Is the Diabetes Epidemic Primarily Due to Toxins?
Joseph Pizzorno, ND
The incidence of diabetes has increased 7 to 10-fold in the past 50 y. Although increased sugar consumption, obesity, and lack of exercise certainly contribute, the effect of environmental toxins may be far greater. The data are so compelling that some researchers now label these toxins as diabetogens. This editorial summarizes the research showing which toxins are the worst offenders, how they disrupt blood sugar control, where they come from, how to assess body load, and strategies for detoxification and excretion.
The Diabetes Epidemic
According to the Centers for Disease Control and Prevention (CDC), the incidence of diabetes has increased from 0.9% in 1958 to 7.2% in 2013, representing an 8-fold increase. This diabetes epidemic is well demonstrated in Figure 1. The problem, of course, is that this is only the tip of the iceberg as the incidence of metabolic syndrome is even higher and many people have diabetes which has not yet been diagnosed.
Some might dismiss this because of increased sugar consumption. But a close look at Figure 2 casts serious doubt on this as the primary, even most important, cause. The diabetes epidemic started 4 decades after the sugar consumption began to increase and shows little correlation. I am not asserting sugar does not contribute to diabetes. But if this were the primary driver, one would have expected the epidemic to start decades earlier.
Another possibility is the increased incidence of obesity which is a known major risk factor for diabetes. However, the obesity epidemic appears because of the same causes as diabetes: diabetogens, many of which are also called obesogens. Of particular significance is the surprising observation that obese people with low levels of persistent organic pollutants (POPs) do not have an increased risk of diabetes.3
In contrast, as can be seen in Figure 3, the diabetes epidemic does correlate with the rate of release of POPs into the environment. Of course, correlation does not prove causation.
More convincing is the correlation between body load of POPs and risk of metabolic syndrome as seen in Figure 4, and the association is synergistic. When POP levels versus diabetes risk is examined, the case becomes even more compelling, as shown in Figure 5. For example, those in the top 10% of trans-nonachlor level have a remarkable 12-fold increased risk.
Diabetogens: Toxins That Disrupt Blood Sugar Control
As near as I can determine, the term diabetogen was coined in 1961 by GD Campbell of the Diabetic Clinic in King Edward VIII Hospital (Congella, Durban, South Africa).7 He posted a letter in the British Medical Journal describing his efforts to determine the cause of an inexplicably high incidence of “connubial” diabetes in married Natal Indians. His investigative work lead him to their high consumption of mustard oil, which consisted of a simple vegetable oil flavored with a synthetic substance containing 95% allyl isothiocyanate. He postulated that the chemical’s chelation of free sulfhydryl (SH) groups in the gut resulted in decreased availability of SH groups, which he thought would impair carbohydrate metabolism. Although he apparently focused on the wrong molecule, his observation of food contamination as a cause of diabetes was right on.
Currently, I am working on 2 new books: for consumers, The Toxin Solution (coming February 2017); and for health care professionals, Clinical Environmental Medicine (coming Dececember 2017), coauthored with Walter Crinnion, ND. As part of the process, I have been working with 2 smart recent Bastyr University graduates (Drs Cirovic and Bender) to help me dig into the research to answer the question, “What percentage of chronic disease may be due to toxins?” The numbers we are finding are simply stunning (lots of content for future editorials).
The methodology we used to determine the percentage of disease potentially because of specific toxins utilizes the following formula:
where p = underlying prevalence of risk factor in the population; rr = relative risk (risk of contracting a disease in an exposed population divided by the risk of contracting the disease in an unexposed population); and AF = attributable fraction (ie, % of disease because of the toxin).
This is the same formula used to determine, for example, the percentage of lung cancer because of smoking.8 As you might expect, determining these numbers requires quite a lot of research time. Table 1 shows what we have TENTATIVELY found for diabetes. I included a few of the references. Please be clear that this is an early look. Challenges finding the numbers we need, nonindependence of the toxins, and difficulty finding unexposed controls makes rigor very difficult. It would be better if we could include error ranges, but we have not progressed that far. Nonetheless, what we have found is very important.
Table 1. Tentative Estimate of Contribution of Key Diabetogens to Diabetes9-11
|Toxin||% of Diabetes|
|Dioxins (other than PCBs)||4|
Abbreviations: BPA, bisphenol A; PCB, polychlorinated biphenyls; OCPs, organochlorine pesticides; PAHs, polycyclic aromatic hydrocarbons.
