The Pesticides Inside Us

After a study by the Environmental Working Group found 287 different industrial chemicals in the umbilical cords of babies born in America, the idea of obesogenic POPs (persistent organic pollutants) was taken seriously. Once scientists began to suspect environmental chemicals as obesity agents, many research projects were designed and performed.

The Institute for Agriculture and Trade Policy announced:

A number of chemicals known to disrupt hormones also appear to be obesogens… Chemicals can affect the size and number of fat cells or the hormones that regulate appetite and metabolism. They can also cause changes in gene expression, or epigenetic changes, which can have intergenerational impacts. Prenatal and early life exposures to chemical obesogens are especially impactful, as they may alter metabolism and development of fat cells over a lifetime…

The American Chemistry Council pooh-poohed this line of research, wagged its finger and pontificated:

Attempts to link our national obesity problem to minute exposures to chemicals found in common, everyday products are a distraction from the real efforts under way to address this important national health issue.

But if causative factors for this important national health issue can start in the womb, as seems likely, surely an effort to address that very basic cause is too significant to be labeled a distraction.

It is the nature of a corporation to be more interested in looking for a cure, because a cure is a product — a pill or fitness tracker or elliptical machine or one of a thousand other objects that companies make and sell to customers who don’t want to be fat. Prevention, on the other hand, means getting rid of some of their products, like nursing bottles and sippy cups made with BPA. (Manufacturers of those items did in fact stop using the chemical, one step ahead of regulation by the Food and Drug Administration.) Prevention usually means abstaining from something harmful, and abstention doesn’t spend money in the marketplace.

What makes this line of inquiry so problematic is that cause and effect are not dramatically and immediately apparent. Following a chain of events, when thousands of potential variables can interfere, is very difficult. In many cases, the effects of prenatal exposure lie dormant for many years, so proving causation is a monumental challenge.

Environmental poisons

The herbicide atrazine is a mitochondrial toxin, and rat studies found that when atrazine exposure goes up so do insulin resistance and obesity. The thing is, we don’t want our mitochondria to be dysfunctional, because they act as the digestive systems and lungs of our individual cells, and without the energy they generate, nothing much else can happen.

Almost everyone in America harbors inside his or her body a measurable amount of the chemical DDE, a metabolite of the insecticide DDT. Higher blood levels of DDE correlate with higher diabetes rates. This is one of the substances that has been examined in many prenatal studies, and the consensus is that fetal exposure is a strong indicator of obesity in later life. Since DDT use has been banned here for 35 years, this is a striking and scary illustration of how persistently these witch brews can hang around.

HCB, a byproduct of manufacturing processes that use chlorine (found in fungicide and wood preservative), has an equally bad reputation as something to be avoided by fetuses, who unfortunately have no choice in the matter. In one study, the blood of newborn infants was analyzed for its presence. Six years later, a followup study showed that the babies with the highest blood levels of HCB were two or three times as likely to be obese.

Another common pesticide, TFZ (triflumizole) is sprayed on many vegetables and fruits, including cucumbers, grapes, watermelons, cherries, strawberries, and apples. Like many other chemicals, it too has been accused of leading to obesity. Given that there are so many clues, further research is definitely indicated. All these substances need to be either definitely indicted, or eliminated from the list of suspects.

Your responses and feedback are welcome!

Source: “The Obesity Era,”, 06/19/13
Source: “Chemicals and Obesity,”, 07/08/13
Source: “Study ties BPA in cans and bottles to childhood obesity but doesn’t prove it’s a cause,”, 09/18/12
Source: “Obesity/Diabetes Epidemic: Rise of the Obesogens,”, 06/29/11
Source: “Can Pesticides Make Your Kids Fat?,”, 11/09/12
Photo credit: Austin Valley via Visualhunt/CC BY

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About Dr. Robert A. Pretlow

Dr. Robert A. Pretlow is a pediatrician and childhood obesity specialist. He has been researching and spreading awareness on the childhood obesity epidemic in the US for more than a decade.
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Dr. Pretlow’s invited presentation at the American Society of Animal Science 2020 Conference
What’s Causing Obesity in Companion Animals and What Can We Do About It

Dr. Pretlow’s invited presentation at the World Obesity Federation 2019 Conference:
Food/Eating Addiction and the Displacement Mechanism

Dr. Pretlow’s Multi-Center Clinical Trial Kick-off Speech 2018:
Obesity: Tackling the Root Cause

Dr. Pretlow’s 2017 Workshop on
Treatment of Obesity Using the Addiction Model

Dr. Pretlow’s invited presentation for
TEC and UNC 2016

Dr. Pretlow’s invited presentation at the 2015 Obesity Summit in London, UK.

Dr. Pretlow’s invited keynote at the 2014 European Childhood Obesity Group Congress in Salzburg, Austria.

Dr. Pretlow’s presentation at the 2013 European Congress on Obesity in Liverpool, UK.

Dr. Pretlow’s presentation at the 2011 International Conference on Childhood Obesity in Lisbon, Portugal.

Dr. Pretlow’s presentation at the 2010 Uniting Against Childhood Obesity Conference in Houston, TX.

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