with our first editor, but we ended up in the hands of another editor when the paperback came out.� Editor Number Two hated all the stuff on the Paleolithic diet and the data from the ancient Egyptians.� This info was the first time in the popular press that the pre- verses post-agricultural diet was used as an argument for low-carb dieting.� And she wanted to ditch it from the book.� We went postal on her, so she ended up agreeing to leave it but only if we buried it in the very back of the book as an Epilogue.� That was one of the chapters of the book I wrote, and I thought it was pretty exciting information.� So, apparently did many others. But not this editor.� Sadly, she is not unusual.� Most want to conform to the genre.

Drs. Volek and Phinney self-published their book, and, as a consequence, could write it however the flip they wanted.� It is extremely well written and suffers none of the usual flaws of a self published book.� And it lays out the rationale for a low-carb diet as the treatment of obesity and other related disorders in a linear fashion instead of adhering to the typical diet book format.

As I finished writing the above paragraph, I clicked over and checked for comments on my latest post and found one with the following line:

This low-carb world can be a lonely place if one needs a navigator�

I can think of no better navigators than the authors of this book. Both of them have done a large part of the hardcore research on low-carb dieting that is in the medical literature today.� Go to PubMed and enter Volek JS or Phinney SD in the search window, hit �Search,� and you will be rewarded with more peer-reviewed scientific papers on low-carb dieting than you will have time to read.� Many of the experiments described in these papers are explained in easy to understand language in their book.

Disclosure: Both Dr. Volek and Dr. Phinney are friends and colleagues of mine.� But they did not send me a copy of their book for review.� I purchased it from Amazon and paid the full price of $29.95 (it is now $19.95).� I bought it months ago and carried it with me all over Europe and on a half dozen other trips since but didn�t have time to even crack it until I was on the last leg back from our holiday trek.� It sounds clich�, but I couldn�t put it down.� I read and annotated the entire book over the course of two long flights.� Virtually anything anyone could want to know about the science behind low-carbohydrate dieting can be found in this book.

I�ll give you just one example.� It is common knowledge among many nutritionist, doctors and journalists that saturated fats are bad for us.� Most believe eating saturated fats leads to higher levels of saturated fats in the blood, which they inevitably describe as �artery-clogging saturated fat’.� Drs. Volek and Phinney, who certainly don�t believe this nonsense, understand adaptation to a low-carbohydrate diet changes the way the human body metabolizes different fats.� Eating more fat on a low-carbohydrate diet speeds up the burning of fat in general and saturated fat in particular.

There are only three things the body can do with saturated fat from the diet (or saturated fat made from dietary carbohydrate — and, yes, the body can and does make saturated fat from dietary carbohydrate).� It can burn them, store them, or convert them to a mono-unsaturated fat.� When people go on low-carbohydrate diets, they reduce their insulin levels, which in turn allows fat to escape from the fat cells to become the body�s primary fuel.

But what happens when a person increases saturated fat intake as part of a low-carbohydrate diet?� Drs. V & P knew that saturated fat burning would increase, but would enough burn to offset the extra amount of saturated fat coming in as part of a high-fat, low-carbohydrate diet?

To find out, they put 20 subjects on a low-carbohydrate diet for 12 weeks and another 20 subjects on a low-fat, high-carbohydrate weight loss diet for the same length of time.� The subjects in the low-carb group consumed three times the saturated fat per day (36 g vs 12 g) as did those in the low-fat group.� The blood from the subjects in both groups was then tested to determine total triglyceride level and specific fatty acid composition.

What did the good docs find?

In the serum samples done at baseline and again after 12 weeks, serum triglycerides� in the low fat group went from 187 to 151 mg per 100 ml, a tidy 19% reduction.� But in the low carb group, the before and after values were 211 and 104, a whopping 51% fall.� Both visually (just looking at the numbers) and statistically, the low carbohydrate group had a much greater (better) reduction in serum triglycerides.

The above should come as no surprise, because everyone knows that a low-carb diet reduces triglyceride levels.� But what about the amount of saturated fat in the blood?

As a proportion of the total, the low carb group had 33% saturates [saturated fatty acids] at baseline and 29% after 12 weeks, whereas the low fat group started at 30 and ended at 29%.� So after 12 weeks of dieting, the proportion of saturated fats in the blood triglycerides was the same for both groups despite the fact that the low carb group was eating three times as many grams per day of saturated fat in their diet.

