CME INDIA Presentation by Dr. N.K. Singh, MD, FICP, Director, Diabetes and Heart Research Centre, Dhanbad, Jharkhand, India. Editor, www.cmeindia.in.

“In the midst of a pandemic, a polluted planet, increasing diseases like cancer, asthma, heart disease, on World Health Day 2022, WHO will focus global attention on urgent actions needed to keep humans and the planet healthy and foster a movement to create societies focused on well-being.” – WHO 

WHO Theme 2022 is very alarming?

• Why are we looking at environmental Pollutants?
  • Persistent Organic Pollutants
  • Air Pollution
  • Noise Pollution
• Limited evidence to suggest that increase in food intake and decrease in energy expenditure are of large enough magnitude to explain the SPEED of increase in prevalence of diabetes or obesity [Macallister et al 2011]

Why we consider out of traditional perspectives?

1. T2D and prediabetes are increasingly observed among children and adolescents.
2. A common assumption is that lifestyle changes characterized by excess energy intake and a lack of exercise have led to the obesity epidemic and, in turn, to the diabetes epidemic. However, there is considerable evidence suggesting that individuals with similar degrees of obesity can have strikingly different risks of T2D.
3. It is particularly noteworthy that whereas 80% of T2D patients are obese, approximately 75– 80% of obese people never develop T2D.
4. Insulin resistance, a prediabetic state, varies 6-fold among obese persons.
5. Although causal relationships between genetic factors and T2D have been eagerly sought, the data from genome-wide association studies have shown that genetic variants might explain statistically only about 10% of the phenotypic variability
6. Thus, obesity itself is not a sufficient cause of T2D. Neither is genetics sufficient in the vast majority of cases.

Monster out of Control

• The worldwide explosion of the rates of diabetes and other metabolic diseases in the last few decades cannot be fully explained only by changes in the prevalence of classical lifestyle-related risk factors, such as physical inactivity.
• For this reason, it has been recently proposed that other “non-traditional” risk factors could contribute to the diabetes epidemics.
• An increasing number of reports indicate that chronic exposure to and accumulation of a low concentration of environmental pollutants (especially the so-called persistent organic pollutants (POPs)) within the body cause diabetogenesis.

What are Persistent Organic Pollutants?

Persistent organic pollutants (POPs) a group of chemical substances that have the following common properties:

• Resistance to biodegradation.
• Wide-range transportation.
• High lipophilicity.
• Bioaccumulation in fat.
• Biomagnification in the food chain.

Story Getting Unfolded

Meat, fish and dairy products are a major source of POPs

Over 1000 high quality recent scientific papers point to unknown mystery

Organic Pollutants and Type 2 Diabetes

Where do we stand in 2022?

• A systematic review identified 22 studies on pesticides and type 2 diabetes.
• Data suggests an association between organochlorine exposure and type 2 diabetes.
• DDE, heptachlor, HCB, DDT, and trans-nonachlor show similar associations with type 2 diabetes.
• Mechanistic studies support a link between organochlorines and insulin resistance.

Be alert to avoid Phthalates

BPA – Very notorious

CME INDIA Learning Points

• A growing body of evidence links T2D to background exposure to environmental chemicals, in particular chlorinated POPs.
• As typical chemicals contaminating adipose tissues as well as all lipid compartments in biological systems, the available epidemiological and experimental evidence largely shows that background contamination from POP mixtures including OC pesticides and PCBs is strongly associated with the development of T2D.
• Inconsistencies concerning findings for specific individual POPs may arise due to different patterns of POP mixtures between and within populations despite high correlations among serum concentrations of many individual POPs.
• Differences in the shape of the dose-response curves among human studies may reflect an inverted U-shaped association secondary to mitochondrial dysfunction or their endocrine-disrupting properties.
• The bottom line is that low-dose effects of POPs appear to be quite real in humans. However, at present human evidence on POPs and obesity remains insufficient.
• The evidence about the potential influence of POPs in the pathogenesis of T2D can no longer be ignored.
• New results also support a potential role of POPs in T1D etiology and demonstrate a high sensitivity of pancreatic β-cells to POPs.

CME INDIA Tail Piece

References:

1. Sims EA. Are there persons who are obese, but metabolically healthy? Metabolism. 2001;50(12):1499 –1504.
2.  Gregg EW, Cheng YJ, Narayan KM, Thompson TJ, Williamson DF.The relative contributions of different levels of overweight and obesity to the increased prevalence of diabetes in the United States: 1976 –2004. Prev Med. 2007; 45(5):348 –352.
3.  McLaughlin T, Abbasi F, Lamendola C, Reaven G. Heterogeneity in the prevalence of risk factors for cardiovascular disease and type 2 diabetes mellitus in obese individuals: effect of differences in insulin sensitivity. Arch Intern Med. 2007;167(7):642– 648.
4.  Billings LK, Florez JC.The genetics of type 2 diabetes: what have we learned from GWAS? Ann NY Acad Sci. 2010; 1212:59 –77. 7. Thayer KA, H
5. PM Lind and L Lind (2018) Diabetologia DOI 10.1007/s00125-018-4621-3
6. Provvisiero et al. 2016). Int J Environ Res Public Health.2016 Oct 6;13(10).
7. Bresson SE, Isom S, Jensen ET, Huber S, Oulhote Y, Rigdon J, Lovato J, Liese AD, Pihoker C, Dabelea D, Ehrlich S, Ruzzin J. Associations between persistent organic pollutants and type 1 diabetes in youth. Environ Int. 2022 Mar 16;163:107175. doi: 10.1016/j.envint.2022.107175. Epub ahead of print. PMID: 35303528.
8. Lee Yu-Mi et al.Persistent Organic Pollutants and Type 2 Diabetes: A Critical Review.Frontiers Endocrinology.(9)2018.https://www.frontiersin.org/article/10.3389/fendo.2018.00712   

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