Obesogens and the Obesity Pandemic: A focus on prevention

May 19, 2022
12:00 pm US Eastern Time

According to the World Health Organization, obesity prevalence has almost tripled since 1975 with more than 1.9 billion adults, 340 million children ages 5-19, and 39 million children under 5 years of age estimated to be overweight or obese. During this webinar Robert H. Lustig, MD, MSL, Jerrold J. Heindel, PhD, and Chris Kassotis, PhD,  presented a set of newly published reviews on the impact of obesogens. They also discussed how reducing exposures to these hormone disrupting chemicals found in consumer and industrial products like makeup, shampoos, soaps, plastics, cleaners, pesticides, food packaging and more can play a critical role in preventing obesity.

Obesity I: Overview and molecular and biochemical mechanisms

While many attribute obesity primarily to an excess of calories and secondarily to two behaviors (gluttony and sloth), scientific evidence demonstrates the importance of hormone-receptor interactions in adiposity, which is unrelated to either behavior or calories. Dr. Robert H. Lustig covered four specific hormone paradigms: 1. The role of hormones and receptors in the development and growth of adipose tissue; 2. the difference between obesity and chronic disease, and the role of three different fat depots in either disease pathogenesis or prevention; 3. The role of insulin in leptin resistance; and 4. Specific time windows of hormone sensitivity (e.g. the fetal and postnatal periods). 

Obesity II: Establishing causal links between chemical exposures and obesity

Obesity is a multifactorial disease with both genetic and environmental components. The prevailing view is that obesity results from an imbalance between energy intake and expenditure caused by overeating and insufficient exercise. Dr. Jerrold J. Heindel discussed another environmental element that can alter the balance between energy intake and energy expenditure: obesogens. Obesogens are a subset of environmental chemicals that act as endocrine disruptors affecting metabolic endpoints. The obesogen hypothesis posits that exposure to endocrine disruptors and other chemicals can alter the development and function of the adipose tissue, liver, pancreas, gastrointestinal tract, and brain, thus changing the set point for control of metabolism. Obesogens can determine how much food is needed to maintain homeostasis and thereby increase the susceptibility to obesity. The most sensitive time for obesogen action is in utero and early childhood, in part via epigenetic programming that can be transmitted to future generations. This webinar explored the evidence supporting the obesogen hypothesis and highlighted knowledge gaps that have prevented widespread acceptance as a contributor to the obesity pandemic. Critically, the obesogen hypothesis changes the narrative from curing obesity to preventing obesity.

Obesity III: Obesogen Assays: Limitations, Strengths, and New Directions

Despite a growing need for well-understood models for evaluating adipogenic and potential obesogenic contaminants, there has been a reliance on decades-old in vitro models that have not been appropriately managed by cell line providers. There has been a quick rise in available in vitro models in the last ten years, including commercial availability of human mesenchymal stem cell and preadipocyte models; these models require more comprehensive validation but demonstrate real promise in improved translation to human metabolic health. While diverse rodent models exist for evaluating putative obesogenic and/or adipogenic chemicals in a physiologically relevant context, Dr. Chris Kassotis discussed how increasing capabilities have been identified for alternative model organisms such as Drosophila, C. elegans, zebrafish, and medaka in metabolic health testing. These models have several appreciable advantages, including most notably their size, rapid development, large brood sizes, and ease of high-resolution lipid accumulation imaging throughout the organisms, and are anticipated to expand the capabilities of metabolic health research.

This webinar was moderated by Génon Jensen, Executive Director of Health and Environment Alliance (HEAL). It lasted for 70 minutes and was recorded for our call and webinar archive.

This webinar series is sponsored by the EDC Strategies Partnership. The EDC Strategies Partnership is co-chaired by Sharyle Patton (Commonweal Biomonitoring Resource Center), Jerry Heindel (Commonweal HEEDS, Healthy Environment and Endocrine Disruptor Strategies), Genon Jensen (HEAL, Health and Environment Alliance), Sarah Howard (HEEDS and the Commonweal Diabetes and Environment Program), and Hannah Donart (Commonweal CHE, Collaborative on Health and the Environment). To see a full list of past calls and webinars related to EDCs and listen to or view recordings, please visit our partnership page. For updates and more information on upcoming webinars, sign up for our HEEDSHEAL, and CHE newsletters!

Featured Speakers

Robert H. Lustig, MD, MSL,is Emeritus Professor of Pediatrics in the Division of Endocrinology, and Member of the Institute for Health Policy Studies at UCSF. Dr. Lustig is a neuroendocrinologist, with expertise in metabolism, obesity, and nutrition. He is one of the leaders of the current “anti-sugar” movement that is changing the food industry. Dr. Lustig graduated from MIT in 1976, and received his M.D. from Cornell University Medical College in 1980. He also received his Masters of Studies in Law (MSL) degree at University of California, Hastings College of the Law in 2013. He is the author of the popular books Fat Chance (2012), The Hacking of the American Mind (2017), and the just released bookMetabolical: The Lure and the Lies of Processed Food, Nutrition, and Modern Medicine,. He is the Chief Science Officer of the non-profit Eat REAL, he is on the Advisory Board of the Center for Humane Technology, Simplex Health, Levels Health, and ReadOut Health, and he is the Chief Medical Officer of BioLumen Technologies, Foogal, Perfact, and Kalin Health.

Jerrold  (Jerry) J. Heindel has a PhD in Biochemistry from the University of Michigan and worked in the area of reproductive biology and toxicology while on the faculty at the University of Texas Medical School at Houston and the University of Mississippi. He moved to the National Institute of Environmental Health Sciences ( NIEHS) NIH in Research Triangle Park, NC, and headed their Reproductive and Developmental Toxicology group. He then moved to the Division of Extramural Research and Training at NIEHS. He was a Scientific Program Administrator responsible for developing and administering the NIEHS grants program in endocrine disruption, the developmental basis of diseases and obesity and diabetes. He is now retired from NIEHS and is currently the director of the Commonweal Program, Healthy Environment and Endocrine Disruptor Strategies, www.heeds.org. Email: jerryheindel@gmail.com

Chris Kassotis, PhD,is an Assistant Professor in the Institute of Environmental Health Sciences and Department of Pharmacology at Wayne State University in Detroit. He completed his PhD at the University of Missouri working with Susan Nagel and Fred vom Saal to assess unconventional oil and gas operations as a novel source of endocrine disrupting chemicals, and the potential for adverse human and animal health outcomes from exposure. He then pursued postdoctoral training with Heather Stapleton's group at Duke and Seth Kullman's lab at North Carolina State to assess the adipogenic/obesogenic activity of complex chemical mixtures (e.g. indoor house dust) via a combination of cell and zebrafish models. Now in his independent laboratory, he is pursuing novel environmental sources of endocrine disruptors and/or metabolic disruptors, examining mixture effects from combinations of these chemicals, and determining underlying molecular mechanisms. His laboratory is currently funded by an R00 through NIEHS to better understand metabolic disruption potential of ethoxylated surfactants used widely in household cleaning products and detergents, and other grants to assess combination effects on metabolic health outcomes from complex mixtures of pollutants in cell and zebrafish models.