Diabetes is a disabling and deadly disease that now affects more people than ever. In the US alone, and according to the 2007 prevalence estimates from the Centers for Disease Control and Prevention (CDC) in Atlanta, GA, the number of Americans with diabetes recently hit the 24-million mark-that's an increase of more than 3 million sufferers in just under two years. The picture's just as bleak in the UK, with figures skyrocketing to nearly 2.5 million, according to health charity Diabetes UK. That's a rise of more than 167,000 in the last year alone. At this rate, by 2030, an estimated 350 million people worldwide will be diabetic (BMJ, 2008; 336: 1180-5).
Scientists have attributed this global epidemic mainly to various lifestyle factors such as obesity, an unhealthy diet and lack of exercise. Indeed, obesity is thought to be the primary risk factor because 90 per cent of diabetics are seriously overweight.
New evidence, however, suggests that our environment may also be contributing to these soaring rates of diabetes prevalence. Studies show that exposure to commonly encoun-tered environmental toxins, such as arsenic, dioxins and even electrical pollution, can dramatically increase the risk of developing the disease.
Just how major a role environmental pollution plays in the development of diabetes was suggested by a recent American study that looked at people's exposure to arsenic, a toxic trace element commonly found in drinking water supplies around the world.
Using data from the 2003-2004 US National Health and Nutrition Examination Survey (NHANES)-population-based surveys carried out by the CDC at various times-it was revealed that type 2 diabetics had 26-per-cent higher levels of arsenic
in their urine than non-diabetics, and the arsenic was most likely derived from drinking water. Or, looking at it from another point of view, people who had the highest levels of arsenic in their urine had nearly four times the risk of developing type 2 diabetes compared with those who had the lowest levels (JAMA, 2008; 300: 814-22).
Earlier studies-carried out in Taiwan, Bangladesh and Mexico-had already established a link between arsenic in drinking water and diabetes. People living in areas with extremely high levels of arsenic in the water were up to 10 times more likely to develop the disease (Am J Epidemiol, 1994; 139: 484-92; Am J Epidemiol, 1998; 148: 198-203; Environ Res, 2007; 104: 383-9).
The new study, however, is among the first to report an increased diabetes risk for people living in areas where arsenic levels are low. Considering the fact that millions of people worldwide are exposed to such levels, these findings are disturbing.
Besides drinking water, we are also exposed to arsenic through mineral water, wine, certain foods (especially marine foods) and pressure-treated lumber (Diabetes Spectrum, 2002; 15: 109-12; J Long Term Eff Med Implants, 2005; 15: 209-23). These sources have yet to be associated with diabetes, but they no doubt add to the body's arsenic burden.
It may be that minimizing our exposure to arsenic wherever possi-ble has an important part to play in the prevention of diabetes.
Persistent organic pollutants
Another toxin-or rather, family of toxins-that might be fuelling the diabetes epidemic is what are known as 'persistent organic pollutants' (POPs). These are chemical agents that persist in the environment and bioaccumulate through the food web. Dioxins, polychlorinated biphenyls (PCBs), dichlorodiphenyldichloro-ethylene [DDE, the main degradation product of the pesticide dichloro-diphenyltrichloroethane (DDT)], trans-nonachlor, hexachlorobenzene and the hexachlorocyclohexanes (including lindane) are some of the POPs most commonly found in the general population (Lancet, 2006; 368: 558-9).
Until recently, the contribution of POP exposure to the incidence of diabetes has received little attention. But several reports have emerged, documenting elevated diabetes in people who are either occupationally or accidentally exposed to high levels of these pollutants.
Some of the best evidence comes from studies of US Air Force personnel who were involved in spraying the herbicide and defoliant Agent Orange-which includes TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin), one of the most toxic chemicals known to man-during the Vietnam War. Scientists found that glucose abnormalities, diabetes prevalence and use of medications to control diabetes were all significantly increased with dioxin exposure. Those with the greatest exposure had a 50-per-cent higher risk of developing diabetes (Epidemiology, 1997; 8: 252-8).
