(Beyond pesticides, September 2, 2021) A study from McMaster University (Canada) shows that exposure to chlorpyrifos, a recently banned and commonly used insecticide, promotes the development of obesity, even at low doses. Obesity usually occurs as a result of a calorie imbalance between food intake, absorption and energy expenditure. Although various factors can promote obesity, researchers suggest that environmental toxins like chlorpyrifos play a role in the development of obesity by suppressing proteins / enzymes.
According to the Center for Disease Control, 42% of the American population is obese and at risk for type 2 diabetes, cardiovascular (heart) disease, stroke, several cancers, and other critical health conditions. Therefore, research like this highlights the importance of studying how exposure to toxic chemicals can impact health to prevent the harmful consequences of disease. The researchers note: “These studies suggest that the effects of environmental toxicants on the development of obesity may have been underestimated, as all studies to date have been conducted in mice housed at RT. [room temperature]. Future studies examining the mechanisms leading to reductions in -AR [beta adrenergic receptors] signaling and whether there are associations between BAT [brown adipose tissue] metabolic activity and CPF [chlorpyrifos] in humans will be important.
Several environmental pollutants are linked to the development of obesity via effects on intestinal health, the endocrine (hormone) and metabolic system, and the development of adipose (fatty) tissue. However, few studies examine the impact of environmental toxins on the activation of brown adipose tissue (BAT) and the body’s ability to burn calories (thermogenesis). So the researchers used a step-by-step screening approach to assess 34 pesticides and herbicides commonly used in brown fat cells (brown adipose tissue). In addition, scientists specifically tested the effects of chlorpyrifos in mice on high calorie diets.
The study found that chlorpyrifos (an organophosphate insecticide) suppresses the decoupling protein 1 (UCP1), responsible for regulating BAT thermogenesis, at concentrations as low as 1 (picomolar) pM. The main route of exposure is diet, as the main cause of obesity is the suppression of diet-induced thermogenesis. Notably, the study focuses on thermoneutral housing for the participating mice, which better mimic human conditions modeling the development of metabolic diseases. Thus, exposure to chlorpyrifos alters BAT activation in thermoneutral mice following a high fat diet, leading to an increased risk of obesity, non-alcoholic fatty liver disease (NAFLD) and insulin resistance. Chlorpyrifos alters protein modifying enzymes, the protein kinases responsible for maintaining UCP1 function, thereby causing BAT to activate and calorie burning suppression. (See “Pesticides and the Obesity Epidemic.”)
The rate of obesity is increasing and has been for the past five decades. Although general overeating and lack of exercise are attributed to obesity, researchers find that the current obesity epidemic has other factors contributing to development. Besides genetics, exposure to obesogenic compounds like pesticides can promote the development of obesity. These compounds regularly cause reproductive, cardiovascular and endocrine (hormonal) problems in exposed people, especially farmers. Bruce Blumberg, Ph.D., professor of developmental and cell biology, University of California, Irvine, defines obesogens “as chemicals that inappropriately stimulate fat cell development or the storage of fat in those cells. , either directly by modifying the way the cells function, or indirectly altering appetites linked to metabolism. Many obesogenic compounds are endocrine disruptors that directly impact hormone and receptor function and include pesticides like organochlorines, organophosphates, carbamates, and pyrethroids. Additionally, endocrine disruption can negatively impact reproductive function, nervous system function, metabolic / immune function, hormone related cancers, and fetal / body development.
Several studies establish a link between exposure to pesticides and endocrine disruption with epigenetic effects (non-genetic influence on gene expression). As early as 15 years ago, a Washington State University study linked exposure to pesticides to multigenerational impacts on male fertility in rodents. According to several studies, exposure to glyphosate has harmful effects over several generations causing negligible observable effects on pregnant rodents but serious effects on the next two generations. These impacts include reproductive (prostate and ovary) and kidney disease, obesity, and birth defects. Therefore, obesogenic compounds also have an impact on the general population and have implications for the health of future generations. For example, studies show that ancestral exposure to DDT increases the risk of breast cancer and cardiometabolic disorders – promoting an epigenetic inheritance of obesity – for up to three successive generations. Although the United States banned DDT more than five decades ago, the insecticide is still persistent in the environment in all ecosystems and remains in use in some countries. Like DDT, exposure to other POPs such as per- and polyfluoroalkylated substances (PFAS) during pregnancy can increase cardiometabolic disorders such as obesity, diabetes and cardiovascular disease in children. Since residues of DDT / DDE, commonly used pesticides and other chemical pollutants contaminate the environment, exposure to these chemical mixtures can synergize to increase toxicity and disease effects.
