Environment, Chemical Exposures, Nutrition and Health

Why supplements including anti-oxidants should be taken seriously.

2013-12-18T04:40:00.001-08:00

Why supplements including anti-oxidants should be taken seriously. Originally published in WODMASTERS. Click for complete article.

Products that are classified as drugs/medicine are required to meet standards of quality and consistency in manufacturing and of safety. Studies are done in vitro, on animals, and finally on humans. Drug interactions are checked. Information is gathered on how the drug is metabolized. Drugs are sometimes metabolized into something deadly before being rapidly metabolized into something safe. Tylenol is an example. Not a problem unless something, like alcohol, blocks a metabolic step and traps Tylenol in its deadly form. This is why people sometimes die when they drink alcohol and then take Tylenol. This should be common knowledge, but it isn’t, yet.
Another important thing to know about a drug or supplement is its “Effective Dose.” How much is needed to give a desired effect? How much selenium is needed for health? How much is too much? How much is “optimal”? These are unanswered questions for many nutritional supplements. What happens if you take too much? Frequently the answer to that question is unknown as well.
Anti-Oxidants should not be assumed to be safe. Recent research has indicated that anti-oxidants, like oxidants, can harm DNA. DNA damage can lead to cancer, the very thing anti-oxidants in nutritional supplements are supposed to prevent.
The last point to raise for this article is a manufacturing issue. Like most people, I used to assume that vitamins and supplements contained what was written on the package. But this is not always the case. An example is the recent report of human growth factors added to deer antler velvet supplements. It is hard to believe human growth factors were accidentally added to deer antler velvet supplements. You’d have to hear the manufacturer out on that one. However, problems like poor mixing and poor calculations can and do happen. Our research group found that out the hard way when we tried to use a well-known brand of vitamins for a human health study.

So, how much of what is in a multi-vitamin? How much of what is in Deer Antler Velvet, DHEA supplements, or “high performance packets?” Deer antler velvet, especially if it is secretly spiked with human growth hormone may quite unsafe. Secret additions to supplements may or may not be added carefully or consistently. There is no way to know unless you are the one doing the spiking . . . or if you have the technical expertise and expensive equipment needed to test it yourself.

New Video on The Economic Costs of Obesity

2013-06-15T07:18:00.001-07:00

The producers (?) of this video asked if we would post it on our blog. The organization is called Academic Earth. The video discusses obesity and brings up some interesting statistics on agricultural subsidies. Apparently, fresh fruit and vegetables don't get much in the way of subsidies. This may make them more expensive for consumers. The final result is that calories from junk food are cheaper than calories from healthy food. They also bring up some disturbing numbers about changes in caloric intake since the 1970s.

If this is true (and it probably is) why has it happened? Changes in family structure and habits? Environmental chemicals that interfere with metabolism or satiety? Lack of exercise? The development of eating as a recreational activity? Eating out more? Being too busy to cook or not knowing how to cook? Its an interesting and sometimes frightening topic. Here is the video. What do you think?

Created by AcademicEarth.org

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New Book: The Rise of the U.S. Environmental Health Movement by Dr. Kate Davies

2013-04-05T09:20:00.001-07:00

Author Dr. Kate Davies

A new book on the history of the US Environmental Health Movement has just been published. The Title is: The Rise of the US Environmental Health Movement. The book is described as the first of its kind and will offer a thorough examination of the environmental health movement. Environmental health in this context refers to the impact of the environment on human health. Many people are concerned about synthetic chemicals in air, food and water. A good understanding of how chemicals impact (or do not impact) health is important. It is also important to understand history. Unfortunately, there is a lot if misleading or inaccurate information out there. Disinformation fuels conspiracy theories and a generally poor approach to problem solving. Dr. Davies' writing is clear, rational and refreshing. The book is highly recommended.

Dr. Davies' book describes how people first became aware of environmental health problems. And how they organized to effect change. There are some very interesting stories there and some very interesting struggles.

In some ways things are vastly different today than they were just a few decades ago. Companies are much more cautious about introducing new chemicals into the environment. Testing for potential problems is much easier today. This helps companies avoid producing or using chemicals that come back to bite them in the ass. Advances in chemistry have also made it much easier for companies to develop less toxic alternatives. The history of the US environmental health movement also examines how chemical companies and other responsible parties attempted to undermine what were usually poorly funded and poorly organized grass-roots activists. The fights go on. Both sides have become more sophisticated in their political and public relations battles. A better understanding of history and science among all parties should help take us away from battles and towards rational approaches to the resolution of problems that effect us all.

Protecting Children from Celiac Disease and a Child's View the problem.

2012-10-05T11:57:00.001-07:00

Protecting children from Celiac Disease:

I've written several articles about gluten, microbes and auto-immunity. All those interactions are interesting to think about. To me this has been like tinkering with puzzles. Celiac disease is a problem of auto-immunity and exposure to the plant protein gluten. It can be a rough road to follow, especially for children. They can't eat the same things other kids eat, and other kids and even adults may not understand that something that seems so normal to them, like a cupcake or sandwich, can cause serious pain and discomfort for a celiac child. This website, "Growing Up Gluten Free" is written and maintained by a child with celiac disease. It helped me understand what life is like for kids like her.

Two children enjoy a Box lunch at CrossFit Seven in Fort Worth, TX.

Celiac disease is more common in people of European descent and probably has a strong genetic component. However, there are other factors involved as well. An individual may be predisposed to developing Celiac disease but not get it unless a combination of other factors line up as well. One thing I had written about in an earlier post was the possibility that gut flora (microbial species and ratios of species) might influence the development of Celiac disease. Intestinal flora in infants will be dependent on whether the infant was born by C-section and on whether he or she was breast fed or bottle fed. The infant digestive system is not completely developed at birth. It is suited for breast milk. New research published this month (October 2012) supports a role for bacterial ecology in Celiac Disease. Delaying introduction of wheat until the infant reaches 12 months of age appears to reduce risk that a genetically at-risk child will develop the disease. Children with a genetic predisposition to Celiacs may take longer to develop an intestinal ecology favorable for wheat (and possibly other foods) than other children. The study was a joint project of the University of Maryland School of Medicine and the Universita` Politecnica delle Marche, in Ancona, Italy.

A Systematic Review of infant feeding practices and incidence of Celiac (Coelicac) disease has also been published very recently (Szajewska et al. 2012). The authors suggest that the best time to introduce wheat into an infant's diet is between 4 and 7 months, and that it should be done while the child is still breastfeeding. Introducing wheat before a child is under 4 months increases the likelihood that he or she will develop Celiac Disease. Likewise, delaying introduction until a child is older than seven months may also increase risk of Celiac's.

There are lots of unknowns still. The Szajewska paper does a great job of defining what they are.

