Yervand Kondrahjian | Staff Writer
According to a 2013 study done by Isfahan University of Medical Sciences, obesity is growing in populations of different economic levels. Because of its adverse effects, it has become a human health crisis at both the individual and public levels. With its prevalence being higher than that of undernutrition, it has been ranked by the World Health Organization (WHO) as one of the top 10 health risks worldwide. Over the past four decades, we have observed the growth of the obesity epidemic and a concurrent increase of industrial chemicals in the environment. In fact, studies propose that substances such as endocrine-disrupting chemicals (EDCs), which alter the functioning of hormones, may have to do with the development of obesity. Further evidence suggests the presence of chemicals termed “obesogens”: molecules with adverse effects on lipid metabolism and adipogenesis that lead to obesity. According to the environmental obesogen hypothesis, individuals who are exposed early in life to substances such as EDCs are prone to gain fat mass and excess weight. Such chemicals interfere with weight homeostasis by changing weight-controlling hormones, modifying sensitivity to neurotransmitters, or altering the sympathetic nervous system activity.
Environmental obesogens are classified as chemical simulators of metabolic hormones or brain neurotransmitters. Evidence from experimental and laboratory studies has shown that there is an association between environmental/obesogenic chemicals and obesity. In fact, chemicals, such as heavy metals, some solvents, pesticides, BPA, organophosphates, phthalates, PCB, PBBs, and many other substances have disruptive effects on the homeostasis of energy balance, glucose and lipid metabolism, and control of adipogenesis.
The effects of obesogen chemicals in human studies have shown conflicting results, though. For instance, the obesogenic effects of phthalates, which are esters mainly added to plastics to increase their flexibility, transparency, durability, and longevity have been examined. A significant link between several phthalates metabolites (monobenzyl phthalate (MBzP), mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), and mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP) and measures of abdominal obesity and insulin resistance has been found in men but not in women, as revealed by a cross-sectional data from the National Health and Nutrition Examination Survey (NHANES) in the USA. Another cross-sectional study, which examined 90 girls whose age ranged between 6 and 8 years, revealed slightly higher concentrations of some phthalate metabolites such as monoethyl phthalate (MEP), mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), and mono-n-butyl phthalate (MBP) among overweight girls than in their other counterparts. However, the difference was not statistically significant. Some studies have shown that despite phytoestrogens’ (notably soy products) beneficial health effects, they may also act as obesogen chemicals.
Different age groups are variably exposed to these chemicals whose effects during fetal and infancy periods may be irreversible and long-lasting for adulthood. Exposure to different doses of these environmental endocrine-disrupting chemicals in different periods of life interacts with some endocrine signaling mechanisms. This in turn leads to eternal undesirable health effects and obesity. Such health consequences may become obvious not only in childhood but also in adulthood, and even in succeeding generations.
Chemical obesogens function through various factors such as leptin, ghrelin, melanocyte-stimulating hormones, neuropeptide Y, amphetamine-regulated transcript, agouti-related protein, and cocaine. It can also function by inhibiting aromatases such as the P450 family members (CYP19 and CYP3A1) or through modifying the expression of various receptors for steroid hormones, retinoic X, peroxisome proliferator-activated, and glucocorticoids. Exposure to obesogen chemicals might affect the steroid hormone receptors, or alter serum levels of metabolic hormones, or even influence nuclear receptor signaling pathways in preadipocytes, which would lead to adipocyte differentiation and thus a tendency to excess weight.
The systemic reactions to exposure to environmental chemical factors can potentially increase the risk for obesity-related health effects, such as metabolic syndrome, insulin resistance, prediabetes, diabetes, oxidative stress, prehypertension, hypertension, and nonalcoholic fatty liver diseases, even in the pediatric age group. Also, these chemicals can have an impact on intrauterine growth retardation, low birth weight, and prematurity, which are considered predisposing factors for obesity and adult chronic diseases.
So, environmental factors have various health consequences. Fast changes in lifestyle habits, along with increased energy intake and decreased energy expenditure are deemed responsible for excess weight. However, the rapid rising trend of obesity in various age groups and in populations with different lifestyle habits and diverse socioeconomic levels necessitates that global obesity epidemic be considered as a multifactorial and complex disorder, which requires the emphasis of public health interventions for environmental protection.
References
Kelishadi, R., Poursafa, P., & Jamshidi, F. (2013). Role of environmental chemicals in Obesity: A systematic review on the current evidence. Journal of environmental and public health. Retrieved November 10, 2021, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3687513/.