Adding up the numbers shows potentially the whole epidemic is apparently due to the massive increase in body load of toxins. A big caveat is that there is a real problem with nonindependence of the correlations and that many of these diabetogens are also being labeled obesogens, as there is substantial overlap of mechanisms of damage. Nonetheless, even if we do not know the exact percentage contribution of each toxin, their role in the epidemic appears undeniable.
Mechanisms of Blood Sugar Control Dysregulation
There are many mechanisms for blood sugar control disruption by these toxins. They can be loosely divided into 2 broad categories: impaired insulin sensitivity and decreased insulin production. Although I have allocated these toxins to the 2 categories, the reality is that all of them have multiple ways in which they disrupt blood sugar regulation.
Decreased Insulin Production
As can be seen in Figure 6, there is a direct correlation between the amount of arsenic in a person’s body (toenail arsenic is the best measure of body load) and risk of diabetes. The primary mechanism appears due to damaging pancreatic β cells with resultant decreased production of insulin.12
Impaired Insulin Sensitivity
Bisphenol A (BPA) blocks insulin receptor sites causing insulin resistance.14 This increases not only the incidence of diabetes, but also obesity, especially the worst type—accumulation of visceral fat—as well demonstrated by increasing waist-to-hip ratio as shown in Figure 7.
Impaired insulin sensitivity is the typical mechanism of damage for all the POPs, which is why they are also implicated in the obesity epidemic.16-19
Sources of the Diabetogens
Arsenic exposure occurs primarily through diet and water. A surprising 13 million in the United States use public water exceeding Environmental Protection Agency (EPA) limit of 10 µg/L. As can be seen from Figure 8, many water supplies have not been tested and the data on private water supplies are very limited, so the total exposure is likely much higher. Seafood, rice, mushrooms, and poultry are main food sources.20 Seafood contains primarily arsenobetaine, an organic form, which is considered less toxic. Even some organically grown rice has been found to have elevated levels.21
BPA is used in the production of polycarbonate plastics. These plastics are used in many ways, such as food and drink packaging, including canned foods and water bottles, compact discs, implanted medical devices, and even in some dental sealants and composites. Figure 9 shows the comparison between urinary BPA after consumption of 2 servings of soy milk in canned versus in glass and one 12-oz serving daily for 1 week of fresh soup compared with canned soup. The threshold for doubling of risk for diabetes is 5.0 µg/L urine
Dioxins are a large class of highly toxic POPs. They are by-products of several industrial processes and new-to-nature molecules made for specific purposes. They include such classes of molecules as polychlorinated dibenzo-p-dioxins (PCDDs); polychlorinated dibenzofurans (PCDFs), or furans; and polychlorinated/polybrominated biphenyls (PCBs/PBBs)
Everyone who eats conventionally grown foods is exposed to organochlorine pesticides (OCPs). The exposure is even higher for those drinking water and breathing in farming areas.
Although banned in 1977, PCBs were manufactured from 1929 and have heavily contaminated the environment. PCBs, like other POPs, are very difficult to breakdown in the environment as well as in living organisms. Because of their nonflammability, chemical stability, high boiling point, and electrical insulating properties, PCBs were used in hundreds of industrial and commercial applications including electrical, heat transfer, and hydraulic equipment; as plasticizers in paints, plastics, and rubber products; in pigments, dyes, and carbonless copy paper; and in many building materials.23 As can be seen in Figure 10, PCBs accumulate with age. This correlates well with the increasing incidence of diabetes with age. This is despite most PCBs and dichlorodiphenyltrichloroethane (DDT) having been banned since the late 1970s.
Phthalates are a family of organic chemicals used as plasticizers (to increase flexibility, transparency, and durability) and for multiple manufactured product purposes, such as to solubilize and stabilize fragrances in cosmetics. Diet is the main source of phthalates as they easily contaminate fatty foods such as milk, butter, and meats when in plastic containers. Diethyl phthalate and dibutyl phthalate are especially common in health and beauty aids, except in Europe where they have now been banned due the very large amount of research showing their toxicity, regardless of the source. As can be seen in Figure 11, phthalate levels in the blood directly correlate with use of health and beauty aids.
Polycyclic Aromatic Hydrocarbons
Polycyclic aromatic hydrocarbons (PAHs) are a group of hydrocarbons with multiple aromatic rings. They include such molecules such as napthalene, fluorene, anthracene, phenanthrene, fluoranthene, pyrene, benzo[a]anthracene, chrysene, benzo[a]pyrene, benzo[b]fluoranthene, benzo[e]pyrene, benzo[j]fluoranthene, benzo[k]fluoranthene, dibenzo[a,h]anthracene, indo[123-cd]pyrene, and dibenzo[al]pyrene. They are the primary carcinogens in cigarette smoke and are found in charbroiled food, in smoked meats, in the air in cities, and wherever fossil fuels are burned.26 They are such a health hazard that a PubMed search yields almost 400 000 studies.
