How Everyday Chemicals Are Fueling the Diabetes and Obesity Epidemic
The air we breathe, the food we eat, and the products we use might be quietly reshaping our metabolism.
We've long understood that poor diet, sedentary lifestyles, and genetics play crucial roles in the development of obesity and diabetes. But a growing body of scientific evidence reveals a more complex picture: environmental chemicals, from permanent stains on our furniture to microscopic particles in our air, may be significant but overlooked contributors to these global epidemics.
Beyond the usual suspects of calories and exercise, our modern environment presents a cocktail of synthetic substances that can disrupt the delicate systems regulating our weight and blood sugar. This article explores the science behind these invisible risk factors and how they might be hindering our best efforts to stay healthy.
Several classes of chemicals have come under scientific scrutiny for their potential to interfere with metabolic processes. Among the most concerning are per- and polyfluoroalkyl substances (PFAS), often called "forever chemicals" due to their persistence in the environment and human bodies 1 5 .
Used in everything from nonstick cookware and stain-resistant furniture to waterproof clothing and food packaging, these chemicals don't break down easily and accumulate in our bodies over time 5 . Mount Sinai researchers found that each increase in PFAS exposure was linked to a 31% increase in type 2 diabetes risk 1 7 .
"Forever chemicals" found in nonstick cookware, stain-resistant fabrics, and food packaging.
Chemical Diabetes RiskPlasticizers used in various consumer products and packaging materials.
Chemical Obesity RiskIncluding certain pesticides that persist in the environment and food chain.
Chemical Diabetes RiskFrom vehicle exhaust and industrial processes that can enter the bloodstream.
Pollutant Diabetes RiskThese substances are increasingly classified as metabolic disruptors or obesogens – chemicals that can promote obesity by altering fat cell development, hormone regulation, or appetite signals 9 .
Recent research from the Icahn School of Medicine at Mount Sinai provides compelling evidence about how "forever chemicals" may be influencing diabetes risk. The study, published in eBioMedicine in 2025, offers a revealing glimpse into this relationship 1 7 .
The research team conducted what's known as a nested case-control study within the BioMe database, a massive collection of health records from more than 70,000 participants 1 7 .
Nested case-control within BioMe database enabled analysis of exposure before disease onset.
180 people recently diagnosed with type 2 diabetes were matched with similar individuals without diabetes.
Using stored blood samples, researchers measured PFAS levels in all participants.
The findings were striking. Participants with higher levels of PFAS in their blood samples were at significantly greater risk of developing type 2 diabetes 1 5 .
Specifically, the research revealed that each increase in the range of PFAS exposure was associated with a 31% increase in type 2 diabetes risk 1 7 . This association held even when accounting for other known risk factors.
Perhaps even more revealing was the discovery of metabolic irregularities in amino acid biosynthesis and drug metabolism that might explain how PFAS affect the body's ability to regulate blood sugar 1 7 . This suggests these chemicals aren't just correlated with diabetes but may actively contribute to its development by disrupting fundamental metabolic processes.
| Research Aspect | Finding | Significance |
|---|---|---|
| Study Design | Nested case-control within BioMe database | Enabled analysis of exposure before disease onset |
| Participant Number | 180 with diabetes + 180 matched controls | Provided substantial statistical power |
| Key Result | 31% increased diabetes risk per PFAS range increase | Revealed dose-response relationship |
| Proposed Mechanism | Disruption of amino acid biosynthesis & drug metabolism | Suggested biological plausibility for the association |
The Mount Sinai study represents just one piece of a much larger puzzle. Research spanning decades has identified multiple ways environmental chemicals can interfere with our metabolism.
The problem appears to be particularly pronounced during developmental periods. The "developmental obesogen" hypothesis suggests that chemical exposures early in life may increase obesity risk by altering the differentiation of fat cells or the development of neural circuits that regulate feeding behavior 9 . These effects may only become fully apparent when combined with consumption of a high-calorie diet later in life 9 .
