Environmental Toxicants – A Factor in the Development of Diabetes?
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Data shows a relationship between diabetes and environmental contaminants – so, what can you do to protect yourself?
The first Global Report on Diabetes, recently published by the World Health Organization (WHO), highlighted several alarming statistics: the incidence of diabetes has doubled since 1980, and as of 2012, it was the eighth leading cause of death worldwide among both sexes, and the fifth leading cause of death in women. Diabetes was responsible for 1.5 million deaths in 2012, more than 43% of which occurred in individuals under 70 years of age.
As the report explains, the increase in type-2 diabetes (T2DM) mirrors the likewise alarming increasing prevalence of obesity, with 1 in 3 adults over the age of 18 overweight and 1 in 10 obese. Excessive body fat is the strongest risk factor for the development of T2DM, while other risk factors include higher waist circumference, higher body mass index (BMI), and being an active smoker. Dietary patterns that include a high intake of saturated fat and total fat, low consumption of fiber, and high intake of sugar-sweetened beverages are also risk factors for T2DM and/or excess body weight. Early childhood nutrition also affects the risk of development of T2DM later in life.
One factor not considered in the WHO overview of diabetes, however, is the potential impact of environmental risk factors on the development of the disease.
Environmental toxicants and diabetes
Exposure to environmental toxicants can occur through the air, contact with the skin, contaminated drinking water, and food. Many environmental pollutants do not degrade over time, and thus continue to accumulate in the environment; these chemicals are classified as persistent organic pollutants (POPs).
In a survey of 2,016 adult participants, performed by the National Health and Nutrition Examination Survey (NHANES), diabetes prevalence was strongly associated with blood concentrations of six persistent organic pollutants.
In a survey of 2,016 adult participants, performed by the National Health and Nutrition Examination Survey (NHANES), diabetes prevalence was strongly associated with blood concentrations of six POPs.[1] Interestingly, obese persons who did not have elevated POPs were not at elevated risk of diabetes. This suggests that the POP exposure, rather than the obesity, was responsible for the increased risk.[2]
Environmental toxicants have the ability to affect genetic transcription, disrupting DNA methylation and altering the organization of chromatin which normally serves to prevent DNA damage and control gene expression. Exposure to environmental pollutants can lead to epigenetic changes, which have the potential to affect more than just one generation.[3],[4] In addition to obesity and diabetes, environmental toxicants have been associated with several types of cancer,[5] respiratory disease,[6] cardiovascular disease,[7] infertility,[8] allergies,[9] autoimmune disease, and many other conditions.[10]
Endocrine-disrupting chemicals (EDCs) wreak havoc on the hormones, and can negatively affect male and female reproductive health, sexual development, risk of breast and prostate cancer, neuroendocrinology, thyroid function, metabolism, and cardiovascular health.[11] EDCs include pollutants like organochlorinated pesticides and industrial chemicals, plastics and plasticizers, fuels, and many other chemicals.[12]
Exposure to bisphenol A (BPA), a known endocrine disruptor, has been linked to obesity, diabetes, cardiovascular diseases, polycystic ovarian disease (PCOS), and low sperm count.
Exposure to bisphenol A (BPA), a known endocrine disruptor, has been linked to obesity, diabetes, cardiovascular diseases, polycystic ovarian disease (PCOS), and low sperm count.[13] BPA is found in the polycarbonate plastics that are used in many types of food and drink packaging including food storage containers, water bottles, the internal protective coating of canned foods, and baby bottles. The degree to which BPA leaches from these materials into food depends mostly on the temperature it is exposed to, with hotter food leading to higher amounts. BPA can also be found in the breast milk of mothers with high levels of exposure.[14]
In data analyzing 4,389 adults with diabetes, higher urinary BPA levels were associated with higher hemoglobin A1c (HbA1c) levels, a blood marker monitored in diabetics.[15] In another recent study, increased exposure to BPA was associated with insulin resistance in overweight or obese children.[16] BPA inhibits the release of adiponectin, which helps to protect humans from obesity, diabetes, and heart disease.[17] Mice exposed to BPA in the prenatal and newborn period developed glucose intolerance.[18]
BPA can also be found in the breast milk of mothers with high levels of exposure.
Dioxins are persistent organic pollutants classified as EDCs.[19],[20] In both men and women, a high serum dioxin level was shown to be an independent risk factor for the development of diabetes, independent of age and weight.[21] Dioxins are absorbed and stored in adipose tissue, therefore they accumulate in the fat of the animals we eat, as well as our bodies. More than 90 percent of human dioxin exposure is through food.