Sellitto M, Bai G, Serena G, Fricke WF, Sturgeon C, Gajer P, White JR, Koenig SS, Sakamoto J, Boothe D, Gicquelais R, Kryszak D, Puppa E, Catassi C, Ravel J, & Fasano A (2012). Proof of concept of microbiome-metabolome analysis and delayed gluten exposure on celiac disease autoimmunity in genetically at-risk infants. PloS one, 7 (3) PMID: 22432018

Szajewska H, Chmielewska A, Pieścik-Lech M, Ivarsson A, Kolacek S, Koletzko S, Mearin ML, Shamir R, Auricchio R, Troncone R, & PREVENTCD Study Group (2012). Systematic review: early infant feeding and the prevention of coeliac disease. Alimentary pharmacology & therapeutics, 36 (7), 607-18 PMID: 22905651

Correlation and Causality: Alcohol and Diabetes to BPA and Estrogen Disruption

2012-09-25T08:57:00.000-07:00

Alcohol and Diabetes:

From a purely health-oriented perspective, alcohol is one of those things where a little seems to be good and more than a little puts you at risk for a bad health outcome. One of the positive things small regular intake can do for you is protect you from diabetes. There is good epidemiological evidence that this is the case. Light drinkers are less likely to develop diabetes than those who abstain.

Samples prepared for analysis.

As most people know, just because two things occur together does not mean that one caused the other. Correlation and causality are two different things. It is important to keep this in mind when reading about human health studies in the news. Epidemiology is a wonderful tool however, and provides clues to problems that might have gone unnoticed. In addition to identifying potential problems correlational (and epidemiological) studies are important in evaluating how a problem identified in the lab may be harming people in the real world. Are light drinkers more likely to eat better, exercise better, be healthier than those who drink more alcohol or even none at all?

An important next step is figuring out why the correlation exists. Here is a case where epidemiology observed something (low alcohol = less diabetes, high alcohol = more diabetes) and experimental study identified a physiological reason that explains those observations. He et al. (2007) discovered that light alcohol intake activates a biochemical pathway that has a positive influence on removal of blood sugar from the blood stream. Higher alcohol intake disrupts glucose management by activating an additional protein that blocks the positive effects seen with light alcohol intake. This discovery helps explain why you can see two different outcomes with alcohol. At first light it may have seemed that scientific studies conflicted each other. The appearance of contradiction may lead some people to throw up their hands and decide to disregard health news or science in general.

Sometimes we need to keep working at the puzzle.

There may be a similar issue with environmental contaminants. Sometimes a relationship is observed and someone publishes on it, and there there are a flurry of other studies that confirm or don't confirm the relationship, expand it or limit it. Identifying the mechanism and understanding how it works under varied circumstances becomes essential. There are now many correlational studies that show that Bisphenol A (BPA) intake is associated with health problems. There are also mechanistic studies that show how BPA interacts with estrogen receptors and causes things to go arwy. One could stop here and take steps to remove BPA from use. Environmentalists and children's health advocates could claim victory. This might result in fewer birth defects, less obesity, less diabetes, fewer behavioral problems in children etc. But it might not.

Plastics are more complex than they seem. Even without BPA many of the chemicals that go into or are released from different plastics may be may activate estrogen receptors. Would people be exposed to less estrogenic chemicals if BPA is banned? We still don't know. While many studies have used data on concentrations of BPA or BPA-metabolites, to the best of my knowledge no one has looked at total exposures to estrogenic chemicals originating from plastics. (There are also estrogenic chemicals from sources other than plastics too). Does removing BPA from a plastic actually make it less estrogenic? Is BPA, rather than other chemicals coming off of plastics, the main source of dietary exposures to estrogenic compounds?

Plastics are amazing, really, and have made many positive and important contributions to our economy and quality of life. For information on how plastics benefit the environment and contribute to quality of life take a look at this pdf from the British Plastics Federation. Its taken tremendous effort and ingenuity to develop polymers. We can figure out where they might cause problems in the environment or in human health by continuing polymer research and including within, cell and molecular studies. We should not have to leave epidemiology to discover problems that could have been avoided after the fact.

He L, Marecki JC, Serrero G, Simmen FA, Ronis MJ, & Badger TM (2007). Dose-dependent effects of alcohol on insulin signaling: partial explanation for biphasic alcohol impact on human health. Molecular endocrinology (Baltimore, Md.), 21 (10), 2541-50 PMID: 17622585

Nguyen KH, Lee JH, & Nyomba BL (2012). Ethanol causes endoplasmic reticulum stress and impairment of insulin secretion in pancreatic β-cells. Alcohol (Fayetteville, N.Y.), 46 (1), 89-99 PMID: 21840159

What are obesogens?

2012-09-15T06:51:00.000-07:00

Living things are delicate, resilient and tenacious. Their chemistry is fascinating. We are molecular machines, in a sense, and fine tuned to interact with the external world. The chemical systems that make us who and what we are took many millions of years to develop. It is incredible that we are now able to synthesize molecules by ingenuity. Chemical engineering, pharmaceutical companies and even the much maligned agrochemical industry have, and are, incredibly important to where we stand now. The drugs, and even pesticides, that have been produced have saved countless lives. It is just now that we have calmed down a little from the excitement of synthesizing new molecules, and started looking at the unintended effects these new molecules have on biochemistry. Things that alter our biochemistry can alter our health. Sometimes they can alter the developmental paths we follow in utero. It would be wonderful if inadvertent exposures to new molecules had beneficial effects. Its possible. As with most things, the good things that happen by accident usually go unnoticed. However, as in most situations, it is far easier to be destructive than constructive.

So, back to the post title: what are obesogens?

Obesity can make your life harder than it needs to be

Obesogens are chemicals that change the way fats (lipids) are handled. Exposure, especially early in life, may influence patterns of fat distribution, the way the body uses fat, and/or the way fat is synthesized. It is possible that some chemicals might make us develop as lean, fat burning machines. This would be a huge problem if we ever have a famine, but that is not our current issue. Obesity, and its associated health problems, is on the rise. Some of the chemicals that may be acting as obesogens in people are:

Organotins (used in marine paints, production of plastics, pesticides.Exposure may come through seafood, produce, drinking water and plastics.

Bisphenol A (BPA): from plastics.

Phthalates: from plastics

Perfluoroalkyll compounds (PFCs): water repellant fabrics, stain preventing treatments.

How to avoid obesogens.

Avoid plastics when possible. Avoid fabrics treated with water repellants or stain blockers. Avoid carpet treatments.

Grün F, & Blumberg B (2006). Environmental obesogens: organotins and endocrine disruption via nuclear receptor signaling. Endocrinology, 147 (6 Suppl) PMID: 16690801

Thayer KA, Heindel JJ, Bucher JR, & Gallo MA (2012). Role of environmental chemicals in diabetes and obesity: a National Toxicology Program workshop review. Environmental health perspectives, 120 (6), 779-89 PMID: 22296744

Plastics, Diabetes and Obesity

2012-09-09T08:57:00.001-07:00

Things start to get interesting when the results human epidemiology and animal exposure studies meet. Epidemiology studies of human exposures to a xenoestrogen like BPA show relationships between exposure and diabetes, or exposure and obesity. But it is very difficult to say that exposure to a plastics component causes obesity, diabetes or heart disease. People who are exposed to a lot of xenoestrogens may eat more canned food and have more BPA (or similar) circulating in their systems, but people who eat a lot of canned and packaged food may also eat poorly, exercise less, and/or be less educated compared to someone who has very little plastics exposure.