Diabetogen Body Load Assessment
A number of laboratory tests are available to determine total body load of toxins as well as the level of specific toxins. These include both conventional laboratory tests and toxin-specific tests.
Conventional Laboratory Tests. Determining which patients have elevated body load of toxins can be inferred from several conventional laboratory tests. The grim reality is that the “normal” range is actually indicative of adaptation to toxic load. Perhaps the most important easily available lab tests indicative of the load of toxins that cause diabetes is γ-glutamyl transferase (GGT), also known as GGTP. This enzyme recycles glutathione for detoxification of POPs and is induced in proportion to exposure. One particularly illustrative study followed men for 4 years to determine the predictive value of GGT for development of diabetes. As Figure 12 shows, the correlation is very strong.
As can be seen in Figure 13, in diabetics there is a very strong correlation between GGT and hemoglobin A1c (HbA1c), which is indicative of poorer blood sugar control the higher the level of toxins.
Other conventional laboratory tests indicative of toxic load include complete blood count (CBC), high-sensitivity C-reactive protein (hsCRP), platelet count, homocysteine, alanine transaminase (ALT), and bilirubin. The number of tests continues to increase as researchers study this area.
Toxin-Specific Laboratory Tests. The best test to determine body load of arsenic is by measuring the amount in toenails. Blood and urine levels typically only indicate acute exposure. As noted above, there is a direct correlation between toenail arsenic and diabetes. The best way to determine body load of chemical toxins is with fat biopsy. Fortunately, much more easily available and more patient tolerant is urinary measurement. A number of laboratories now directly measure multiple industrial toxins in urine and blood.
Detoxification and Excretion of Diabetogens
A number of liver enzymes metabolize chemical toxins. This typically results in either complete breakdown but more often excretion of conjugated compounds directly into the urine.
There are essentially 5 types of strategies for decreasing body load of toxins:
- Avoidance (the best!).
- Increasing glutathione production (facilitates phase 2 conjugation and helps protect from the oxidation and inflammation which facilitate the damage to blood sugar regulation).
- Increasing dietary fiber (helps bind toxins in the gut to facilitate excretion from the body).
- Toxin-specific interventions to increase detoxification/elimination.
- Toxin-specific interventions to prevent the damage they cause.
The importance of avoidance cannot be overstated. Although some of these toxins have half-lives of hours to days, some take months to even years. Once in the body, many are very difficult to eliminate and accumulate in fat stores. The following toxin-specific interventions presuppose glutathione support and increasing dietary fiber.
As methylation is the normal mechanism for excretion of arsenic, methyl donors would seem like a good idea. However, the research is mixed. Resveratrol has been shown in cell cultures to protect against arsenic-induced oxidative damage.29 B vitamins have been shown to increase urinary excretion of arsenic in humans.30 In a rat model, curcumin protects against multiple mechanisms of arsenic damage.31
In an interesting rat study, probiotics Bifidobacterium breve and Lactobacillus casei were shown to bind BPA in the gut and increase excretion in the stools.32 Both α-tocopherol and α-lipoic acid have been shown in a rat model to decrease BPA toxicity as has N-acetylcysteine (NAC).33,34
Dioxins (Other Than PCBs)
Quercetin has been shown in animal studies to protect against the oxidative stress induced by dioxins.35 Vitamin C has been shown in human cell cultures to suppress dioxin carcinogenesis.36
NAC has been shown in human cells to decrease glutathione depletion by OCPs.37 Gallic acid and quercetin have been shown to alleviate lindane-induced cardiotoxicity in rats.38
Epigallocatechin gallate (EGCG) and quercetin have been shown in human cell lines to protect against DNA damage from PCBs.39 PCB-induced oxidative stress and cytotoxicity in cell lines can be mitigated by NAC.40 In cell cultures, quercetin blocks the inflammatory induced by PCBs.41
In rats, α-lipoic acid, resveratrol, and curcumin protect against the testicular toxicity induced by phthalates.42,43
Polycyclic Aromatic Hydrocarbons
Finally, a human study—probably because this class of toxins has been recognized for decades as the primary carcinogens in tobacco smoke. Antioxidants such as vitamin C and vitamin E at modest daily dosages of 500 mg and 400 IU daily have been shown to protect women smokers from DNA damage.44 In human epithelial cells, curcumin protects against DNA damage from PAHs.45 Quercetin has been shown to enhance the protective effects of β-carotene for DNA from PAHs.46 Epicatechins have been shown in mucosal cell cultures to protect against DNA damage.47
Bile Sequestrants. Although the approaches above all used natural medicines, there is also an intriguing drug option. Bile sequestrants, which were designed to decrease cholesterol levels, have in limited studies been shown to also decrease body load of several POPs. Five grams per day of colestimide was shown to decrease body load of PCBs by 23% after 6 months.48 Interestingly, those in the control group suffered a 24% increase.