Other environmental chemicals such as polycyclic aromatic hydrocarbons and volatile organic compounds have been shown to cause oxidative stress in a dose-response fashion. Oxidative stress contributes to insulin resistance, a hallmark of metabolic syndrome and type 2 diabetes.[22],[23]
Natural agents that minimize harm
Lifestyle changes to reduce exposure to harmful compounds such as these may have beneficial effects on health. In addition, certain natural products have been shown to help mitigate the harm caused by environmental toxicants.
N-acetylcysteine, an antioxidant that also provides cysteine for the production of glutathione, has been found to attenuate the inflammation, oxidative damage, and related cognitive dysfunction associated with BPA exposure.[24],[25] Quercetin, a natural compound that is also available as a supplement, has evidence it helps mitigate oxidative damage to the liver and kidneys that can be caused by BPA.[26] In addition, silymarin, found in milk thistle, helps protect against the oxidative damage induced by environmental contaminants.[27],[28]
N-acetylcysteine, an antioxidant that also provides cysteine for the production of glutathione, has been found to attenuate the inflammation, oxidative damage, and related cognitive dysfunction associated with BPA exposure.
Berberine, a compound found in botanicals such as Oregon grape, goldenseal, and barberry, has a multitude of actions that may help reduce damage from these environmental compounds as well as clinical evidence of its benefits for diabetics.[29] It serves as an antioxidant and anti-inflammatory agent,[30],[31] improves insulin resistance, promotes insulin secretion, inhibits gluconeogenesis (glucose production) in the liver, and stimulates glycolysis (glucose breakdown) in peripheral tissue cells.[32] Berberine also helps balance the gut microbiota and regulates cholesterol production.[33]
Lipoic acid is one additional antioxidant that helps protect against BPA toxicity.[34] Studies show that lipoic acid can mitigate the peripheral neuropathy complications of diabetes, reduce HbA1c levels, support blood vessel health, and improve glucose utilization.[35],[36],[37]
Summary
Environmental toxicants in our air, water, and food produce oxidative stress and contribute to insulin resistance, but natural substances can help mitigate the harm. N-acetylcysteine, quercetin, silymarin (milk thistle), berberine, and lipoic acid have antioxidant and healing properties. These agents have been shown to protect tissues against damage caused by persistent organic pollutants and endocrine disruptors. Many of these agents can be used as supplements, and in addition to dietary and lifestyle changes, offer a holistic approach for protecting the body against chemical exposures.
Click here to see References
[1] Lee DH, et al. A strong dose-response relation between serum concentrations of persistent organic pollutants and diabetes: results from the National Health and Examination Survey 1999-2002. Diabetes Care. 2006 Jul;29(7):1638-44.
[2] Carpenter DO. Environmental contaminants as risk factors for developing diabetes. Rev Environ Health. 2008 Jan-Mar;23(1):59-74.
[3] Feinberg AP, et al. Phenotypic plasticity and the epigenetics of human disease. Nature. 2007 May 24;447(7143):433-40.
[4] Skinner MK, et al. Epigenetic transgenerational actions of environmental factors in disease etiology. Trends Endocrinol Metab. 2010 Apr;21(4):214-22.
[5] Irigaray P, et al. Lifestyle-related factors and environmental agents causing cancer: an overview. Biomed Pharmacother. 2007 Dec;61(10):640-58.
[6] Khafaie MA, et al. Critical review of air pollution health effects with special concern on respiratory health. J Air Pollution Health. 2016 May 29;1(2):123-36.
[7] Bhatnagar A, et al. Environmental cardiology: studying mechanistic links between pollution and heart disease. Circ Res. 2006 Sep 29;99(7):692-705.
[8] Mendiola J, et al. Exposure to environmental toxins in males seeking infertility treatment: a case-controlled study. Reprod Biomed Online. 2008 Jun;16(6):842-50.
[9] Diaz-Sanchez D, et al. Diesel fumes and the rising prevalence of atopy: an urban legend? Curr Allergy Asthma Rep. 2003 Mar;3(2):146-52.
[10] Schug TT, et al. Endocrine disrupting chemicals and disease susceptibility. J Steroid Biochem Mol Biol. 2011 Nov;127(3-5):204-15.
[11] Ngwa EN, et al. Persistent organic pollutants as risk factors for type 2 diabetes. Diabetol Metab Syndr. 2015 Apr 30;7:41.
[12] Diamanti-Kandarakis E, et al. Endocrine-disrupting chemicals: an Endocrine Society scientific statement. Endocr Rev. 2009 Jun;30(4):293-342.
[13] Fenichel P, et al. Bisphenol A: an endocrine and metabolic disruptor. Ann Endocrinol (Paris). 2013 Jul;74(3):211-20.
[14] Geens T, et al. A review of dietary and non-dietary exposure to bisphenol-A. Food Chem Toxicol. 2012 Oct;50(10):3725-40.