These and other, similar obser-vations led the US Department of Veterans Affairs to recognize type 2 diabetes as a disease related to herbicide exposure in 2001 (Rev Environ Health, 2008; 23: 59-74).
Even low-level dioxin exposure has been linked to an increased risk of diabetes, as shown by a study of just over 1000 US veterans who never had contact with dioxin-contaminated herbicides and whose serum dioxin levels were within the range of background exposure typically seen in the US population. Compared with people who had the lowest levels of dioxin, those with the highest levels were nearly twice as likely to have diabetes (Epidemiology, 2000; 11: 44-8).
In addition to dioxin, a number of other members of the POP family have been associated with diabetes, including PCBs and chlorinated pesticides (Rev Environ Health, 2008; 23: 59-74).
However, one of the most compelling findings to date is a recent analysis, led by Korean researcher Duk-Hee Lee, that looked at a combination of POPs in a random sample of the general US population. Again, using data from the 2003-2004 NHANES-the same survey used in the latest arsenic study-Lee and his colleagues inves-tigated the prevalence of diabetes (types 1 and 2 combined) in relation to six common contaminants: 2,2',4,4',5,5'-hexachlorobiphenyl (PCB153); 1,2,3,4,6,7,8-heptachloro-dibenzo-p-dioxin (HpCDD); 1,2,3,4,6, 7,8,9-octachlorodibenzo-p-dioxin (OCDD); oxychlordane; p,p'-dichloro-diphenyltrichloroethane (DDE); and trans-nonachlor. These POPs were selected because they were detect-able in at least 80 per cent of the survey participants.
What they found was a strong, positive association between diabetes and all six POPs studied-especially PCB153, oxychlordane and trans-nonachlor. Individuals with the highest concentrations of these chemicals in their blood serum had a more than fivefold greater risk of diabetes than those with the lowest concentrations.
Even more alarming, when the researchers looked at the impact of the six POPs combined, participants in the highest category of exposure were nearly 40 times more likely to have diabetes (Diabetes Care, 2006; 29: 1638-44).
The study's most interesting finding, however, was what it didn't find. Surprisingly, there was no association between obesity and diabetes among participants with undetectable levels of POPs. Obesity was a risk factor for diabetes only if people had blood concentrations of these toxins above a certain level. This suggests that the role played by obesity in diabetes is not as significant as is widely believed.
Indeed, according to a review including the Lee et al. study, published in the prestigious peer-reviewed journal The Lancet, "This finding might imply that virtually all the risk of diabetes conferred by obesity is attributable to persistent organic pollutants, and that obesity is only a vehicle for such chemicals. This possibility is shocking" (Lancet, 2006; 368: 558-9).
Shocking, indeed. But at least one scientist has observed that there may be a plausible explanation for the apparent association between obesity and diabetes, even if the true culprits are the POPs. As David Carpenter-from the Institute for Health and the Environment at the University at Albany in New York-notes, "Most obesity comes from excessive consumption of animal fats, and animal fats contain most of the POPs that are taken in with our diet" (Rev Environ Health, 2008; 23: 59-74). So, it appears that, as people become fatter, the more toxic POPs their bodies retain-and this increases their risk of diabetes.
This theory is supported by the Lee et al. results, which found that the association between POPs and diabetes was much stronger among obese participants compared with their lean compatriots (Diabetes Care, 2006; 29: 1638-44).
Where the theory appears to stumble, however, is when we consider exercise-known to be an important factor in diabetes prevention. "[I]f the POPs, not the obesity, is the major risk factor for diabetes," says Carpenter, "then explaining how exercise can help prevent diabetes is very difficult" (Rev Environ Health, 2008; 23: 59-74). Still, there are possible explanations. Perhaps exercisers also adopt a healthier diet that includes less animal fat. Or maybe it's to do with the fact that exercise increases the oxygen supply, which assists the detoxification process (Alt Comp Ther 2002; 8: 218-23). Clearly, more research is needed to understand all potential influences on the disease.