But there�s more.� Because the low carb group ended up with blood triglycerides of 104 mg per 100 ml compared to the low fat group�s 151, they actually had about 30% less total triglycerides circulating in their serum.� So although the two groups had similar relative proportions of saturates, this means that the absolute serum content of saturates in the low-carb group was 30% lower than the low fat diet group.� So what we found, in a nutshell, is that despite a higher intake of saturated fat, the proportionate blood level of saturated fats did not increase, and their absolute levels fell dramatically with the low carbohydrate diet.

The bottom line on this point is that when our metabolism adapts to a low carbohydrate diet, saturated fats become a preferred fuel for the body, and their levels in blood and tissue triglyceride pools actually drops.

To summarize, a three times higher intake of saturated fats leads to a 30% drop in saturated fats in the blood of those following a low-carb diet as compared to those following a low-fat, high-carb diet.

Which means, of course, that if you want to decrease the artery-clogging saturated fats (should that be what you want to call them) in your blood, a low-fat, high-carb diet, the very diet almost every health care professional recommends for the job, isn�t the way to do it.� All you have to do is simply follow a low-carb diet.

The description of what happens to saturated fats in the blood during a low carb diet took two pages out of a 300 page book, so you can imagine how much content the entire book contains.

There is so much invaluable information in this book that I�m having to fight back the impulse to quote the whole thing.� You�ll learn

why you need more sodium on a low-carb diet and why the sodium prevents lean tissue loss,
why you need to increase fat intake during maintenance,
why a low-carb diet decreases inflammation,
why the low-carb, high-fat diet improves gall bladder function,
why excess carbohydrate converts to saturated fat and how,
what all the lipid parameters mean and how they�re affected by a low-carb diet,
and what the Paleolithic evidence tells us about diet.

And this list is just scratching the surface.� As I read this book, I kept marking parts that I needed to use for this blog.� In going back through, I would have to practically reprint the whole thing to give you just the important parts because the entire book is a gem.

Unlike most traditional diet books, The Art and Science of Low Carbohydrate Living doesn�t contain a lengthy section on how to execute a low carb diet.� There are plenty of books out there – some written by MD and me – that do that.� The book does have about 10 pages of the authors� favorite recipes for low-carb foods and a seven day meal plan incorporating many of these recipes. (Another disclosure:� The authors recommend Protein Power as a good book on low-carb dieting, but I would have written this review the same had they never mentioned our book.)

The strength of this book isn�t in its meal plans and recipes, although those are delicious, it is in the wealth of information about all aspects of low-carb dieting.� If you have a question, almost any question, about any facet of low-carbohdyrate dieting, this book will have the answer.� And the answer will grounded in science, and in many cases from work done by these two scientists on the front lines of low-carbohydrate research.

As far as I am concerned, if you are planning on going on a low-carb diet and can afford only one book, make The Art and Science of Low Carbohydrate Living that one book.� If you are a long time low-carber, this is the one essential reference book you should have on your shelf.

If you are getting going on a low-carb diet the first part of this year, grab this book before you do another thing.� Once you see the world of benefits that will accrue to you from following such a diet, you will probably be able to overcome any depression that may have been inflicted on you from my last post.� So don�t hold off, grab a copy of this book today.� You will be very glad you did.

The post The best low-carb book in print appeared first on The Blog of Michael R. Eades, M.D..

The best and easiest way to stay slim is to never become obese in the first place.

What I mean by making this seemingly obvious statement is that when a person goes from being normal weight to being overweight it is an indication that something metabolically has gotten broken.� At this point, no one knows for sure what gets broken, but many (and I count myself in this ever growing group) believe the damage occurs in the mitochondria, the organelles within the cells that are the energy furnaces.� Once whatever it is that gets broken breaks, it is difficult from that point on to lose weight and maintain weight loss without effort.

The study I mentioned above showed that the non-obese didn�t really gain anything over the Thanksgiving through New Year�s holidays, and I�m sure it�s not because they didn�t go face down in the fudge.� They didn�t gain because their metabolic systems were working properly.

MD and I both had our struggles with excess weight starting a few of decades ago.� We were both thin, both ate whatever we wanted, and both never gained weight.� Until, that is, our metabolic systems became damaged.� Once that happened, we ballooned, then lost, then have fought it since.� We both have kept our weight under control for years now with a few exceptions here and there by judiciously following a low-carbohydrate diet.� Since we�ve both stayed pretty much in the normal weight range for at least the last several years, we decided to try an experiment over the holidays.� And not over the entire Thanksgiving to New Year�s stretch but for a fairly short stretch between Dec. 20-Jan 2.� We had planned to make a multi-state trek to visit relatives over this period, so we decided that while we were traveling, we were going to eat like normal Americans just to see what would happen.