[15] Silver MK, et al. Urinary bisphenol A and type-2 diabetes in U.S. adults: data from NHANES 2003-2008. PLoS One. 2011;6(10):e26868.
[16] Bertoli S, et al. Human bisphenol A exposure and the “diabesity phenotype.” Dose Response. 2015 Jul 31;13(3):1559325815599173.
[17] Hugo ER, et al. Bisphenol A at environmentally relevant doses inhibits adiponectin release from human adipose tissue explants and adipocytes. Environ Health Perspect. 2008 Dec;116(12):1642-7.
[18] Alonso-Magdalena P, et al. The estrogenic effect of bisphenol A disrupts pancreatic beta-cell function in vivo and induces insulin resistance. Environ Health Perspect. 2006 Jan;114(1):106-12.
[19] Remillard RB, et al. Linking dioxins to diabetes: epidemiology and biologic plausibility. Environ Health Perspect. 2002 Sep;110(9):853-8.
[20] Calvert GM, et al. Evaluation of diabetes mellitus, serum glucose, and thyroid function among United States workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin. Occup Environ Med. 1999 Apr;56(4):270-6.
[21] Huang CY, et al. Association between dioxin and diabetes mellitus in an endemic area of exposure in Taiwan: a population-based study. Medicine (Baltimore). 2015 Oct;94(42):e1730.
[22] Hong YC, et al. Community level exposure to chemicals and oxidative stress in adult population. Toxicol Lett. 2009 Jan 30;184(2):139-44.
[23] Kabuto H, et al. Exposure to bisphenol A during embryonic/fetal life and infancy increases oxidative injury and causes underdevelopment of the brain and testis in mice. Life Sci. 2004 Apr 30;74(24):2931-40.
[24] Jain S, et al. Protective effect of N-acetylcysteine on bisphenol A-induced cognitive dysfunction and oxidative stress in rats. Food Chem Toxicol. 2011 Jun;49(6):1404-9.
[25] Yang YJ, et al. Bisphenol A exposure is associated with oxidative stress and inflammation in postmenopausal women. Environ Res. 2009 Aug;109(6):797-801.
[26] Sangai NP, et al. Testing the efficacy of quercetin in mitigating bisphenol A toxicity in liver and kidney of mice. Toxicol Ind Health. 2014 Aug;30(7):581-97.
[27] Kiruthiga PV, et al. Silymarin protection against major reactive oxygen species released by environmental toxins: exogenous H2O2 exposure in erythrocytes. Basic Clin Pharmacol Toxicol. 2007 Jun;100(6):414-9.
[28] Surai PF, et al. Silymarin as a natural antioxidant: an overview of the current evidence and perspectives. Antioxidants (Basel). 2015 Mar 20;4(1):204-47.
[29] Lan J, et al. Meta-analysis of the effect and safety of berberine in the treatment of type 2 diabetes mellitus, hyperlipemia and hypertension. J Ethnopharmacol. 2015 Feb 23;161:69-81.
[30] Li Z, et al. Antioxidant and anti-inflammatory activities of berberine in the treatment of diabetes mellitus. Evid Based Complement Alternat Med. 2014;2014:289264.
[31] Pang B, et al. Application of berberine on treating type 2 diabetes mellitus. Int J Endocrinol. 2015;2015:905749.
[32] Wang Y, et al. Hypoglycemic and insulin-sensitizing effects of berberine in high-fat diet- and streptozotocin-induced diabetic rats. Metabolism. 2011 Feb;60(2):298-305.
[33] Han J, et al. Modulating gut microbiota as an anti-diabetic mechanism of berberine. Med Sci Monit. 2011 Jul;17(7):RA164-7.
[34] El-Beshbishy HA, et al. Lipoic acid mitigates bisphenol A-induced testicular mitochondrial toxicity in rats. Toxicol Ind Health. 2013 Nov;29(10):875-87.
[35] Packer L, et al. Molecular aspects of lipoic acid in the prevention of diabetes complications. Nutrition. 2001 Oct;17(10):888-95.
[36] Poh ZX, Goh KP. A current update on the use of alpha lipoic acid in the management of type 2 diabetes mellitus. Endocr Metab Immune Disord Drug Targets. 2009 Dec;9(4):392-8.
[37] Sola S, et al. Irbesartan and lipoic acid improve endothelial function and reduce markers of inflammation in the metabolic syndrome: results of the Irbesartan and Lipoic Acid in Endothelial Dysfunction (ISLAND) study. Circulation. 2005 Jan 25;111(3):343-8.
The information provided is for educational purposes only. Consult your physician or healthcare provider if you have specific questions before instituting any changes in your daily lifestyle including changes in diet, exercise, and supplement use.
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Dr. Carrie Decker
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