Yet another possible culprit in the growing wave of diabetes is the endocrine-disrupting chemical bis-phenol A (BPA), used in the product-ion of plastic consumer products, and in the epoxy resins that line food and drink cans. The chemical is pervasive in the environment and in people, too-primarily because it leaches from containers into the food we eat (see WDDTY vol 18 no 8). US studies have found detectable levels of BPA in more than 90 per cent of the general population (JAMA, 2008; 300: 1303-10).
Most studies of the health effects of BPA have focused on its well-known oestrogenic activity. BPA and other endocrine disruptors diminish sperm production, accelerate the onset of puberty and damage sexual organs (Environ Health Perspect, 2006; 114: A48-9). However, newer reports have shown additional modes of action, one of which is disruption of glucose metabolism.
One animal study found that BPA-given at a dose well below the lowest observed adverse-effect level currently accepted by the US Environmental Protection Agency (EPA)-nevertheless interfered with the function of pancreatic beta cells (responsible for the storage and release of insulin, the main hormone involved in blood glucose metab-olism), thereby inducing the insulin resistance that precedes type 2 diabetes. The researchers concluded that "this altered blood glucose homeostasis by BPA exposure may enhance the risk of developing type 2 diabetes" (Int J Androl, 2008; 31: 194-200; Environ Health Perspect, 2006; 114: A48-9).
This was confirmed by another study which found that just four days of low-dose BPA injections produced insulin resistance in mice (Environ Health Perspect, 2006; 114: 106-12).
As usual, animal findings do not necessarily apply to humans. How-ever, a recent study reported in the prestigious Journal of the American Medical Association found a signifi-cant link between BPA and diabetes in the general US population. Using NHANES data, researchers looked at 1455 adults, aged 18 to 74 years, to examine the associations between urinary BPA and health status.
After adjusting for potential confounders, they found that higher BPA concentrations were signifi-cantly related to a diagnosis of diabetes, with a 39-per-cent greater risk. The link between BPA and cardiovascular disease was also evident (JAMA, 2008; 300: 1303-10).
These findings are also consistent with the findings on POPs-and perhaps with the obesity-pollution hypothesis as well. It may be that obese people are at greater risk of diabetes not because of the excess weight per se, but because they consume more food contaminated with BPA. Indeed, the researchers found that participants with a BMI
of 35 kg/m2 or more had almost twice the levels of BPA as those with a BMI of 18.5-24.9 kg/m2.
The precise relationship between obesity, environmental toxins and diabetes has yet to be established, but the research so far indicates that it's a connection that cannot be ignored.
There are, no doubt, plenty of other widespread environmental contam-inants that could be contributing to diabetes-but few of us would think of electricity. Scientist Magda Havas, of Trent University in Ontario, Canada, has been researching a form of electromagnetic pollution known as 'dirty electricity', and her findings add another piece to the diabetes puzzle.
Dirty electricity refers to surges of high-frequency voltage or electro-magnetic radiation that 'contam-inate' the normal 50-60 Hz power lines around us. These surges are generated by electrical equipment such as computers, plasma TVs, energy-efficient lighting and dimmer switches.
Advances in technology have allowed scientists to measure dirty electricity and it appears that this ubiquitous pollutant is 'biologically active'-in other words, it's potentially harmful to health.
Havas' research has linked dirty electricity to a variety of health conditions, including asthma, attention-deficit/hyperactivity disorder (ADHD) and multiple sclerosis (Electromagn Biol Med, 2006; 25: 259-68). But one of the most compelling relationships is between dirty electricity and diabetes.