Fifteen grams per day of olestra, administered via 22 Pringles Light crisps, for 12 months decreased body load of PCBs and dichlorodiphenyldichloroethylene (DDE) (the breakdown product in the body of DDT) by 9%.49 This is particularly important as the body half-life of DDE is more than 10 years.
The astute reader will have noticed that few of these interventions have been studied in human clinical trials and that the limited research appears to have been on protection rather than detoxification/excretion. I think this inexplicable research deficiency reflects the lack of recognition in much of the research community of the substantial human damage being done by environmental toxins. We are way past the “yellow canary” stage of reactivity to toxins—the whole population is now clearly being affected.
Glutathione. Finally, glutathione plays a critical role in protection from the oxidative effects of these toxins and facilitation of their detoxification through phase 2. Ways to increase endogenous synthesis will be discussed in a future editorial.
As near as I can determine from the research, the diabetes epidemic is likely due to the ever-increasing body load of toxins. Although only 7 are discussed here, the list is almost certainly to increase as the research evolves. Most of these chemical toxins are very difficult to get out of the body, hence the title of persistent organic pollutants. Foundational to excretion and detoxification are supplementing with NAC to promote glutathione production and increasing dietary and supplemental fiber, augmented by the appropriate intervention for those toxins with the highest body load.
- Centers for Disease Control and Prevention. Diabetes statistics. CDC Web site. http://www.cdc.gov/diabetes/statistics/slides/long_term_trends.pdf. Accessed May 1, 2016.
- Guyenet S. By 2606, the US diet will be 100 percent sugar. Whole Health Source Web site. http://wholehealthsource.blogspot.com/2012/02/by-2606-us-diet-will-be-100-percent.html. Published February 18, 2012. Accessed August 3, 2016.
- Lee DH, Lee IK, Song K, 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;29(7):1638-1644.
- Neel BA, Robert M. Sargis RM. The paradox of progress: Environmental disruption of metabolism and the diabetes epidemic. Diabetes. 2011;60(7):1838-1848
- Ukropec J, Radikova Z, Huckova M, et al. High prevalence of prediabetes and diabetes in a population exposed to high levels of an organochlorine cocktail. Diabetologia. 2010;53(5):899-906.
- Lee DH, Lee IK, Song L, 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;29(7):1638-1644.
- Campbell GD. Connubial diabetes and the possible role of “oral diabetogens.” BMJ. 1961;1(5238):1538-1539.
- Levin M. The occurrence of lung cancer in man. Acta Unio Int Contra Cancrum. 1953;9(3):531-541.
- Navas-Acien A, Silbergeld EK. Pastor-Barriuso R, Guallar E. Arsenic exposure and prevalence of type 2 diabetes in US adults. JAMA. 2008;300(7):814-822.
- Song Y, Chou EL, Baecker A, et al. Endocrine-disrupting chemicals, risk of type 2 diabetes, and diabetes-related metabolic traits: A systematic review and meta-analysis. J Diabetes. 2016;8(4):516-532.
- Ranjbar M, Rotondi MA, Ardern CI, Kuk JL. Urinary biomarkers of polycyclic aromatic hydrocarbons are associated with cardiometabolic health risk. PLoS One. 2015;10(9):e0137536.
- Liu S, Guo X, Wu B, et al. Arsenic induces diabetic effects through beta-cell dysfunction and increased gluconeogenesis in mice. Sci Rep. November 2014;4:6894.
- Pan WC, Seow WJ, Kile ML, et al. Association of low to moderate levels of arsenic exposure with risk of type 2 diabetes in Bangladesh. Am J Epidemiol. 2013;178(10):1563-1570.
- Wang T, Li M, Chen B, et al. Urinary bisphenol A (BPA) concentration associates with obesity and insulin resistance. J Clin Endocrinol Metab. 2012;97(2):E223-E227.
- Savastano S, Tarantino G, D’Esposito V, et al. Bisphenol-A plasma levels are related to inflammatory markers, visceral obesity and insulin-resistance: A cross-sectional study on adult male population. J Transl Med. May 2015;13:169.