We didn�t go out of our way to overindulge in anything.� We had a maybe two hamburgers with the bun and had two or three orders of fries (I�m talking about during this entire period – not every day).� We had a Christmas cookie or two, downed several pieces of fudge, drank a bunch of eggnog, ate some fruitcake, and had a couple of bowls of ice cream.� And MD had a little more wine than usual while I probably doubled up on my Jameson.� Other than those indulgences we ate what would be considered sensibly by most people.� We ate some mashed potatoes, grits (we were in the South), beans (not the green bean variety), more fruit than usual and meat of one sort or another.� Pictured below is my plate (which I doubled down on) on New Year�s day.

As you can see, I ate ham, cheese grits, black-eyed peas, curried fruit, and corn bread.

The point of this exercise was to see what would happen to us if we followed a sort of modified typical American diet.� We avoided trans fats and vegetable oils as much as we could and had absolutely no soft drinks.� We had no breakfast cereals of any kind and took it easy on the wheat, but we did eat a little bread occasionally.� Except for the bits of fudge and other Christmas goodies we consumed – all of which were homemade using butter and/or lard as the fat source – we didn�t really go overboard on the sweets.� Our fructose intake was doubtless considerable less than that the average American, especially during that time of year.

So what happened to us during this couple of weeks of much better than average typical American dieting?

We gained weight!� And a fair amount of it.

I don�t know exactly how much we each gained because neither of us ever weighs – we go more by how our clothing fits.� (We didn�t plan on starting this little experiment before we left or we probably would have weighed.� We started it once we were already on the road.)� When I left on the plane, I wore a freshly laundered pair of jeans that fit loosely around my waist and that scrunched up a bit when I tightened my belt.� When we flew home, I wore the same pair of jeans (also freshly laundered), and they were tight around my waist and my belly actually spilled over a little.� MD had the same experience except her weight distribution was a little different.

If I had to guess, I would say we both gained somewhere around five or six pounds.� We were clearly at the top of the range of weight gain as described by the study I linked to earlier, and it happened in two weeks not the six weeks as it did in the study.� Which would indicate that we fall into the obese category, since the obese are the ones who most readily gain weight over the holidays.

But we aren�t really obese, or at least weren�t when we started.� But we obviously have the same metabolic defect that the obese have.� Our metabolic machinery has been damaged.� And even though we�ve keep our weight under control for years, the problem is still there, lurking in the weeds, ready to strike the moment we drop our defenses.

The take home message here is, to paraphrase Wendell Phillips, eternal vigilance is the price of thinness.� At least after you�ve once become obese.

So, MD and I are back on a rigid version of our own program, we are taking Metabosol, and, with the exception of a party we attended last night, are eschewing booze until we get back to our regular sizes.� Some of my GERD symptoms re-appeared during our modified debauch and I was thankful I had an old bottle of out-of-date Protexid to see me through.� One day of solid low-carb, and no more GERD, thank God.� And already after just a few days our clothing is starting to fit again.

If you are one of the many who are committed to a program of weight loss and rehabilitation this January, know that MD and I are right in there with you.

I want to forewarn you, though, that you�ve got to get your head right if you seriously plan to succeed.� Don�t be a Tara Parker-Pope.

I�ve had a number of people send me the link to her long piece in last week�s New York Times Magazine (Parker-Pope is a health columnist for the New York Times) about her struggles to lose weight and to maintain her weight loss once she is finally able to shed a little.� In the article she describes her despair as she tried first this program then that to lose weight.� She fits perfectly the description of so many patients I�ve dealt with over the years.

Once your metabolism is broken, it�s difficult� to lose weight (other than the first time or two you try it) and even more difficult to keep it off.� In order to be successful, you�ve got to make a real commitment and stick to it.� You can�t drift here and there as Parker-Pope has done looking for some magic regimen that is going to �melt the fat away.�� It ain�t going to happen.� It takes a lot of hard work and resolve to see it through.� Even with a low-carb diet.

As you can see from the vintage ad above, Tara Parker-Pope is not the first to look for a miracle cure for excess �flesh.�� But she is at a bit of a disadvantage in that by virtue of her position she can pick up the phone and call the head of nutrition at Harvard, Yale, Johns Hopkins or any big institution and ask for advice for a column she�s writing.� Unfortunately, the advice she will get from most of these people is totally the mainstream academic party line and more than likely incorrect.� And, if she�s like many patients I�ve dealt with, as soon as she discovers that whatever she is doing entails real work, she will start looking for the next magic fix, only to be disappointed in that.� She will, as she describes, roller-coaster around weight-wise, quickly regaining whatever she loses, and end up fat, sad and miserable.� The only difference between Tara Parker-Pope and the millions of other people out there in her shoes is that she has a powerful platform to express the despair and hopelessness she feels to a large readership.� (I noticed that for a few days her piece was the most emailed of all the articles in the New York Times, which speaks to just how many people are struggling.)