This is why animal studies are so important. When the results of controlled animal studies are similar to trends we are observing in people the case for concern about a particular chemical jumps. Many people oppose animal studies for ethical reasons, but sometimes leaving questions unanswered is unethical as well.

There is increasing evidence that chemicals in the environment may be contributing to diabetes and obesity. This is not to say that there is no such thing as good habits, but biochemical variables, set during early life, may make it harder to regulate things like blood sugar and weight. For current reviews and discussion take a look at:

Here is animal evidence for a relationship between exposure to bisphenol A, (and possibly other chemicals that are structurally similar) and diabetes: Bisphenol A Exposure during Pregnancy Disrupts Glucose Homeostasis  in Mothers and Adult Male Offspring. As discussed in previous posts, nearly everyone is exposed to Bisphenol A (BPA) and probably to other xenoestrogens through consumption of food and beverages packaged in plastic. It is an interesting study. It shows that exposures during pregnancy will affect offspring into adulthood. Whether or not this is happening in people is unknown, and not testable.

Katzenellenbogen JA (1995). The structural pervasiveness of estrogenic activity. Environmental health perspectives, 103 Suppl 7, 99-101 PMID: 8593885

Newbold RR (2010). Impact of environmental endocrine disrupting chemicals on the development of obesity. Hormones (Athens, Greece), 9 (3), 206-17 PMID: 20688618

Alonso-Magdalena P, Vieira E, Soriano S, Menes L, Burks D, Quesada I, & Nadal A (2010). Bisphenol A exposure during pregnancy disrupts glucose homeostasis in mothers and adult male offspring. Environmental health perspectives, 118 (9), 1243-50 PMID: 20488778

Xenoestrogens and Plastics

2012-09-06T15:57:00.000-07:00

This post covers one of the problems posed by endocrine disruptors (ECDs) that I don't think has gotten a lot attention, or at least broad enough attention. This is the issue of estrogen-mimics. These are also known as Xenoestrogens. A lot of people seem to be aware of BPA and take steps to avoid it. However, BPA is a relatively small part of the story. Plastics labeled BPA-free may not be Estrogen Activity-Free at all (Yang et al. 2011). Normal estrogen acts by docking at an estrogen-receptor, like a lock fitting into a key, and turns on various biochemical pathways. These pathways play important roles in maintaining normal function in various tissue, allow girls to develop normally through puberty, make reproduction possible, organize behavioral responses and neurological function among other things.

The problem with xenoestrogens is that the body can't tell the difference between these molecules and natural estrogen. Its an issue of molecular structure or shape (Katzenellenboggen 1995). That means biochemical pathways can be turned on at inappropriate times, upsetting the normal course of development, including brain development. It may also mean that more estrogen activity is happening because estrogen-regulated cell activity is ramped up. This might mean more cell division and change in estrogen-sensitive tissue, which can increase risk of breast cancer. There is also evidence that xenoestrogens can harm male development as well (Ogura et al. 2007).

A normal three-year old performs with her toy cat

Many chemicals have estrogen-activity. Some chemicals are more estrogenic than others. Household products, dusts, plastics, cosmetics, personal care products may all contain estrogenic chemicals. Note that, dust aside, there are products that don't contain estrogenic chemicals. For example, plastics can be produced that do not have estrogenic activity.

It may just be hard to find them. For example, the only company I know of that produces a plastic water bottle that is independently certified as Estrogen Activity Free is a small company called The Water Geeks. The Headline on the Link says BPA-Free, but these are Estrogen-Activity Free as well. A small company, Certichem, run by a bunch of University of Texas professors, certifies chemicals as Estrogen-Actity Free. They also test things for androgen and anti-androgen activity as well.

BPA-Free is great, but BPA bottles and cans are not necessarily Estrogen-Activity Free. I try to use glass, which is not always practical or even permitted in some situations. We probably don't want to see fields of pee-wee soccer players running around with glass bottles, and a lot of boxes probably don't want to see exhausted athletes staggering around with glass either.

The Environmental Working Group provides a website that will help you identify products that contain fewer ECDs. They also have a lot of other well-written and informative material on the topic of chemicals in the environment. You can read more about Endocrine Disruption and the concerns of the scientific and medical communities in this pdf published by The Endocrine Society.

Katzenellenbogen JA (1995). The structural pervasiveness of estrogenic activity. Environmental health perspectives, 103 Suppl 7, 99-101 PMID: 8593885

Yang CZ, Yaniger SI, Jordan VC, Klein DJ, & Bittner GD (2011). Most plastic products release estrogenic chemicals: a potential health problem that can be solved. Environmental health perspectives, 119 (7), 989-96 PMID: 21367689

Ogura Y, Ishii K, Kanda H, Kanai M, Arima K, Wang Y, & Sugimura Y (2007). Bisphenol A induces permanent squamous change in mouse prostatic epithelium. Differentiation; research in biological diversity, 75 (8), 745-56 PMID: 17459086

Ogura Y, Ishii K, Kanda H, Kanai M, Arima K, Wang Y, & Sugimura Y (2007). Bisphenol A induces permanent squamous change in mouse prostatic epithelium. Differentiation; research in biological diversity, 75 (8), 745-56 PMID: 17459086

What are endocrine disruptors?

2012-09-06T07:17:00.000-07:00

The next several posts will be devoted to the subject of endocrine disruption with a focus on environmental chemicals that interfere with sex steroids, chiefly estrogens and androgens. Most people are probably familiar with estrogen and testosterone. These are steroids produced by the human body (and the bodies of other species) that play important roles in sexual development and reproduction. They also play many other related roles, influence growth and tissue maintenance, neurological function and behavior.

An endocrine disruptor is a chemical agent that interferes with very complex, inter-regulating and intertwined endocrine systems. Interference with one steroid hormone can produce chain reactions that impact other hormones that, in turn, influence other systems and other hormones. For example, Bisphenol A, an estrogen mimic will change production of Prolactin (Steinmetz et al. 1997).

A young boy ponders something.

The effects of endocrine disruptors can be strongest during critical periods such as fetal development, infancy, adolescence, conception and pregnancy. These are times of important changes that will have long-term consequences for a child (fry, larvae, pup, chick etc.) and its future children. Thousands of chemicals have been found to be endocrine disruptors. Some of them are very resistant to degradation and remain in the environment and in people's bodies for decades or longer. Many of these are no longer in use even though with can still easily detect them. They were found to be a threat to health and were banned and/or replaced with something less dangerous. There are many other chemicals in use that have not been tested. There are others that are current foci of research and debate. These chemicals were not developed to cause harm to humans (at least not most of them), rather they were found to be harmful after they were already in use. An example that you may be aware of is the plastics additive Bisphenol A.

