An obesogen is a chemical that makes an organism to gain fat. For example, bisphenol A, certain phthalates, and most organophosphate flame retardants can be such agents. They can induce the production of new fat cells and/or encourage the storage of more fat. Over the past 20 years, calorie intake has not changed or has slightly decreased, but obesity has increased, and not just among humans. Body weight of animals such as dogs, cats, rodents, and non-human primates are also increasing. The primary regulator of fat cell formation (adipogenesis) is considered to be peroxisome proliferator activated receptor gamma (PPAR-γ). A long list of environmental contaminants bind to this fat receptor - plasticisers, phthalates, BPA and its analogues, flame retardants, and per- and poly-fluoroalkyl substances (PFAS), all are obesogens.

Obesogens can alter appetite control, impact the microbiome, or alter how much energy the body burns at rest (basal metabolic rate) via the thyroid hormone receptor. Basal metabolic rate represents 70% of an average person’s energy expenditure, so lowering it has a significant impact on weight. Oestrogen and androgen receptors, glucocorticoid receptors, and the retinoid X receptor, which promotes adipocyte formation and adipocyte precursor proliferation, are also sensitive to obesogenic chemicals.

Oestrogen and androgen receptors, glucocorticoid receptors, and the retinoid X receptor, which promotes adipocyte formation and adipocyte precursor proliferation, are also sensitive to obesogenic chemicals. Obesogens are present everywhere in our environment. They are found in dust, water, processed foods, food packaging, cosmetics and personal care products, as well as in furniture and electrical appliances, air pollutants, pesticides, plastics, and softeners.

Numerous studies have shown that obesogenic compounds have an impact on obesity. Tributyltin chloride promoted fat formation in mice. The mice that received tributyltin did not eat more or move less than the untreated mice, but they used calories differently and stored more fat. Mice fed with DEHP (diethylhexyl phthalate) ate more food, gained weight, and accumulated more abdominal fat.

In a US clinical trial that examined the weight loss of more than 600 overweight and obese adults using four diets, it was found that plasma PFAS concentration did not affect the degree of weight loss over the six months of the diet, but women who had higher levels of the compound at the beginning of the trial gained significantly more weight back. Moreover, people with higher levels of perfluoroalkyl compounds in their plasma have lower resting metabolic rate and regain their weight much faster after dieting.

In another study, BPA affected PPAR and lipid accumulation in vitro, while low-dose BPA exposure before birth in male mice increased body weight, food intake, and the number of fat cells, as well as insulin levels.

In a US study, the effect of household dust on mouse fat cells was examined. 10 out of 11 dust samples stimulated triglyceride accumulation in preadipocyte mouse cells.

In a study in Canada, children whose mothers regularly consumed drinks containing nonnutritive sweeteners during pregnancy had a higher body mass index and more body fat tissue by age three. Researchers fed pregnant mice with sucrose, aspartame, or sucralose. Male offspring of mice fed with sucrose, aspartame, and sucralose showed 50%, 47%, and 15% more body fat, respectively.

Estimating how much chemicals may be contributing to the global obesity epidemic is difficult. While obesogens are not the sole causes of the obesity problem, these chemicals deserve more attention and potentially stricter regulation.