Chemicals can induce oxidative stress and systemic inflammation, both hallmarks of metabolic impairment 6 .
Many environmental chemicals act as endocrine disruptors, altering normal hormone function.
Chemicals can impair mitochondrial function, thereby lowering metabolic rate .
Exposure can cause epigenetic modifications that change how genes related to metabolism are expressed 6 .
| Chemical Class | Common Sources | Potential Metabolic Effects |
|---|---|---|
| PFAS ("Forever Chemicals") | Nonstick cookware, stain-resistant fabrics, food packaging | Increased diabetes risk, disrupted fat and glucose regulation 1 5 |
| Particulate Matter | Vehicle exhaust, industrial processes, construction | Insulin resistance, systemic inflammation, elevated HbA1c 6 |
| Heavy Metals | Contaminated water, certain foods, industrial sites | Impaired insulin secretion, disrupted glucose uptake 6 |
| Phthalates | Plastics, personal care products | Potential interference with fat loss during dieting |
Perhaps one of the most concerning findings is that chemical exposure might not only promote weight gain and metabolic problems but could also interfere with weight loss efforts.
A 2024 systematic review examined whether environmental chemicals might impede the effectiveness of dietary interventions for obesity and diabetes . While evidence is still emerging, some studies found that certain chemicals were associated with:
During calorie restriction (particularly with phthalates and parabens)
After initial loss (associated with PFAS)
Despite weight loss (linked to organochlorines)
This suggests that for some individuals struggling to lose weight despite strict dieting, chemical exposures might represent a previously unappreciated barrier. When people lose weight, lipophilic contaminants (fat-loving chemicals) stored in adipose tissue are mobilized, leading to a spike in circulating levels that might paradoxically dampen some health benefits of weight loss .
Understanding the relationship between chemicals and metabolic disease requires sophisticated tools and methods. Researchers in this field utilize an array of specialized approaches:
| Tool/Method | Function | Application Example |
|---|---|---|
| Silicon Wristbands | Passive sampling devices that absorb chemicals from the environment | Measuring pesticide exposure in pregnant women by analyzing chemicals detected on wristbands 2 |
| Population Lifecourse Exposure-to-Health-Effects Model (PLETHEM) | Open-source modeling platform for creating PBPK (physiologically based pharmacokinetic) models | Predicting how chemicals move through the body and estimating potential human health risks 4 |
| High-Throughput Screening | Automated testing of thousands of chemicals for biological activity | Using Tox21 program to identify which chemicals might perturb biological processes related to diabetes and obesity 9 |
| Metabolomic Analysis | Comprehensive measurement of small molecule metabolites in biological samples | Identifying metabolic irregularities in amino acid biosynthesis related to PFAS exposure 1 |
| Epidemiological Databases | Large collections of health records and biological samples | Conducting nested case-control studies within biobanks like Mount Sinai's BioMe database 1 7 |
The growing evidence linking environmental chemicals to obesity and diabetes has significant implications for both public policy and individual choices.
From a policy perspective, these findings underscore the importance of preventing chemical exposures to promote public health 1 . This might include stricter regulation of certain chemicals, improved labeling requirements, and support for the development of safer alternatives.
Choosing fresh foods over processed foods that may contain packaging chemicals.
Using glass or stainless steel containers instead of plastic for food storage.
Selecting furniture and clothing without stain-resistant or waterproof coatings when possible.
Supporting regular policy reviews of chemical safety data.
As Dr. Damaskini Valvi, senior author of the Mount Sinai study, notes, this research can help "design more effective interventions for the early prevention of type 2 diabetes in the future, taking into account individuals' exposures to environmental chemicals along with other well-known genetic, clinical, and lifestyle factors" 1 7 .
The science makes clear that addressing the obesity and diabetes epidemics will require looking beyond traditional risk factors to consider the complex interplay between our bodies and the chemical environment we've created. By acknowledging these connections, we move closer to truly comprehensive approaches to prevention and treatment.