23
Jun
As Obesity Drug Market Grows, Action Urges Prevention by Ending Obesogenic Chemicals in Food Production
(Beyond Pesticides, June 23, 2026) With new medications (including those containing GLP-1-receptor-agonist or glucagon-like peptide-1) exploding onto the market to treat obesity and serious related health threats, it is easy to lose sight of critical policy issues that allow the ongoing introduction of obesogenic pesticides and other chemicals (endocrine disrupting chemicals that affect metabolism and fat storage) into the food supply. The science on obesity has found that the most common form is attributable to a combination of genetic and environmental factors.
Because there are many factors, the blame for the obesity epidemic cannot be attributed solely to diet broadly, but may relate directly to pesticide and toxic chemical exposures, including chemical residues in food, that may lead to Type 2 diabetes, heart disease, high blood pressure, kidney failure, a breakdown of cartilage and bone within joints, and other metabolic disorders. An increasing body of research shows that exposure to certain pesticides and environmental contaminants initiates various changes in metabolism leading to obesity—not only in the exposed person, but also in offspring.
With all the media attention on a medical cure for obesity, Beyond Pesticides has launched an action to: Urge lawmakers and policymakers to support policies that contribute to obesity prevention by eliminating endocrine disrupting chemicals and promoting the growth of organic food production.
The National Institute of Diabetes and Digestive and Kidney Diseases at the National Institutes of Health cites data that finds, “Obesity is a chronic disease that affects more than 4 in 10 adults in the United States, and nearly 1 in 10 Americans have severe obesity.” With about 43% of adults classified as overweight or obese, a long list of recognized health impacts, and many finding that restricting calories and increasing exercise do not help them lose weight, people are increasingly turning to pharmaceutical approaches to weight loss. One study states that medications with GLP-1 “can reduce body weight in obese patients by between 15% and 25% on average after about 1 year.” Obesity drugs come with side effects. An increasing body of science suggests that a societal focus on preventing obesogen use would help to reduce the need for clinical intervention.
Bruce Blumberg, PhD, University of California, Irvine, first hypothesized the theory on the role environmental chemicals play in promoting obesity in 2006. (See Daily News and The Obesogen Effect.” Coining the term “obesogen,” Dr. Blumberg found that a chemical his team was researching for other issues, a now-banned broad-spectrum biocide/pesticide called tributyltin (TBT), happened to be make laboratory mice fat. Since then, research on the issue continues to expand significantly, and government bodies such as the National Institute for Environmental Health Sciences have recognized the role pesticides and other chemicals play in weight gain and the global obesity epidemic.
Obesogens are endocrine disrupting chemicals that promote obesity following exposure. Endocrine disruption in general and obesity specifically are public health concerns, and there is a wide body of science linking pesticide and other chemical exposures to these effects. The current list of identified environmental obesogens includes pesticide active ingredients such as thiamethoxam, atrazine, permethrin, and glyphosate, as well as contaminants and other ingredients that may be found in pesticide products, such as dioxins, phthalates, per- and polyfluoroalkyl substances (PFAS), alkylphenols, and polyaromatic hydrocarbons (PAHs). In addition to the effects of a single obesogen, two or more obesogens may have a synergistic effect, as shown by the interaction of tributyltin (TBT) and perfluorooctanesulfonate (PFOS). Among the implicated chemicals are those known to leach from plastic food packaging materials.
Obesogens have a diverse spectrum of actions. They are defined functionally as chemicals that promote obesity by increasing the number of fat cells and/or the storage of fat in existing adipocytes. Obesogens can also act indirectly to promote obesity by shifting energy balance to favor calorie storage, by altering basal metabolic rate, by altering gut microbiota to promote food storage, and by altering hormonal control of appetite and satiety.
These changes may occur as a result of direct exposure, in utero exposure, or because of genetic or transgenerational effects. J.J. Heindel, PhD, and others find that susceptibility to obesity starts during development (in utero and the first few years of life), and that obesogens alter developmental programming, disrupting the set point for weight gain later in life. As stated by the researchers, “[I]t is well documented that while it is possible to lose weight and keep it off for an extended time, the vast majority of people will gain the weight back, perhaps indicating they are fighting against a set point or sensitivity to develop these metabolic problems that favors calorie storage over the long term.”
The inability of the U.S. Environmental Protection Agency (EPA) to prevent exposure to obesogens through the use of pesticides is one more failure of the agency to carry out its mandated consideration of endocrine disrupting pesticides. It is evidence of a failed pesticide regulatory system that does not consider and promote nontoxic and beneficial alternatives, such as organic agriculture and land management—which the agency could do under its mandate to protect against “unreasonable adverse effects” to people and environment in the Federal Insecticide, Fungicide and Rodenticide Act (FIFRA).
While childhood obesity is recognized as a serious problem, the National School Lunch Program of the U.S. Department of Agriculture (USDA)—although improved by the Healthy, Hunger-Free Kids Act of 2010—still provides lunches laced with obesogenic pesticides. To take meaningful steps against childhood obesity, school lunches must be organic.