Bisphenol A is commonly called BPA. After years of debate and conflict among interested parties BPA has been banned from baby bottles in the US. Manufacturers are adapting and produced new products. Consumers can easily find BPA-Free materials and it seems likely that BPA will leave many markets. While BPA may be in decline the issue of endocrine disruptors is far from resolved. The plastic products used to make some BPA-Free plastics also appear to be endocrine disruptors (Yang et al. 2011.) Some of them appear to be more disruptive than the BPA-laced plastics they are meant to replace. It would be better to produce Endocrine-Disruptor-free products Instead of BPA-Free products

It is very difficult to pull something out of the market once it is already there. People's livelihoods have become dependent on continuing use, reputations are at stake, there may be millions of dollars spent on legal fees, on efforts to fund studies that would show that the product in question was harmless after all, and then more time and more money spent arguing why banning a product would be unfeasible and not worth the cost of replacing it, developing alternative technology, or cleaning up environmental messes. Banning chemicals after they become part of the economy is hugely wasteful, makes people on both sides of the playing field upset and erodes public confidence. We may discuss this in greater detail later, but for now, just be aware that the chemical problem of endocrine disruptors is also an economic and then a political problem as well. This should be resolved eventually, but until then, we may have a very interesting, and for some a painful, ride. Steinmetz R, Brown NG, Allen DL, Bigsby RM, & Ben-Jonathan N (1997). The environmental estrogen bisphenol A stimulates prolactin release in vitro and in vivo. Endocrinology, 138 (5), 1780-6 PMID: 9112368 Yang CZ, Yaniger SI, Jordan VC, Klein DJ, & Bittner GD (2011). Most plastic products release estrogenic chemicals: a potential health problem that can be solved. Environmental health perspectives, 119 (7), 989-96 PMID: 21367689

Steinmetz R, Brown NG, Allen DL, Bigsby RM, & Ben-Jonathan N (1997). The environmental estrogen bisphenol A stimulates prolactin release in vitro and in vivo. Endocrinology, 138 (5), 1780-6 PMID: 9112368

Yang CZ, Yaniger SI, Jordan VC, Klein DJ, & Bittner GD (2011). Most plastic products release estrogenic chemicals: a potential health problem that can be solved. Environmental Health Perspectives, 119 (7), 989-96 PMID: 21367689

Are Silver Nanoparticles in Clothing Safe?

2012-07-15T12:57:00.000-07:00

Silver nanoparticles are woven into high-tech athletic clothing as a means of controlling bacteria and odors. Silver has low toxicity for people, but is able to kill bacteria. How it kills bacteria is not completely understood, but it is believed to cause oxidative stress. Oxidative stress is harmful for us as well, but bacteria can be killed at lower levels than can hurt us. Still, oxidative stress is not good. That's why anti-oxidants are protective against cancer and effects of cell damage. Silver nanoparticles are used in topical antibiotics to treat life threatening infections in burn patients. Better to risk a little oxidative stress from silver nanoparticles than to die from an infection.

So, is it a good idea to put silver nanoparticles in clothes? No one knows the answer to this question. But there are a few answers to a few related questions. For example, do the silver nanoparticles embedded in fabrics some off the cloth and end up in wastewater? Do the particles come off the cloth and enter peoples bodies? Are there any known health effects from exposure to silver nanoparticles? If the particles stay in the fabric there is probably little to worry about. Let's take a look:

Do Silver nanoparticles come off the fabrics in which they are embedded? Apparently they do, but different fabrics lose nanoparticles at different rates, at least during the wash cycle. Benn TM, & Westerhoff P (2008). Nanoparticle silver released into water from commercially available sock fabrics. Environmental science & technology, 42 (11), 4133-9 PMID: 18589977
Can silver nanoparticles be absorbed through people's skin? Apparently they can. Silver nanoparticles are being used a a topic anti-biotic in burn patients. Infection is a major, major factor in recovery (and mortality) for burn patients. Brandt O, Mildner M, Egger AE, Groessl M, Rix U, Posch M, Keppler BK, Strupp C, Mueller B, & Stingl G (2012). Nanoscalic silver possesses broad-spectrum antimicrobial activities and exhibits fewer toxicological side effects than silver sulfadiazine. Nanomedicine : nanotechnology, biology, and medicine, 8 (4), 478-88 PMID: 21839058
How long do silver nanoparticles stay in a person once they get there? This is an important question. If they stay around a long time, they can do damage for a long time. If they leave quickly they would be less dangerous. Same thing goes for a lot of other substances. The answer to this question appears to be unknown
Are there any known health effects if silver nanoparticles are absorbed? Lim DH, Jang J, Kim S, Kang T, Lee K, & Choi IH (2012). The effects of sub-lethal concentrations of silver nanoparticles on inflammatory and stress genes in human macrophages using cDNA microarray analysis. Biomaterials, 33 (18), 4690-9 PMID: 22459196. Silver nanoparticles appear to have harmful effects on some human (and animal) cells. (Comparative in vitro cytotoxicity study of silver nanoparticle on two mammalian cell lines- citation)

While its been demonstrated that the particles can harm cells, tissues or organs we don't know how much would be needed to harm health. The amount of silver nano-particles absorbed from clothing may not be high enough to matter. Its an unanswered question. We'll probably hear more about this in coming years. For now you'll have to rely on your own judgement.

High Fat Diet, Cholesterol, the Swiss and the Australian Aboringinals

2012-05-20T08:16:00.001-07:00

Perusing Google News with morning I came across an article claiming that "Research Shows CrossFit Diet/Exercise Reduces Risk of Heart Disease". I clicked on that one immediately because, to the best of my knowledge, no scientific research has been published on relationships between high intensity CrossFit-type training and cardiovascular disease. If one were to do a search today on Web of Knowledge using the search term "Crossfit" you would get a single hit:

Jansen, J., van Dam, N., Hoefsloot, H., & Smilde, A. (2009). Crossfit analysis: a novel method to characterize the dynamics of induced plant responses BMC Bioinformatics, 10 (1) DOI: 10.1186/1471-2105-10-425

I'm sure the intentions of whoever wrote the press release were good . . . but . . . it is quite a stretch. Still, interesting that it made it into Google News. The research the author discusses has nothing to do with Crossfit. The press release does, however, attempt to associate a high-fat diet (promoted by some Crossfitters as healthy than other diets) with lower incidence of cardiovascular disease by comparing incidence of disease between residents of Switzerland and Australian aboriginals living in modern Australia. The claim was that a high-fat dining Swiss have less cardiovascular disease than the presumed low-fat dining Australian Aboriginals and that, therefore, high-fat diets are healthier than low-fat diets.

I have not looked up the statistics for the Swiss, but Australian Aboriginals have been suffering increasing rates of cardiovascular disease over at least the last 30 years. Few modern Aboriginals are likely to be following a traditional Aboriginal diet. It is extremely unlikely that the increasing rate of heart disease observed in Australian Aboriginals has been caused by low intake of dietary fat. Aboriginals are suffering from increasing obesity and diabetes just like so much of the rest of the world. The high incidence of cardiovascular disease in Aboriginals may be due to genetic factors and a change to a Western-type diet but extremely unlikely to be caused by a low-fat diet (especially since they are not eating this way anymore anyway). There are also obviously many other differences between the Swiss and the Aboriginals (differences in poverty levels, availability of lederhosen and differences in other possibly important variables like intake of strong coffee and chocolate).

