Review ArticleEnvironmental Health & Obesity

Obesogens as an Environmental Risk Factor for Obesity

Introduction

Obesity has reached pandemic proportions globally, imposing enormous burdens on public health systems and individual well-being through its associations with type 2 diabetes, cardiovascular disease, metabolic syndrome, and various cancers. The prevailing medical paradigm has long framed obesity primarily as a consequence of energy imbalance — the simple excess of caloric intake over energy expenditure. While diet and physical activity undeniably play central roles, this framework alone fails to fully explain the rapid escalation of obesity prevalence worldwide over recent decades, including in Malaysia where obesity rates have risen substantially.

This review, published in the Malaysian Journal of Public Health Medicine, examined the emerging concept of obesogens — environmental chemicals that may promote obesity through mechanisms distinct from, and additive to, traditional dietary and lifestyle factors. The obesogen hypothesis, first formally articulated by researchers studying endocrine-disrupting chemicals (EDCs), proposes that certain environmental pollutants can alter the body’s regulation of fat storage, metabolic set points, and appetite control, thereby predisposing exposed individuals to weight gain and obesity.

Defining Obesogens

An environmental obesogen is defined as a chemical that can alter lipid homeostasis to promote adipogenesis (the formation of new fat cells) and lipid accumulation. Many obesogens are classified more broadly as endocrine-disrupting chemicals — synthetic compounds capable of interfering with normal hormonal function and producing adverse health effects. The distinction is that obesogens specifically act through pathways relevant to energy metabolism and fat tissue biology.

Obesogens operate through multiple mechanisms. Some act directly on adipocyte biology by increasing the commitment of precursor stem cells to the adipocyte lineage, promoting the differentiation of pre-adipocytes into mature fat cells, or enlarging existing adipocytes. Others work indirectly by altering basal metabolic rate, shifting energy balance toward caloric storage, or modifying the hormonal regulation of appetite, satiety, and food preferences through effects on the brain, pancreas, liver, gastrointestinal tract, and muscle tissue.

Key Obesogenic Chemicals

Bisphenol A (BPA)

BPA is one of the most widely studied potential obesogens. Found extensively in polycarbonate plastics, epoxy resins lining food cans, thermal receipt paper, and numerous consumer products, BPA exposure is nearly ubiquitous in modern populations. Research has demonstrated that BPA can promote adipogenesis, disrupt lipid and glucose metabolism, and interfere with insulin signalling. Epidemiological studies have found associations between urinary BPA levels and increased body mass index, particularly in children and women.

Phthalates

Phthalates, used as plasticisers in flexible polyvinyl chloride (PVC) products and as solvents in personal care items, represent another major class of suspected obesogens. These compounds can leach from products into food, water, and air. Research has demonstrated relatively consistent associations between phthalate exposure and obesity outcomes in children, though results in adult populations have been more heterogeneous.

Tributyltin (TBT)

TBT, an organotin compound historically used as an antifouling agent in marine paints, represents one of the best-characterised obesogens in experimental models. TBT activates the retinoid X receptor (RXR) and peroxisome proliferator-activated receptor gamma (PPARγ), a master regulator of adipogenesis, at nanomolar concentrations. Animal studies have demonstrated that prenatal TBT exposure can programme increased fat mass that persists into adulthood and across generations.

Perfluoroalkyl Substances (PFAS)

PFAS, commonly referred to as “forever chemicals” due to their environmental persistence, have been associated with altered lipid profiles and increased adiposity in some epidemiological studies. These compounds are found in non-stick cookware, water-resistant fabrics, food packaging, and firefighting foams, resulting in widespread human exposure.

Organochlorine Pesticides

Legacy organochlorine pesticides, including DDT and its metabolites, persist in the environment and bioaccumulate through food chains despite being banned or restricted in many countries. These compounds have been associated with metabolic disruption and diabetes risk, though evidence specifically linking them to obesity outcomes has been more variable across studies.

Developmental Programming and Epigenetic Effects

One of the most concerning aspects of obesogen exposure is its potential to produce lasting metabolic effects through developmental programming. Exposure during critical windows — particularly the prenatal period and early infancy — may permanently alter the trajectory of adipose tissue development, metabolic regulation, and energy homeostasis. This concept aligns with the broader Developmental Origins of Health and Disease (DOHaD) framework, which recognises that early-life environmental exposures can programme lifelong disease susceptibility.

Epigenetic modifications — changes in gene expression that do not involve alterations to the DNA sequence itself — represent a key mechanism through which obesogen exposure may exert lasting effects. These modifications, including DNA methylation and histone modifications, can alter the expression of genes involved in adipocyte differentiation, metabolic regulation, and appetite control. Importantly, some animal studies have demonstrated that epigenetic changes induced by obesogen exposure can be transmitted across generations, raising the possibility of transgenerational obesogenic effects.

Relevance to the Malaysian Context

Malaysia has experienced a rapid rise in obesity prevalence over recent decades, with the National Health and Morbidity Survey documenting significant increases in both adult and childhood obesity. While dietary shifts toward higher caloric intake and reduced physical activity are well-recognised contributors, the obesogen hypothesis suggests that environmental chemical exposures may constitute an additional, underappreciated factor in Malaysia’s obesity epidemic.

Malaysia’s economic development and industrialisation have been accompanied by increased use of plastics, processed foods, and consumer chemicals — all potential sources of obesogenic exposure. The tropical climate and agricultural practices in the region may also influence exposure patterns to certain pesticides and persistent organic pollutants. Understanding the potential contribution of environmental obesogens to Malaysia’s obesity burden is therefore relevant for developing comprehensive prevention strategies.

Implications for Public Health

The obesogen hypothesis carries several important implications for public health policy and practice. First, it suggests that obesity prevention strategies focused exclusively on diet and exercise, while necessary, may be insufficient if environmental chemical exposures are simultaneously promoting adipogenesis and metabolic disruption. Second, the evidence for developmental programming effects underscores the particular importance of reducing obesogen exposure during pregnancy and early childhood. Third, the identification of specific obesogenic chemicals provides actionable targets for regulatory intervention, including restrictions on BPA, phthalates, and other compounds in food-contact materials and consumer products.

The precautionary principle suggests that, given the growing evidence base and the difficulty of reversing obesity once established, proactive measures to reduce population-level exposure to suspected obesogens are warranted even as research continues to refine our understanding of dose-response relationships and mechanisms of action.

Limitations

This review acknowledged several important limitations in the obesogen literature. Much of the mechanistic evidence comes from animal studies, and the translation of these findings to human populations is complicated by differences in metabolism, exposure levels, and confounding factors. Epidemiological studies face challenges in accurately assessing chemical exposures over the relevant time periods. The multicausal nature of obesity makes it difficult to isolate the contribution of any single environmental factor, and the interaction between genetic susceptibility, dietary patterns, and chemical exposures remains poorly understood.

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