Beyond Pesticides action: Urge lawmakers and policymakers to support policies that contribute to obesity prevention by eliminating endocrine disrupting chemicals and promoting the growth of organic food production.
Letter to U.S. Environmental Protection Agency
Contrary to popular opinion, the blame for the obesity epidemic cannot be attributed solely to diet broadly, but links directly to pesticide and toxic chemical exposures, including residues in food, that may lead to Type 2 diabetes, heart disease, high blood pressure, kidney failure, a breakdown of cartilage and bone within joints, and other metabolic disorders. An increasing body of research shows that exposure to certain pesticides and environmental contaminants initiates various changes in metabolism leading to obesity—not only in the exposed person, but also in offspring.
With about 43% of adults classified as overweight or obese, a long list of recognized health impacts, and many finding that restricting calories and increasing exercise do not help them lose weight, people are increasingly turning to pharmaceutical approaches to weight loss. These drugs come with side effects that may also be harmful. An increasing body of science suggests that a societal focus on prevention, targeting contaminants, would be a more effective strategy and reduce the need for clinical intervention.
Since Bruce Blumberg, PhD, first hypothesized the obesity-promoting role of environmental chemicals in 2006, research on the issue continues to expand significantly, and government bodies such as the National Institute for Environmental Health Sciences recognize the role pesticides and other chemicals play in the global obesity epidemic.
Obesogens are endocrine disrupting chemicals that promote obesity following exposure. Endocrine disruption in general and obesity specifically are public health concerns, and there is increasing science linking pesticide and other chemical exposures to these effects. The current list of identified environmental obesogens includes pesticide active ingredients such as thiamethoxam, atrazine, permethrin, and glyphosate, as well as contaminants and other ingredients that may be found in pesticide products, such as dioxins, phthalates, per- and polyfluoroalkyl substances (PFAS), alkylphenols, and polyaromatic hydrocarbons (PAHs). In addition to the effects of a single obesogen, two or more obesogens may have a synergistic effect, as shown by the interaction of tributyltin (TBT) and perfluorooctanesulfonate (PFOS).
Obesogens promote obesity by increasing the number of fat cells and/or the storage of fat in existing adipocytes. They can also act indirectly to promote obesity by shifting energy balance to favor calorie storage, by altering basal metabolic rate, by altering gut microbiota to promote food storage, and by altering hormonal control of appetite and satiety.
These changes may occur as a result of direct exposure, in utero exposure, or because of transgenerational effects. J.J. Heindel, PhD and others find that susceptibility to obesity starts during development (in utero and the first few years of life), and that obesogens alter developmental programming, disrupting the set point for weight gain later in life. As stated by the researchers, “[I]t is well documented that while it is possible to lose weight and keep it off for an extended time, the vast majority of people will gain the weight back, perhaps indicating they are fighting against a set point or sensitivity to develop these metabolic problems that favors calorie storage over the long term.”
EPA has failed to carry out its mandated consideration of endocrine disrupting pesticides and thus failed to prevent exposure to obesogens. The pesticide regulatory system fails to consider and promote nontoxic and beneficial alternatives, such as organic agriculture, as mandated in the Federal Insecticide, Fungicide and Rodenticide Act (FIFRA), to protect against “unreasonable adverse effects” to people and the environment.
Please ensure that pesticide risk assessments include the harms arising from exposure to obesogens. Please also ensure that the baseline against which “benefits” of pesticides are measured is organic agriculture.
Thank you.
Letter to U.S. Congress
Contrary to popular opinion, the obesity epidemic cannot be attributed solely to diet broadly, but links directly to pesticide and toxic chemical exposures, including residues in food, that may lead to Type 2 diabetes, heart disease, high blood pressure, kidney failure, a breakdown of cartilage and bone within joints, and other metabolic disorders. Research shows that exposure to certain pesticides and environmental contaminants initiates various changes in metabolism leading to obesity—not only in the exposed person, but also in offspring.
With about 43% of adults classified as overweight or obese, a long list of recognized health impacts, and many finding that restricting calories and increasing exercise do not help them lose weight, people are increasingly turning to pharmaceutical approaches to weight loss. These drugs come with side effects that may also be harmful. An increasing body of science suggests that a societal focus on prevention, targeting petrochemical contaminants, would be a more effective strategy and reduce the need for clinical intervention.
Since Bruce Blumberg, PhD first hypothesized the obesity-promoting role of environmental chemicals in 2006, research has expanded significantly, and government bodies such as the National Institute for Environmental Health Sciences recognize the role pesticides and other chemicals play in the global obesity epidemic.
Obesogens are endocrine disrupting chemicals that promote obesity following exposure. The current list of identified environmental obesogens includes pesticide active ingredients such as thiamethoxam, atrazine, permethrin, and glyphosate, as well as contaminants and other ingredients that may be found in pesticide products, such as dioxins, phthalates, per- and polyfluoroalkyl substances (PFAS), alkylphenols, and polyaromatic hydrocarbons (PAHs). In addition to the effects of a single obesogen, two or more obesogens may have a synergistic effect, as shown by the interaction of tributyltin (TBT) and perfluorooctanesulfonate (PFOS).