Rowley K, Walker KZ, Cohen J, Jenkins AJ, O'Neal D, Su Q, Best JD, & O'Dea K (2003). Inflammation and vascular endothelial activation in an Aboriginal population: relationships to coronary disease risk factors and nutritional markers. The Medical journal of Australia, 178 (10), 495-500 PMID: 12741936 O'Dea K (1991). Westernisation, insulin resistance and diabetes in Australian aborigines. The Medical journal of Australia, 155 (4), 258-64 PMID: 1875844

Estrogen and Progesterone in Waterways

2011-11-17T07:49:00.000-08:00

In the last post, I was speculating about how estrogens from effluent might end up in way water ways and end up increasing the incidence of prostate cancer. I wondered if the problem (if it there is anything more than a chance association) might be progesterone from birth control pills rather than estrogen. Progesterone is markedly non-soluble in water so it seemed unlikely at first thought. Poking around a little, progesterone might end up in sewage effluent after all. The three studies below report on fecal and/or urinary progesterone, conjugated progesterone or "progesterone metabolites" in animals. So . . . maybe progesterone contamination of water might be relevant. And, not all sewage is filtered and treated. I recently watched someone emptying a truckload of portapotties into one of our local creeks. (Yes, I called the police, who told me it was not their problem.) Don't know if anyone has looked at this or not. If you know, please have at it in comments.

deCatanzaro D, Muir C, Beaton EA, & Jetha M (2004). Non-invasive repeated measurement of urinary progesterone, 17beta-estradiol, and testosterone in developing, cycling, pregnant, and postpartum female mice. Steroids, 69 (10), 687-96 PMID: 15465115Kinoshita K, Inada S, Seki K, Sasaki A, Hama N, & Kusunoki H (2011). Long-term monitoring of fecal steroid hormones in female snow leopards (Panthera uncia) during pregnancy or pseudopregnancy. PloS one, 6 (5) PMID: 21559303Brown JL, Wasser SK, Wildt DE, & Graham LH (1994). Comparative aspects of steroid hormone metabolism and ovarian activity in felids, measured noninvasively in feces. Biology of reproduction, 51 (4), 776-86 PMID: 7819459google-site-verification: googleaa234ad89e44d776.html

Response to a friend on significance of Triclosan in drinking water

2011-11-16T08:36:00.000-08:00

Sorry Friend. That was a poor response to your question about the significance of Triclosan following news of the chemical as an androgen blocker in water.

Triclosan is a thyroid disruptor and according to recent reports, an androgen blocker. As an anti-androgen, exposure could be important to male fetuses, since it could potentially interfere with development of the genito-urinary system, which could mean birth defects like hypospadias, small phallus, or non-obvious problems like changes in numbers and proportions of cells that would, later in life, produce sperm and testosterone. Thyoid inhibition has its own effects on development of the male reproductive system as well. So there might be some interesting interactive effects if both thyroid hormones and androgens are impacted. If that would occur you'd see reduced fertility. In an adult lowered testosterone would lead to other problems.

Blocking androgens, on the upside, might lead to less prostate cancer. It would be interesting to see if Dial Soap or other triclosan-containing products use this as a marketing point. "protects against body odor, gingivitis AND prostate cancer" Let's guess not.

Lastly, there was also an article out recently that associates rates of prostate cancer with presumed levels of estrogen (presumably from urine from women on birth control) in water supplies (Margel & Fleshner 2011). This was unexpected to me, until I thought about the pathway through which testosterone is produced. Testosterone can be synthesized from Progesterone, which is also present in birth control pills. So, it may be the progesterone, rather than estrogen, that is causing the problem. Progesterone is not water soluble, so its unlikely to be found in water systems unless conjugated to something else or incorporated in something else, so this is just speculation on my part.

Back to Triclosan. You can find some basic information on what kinds of products contain Triclosan at the Environmental Working Group Website. Its dated 2008, but the basic information may be useful.

For all of this, note that, for Triclosan, the picture is far from clear, as recent papers also report Triclosan enhancing androgenic activity in vitro (Christen et al. 2010) and as having estrogenic activity (Jung et al. 2011). Neither of those qualities is desirable in an environmental contaminant.
Best wishes,

Margel, D., & Fleshner, N. (2011). Oral contraceptive use is associated with prostate cancer: an ecological study BMJ Open, 1 (2) DOI: 10.1136/bmjopen-2011-000311

Christen V, Crettaz P, Oberli-Schrämmli A, & Fent K (2010). Some flame retardants and the antimicrobials triclosan and triclocarban enhance the androgenic activity in vitro. Chemosphere, 81 (10), 1245-52 PMID: 20943248

Jung EM, An BS, Choi KC, & Jeung EB (2011). Potential estrogenic activity of triclosan in the uterus of immature rats and rat pituitary GH3 cells. Toxicology letters PMID: 22062131

Rostkowski, P., Horwood, J., Shears, J., Lange, A., Oladapo, F., Besselink, H., Tyler, C., & Hill, E. (2011). Bioassay- directed identification of novel antiandrogenic compounds in bile of fish exposed to wastewater effluents. Environmental Science & Technology DOI: 10.1021/es202966c

Selenium, Brazil Nuts and Testosterone

2011-05-01T13:25:00.000-07:00

There seems to be a lot out in the popular press or online material that incresing selenium intake will increase a healthy man's testosterone production (example and example II from Forbes Magazine: what were they thinking?), but little, if anything, in the scientific literature to support that idea. (I like the scientificky approach used by that website, especially the graph that shows no effect, and no indication of variability in the data points). However, elevated testosterone, long term, will increase risk of testicular and prostate cancer. There has also been recent emphasis on consumption of brazil nuts as a natural source of selenium that will boost testosterone and increase virility.

Selenium is protective against prostate cancer, and good for testicular development (fetal period . . . sorry guys) and possibly protective against other oxidative-stress-induced ailments, testicular or not. On the other hand, selenium, at high concentrations can result in DNA damage, and thus increase risk of cancer. The problem with supplementing, either through tablets, or through consumption of a natural product high in selenium, is that we do not know where the lines of good and evil cross.

As for Brazil nuts, selenium concentrations in any plant should be dependent on the concentration of selenium in the soil in which it grows, therefore, the concentration of selenium in Brazil nuts probably varies. This turns out to be the case, with nuts grown in Manaus-Belem more than ten times higher in selenium than those grown in Acre-Rondia. Someone consuming Brazil nuts may or may not be making a significant increase in selenium intake.
Chang, J. (1995). Selenium content of Brazil nuts from two geographic locations in Brazil Chemosphere, 30 (4), 801-802 DOI: 10.1016/0045-6535(94)00409-N

ATIF, F., YOUSUF, S., & AGRAWAL, S. (2008). Restraint stress-induced oxidative damage and its amelioration with selenium European Journal of Pharmacology, 600 (1-3), 59-63 DOI: 10.1016/j.ejphar.2008.09.029

Brozmanová J, Mániková D, Vlčková V, & Chovanec M (2010). Selenium: a double-edged sword for defense and offence in cancer. Archives of toxicology, 84 (12), 919-38 PMID: 20871980
Henderson, B. (2000). Hormonal carcinogenesis Carcinogenesis, 21 (3), 427-433 DOI: 10.1093/carcin/21.3.427

Schistosomiasis may be protective against Auto-Immune Disease

2011-02-09T07:14:00.000-08:00

Following up here on the associations between parasite infection and reduced incidence of autoimmune diseases such as diabetes, thyroid disorders, arthritis and possibly asthma, this time with a specific focus on Schistosome infection. Schistosomias is a common infection in many areas of the developing world, and is thought to be the second most important human parasite after malaria. Infection may be sub-clinical with little or no indication of infection.

