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Can BPA make you gain weight? It might change your activitystat.

Activitystat is a setpoint for a person’s general activity level.

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Have you ever wondered why some people are very active while others prefer to conserve their energy?  People tend to keep preferred levels of activity, almost as part of their personalities.  Those who are highly active may prefer lots of sports or just lots of fidgeting.  They get antsy when confined. Others relax whenever possible.  The ActivityStat is a term for a person’s general level of activity.  “The ActivityStat hypothesis” suggests that when physical activity is increased or decreased in one domain, there will be a compensatory change in another domain, in order to maintain an overall stable level of physical activity or energy expenditure over time.”  The ActivityStat leads people to maintain a certain level of activity.  A person whose ActivityStat is high would probably fidget more or get up 20 times to get coffee when confined.   Person whose ActivityStat is low might reduce activity for the rest of the day after a workout or play session.  What determines a person’s activitystat is unknown.  It might be genetic.  But it may also be influenced by the environment.

The obesity epidemic is disturbing and fascinating as well.  And while many have been quick to blame parents, the internet, schools and “moral failings,” there is growing evidence that unseen and poorly understood factors are involved, at least in part.  These factors include current or early exposure to chemicals that have entered the environment or otherwise found their way to our food and water supplies.  BPA, found in some plastics, has been a hot-button chemical.  It was one of the first identified as an “endocrine disruptor” (a chemical that interacts with hormones or their receptors).  While there has been a ton of research on BPA, new things keep turning up:  male rats exposed to BPA very early in life, don’t move around as much as unexposed rats.

Can BPA make you gain weight?  BPA also increases fat cells.

While BPA may decrease your activity stat, it also increases fat cells.  At least in vitro (this is cells in a dish, rather than in a living animal).  When a person is exposed to BPA, the body gets rid of it pretty quickly.  It converts it to something called BPA-G.  Until recently it was thought the BPA-G was harmless and could be urinated away.  BPA-G added to a cell culture of potential fat cells caused the not-yet-fat cells to turn into fat cells.  It also caused them to start making more fat.  There may be no need to fear the occasional drink from a plastic water bottle.  But people should probably stay away when possible.  Especially pregnant women.  Even if it says BPA-free on the label.  We are just learning about BPA-free plastics, and it looks like they are much like BPA.  A last word . . . these studies were of cells (or rats) eposed to BPA or BPA-G early on.  The same effect may not be seen in adults.  Or even humans for that matter.  My apologies if this is too technical or not technical enough.  For you geeks, links to the original articles are below.

Andrea B. Kirk

The author on a great hair day.

NOTE:  This is a disclaimer.  I am not a medical doctor, I am a scientist. If you have questions about your health, talk to your medical doctor

Boucher JG, Boudreau A, Ahmed S, Atlas E. In Vitro Effects of Bisphenol A β-D-Glucuronide (BPA-G) on Adipogenesis in Human and Murine Preadipocytes.Environmental Health Perspectives. 2015;123(12):1287-1293. doi:10.1289/ehp.1409143.

Volberg V, Harley K, Calafat AM, et al. Maternal bisphenol A exposure during pregnancy and its association with adipokines in Mexican-American children.Environmental and molecular mutagenesis. 2013;54(8):621-628. doi:10.1002/em.21803.

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Obesity Genetics and Bacteria: Another Piece of a Strange Puzzle

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Obesity genetics and bacteria are strange bedfellows.  The causes of obesity are far more complicated than we thought just a few short years ago.  Diet and exercise are important, for sure.  But scientists are discovering that genetics and the gut microbiome are be key factors too.  The gut microbiome, if you didn’t know, are the trillions of bacteria that reside in our digestive tracts.  New research has uncovered a piece of how genetics and bacteria interact to increase the chances that someone will become obese, or develop diabetes.

Obesity Genetics and Bacteria Nutshell

Most of us will remember that people can’t digest plant fiber.  That is why we don’t bother to eat grass.  Or leaves.  Or at least most leaves . . . the kind on trees.  Or shrubberies.  Cows and other hoofed animals can eat these things because their stomachs are designed differently.  Bacteria in a cow’s stomach have time to ferment grass and such and break down all those long cellulose chains into useable starch for the cow.  It turns out, however, that some gut bacteria in humans can break down plant fiber into short chain fatty acids.   Humans can then take these fatty acids and convert them into fat.

Obesity and Genetics.

Here comes the genetics part:  While we host trillions of bacteria, we also control their populations.   Overgrowth of bacteria is controlled by a gene called TLR5.  People whose TLR5 doesn’t work that well cannot control gut bacteria as well.  About 10% of our population has a mutated TLR5 that just doesn’t work.  At all.   Having this mutation increases your risk of metabolic syndrome: obesity, diabetes and cardiovascular disease.  Having this mutation also increases fat deposits in the liver.  If you are incredibly geeky (happy emoticom) you can read this “just out” article on genetics and obesity and bacteria here.  If you are less technically oriented, hopefully this information will of help as it is.  If you are struggling with your weight and trying to stay healthy, keep up the good work.   It actually is harder for some people than it is for others.   Different people can actually eat the same thing, and get different amounts of calories out of it.

Back in the old days having this mutation might have been beneficial.  You would have been able to extract more energy from food, which would have been great in times of famine.  But we now live in a time of excess.

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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