- Remillard RB, Bunce NJ. Linking dioxins to diabetes: epidemiology and biologic plausibility. Environ Health Perspect. 2002;110(9):853-858.
- Tang M, Chen K, Yang F, Liu W. Exposure to organochlorine pollutants and type 2 diabetes: A systematic review and meta-analysis. PLoS One. 2014;9(10):e85556.
- Weinhold B. PCBs and diabetes: Pinning down mechanisms. Environ Health Perspect.2013;121(1):A32.
- Grün F, Blumberg B. Perturbed nuclear receptor signaling by environmental obesogens as emerging factors in the obesity crisis. Rev Endocr Metab Disord. 2007;8(2):161-171.
- Jomova K, Jenisova Z, Feszterova M, et al. Arsenic: Toxicity, oxidative stress and human disease. J Appl Toxicol. 2011;31(2):95-107.
- Holtcamp W. Suspect sweetener: Arsenic detected in organic brown rice syrup. Environ Health Perspect.2012;120(5):A204.
- Centers for Disease Control and Prevention. Arsenic toxicity. CDC Web site. http://www.atsdr.cdc.gov/csem/arsenic/docs/arsenic.pdf. Accessed August 18, 2015.
- US Environmental Protection Agency. Hazardous waste. EPA Web site. https://www3.epa.gov/epawaste/hazard/tsd/pcbs/about.htm. Accessed February 26, 2016.
- Serdar B, LeBlanc WG, Norris JM, Dickinson LM. Potential effects of polychlorinated biphenyls (PCBs) and selected organochlorine pesticides (OCPs) on immune cells and blood biochemistry measures: A cross-sectional assessment of the NHANES 2003-2004 data. Environ Health. December 2014;13:114.
- Duty SM, Ackerman RM, Calafat AM, Hauser R. Personal care product use predicts urinary concentrations of some phthalate monoesters. Environ Health Perspect. 2005;113(11):1530-1535.
- Caruso JA, Zhang K, Schroeck NJ, et al. Petroleum coke in the urban environment: A review of potential health effects. Int J Environ Res Public Health. 2015;12(6):6218-6231.
- Lee DH, Ha MH, Kim JH, et al. Gamma-glutamyltransferase and diabetes: A 4 year follow-up study. Diabetologia. 2003;46(3):359-364.
- Gohel MG, Chacko AN.Serum GGT activity and hsCRP level in patients with type 2 diabetes mellitus with good and poor glycemic control: An evidence linking oxidative stress, inflammation and glycemic control. J Diabetes Metab Disord. 2013;12(1):56.
- Chen C, Jiang X, Hu Y, Zhang Z. The protective role of resveratrol in the sodium arsenite-induced oxidative damage via modulation of intracellular GSH homeostasis. Biol Trace Elem Res. 2013;155(1):119-131.
- Argos M, Rathouz PJ, Pierce BL, et al. Dietary B vitamin intakes and urinary total arsenic concentration in the Health Effects of Arsenic Longitudinal Study (HEALS) cohort, Bangladesh. Eur J Nutr. 2010;49(8):473-481.
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- Padma V, Poornima P, Prakash C, Bhavani R. Oral treatment with gallic acid and quercetin alleviates lindane-induced cardiotoxicity in rats. Can J Physiol Pharmacol. 2013;91(2):134-140.
- Ramadass P, Meerarani P, Toborek M, et al. Dietary flavonoids modulate PCB-induced oxidative stress, CYP1A1 induction, and AhR-DNA binding activity in vascular endothelial cells. Toxicol Sci. 2003;76(1):212-219.
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- Choi YJ, Arzuaga X, Kluemper CT, et al. Quercetin blocks caveolae-dependent pro-inflammatory responses induced by co-planar PCBs. Environ Int. 2010;36(8):931-934.
- El-Beshbishy HA, Mariah RA, Al-Azhary NM, et al. Influence of lipoic acid on testicular toxicity induced by bi-n-butyl phthalate in rats. Food Chem Toxicol. 2014 Sep;71:26-32
- El-Fattah AA, Fahim AT, Sadik NA, Ali BM. Resveratrol and curcumin ameliorate di-(2-ethylhexyl) phthalate induced testicular injury in rats. Gen Comp Endocrinol. January 2016;225:45-54.
- Mooney LA, Madsen AM, Tang D, et al. Antioxidant vitamin supplementation reduces benzo(a)pyrene-DNA adducts and potential cancer risk in female smokers. Cancer Epidemiol Biomarkers Prev. 2005;14(1):237-242.
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