Osada et al. (2009) reported on lower inflammation and less arthritic response in infected mice. Arthritis can be induced in mice by injecting them with Collagen II. A recent publication by Xiao-Ping Chen's group (He et al. 2010) further report that the inhibitory effect of schistosomiasis is dependent on the life stage of the schistosomes. Schistosomes have a very complex life cycle and apparently some phases are more protective or induce different physiological responses in the host than others. Acute infection and egg-laying by the parasite are associated with less response to the collegen injections. Very interesting.

However, it is not advised that people run out and attempt to infect themselves, which can be pretty horrible and disfiguring. Malnutrition, anemia and lowered IQ have been observed in infected children, and increased incidence of bladder cancer is seen among infected adults. Still, it will be interesting to see where this work goes, and what treatments may be eventually developed. Thank you Osada et al. and He et al.

He, Y., Li, J., Zhuang, W., Yin, L., Chen, C., Li, J., Chi, F., Bai, Y., & Chen, X. (2010). The inhibitory effect against collagen-induced arthritis by Schistosoma japonicum infection is infection stage-dependent BMC Immunology, 11 (1) DOI: 10.1186/1471-2172-11-28

Araújo, M., Hoppe, B., Medeiros Jr, M., & Carvalho, E. (2004). Schistosoma mansoni infection modulates the immune response against allergic and auto-immune diseases Memórias do Instituto Oswaldo Cruz, 99 DOI: 10.1590/S0074-02762004000900005

OSADA, Y., SHIMIZU, S., KUMAGAI, T., YAMADA, S., & KANAZAWA, T. (2009). Schistosoma mansoni infection reduces severity of collagen-induced arthritis via down-regulation of pro-inflammatory mediators International Journal for Parasitology, 39 (4), 457-464 DOI: 10.1016/j.ijpara.2008.08.007

Did Intestinal parasites and poor hygiene protect us from autoimmune diseases?

2011-01-22T13:16:00.000-08:00

Autoimmune diseases are troubling, and often frustrating and painful for health care practitioners and patients. As far as I know, celiac disease is the only autoimmune disorder with a specific and identified trigger: the protein gluten. It has also been pointed out that the incidence of Celiac Disease, the formal name for gluten-triggered autoimmune reactions in the bowel, appears to have been increasing. Some have claimed that humans are not adapted to consumption of plant proteins like gluten, and that inflammatory bowel disorders are the result of the development of agriculture. However, there are a few other possibilities. One is that autoimmune disorders in general have been increasing and that Celiac disease is not increasing at a uniquely faster rate.

A major hypothesis in the development of allergies (inappropriate immune responses to non-pathogens, such as glutten or pollen or dog hair) is lack of exposure to potential allergens early in life. This, perhaps, is the root of the problem: soap, lysol, and a generally high level of cleanliness. Also, a huge change in human habit is the widespread introduction of infant formula to replace breast milk, and early introduction of other foods into infant diets. The ideal window of exposure to gluten is now considered to be between 4 and 7 months and that exposure should be concurrent with continuing breast milk consumption. Introduction to wheat cereals during this period is thought to be protective against celiac disease. Those raising their young children on gluten-free diets in the hope of protecting them from celiac disease, or the adverse effects of inflammation in general, may be taking the wrong route. (See Pinier et al. 2010 and Lopez-Serrano et al. 2010). Let them get a little dirty

Another possiblity, proposed by Elliot and Weinstock (2009) is the current rarity of helminth infection in the Western World. These authors propose that helminth infection was protective against autoimmune diseases like celiac disease by stimulating immune circuits that lower inflammation. I suppose if one were to choose between a gluten-free diet and helminth infection, most would go with the gluten-free diet. However, before you consider loss of bread as the price some pay for the protection of all against intestinal parasites, note that Elliot and Weinstock also propose exploration of the use of helminths for clinical treatment of auto-immune disease.

Elliott, DE and Weinstock JV (2009). Inflammatory bowel disease and the hygiene hypothesis: an argument for the role of helminths Progress in Inflammation Research, 149-178 DOI: 10.1007/978-3-7643-8903-1_9

Pinier M, Fuhrmann G, Verdu E, & Leroux JC (2010). Prevention measures and exploratory pharmacological treatments of celiac disease. The American journal of gastroenterology, 105 (12) PMID: 20877349

López-Serrano P, Pérez-Calle JL, Pérez-Fernández MT, Fernández-Font JM, Boixeda de Miguel D, & Fernández-Rodríguez CM (2010). Environmental risk factors in inflammatory bowel diseases. Investigating the hygiene hypothesis: a Spanish case-control study. Scandinavian journal of gastroenterology, 45 (12), 1464-71 PMID: 20704469

Ketogenic Diets

2011-01-15T12:01:00.000-08:00

I would advocate moderation in just about everything. Ketogenic diets have proven helpful to people with uncontrolled epilepsy and may be of benefit to epileptics in general, to victims of stroke and other forms of brain injury and possibly cancer. They come with other effects that may not be worth the discomfort or unintended risks to healthy people. This includes kidney stones and, in women and girls, amenorrhea. Amenorrhea is associated with bone loss, increasing risk of osteoporosis, and indicates problems in hormone balance. Supplementation with calcium may help with this, but then again, it might not. Physiology can be quite complex, and consumption does not necessarily indicate absorption is occurring. It is quite possible that something that causes hormonal imbalance in women may also cause hormonal imbalance in men. Playing with one’s physiology, when we don’t know the unintended outcomes of such play, may be inadvisable, especially long-term.

I have been a vegetarian for 30 years and an athlete all my life. I have excellent bone density, low blood pressure, low resting heart rate, low fasting blood sugar, excellent blood lipid profile and great strength to body weight ratio. I'm happy and healthy, even though I thoroughly understand I represent but a single data point. I do get a lot of advice from well-meaning friends that I need to eat meat and would be much healthier if I followed a ketogenic diet. Vegetarians, as described in some current diet books, are weak and "skinny-fat". I will leave it at this: The "optimal diet" for one person may not be the "optimal diet" for another, nor the optimal diet for all conditions. Humans are omnivores and physiologically polymorphic and adaptable. This has given us tremendous abilitity to survive in wildly different climes and environments, and has made us such a resilient species. It is also quite possible, that our individual resilience allows our bodies to adjust to dietary and environmental change.

The current state of research indicates no harm though, from short-term ketogenic diets. I have not found much in the way of research on the risks and benefits of long-term ketogenic diets in healthy adults. Anyone who wishes to add a citation, please feel free.