Study results indicate that chlorpyrifos negatively affects metabolic function, playing a role in inhibiting calorie burning or thermogenesis. Suppressing thermogenesis allows calories to build up in fatty tissue rather than being converted into energy. Scientists attribute the obesity epidemic in part to exposure to environmental toxicants. Many of these contaminants are lipophilic and bioaccumulate in fatty adipose tissue. Therefore, these results explain why lifestyle changes regarding diet and exercise rarely support weight loss. Senior author and professor at McMaster University, Gregory Steinberg (PhD), notes that “Chlorpyrifos would only need to inhibit energy use in brown fat by only 40 calories per day to trigger it. obesity in adults, which would result in an additional weight gain of five pounds. per year.”
This study is the first toxicological evaluation to study obesity and obesity-related diseases in rodents under thermoneutral conditions, or the temperature at which an organism does not need to regulate body heat. Thermoneutral conditions are a better predictor of the health effects in humans associated with exposure to chemicals. Previous studies using mice at room temperature fail to capture the extent of health effects associated with obesity, even at chemical concentrations known to cause toxicity in animal studies (i.e. neurotoxic effect and effects on reproduction). However, the researchers found that exposure to actual concentrations of chlorpyrifos under thermoneutral conditions promotes weight gain, noncholic fatty liver disease, and insulin resistance.
The United States Environmental Protection Agency (EPA) recently announced the cancellation of all uses of chlorpyrifos in food production in the United States, as chemical contamination of the general population remained significant even after implementation. residential use restrictions more than two decades ago. However, pesticide markets still contain many chemicals that cause similar neurotoxic health effects, endocrine disruptors, carcinogens. This study is taking place in Canada, which has long banned chlorpyrifos for food. However, imported goods may still contain chemical residues, as this study indicates. In addition, chlorpyrifos residues do not disappear immediately after end use and will persist in our environment for some time. Therefore, studies like this one can help government and health officials understand the mechanism used by toxic chemicals to alter metabolic function, thereby fueling the obesity epidemic.
Understanding the effects that obesogenic pesticides can have on the health of current and future generations is essential. Beyond Pesticides believes that we must mitigate the multigenerational impacts of pesticides on human and animal health. However, there is a lack of understanding behind the cause of pesticide-induced diseases, including the expected delay between chemical exposure, health impacts, and epidemiological data. Therefore, lawmakers and regulators should consider taking a more cautious approach before introducing these chemicals into the environment. With far too many illnesses in the United States associated with exposure to pesticides, reducing pesticide use is an extremely important aspect of safeguarding public health and reducing costs to local communities.
Learn more about the effects of pesticides on human health by visiting Beyond Pesticides’ Pesticide-Induced Disease Database, which supports pesticide addiction abandonment. This database is a fantastic resource for additional scientific literature documenting high rates of body burdens, including obesity, endocrine disruption, cancer, and other chronic diseases and illnesses in people exposed to pesticides. Adopting regenerative organic practices and using the least toxic pest control can reduce harmful exposure to pesticides. Solutions such as buying, growing and supporting organic produce can help eliminate the heavy use of pesticides in the environment. Learn more about the multigenerational impacts of pesticides on our health through the journal Pesticides and You from Beyond Pesticide. Also, watch Michael Skinner’s (Ph.D.) talk on transgenerational epigenetic actions of endocrine disruptors on reproduction and disease presented at the 2014 Beyond Pesticides National Pesticides Forum.
Advocate for the elimination of toxic pesticide use by telling the EPA to ban all uses of chlorpyrifos and other environmental toxins as part of Beyond Pesticides Week action.
All positions and opinions not attributed in this article are those of Beyond Pesticides.
Source: Science Daily, Nature Communication