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Mar 18

Guest commentary, What’s new
Untangling the causes of obesity

Jerry Heindel, PhD photoBy Jerry Heindel, PhD
Director, Healthy Environment and Endocrine Disruptor Strategies (HEEDS)

As researchers look for the reasons to explain the global rise in obesity, one thing has become clear — chemicals in our food, packaging, personal care items, and other products are playing a key role.

Obesity is linked to a variety of preventable health effects, such as type 2 diabetes, heart disease, and even certain types of cancer. Despite the focus on treating obesity with diet and exercise, drugs, and bariatric surgery, obesity is still increasing at alarming rates worldwide, especially in children. 

Evidence is mounting that certain chemicals called obesogens can cause the human (and animal) body to produce more fat than it normally would. Many different chemicals can act as obesogens, including everything from sugar to known bad actor chemicals like bisphenol-A (BPA), phthalates, and flame retardants. Many obesogens do this by impacting the proper functioning of our hormones; they can alter metabolism and promote increased storage of calories. Because of this, obesogens can increase weight gain even if we don’t eat more. 

How scientists study obesity 

In our new analysis, we examined four different models that researchers use in studying obesity. Consistent with these models, we found that exposure to obesogens can result in changes in metabolism leading to weight gain. We proposed an integrated model that puts exposure to obesogens as a key cause of obesity. 

The first model we examined is the “calories in - calories out” idea: you gain weight if you eat more calories than you expend. This model also says that something in the environment has changed over the last 50 or so years, unconsciously altering the brain, leading to increased food consumption and increased weight. The environmental change is not defined, but researchers suspect ultra-processed foods are the culprit. 

The second model states that sugar is the culprit – specifically, high glycemic index carbohydrates that stimulate insulin. The increased insulin stimulates fat storage and increases how much we eat. Since the Western diet is high in sugar and ultra-processed foods, both of these models explain at least some of the current obesity epidemic. 

The third model — the obesogen model — states that obesogens alter metabolism. Most chemicals disrupt hormonal signaling pathways in various tissues that control energy intake, nutrient handling, and body weight. Currently, everyone is born pre-polluted with obesogens and exposure continues throughout life. Exposure to these obesogens at any time can increase weight gain, but when it’s early in life (in utero and early childhood), it disrupts the normal development of fatty tissue, liver, gastrointestinal tract, brain, and tissues regulating metabolism. These permanent changes can lead to obesity later in life, making it easier to gain weight and more challenging to lose it and to keep the weight off. 

The fourth model states that tissues have metabolism sensors that detect when there is sufficient fuel. These sensors produce small amounts of reactive oxygen species that tell the pancreas to release more insulin and fat tissue to make more fat. Both obesogens and ultra-processed foods stimulate production of these reactive oxygen species in inappropriately large amounts, which causes overeating. 

Obesogens are the common thread 

Obesogens are a unifying and key part of the obesity models, affecting all known key activities associated with both the first and second models.

Regarding the “calories in - calories out” model, the changes that cause unconscious altered brain control of appetite can come from ultra-processed foods and obesogens (which also stimulate reactive oxygen species). Concerning the “sugar is the culprit” model, both obesogens and reactive oxygen species stimulate insulin, increasing fat storage. 

In the future, there should be less focus on individual models and more emphasis on a comprehensive model that includes obesogens and reactive oxygen species as essential contributors to obesity.

How we can reduce obesogen exposure 

A new approach is needed — one focusing on prevention.

The good news is that we know many obesogens by name. They include chemicals that come from fossil fuels and plastics (e.g., BPA, phthalates, and PFAS), flame retardants and some food additives, and emulsifiers and colorants found in ultra-processed food. We know where these exposures come from. For many obesogens, we know how they act to increase weight gain.

Decreasing human exposure to obesogens, particularly early in life, will prevent obesity. Personal changes can help, like filtering drinking water and using organic household products, cleaners, and pesticides. Individuals can also try to limit exposures to plastics, canned food, and ultra-processed food.

However, it is unrealistic to expect consumers or clinicians to prevent obesity alone. Instead, policymakers and regulators need to develop public health policies that will regulate and remove these harmful chemicals from products.

Want to learn more? 

EHN’s guide to Obesogens: Chemicals that cause weight gain.

Publication: Obesogens: a unifying theory for the global rise in obesity. Heindel JJ, Lustig RH, Howard S, Corkey BE. Int J Obes (Lond). 2024 Jan 11. doi: 10.1038/s41366-024-01460-3. Open access.

Video: Are we there yet? Unifying model of obesity, by Nicholas Norwitz, about this paper.

Webinar March 19, featuring Dr. Heindel: Obesogens: A unifying theory for the global rise in obesity. The webinar will be recorded and available at that link.

Dr. Heindel coordinated three major review articles on obesogens published in 2022 in the journal Biomedical Pharmacology.


This article is crossposted with Environmental Health News.

Tags: obesityEDCs