Using four case studies, Havas looked at electrically sensitive diabetics and analyzed the changes in their blood sugar levels in response to the amount of dirty electricity in their environment. She discovered that, in an electromag-netically 'clean' environment, type 1 diabetics required less insulin and type 2 diabetics had lower levels of blood sugar. Exposure to dirty electricity, on the other hand, rapidly increased their blood sugar levels.
A particularly interesting piece of evidence is the case of a type 2 diabetic man who was taking no medication, but was monitoring his blood sugar. He found that his blood sugar increased whenever he worked on a computer, then dropped drama-tically after moving away from it. He also reported rapid changes in blood sugar as he walked from a medical clinic (an environment with dirty electricity) to his parked vehicle (no dirty electricity), then back to the medical clinic.
His blood sugar levels changed significantly within those 20 min-utes. Indeed, his endocrinologist diagnosed him as prediabetic when his blood sugar was tested imme-diately upon entering the clinic, but as type 2 diabetes after a 20-minute wait there.
"Measurement of blood sugar needs to be done in an electromag-netically clean environment to pre-vent misdiagnosis and to accurately determine the severity of the disease," concludes Havas (Electro-magn Biol Med, 2008; 27: 135-46).
Besides Havas' research, small studies conducted in healthcare facilities in Canada and Japan show that both type 1 and 2 diabetics can benefit from the installation of special filters to reduce dirty electricity. Within 30 minutes of installing Graham-Stetzer (GS) filters at the Yoyogi Natural Clinic in Tokyo, Japan, the patients' plasma became less viscous and their blood sugar levels dropped. One type 2 diabetic had previously had difficulty regulating his blood sugar, despite medication. Yet, three days after installing four GS filters in his home, his blood sugar dropped significantly and he felt well (Electromagn Biol Med, 2008; 27: 135-46).
According to Havas, these results-along with a growing body of laboratory and observational evidence-suggest that there is a third type of diabetes in which sufferers respond to environmental triggers such as dirty electricity.
"Unlike true Type 1 and Type 2 diabetics whose blood sugar is not affected by dirty electricity," Havas explains, "Type 3 diabetics may be better able to regulate their blood sugar with less medication, and those diagnosed as borderline or pre-diabetic may remain non-diabetic longer by reducing their exposure to electromagnetic energy."
She estimates that as many as 5-60 million diabetics worldwide could benefit from limiting their exposure to dirty electricity (Electro-magn Biol Med, 2008; 27: 135-46).
This means that, in addition to lifestyle and genetics, environmental pollutants may also be contributing to the spiralling rates of diabetes. Many questions remain-such as the precise role played by obesity-but until these are answered, it may be prudent to minimize our exposure to these harmful environmental con-taminants wherever possible.
What is diabetes?
Diabetes is a lifelong metabolic disease caused by too much glucose (sugar) in the blood. This occurs when the body fails to produce or properly use insulin, a hormone produced by the pancreas that is necessary for converting sugar, starches and other foods into energy.
There are two main forms of diabetes-known as type 1 and type 2. Type 1, often called 'early-onset diabetes' because it typically develops in adolescence, results from the loss of function of insulin-producing cells (beta cells) in the pancreas. Type 1 diabetics must receive artificial insulin or they will enter a glucose-induced coma and die.
The majority of people with diabetes, however, don't have this extreme, physiological form of the disease. Any dysfunction of the insulin-glucose system-such as the body not producing enough insulin, or not responding to insulin properly, or producing too much insulin-can cause insulin resistance and eventually type 2 diabetes.
Although type 1 and type 2 diabetes have traditionally been considered two distinct disorders, researchers have recently noted an apparent continuum between the two in that type 2 diabetes is often accompanied by dysfunctional pancreatic beta cells predating insulin resistance (Rev Environ Health, 2008; 23: 59-74).
Much of the research on environmental pollutants and diabetes refers to type 2 diabetes, and this is the type that's increasing at an alarming rate. Nevertheless, some studies-such as those by Magda Havas (see main text)-suggest that certain contaminants might play a role in type 1 diabetes, too.
