In the United States, one-third of adults are now obese, and the majority of people – more than two-thirds - are overweight. And the US is not alone - according to the World Health Organization, the number of obese adults and children worldwide has more than doubled since 1980. Obesity is linked to increased risk of several chronic diseases including diabetes, cardiovascular disease (CVD), cancer, arthritis, and infertility, adding an estimated $200 billion to US healthcare costs as the number of obese individuals continues to rise (1).
While there is no denying the role of sedentary lifestyle and overconsumption of calories, obesity has recently come to be understood as a condition with strong links to toxic environmental exposures. Studies in the past decade show that obesity is a highly complex disease with both causal and contributory links to metabolic dysfunction (2).
Adipose tissue (body fat), was formerly thought to be metabolically inert, but is now recognized as a true endocrine organ involved in several physiological functions, including metabolic regulation and energy storage. Adipose tissue appears to serve not only as the storage site but also as a modulator of lipophilic persistent organic pollutants (POP’s), a group of toxins that includes current and previously used pesticides and industrial chemicals that persist in the environment. By sequestering these pollutants, the fat protects other organs and tissues from their toxic effects. However, as pollutants accumulate, the total body burden increases and the accumulated POP’s are gradually released into the circulation – especially during periods of weight loss (3).
Over time the fat serves as an internal source of exposure to POP’s, many of which have obesogenic and pro-inflammatory effects of their own -modulating differentiation, metabolism and function of white adipose tissue which contribute to continued weight/fat gain and development of obesity-associated diseases. Fat samples from obese patients show higher levels of POP’s correlate with age and longer duration of obesity, and there has been a positive correlation between POP’s and dysglycemia (abnormal blood sugar), hypertension (high blood pressure) and CVD risk (4).
Some of the other mechanisms of environmental toxins that have been shown include:
- Endocrine disruption: through molecular mimicry, chemicals themselves may exert hormone-like action at receptor sites for thyroid, insulin and steroid hormones, which in turn effect body weight and metabolism. Common examples include bisphenol A, phthalates, organotins, and PBDE flame retardants (5,6,7).
- The obesogen hypothesis: Pre-natal and peri-natal exposures to PCB’s, DDT and DDE have been associated with rapid weight gain in first 6 months, higher BMI in infancy, and increased adipocyte differentiation –which means a higher number of fat cells which will stay with them for life.(8)
- Childhood obesity: Early childhood exposures to BPA, a commonly used plasticizer with known estrogenic properties, has been associated with higher child adiposity. Prenatal BPA exposures were associated with increased BMI and adiposity only in boys (9).
- Dysbiosis: Organochlorine pesticides in particular may increase methanobacteriales in the gut, which have been associated with higher body weight and waist circumference in Korean women (10).
- Methylation: Preliminary evidence suggests that supporting methylation may modulate the effects of BPA exposure - a 2007 animal study showed that perturbation of mouse coat color induced by BPA exposure is rescued by methyl donor nutrient supplementation (folic acid, choline, betaine and vitamin B12). (2)
Considering the links between environmental toxins and obesity, incorporating detoxification strategies can help patients that struggle to maintain a healthy weight. Supporting phase 1 and phase 2 of liver detoxification may help to eliminate the stored toxins that inhibit fat loss, and help to safely metabolize and excrete those that are mobilized during fat loss, preventing further inflammation and tissue damage. A protein- and nutrient-supported detoxification program can provide nutrients that promote detoxification while also incorporating diet and lifestyle changes that support lasting weight loss.
DISCLAIMER: The information contained in this article is for informational purposes only, and is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.
1) Janesick, A. S., & Blumberg, B. (2016). Obesogens: an emerging threat to public health. American journal of obstetrics and gynecology, 214(5), 559–65. doi:10.1016/j.ajog.2016.01.182
2) Xue, J., & Ideraabdullah, F. Y. (2016). An assessment of molecular pathways of obesity susceptible to nutrient, toxicant and genetically induced epigenetic perturbation. The Journal of nutritional biochemistry, 30, 1–13. doi:10.1016/j.jnutbio.2015.09.002
3) La Merrill, M., Emond, C., Kim, M. J., Antignac, J.-P., Le Bizec, B., Clément, K., … Barouki, R. (2013). Toxicological function of adipose tissue: focus on persistent organic pollutants. Environmental health perspectives, 121(2), 162–9. doi:10.1289/ehp.1205485
4) Pestana, D., Faria, G., Sá, C., Fernandes, V. C., Teixeira, D., Norberto, S., … Calhau, C. (2014). Persistent organic pollutant levels in human visceral and subcutaneous adipose tissue in obese individuals--depot differences and dysmetabolism implications. Environmental research, 133, 170–7. doi:10.1016/j.envres.2014.05.026
5) Newbold, R. R. (n.d.). Impact of environmental endocrine disrupting chemicals on the development of obesity. Hormones (Athens, Greece), 9(3), 206–17. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/20688618
6) Grün, F., & Blumberg, B. (2006). Environmental obesogens: organotins and endocrine disruption via nuclear receptor signaling. Endocrinology, 147(6 Suppl), S50–5. doi:10.1210/en.2005-1129
7) Hatch, E. E., Nelson, J. W., Stahlhut, R. W., & Webster, T. F. (2010). Association of endocrine disruptors and obesity: perspectives from epidemiological studies. International journal of andrology, 33(2), 324–32. doi:10.1111/j.1365-2605.2009.01035.x
8) Valvi, D., Mendez, M. A., Martinez, D., Grimalt, J. O., Torrent, M., Sunyer, J., & Vrijheid, M. (2012). Prenatal concentrations of polychlorinated biphenyls, DDE, and DDT and overweight in children: a prospective birth cohort study. Environmental health perspectives, 120(3), 451–7. doi:10.1289/ehp.1103862
9) Vafeiadi, M., Roumeliotaki, T., Myridakis, A., Chalkiadaki, G., Fthenou, E., Dermitzaki, E., … Chatzi, L. (2016). Association of early life exposure to bisphenol A with obesity and cardiometabolic traits in childhood. Environmental research, 146, 379–87. doi:10.1016/j.envres.2016.01.017
10) Lee, H.-S., Lee, J.-C., Lee, I.-K., Moon, H.-B., Chang, Y.-S., Jacobs, D. R., & Lee, D.-H. (2011). Associations among organochlorine pesticides, Methanobacteriales, and obesity in Korean women. PloS one, 6(11), e27773. doi:10.1371/journal.pone.0027773