Triclosan induces hypothyroidism and is transfered to infants during lactation.

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.

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

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

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

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

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

Nutritional Stuff, Protein and Vegetarianism

This is not my field but, late at night, when I can't sleep, I sometimes look at articles dealing with nutrition and here are two that piqued my curiosity.
One is that high protein maternal diets may predispose infants (at least rats anyway) to greater risk of obesity later in life.  Maternal consumption of high-prebiotic fibre or -protein diets during pregnancy and lactation differentially influences satiety hormones and expression of genes involved in glucose and lipid metabolism in offspring in rats, British Journal of Nutrition.  Of course there are lots of questions.  The young rats were switched to a "normal" diet after weaning.  What if they had stayed on the same diet their mothers had been on?  For review of fetal programming see Godfrey et al. 2007.  Is the problem when diet changes after an infant as been "programmed" to a particular nutritional condition?  i.e. is it mismatch between fetal expectation and the reality of later life, or is it a problem created by a high protein diet? 

The other is that creatine supplements appear to increase cognitive function in vegetarians:  The influence of creatine supplementation on the cognitive functioning of vegetarians and omnivores also just out in the British Journal of Nutrition.  I'm a vegetarian with ADHD-like traits.  Time to try a supplement?  Opposed on principle, but what the hey, I can use all the cognitive function I can get.

Godfrey KM, Lillycrop KA, Burdge GC, Gluckman PD, & Hanson MA (2007). Epigenetic mechanisms and the mismatch concept of the developmental origins of health and disease. Pediatric research, 61 (5 Pt 2) PMID: 17413851

Ototoxicity

You don't hear much about ototoxicity (pun completely intended), but I think it is fascinating (what???).  Hearing is relatively easy to evaluate and can serve as marker of neurological effect for chemicals targetting the developing nervous system (i.e. harm nerve development in general and you may see poor functioning in general, including poor hearing).  Like other cells in the body, cells involved in hearing are vulnerable to oxidative stress.  Oxidative attack can result in damage to a cell's DNA, which can lead to development of a cancerous cell or, if you are a fetus, in the development of a birth defect.  Your body is not completely defenseless against a cancerous cell.  Abnormal cells normally self-destruct in a process called "apoptosis".  Its when a cell loses the ability to undergo apoptosis that you may have a serious problem. 

When you combine something like Arsenic, which is a great creator of oxidative stress, with exposure to loud noise you get more hearing loss than you would if you were not also exposed to Arsenic.  Heavy metals, mercury and lead, are classic ototoxicants as are some antibiotics and drugs for erectile dysfunction. 

Hearing loss is also seen when environmental chemicals interfere with neurodevelopment.  There is some very interesting work being done in this area by Tomas Trnovec (Slovakia) et al. that focuses on hearing deficits in children exposed to PCBs.  PCBs were bannned in the US decades ago, but continued to be produced by the Soviet Block.  Poor environmental regulation in Eastern Europe has left those countries with some major environmental health problems.  Best wishes to all working in this area.