The chemical connection
The evidence that chemicals might be responsible for the rising rates of diabetes is further supported by the research of Dr Lisa Landymore-Lim, a British chemist specializing in immunology and biomedical chemistry.
As reported in WDDTY vol 17 no 9, Dr Landymore-Lim has amassed a convincing body of evidence that a variety of common drugs-including antibiotics and diuretics-are capable of causing type 1 diabetes.
What's particularly interesting about her research is that these drugs share certain chemical similarities-primarily, an excess of negative charge with an affinity for chelation with zinc ions. The pancreas, being a rich source of zinc, thus becomes a target of attack by zinc-seeking chemicals. Indeed, Dr Landymore-Lim suggests that drugs can cause diabetes by interacting with the zinc in the insulin-secreting beta cells of the pancreas. Thus changed and unrecognizable to the body, which registers these cells as 'foreign', the immune system attacks these cells, ultimately causing the disease. Although pesticides and other environmental chemicals may act differently with beta cells, the general principle may apply. By irrevocably changing beta cells, they may in some way trigger the diabetic process.
How to minimize your risk
- Arsenic. To reduce your exposure to arsenic in drinking water, invest in one
of the many water filters or purification systems that are on the market (see WDDTY vol 19 no 8 for a rated selection). Some filters, such as the Freshwater Pur-Wa Water Distiller (www.freshwaterfilter.com), guarantee 100-per-cent contaminant-free water.
Another approach is to rid your body of arsenic-as well as other potentially harmful heavy metals-by undergoing detox. There are a number of natural ways to do this (see WDDTY vol 19 no 2), but one of the most effective appears to be a homeopathic remedy comprising Chlorella and its growth factor, and Coriandrum sativum leaf tincture. Called HMDTM (Heavy Metal Detox), this product was able to clear arsenic, aluminium, antimony, beryllium, cadmium, lead, mercury, nickel, thallium and uranium from 350 metal-foundry workers-without removing essential minerals (Explore!, 2007; vol 16 no 6). For more information, go to www.heavymetaldetox.net.
- Persistent organic pollutants (POPs). As these include such a wide range of chemicals, pinpointing routes of exposure can be difficult. However, according to scientist David Carpenter, most exposure to POPs is through consumption of animal fats, so limiting the amount of such fats in your diet could reduce the risk of diabetes (Rev Environ Health, 2008; 23: 59-74).
- Bisphenol A (BPA). There are several ways to minimize your exposure to this hazardous chemical.
- Consume fresh, unprocessed foods and avoid canned goods as much as possible
- Avoid polycarbonate plastic food containers marked with the number '7' in the recycling logo, as these usually contain BPA. In general, these are rigid, transparent plastic containers. Plastics that are numbered 1, 2 and 4 are safer, as they don't contain BPA
- Use glass baby bottles, or those made of polypropylene and polyethylene plastics. These pliable, opaque plastics don't contain BPA. Medela-brand bottles used to store breast milk are also BPA-free
- Choose glass instead of plastic for water bottles, too, or get your water from the tap (filtered). Also, avoid metal water bottles as they may be lined with BPA-containing plastic
- Avoid using plastic containers in the microwave. Ceramic, glass and other microwaveable dishware are healthier alternatives
- Avoid storing food and drink in plastic containers. Glass and stainless steel are better, safer choices.
- Dirty electricity. Graham-Stetzer (GS) filters-the brainchild of Professor Martin Graham, at the University of California at Berkeley, and power-quality expert Dave Stetzer-can clean up both the power that enters a building as well as the dirty electricity within that building by shorting out the high-frequency spikes. Studies show that installing these filters results in numerous health benefits, especially for diabetics (Electromagn Biol Med, 2006; 25: 259-68). These filters are available from www.stetzerelectric.com and www.grahamstetzer.co.uk.