Great-grandma’s Pesticides Can Make You Fat

Imagine this: your great- grandmother who loved gardening exposed you to harmful chemicals. And you never even met her.

A 2014 study from Washington State University found that when pregnant rodents were exposed to the pesticide methoxychlor, obesity and other abnormalities were passed on to future generations. Though methoxychlor was banned in 2003 due to its ability to disrupt endocrine systems, its effects may haunt future generations.

The research lead by Michael Skinner has also linked “transgenerational epigenetic inheritance” to other toxins such as plastics, fungicides and BPA.

This adds to the alarm bells sounded in this excerpt from Globesity:

“In 2002, researcher Paula Baillie-Hamilton of Scotland published a seminal paper that stated that the current obesity epidemic could not be explained solely by poor diet and inactivity. She wrote: “What has, up to now, been overlooked is that the earth’s environment has changed significantly during the last few decades because of the exponential production and usage of synthetic organic and inorganic chemicals.”[i] She then named many studies in which chemicals spurred weight gain. The list included more familiar ones like phthalates, bisphenol A (BPA) and pesticides but also others not known to many outside of a lab. How was this happening? Baillie-Hamilton thought the chemicals were changing hormones, neurotransmitters, or the sympathetic nervous system. “Many of these chemicals are better known for causing weight loss at high levels of exposure, but much lower concentrations of these same chemicals have powerful weight-promoting actions,” she reported.

More recently, Retha Newbold of the National Institute of Environmental Health Sciences, part of the National Institutes of Health, added to the alarm. Her charge? Exposure to environmental chemicals during development—before birth—may be contributing to the obesity epidemic.[ii] Fetal life is under siege from chemicals. Though adults also suffer, the unborn are extremely fragile. First, the fetus doesn’t have the protective mechanisms which an adult has: fully developed DNA repair tools, a capable immune system, detoxifying enzymes, complete liver metabolism, and a fully functional blood-brain barrier. Chemicals can pass through the placenta. And worse, the fetus has a fast metabolism, which can add to toxicity.[iii] When cells divide rapidly while being exposed to chemicals, things go wrong. Their marching orders are altered. And these changes, including tendency to obesity, may not appear until adulthood. Or even scarier, the damages may show up way down the road, in the cells of future generations. Genes are altered. Yes, that BPA in your water bottle may figure strongly in your great-grandchild’s life. You may be exposing all your future generations to obesity based on your contact with chemicals. Quite a legacy.

Transgenerational harm is also evident in tributyltins (TBT), compounds in the organotin group.  Humans are exposed through contaminated seafood and shellfish, fungicides on crops, and antifungal agents in wood treatments, industrial water systems, and textiles. TBT exposure in mice before birth caused them to gain more fat later in life.[iv] In 2013, scientists at the University of California Irvine found that those pregnant mice that were fed TBT birthed pups with bigger fat cells and more of them. Most disturbingly, the children and grandchildren of these mice inherited the fat changes in spite of never having been exposed to the chemical. TBT alters genes, which sets future generations up for lifelong struggles with weight. [v]”

[i] Baillie-Hamilton PF. “Chemical toxins: a hypothesis to explain the global obesity epidemic.” J Altern Complement Med. 2002 Apr;8(2):185-92. [ii] Newbold, RR. “Impact of environmental endocrine disrupting chemicals on the development of obesity.” Hormones (Athens). 2010 Jul-Sep;9(3):206-17. Review.[iii] Newbold, RR. “Impact of environmental endocrine disrupting chemicals on the development of obesity.” Hormones (Athens). 2010 Jul-Sep;9(3):206-17. Review. [iv] Grün F, Blumberg B. “Environmental obesogens: organotins and endocrine disruption via nuclear receptor signaling.” Endocrinology. 2006 Jun;147(6 Suppl):S50-5. [v] Chamorro-García R et al.  Transgenerational inheritance of increased fat depot size, stem cell reprogramming, and hepatic steatosis elicited by prenatal exposure to the obesogen tributyltin in mice. Environ Health Perspect. 2013 Mar;121(3):359-66. doi: 10.1289/ehp.1205701. Epub 2013 Jan 11.