Obesogens promote obesity by increasing the number of fat cells and/or the storage of fat in existing adipocytes. They can also act indirectly to promote obesity by shifting energy balance to favor calorie storage, by altering basal metabolic rate, by altering gut microbiota to promote food storage, and by altering hormonal control of appetite and satiety.
These changes may occur as a result of direct exposure, in utero exposure, or because of transgenerational effects. J.J. Heindel, PhD and others find that susceptibility to obesity starts during development, and obesogens alter developmental programming, disrupting the set point for weight gain later in life. As stated by the researchers , “[I]t is well documented that while it is possible to lose weight and keep it off for an extended time, the vast majority of people will gain the weight back, perhaps indicating they are fighting against a set point or sensitivity to develop these metabolic problems that favors calorie storage over the long term.”
EPA has failed to carry out its mandated consideration of endocrine disrupting pesticides, including obesogens. The pesticide regulatory system fails to consider and promote nontoxic and beneficial alternatives, such as organic agriculture, as mandated by the Federal Insecticide, Fungicide and Rodenticide Act (FIFRA), to protect against “unreasonable adverse effects” to people and the environment.
While childhood obesity is recognized as a serious problem, the National School Lunch Program of the U.S. Department of Agriculture (USDA) still provides lunches laced with obesogenic pesticides. To take meaningful steps against childhood obesity, please ensure that school lunches are organic.
Please ensure that EPA’s pesticide risk assessments include the harms of obesogens and that the baseline against which “benefits” of pesticides are measured is organic agriculture.
Thank you.
Letter to U.S. Department of Agriculture
Contrary to popular opinion, the blame for the obesity epidemic cannot be attributed solely to diet broadly, but links directly to pesticide and toxic chemical exposures, including residues in food, that may lead to Type 2 diabetes, heart disease, high blood pressure, kidney failure, a breakdown of cartilage and bone within joints, and other metabolic disorders. An increasing body of research shows that exposure to certain pesticides and environmental contaminants initiates various changes in metabolism leading to obesity—not only in the exposed person, but also in offspring.
With about 43% of adults classified as overweight or obese, a long list of recognized health impacts, and many finding that restricting calories and increasing exercise do not help them lose weight, people are increasingly turning to pharmaceutical approaches to weight loss. These drugs come with side effects that may also be harmful. An increasing body of science suggests that a societal focus on prevention, targeting contaminants, would be a more effective strategy and reduce the need for clinical intervention.
Since Bruce Blumberg, PhD, first hypothesized the obesity-promoting role of environmental chemicals in 2006, research on the issue continues to expand significantly, and government bodies such as the National Institute for Environmental Health Sciences recognize the role pesticides and other chemicals play in the global obesity epidemic.
Obesogens are endocrine disrupting chemicals that promote obesity following exposure. Endocrine disruption in general and obesity specifically are public health concerns, and there is increasing science linking pesticide and other chemical exposures to these effects. The current list of identified environmental obesogens includes pesticide active ingredients such as thiamethoxam, atrazine, permethrin, and glyphosate, as well as contaminants and other ingredients that may be found in pesticide products, such as dioxins, phthalates, per- and polyfluoroalkyl substances (PFAS), alkylphenols, and polyaromatic hydrocarbons (PAHs). In addition to the effects of a single obesogen, two or more obesogens may have a synergistic effect, as shown by the interaction of tributyltin (TBT) and perfluorooctanesulfonate (PFOS).
Obesogens promote obesity by increasing the number of fat cells and/or the storage of fat in existing adipocytes. They can also act indirectly to promote obesity by shifting energy balance to favor calorie storage, by altering basal metabolic rate, by altering gut microbiota to promote food storage, and by altering hormonal control of appetite and satiety.
These changes may occur as a result of direct exposure, in utero exposure, or because of transgenerational effects. J.J. Heindel, PhD, and others find that susceptibility to obesity starts during development (in utero and the first few years of life), and that obesogens alter developmental programming, disrupting the set point for weight gain later in life. As stated by the researchers, “[I]t is well documented that while it is possible to lose weight and keep it off for an extended time, the vast majority of people will gain the weight back, perhaps indicating they are fighting against a set point or sensitivity to develop these metabolic problems that favors calorie storage over the long term.”
EPA has failed to carry out its mandated consideration of endocrine disrupting pesticides and thus failed to prevent exposure to obesogens. The pesticide regulatory system fails to consider and promote nontoxic and beneficial alternatives, such as organic agriculture, as mandated in the Federal Insecticide, Fungicide and Rodenticide Act (FIFRA), to protect against “unreasonable adverse effects” to people and the environment.
Please ensure that pesticide risk assessments include the harms arising from exposure to obesogens. Please also ensure that the baseline against which “benefits” of pesticides are measured is organic agriculture.
Thank you.