Kossoff, E., Zupec-Kania, B., & Rho, J. (2009). Ketogenic Diets: An Update for Child Neurologists Journal of Child Neurology, 24 (8), 979-988 DOI: 10.1177/0883073809337162

Bergqvist AG, Chee CM, Lutchka L, Rychik J, & Stallings VA (2003). Selenium deficiency associated with cardiomyopathy: a complication of the ketogenic diet. Epilepsia, 44 (4), 618-20 PMID: 12681013

Brinkworth GD, Buckley JD, Noakes M, Clifton PM, & Wilson CJ (2009). Long-term effects of a very low-carbohydrate diet and a low-fat diet on mood and cognitive function. Archives of internal medicine, 169 (20), 1873-80 PMID: 19901139

Role of Hormones, Genes, Hybrid Cars and Environmental Factors in Human Cryptorchidism

2011-01-07T19:40:00.000-08:00

Undescended testicles (Cryptorchidism) appear to be of complex origin . . . one of those cases where there are genetic and environmental components, and therefore difficult to figure out. You can consider genetics, exposures to environmental estrogens and anti-androgens and the relations among risk factors. You will not be bored trying to figure this one out. Added to this mix is a previously unconsidered variable: Hybrid Cars.

I teach a course called "Introduction to Research" which is somewhat like boot camp for aspiring academics. I would now only encourage people to go into academia if they are so driven by love or fascination for a subject that they are willing to sacrifice a signifant amount material comfort in its pursuit. I described my 16 year old minivan as dented and rusty, with an interior re-upholstered piece-meal with green fluorescent duct-tape. The starstruck response: a breathless and drawn out "cool . . . " I went on to describe my leaky roof and deceased dishwasher, and received this: "Dr. K, I will come to your house and fix your dishwasher" followed by "and I will drape my body over the hole in your roof next time it rains" from yet another. Undergraduates can be absolutely amazing.

So, to the hybrid part of the cryptorchidism story. The minivan leaks oil, gets not-so-good mileage and I drive about 120 miles a day to commute to the University. This is horrible for the environment, and costs about 1/7th of my income in gasonline alone. It suddenly struck me, during a quiet conversation with a good friend, and sometimes nemesis, that I could get a used Prius and maybe come out ahead financially on the reduction in gas expenditures. "Oh No! I'm Emasculating!" (that wasn't exactly how it was phrased, but you get the point: he has just become cryptorchidic). I only struck up a conversation with him in the first place because he looked like a hippie and a good environmentalist. Just another reminder not to speak to strangers even if they look "nice".

So what's the deal with hybrids and environmentalism that threatens the masculinity of men in Texas? A simple question, that could be answered with a simple "beats the hell out of me" until I started considering bumper stickers:

This is a question that should be posed to an historian, psychologist and/or poli sci person.

Foresta, C., Zuccarello, D., Garolla, A., & Ferlin, A. (2008). Role of Hormones, Genes, and Environment in Human Cryptorchidism Endocrine Reviews, 29 (5), 560-580 DOI: 10.1210/er.2007-0042

Hearing, Reading Disabilities and PCB exposures

2011-01-06T09:09:00.000-08:00

I found this article very exciting. Serum PCB Concentrations and Cochlear Function in 12-Year-Old Children. by Trnovec et al. 2010, in which they describe associations between hearing function and PCB exposures in Slovakian kids. (In regular terms: PCB exposure in children probably causes hearing deficits). My forebears were deaf, graduated from the American School for the Deaf, were members of Deaf Baseball and Football teams, and from all the old pictures we have, seem to have had absolutely fun and wonderful lives, so I've never really considered Deafness a disability. However, hearing deficits make it hard for children to learn to read, and they do not get the full range of information available to children without hearing deficits. This can be a problem that may put them at a disadvantage in terms of conventional measures of school and life success. See Banai et al. 2009 for some recent interesting work in this area.

Trnovec et al. also observed differences between ears (no, not that some kids heads were filled with Kapok and some weren't) with the left ear showing a stronger deficit than the right. This does lead one to wonder if people are left earred or right-earred and that the same effect might not be seen if they had recruited only right-handed or left-handed children. This is also more complex than it seems because you can be right handed and "goofy footed" i.e. left foot dominant. I am goofy footed, but its only apparent when I'm out surfing.

Here is a link for understanding the systems through which Trnovec are evaluating correlations of PCB exposure with hearing. http://www.est-med.com/OAE/understanding-using_OAE%20von%20Kemp.pdf

Trnovec, T., Šovčíková, E., Pavlovčinová, G., Jakubíková, J., Jusko, T., Husťák, M., Jurečková, D., Palkovičová, L., Kočan, A., Drobná, B., Lancz, K., & Wimmerová, S. (2010). Serum PCB Concentrations and Cochlear Function in 12-Year-Old Children Environmental Science & Technology, 44 (8), 2884-2889 DOI: 10.1021/es901918h

Triclosan induces hypothyroidism and is transfered to infants during lactation.

2010-12-30T17:40:00.000-08:00

Triclosan is used in many personal care products as an anti-bacterial agent. You can find it in soaps, toothpaste etc. It is also an endocrine disruptor that effects at least two different (albeit interrelated) systems. Triclosan has some estrogenic effects. Paul et al. (Dec 2010) have demonstrated that triclosan alters thyroid hormone levels early in lactation. Thyroid hormones are especially important during fetal and infant development because they play crucial roles in brain development. Early thyroid hormone deficiency alters neurological function in animals, and in human, reduces IQ and increases ADHD-like behavior. There are many environmental contaminants that interfere with thyroid hormones including PCBs, PBDEs, perchlorate, and nitrate. It is difficult to study the impact of exposures to these chemicals in humans because its hard to know how much people are exposed to over time, and people are probably never exposed to just one agent at a time. Its important to consider additive (or synergistic or antagonistic) effects and not consider them individually. For now, its probably best for pregnant and lactating women to limit their exposure to triclosan. Thank you, Paul et al., for your hard work, and for fitting yet another piece into the puzzle. Here is the U.S. FDA's position on Triclosan safety.
as of today.

Paul KB, Hedge JM, Devito MJ, & Crofton KM (2010). Developmental triclosan exposure decreases maternal and neonatal thyroxine in rats. Environmental toxicology and chemistry / SETAC, 29 (12), 2840-4 PMID: 20954233

Fried food may cause diabetes in thin people too.

2010-12-24T04:41:00.000-08:00

A Taiwanese research group published on the effects of high oxidized frying oil on insulin secretion (reduces insulin secretion)in 2007. In this study they (Chiang et al. 2010) attempt to determine the cause by experimenting with mice. They used three treatment groups:

Low Fat Diet
High Fat Diet
High Oxidized Frying Oil Diet.

The mice fed high oxidized frying oil exhibited reduced insulin secretion and high blood glucose levels. Very important here: their islets of langerhans (the tissue that produces insulin, as well as glucagon) showed evidence of oxidative damage. Glucagon and insulin work together to keep blood sugar stable. It seems likely that oxidative damage would occur throughout the body, so its probably best to avoid fried food even if diabetes or metabolic syndrome is not one of your concerns.

The High Fat diet mice did not show such changes. This implies that a diet high in fried food may put people at risk of diabetes or metabolic disorder by interfering with production of hormones regulating blood sugar, while a high fat diet of unoxidized oil might be just fine. Vitamin E is an important anti-oxidant and is protective against the effects of High Oxidized Frying Oil. Chiang et al. found that adding Vitamin E to the diet reduced the effects of the Oxidized Fat diet. Thanks to all for their hard work.