The underlying message of her piece is that she has tried everything, and it has all been for naught.� Her obesity is a condition beyond her control because she has worked with all the greatest minds in the academic world of obesity treatment and has ended up fatter than when she started.

My contention is that if she would undertake a low-carb diet composed of whole foods (with maybe a shake or two thrown in here or there) and stick with it judiciously she would ultimately achieve success.� At least considerably more success than she has achieved thus far.� But if she followed the best low-carb diet known to man and lost to her ideal weight and body fat percentage, she would still have to continue to watch what she eats for the rest of her life if she were to want to maintain her new slim self.� MD and I just proved that over the past couple of weeks.
I have never been able to understand the mindset of people who think that once they lose to their ideal weight and body fat percentage they can then go back to their old way of eating without regaining all the weight they originally put on by their old way of eating.� It baffles me even more that people can lose considerable amounts of weight on a given diet, then go back to their old way of eating, regain all their weight, and view it as a failure of their weight loss diet.� But they do.

I always took a detailed dietary history of all my patients.� Many had been through two or three (or more) weight loss programs before they came to see me.� I would ask them about all the different programs they had tried, and they would list them out.� And most had had some measure of success on one or more (if not all) of these programs, in many cases having lost anywhere from 60-80 or more pounds, but they, almost to a person, considered these programs failures because they had regained their lost weight.

These people, like Tara Parker-Pope, MD and me, and anyone else who has crossed the Rubicon into the land of obesity have dysfunctional metabolic systems that will probably never be completely normal again.� They, like we, will always have to exercise vigilance to maintain what we maintained so easily before the damage took place.

As I wrote above, the easiest way to deal with obesity is to never become obese in the first place.

Which brings me to a real pet peeve of mine.� I want to go for the throats of people who let their kids eat and drink tons of sugary crap and justify it because their kids don�t gain weight from it.� Who knows when the irreversible damage begins to occur?� I feel the same about adolescents and young adults who seem to feel invincible and are face down in all kinds of crap all the time because they never gain weight.� And they assume, stupidly, that they never will.� But when they do, most will struggle with it for the rest of their lives.

In preparation for my own weight loss, I went back an reread a few of my old posts to gain inspiration.� If you are in the let�s-lose-weight boat this month with MD and me, you might want to read them, too.

Here is one of my favorites about a good friend who really committed to losing weight and turned her life around.� The post also tells you why you should gain control not just for yourself but for others.

Another old post gives some psychological insights as to why it can be difficult right now to give yourself over to a low-carbohydrate diet and some psychological tools to make it easier.

Here is one that gives a few more psychological tools to make dieting easier.

Years ago I wrote a regular column for a now-defunct low-carb magazine.� This piece on what it takes to really make a low-carbohydrate diet work may help with your struggles.

There are the two fairly recent posts on all the tips and tricks you can use to start (or restart) a low-carbohydrate diet.

I�m frequently asked on radio, TV and print interviews what my daily food intake is.� A couple of years ago I decided to do a photo diary of a week�s intake of food during a normal week.� The food I ate that week pretty much mirrors the food I eat now with a couple of exceptions.� The quality of the cooked food is better now because almost everything we eat at home is prepared sous vide for obvious reasons.� I go through periods from time to time in which I really like to have shakes for breakfast.� Then I burn out on them and almost can�t bear the thought.� During the non-shake periods I typically eat three eggs and three or four slices of bacon (Mangalitsa bacon if I can get it) every day for breakfast.� During my week�s photo log, I was in a shake phase, so realize that I am not now in shake phase, so it�s bacon and eggs, but that�s about the only difference.� The week�s diet you�ll see if you take a look is what keeps me at my normal weight.� It�s pretty much what I�m back on now minus the booze and a few of the little extra carb tidbits. Plus, I�m scrupulously avoiding wheat just to see what happens.� As soon as I lose the few pounds I picked up and my jeans are loose again, I�ll be back to this diet in full.

• Photo food diary day 1
• Photo food diary day 2
• Photo food diary day 3
• Photo food diary day 4
• Photo food diary day 5
• Photo food diary day 6
• Photo food diary day 7

If you, like we, have been noshing on more carbs than normal over the holidays, then start anew with us this January.� As I have discovered this first few days, the time I spent dallying with carbohydrates over the previous couple of weeks has reinvigorated my long dormant urge to eat even more carbs.� I�m sure I�m not the only one in this boat.� We all have to remember that this urge is one we have to overcome first by effort and ultimately by habit.� I�m back on track.� Hope you are as well.

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