Ya-Fan Chiang, Huey-Mei Shaw, Mei-Fang Yang, Chih-Yang Huang, Cheng-Hsien Hsieh and Pei-Min Chao (2011). Dietary oxidised frying oil causes oxidative damage of pancreatic islets and impairment of insulin secretion, effects associated with vitamin E deficiency British Journal of Nutrition : 10.1017/S0007114510005039

Chao, P., Huang, H., Liao, C., Huang, S., & Huang, C. (2007). A high oxidised frying oil content diet is less adipogenic, but induces glucose intolerance in rodents British Journal of Nutrition, 98 (01) DOI: 10.1017/S000711450769000X

Autoimmune disease and inhalation of particulates

2010-12-23T05:07:00.000-08:00

Airborne particulate matter appears to increase risk of diabetes, as discussed a few posts down and diabetics appear to have altered immune function according to a number of parameters. Diabetics have now been observed to have stronger indicators of immune response when air pollution levels (particulate matter in this case) are high. Schneider and Alexis (2010 . . . two first authors, congratulations all) observed increased blood levels of endogenous promotors of Activated Protein C Resistance. Diabetics who were also obese, or who did not express GSTm1, (not having this, by the way, increases risk of a wide array of cancers) or who already had elevated HbA1C (this is an indicator of longer-term blood glucose levels) had the strongest response to particulate matter. So, are diabetics more vulnerable to challenges to the immune system? Do these challenges contribute to development of diabetes? Or is there an interplay in each (diabetes and immune response)alters the pattern of the other. Lets hope they don't progressively spiral over time and continued exposure. The cohort was small with only 20 subjects, but it would be interesting to look at response to particulate matter by age, or time since diagnosis of type II diabetes.

Schneider A, Alexis NE, Diaz-Sanchez D, Neas LM, Harder S, Herbst MC, Cascio WE, Buse JB, Peters A, & Devlin RB (2010). Ambient PM2.5-Exposure Up-regulates the Expression of Co-Stimulatory Receptors on Circulating Monocytes in Diabetic Individuals. Environmental health perspectives PMID: 21169129

Inflammation, autoimmune disease, diabetes and gum disease

2010-12-20T08:26:00.000-08:00

The other day I wrote about environmental agents increasing risk of obesity, diabetes and insulin resistance and mentioned an article associating exposure to particulate matter with increased incidence of diabetes and wondered about it. If, as the authors suggest, exposure to particulates results in low-level chronic inflammation, then other causes of chronic inflammation (like gum disease) should also be associated with increased risk of diabetes, insulin resistance or similar. A little poking around, and yes, looks like a hit: Increased Prevalence of Cardiovascular and Autoimmune Diseases in Periodontitis Patients: A Cross-Sectional Study. Just out last month by Nesse et al. at the University of Groningen in The Netherlands. Very cool guys. Congrats on the publication.

Nesse W, Dijkstra PU, Abbas F, Spijkervet FK, Stijger A, Tromp JA, van Dijk JL, & Vissink A (2010). Increased prevalence of cardiovascular and autoimmune diseases in periodontitis patients: a cross-sectional study. Journal of periodontology, 81 (11), 1622-8 PMID: 20583916

A Little More on Lipophilic Chemicals, Diabetes and Obesity

2010-12-17T10:50:00.000-08:00

This is just a little continuation of the post made yesterday in which I wondered if associations between intake of animal protein (vs. vegetable protein) and waist circumference had anything to do with increased exposure of consumers of animal products to environmental contaminants. This is not my area of research . . . but it is an area of research for a lot of other people. Diabetes and/or Insulin Resistance is associated with exposure to Brominated Flame Retardants, Persistent Organic Pollutants, polychlorinated diphenyl ethers, and, interestingly (perhaps because I don't understand the mechanism by which this would occur . . . will have to look into it) airborn particulates. A brief and very readable review of environmental (chemical) causes of diabetes was made in 2008 by Oliver et al.

Jones, O., Maguire, M., & Griffin, J. (2008). Environmental pollution and diabetes: a neglected association The Lancet, 371 (9609), 287-288 DOI: 10.1016/S0140-6736(08)60147-6
Lee, D., Lee, I., Jin, S., Steffes, M., & Jacobs, D. (2007). Association Between Serum Concentrations of Persistent Organic Pollutants and Insulin Resistance Among Nondiabetic Adults: Results from the National Health and Nutrition Examination Survey 1999-2002 Diabetes Care, 30 (3), 622-628 DOI: 10.2337/dc06-2190
Lim, J., Lee, D., & Jacobs, D. (2008). Association of Brominated Flame Retardants With Diabetes and Metabolic Syndrome in the U.S. Population, 2003-2004 Diabetes Care, 31 (9), 1802-1807 DOI: 10.2337/dc08-0850
Pearson JF, Bachireddy C, Shyamprasad S, Goldfine AB, & Brownstein JS (2010). Association between fine particulate matter and diabetes prevalence in the U.S. Diabetes care, 33 (10), 2196-201 PMID: 20628090

Animal vs. Plant Protein, Adiposity, Persistent Organic Pollutants and Endocrine Disruption

2010-12-16T04:23:00.000-08:00

Intake of vegetable protein is negatively correlated with waist circumference and BMI. In contrast, intake of animal protein is positively correlated with waist circumference and BMI, at least in Belgians. There are a lot of questions to raise with this including the possibility that people who eat less animal protein consume less animal fat which can be a rich source of bioactive, lipophilic contaminants which may also be endocrine disruptors that increase adiposity or alter blood lipids. Note Ruzzin et. al.'s April 2010 paper "Persistent Organic Pollutant Exposure Leads to Insulin Resistance Syndrome." (Very nice work! Congratulations to all authors.) Also possible that people who eat a lot of vegetable protein also eat fewer calories, are less sedentary etc. There is also the argument that lean, grass-fed animals (happy cattle, miserable chickens) would eliminate this vulnerability in meat eaters. That would be an interesting study. BMI and blood lipid profiles in matched cohorts of grass-fed/organic animal protein eaters vs. regular grocery store consumers. Anyone . . . ?

Ruzzin J, Petersen R, Meugnier E, Madsen L, Lock EJ, Lillefosse H, Ma T, Pesenti S, Sonne SB, Marstrand TT, Malde MK, Du ZY, Chavey C, Fajas L, Lundebye AK, Brand CL, Vidal H, Kristiansen K, & Frøyland L (2010). Persistent organic pollutant exposure leads to insulin resistance syndrome. Environmental health perspectives, 118 (4), 465-71 PMID: 20064776

Lin, Y., Bolca, S., Vandevijvere, S., De Vriese, S., Mouratidou, T., De Neve, M., Polet, A., Van Oyen, H., Van Camp, J., De Backer, G., De Henauw, S., & Huybrechts, I. (2010). Plant and animal protein intake and its association with overweight and obesity among the Belgian population British Journal of Nutrition, 1-11 DOI: 10.1017/S0007114510004642