Most of us are probably aware that rates of type 2 diabetes are rising rapidly, both in the U.S. and around the world.  Type 2 diabetes used to be a disease of middle and old age, but now we are seeing it in teenagers.  The increasing prevalence of this disease, with its horrible and costly long-term sequelae, is one of the factors leading epidemiological experts to predict a decline in lifespan in the U.S. over the next few generations.

While you might have missed the news about the increasing prevalence of type 2 diabetes, you'd have to have been on an extended sabbatical on another planet to miss the fact that Americans are getting fatter, and fatter at earlier ages.  I won't repeat here the statistics about our increasing girth--they are ubiquitous, and don't add much to what we can perceive for ourselves.  We have been told that obesity is a big risk factor for type 2 diabetes, so it comes naturally to attribute the diabetes epidemic to individuals' bad habits.  And certainly a trip to any conventional supermarket will suffice to convince us that many Americans do indeed have terrible eating habits.  However, research increasingly suggests that obesity alone is not enough to predispose one to type 2 diabetes; instead, obesity may be another symptom of an overall disturbance in our homeostasis, part of the disturbance that also creates diabetes rather than its cause.   New research strongly suggests that environmental toxicity is an often-overlooked factor in creating these pervasive metabolic disruptions.

Body mass index (BMI) is one of the measures scientists and clinicians frequently use to determine if someone is obese.  You can read more about BMI elsewhere; I don't want to digress into a long discussion about it here.  Suffice it to say that a BMI over 25 is generally associated with greater risk of various chronic diseases, and a BMI over 40 is considered morbid obesity.  A recent study published in Clinical Chemistry found that elevated BMI was not in and of itself associated with type 2 diabetes.  As the authors put it, "obesity itself is not a sufficient risk factor for type 2 diabetes."  (Lim, Jt-Sun et al., "A Strong Interaction Between Serum Gamma-Glutamyltransferase and Obesity on the Risk of Prevalent Type 2 Diabetes: Results from the Third National Health and Nutrtion Examination Survey," Clinical Chemistry 2007; 53: 1092-98)

What seems to tip people over into increased risk of developing diabetes is a combination of elevated BMI and elevated serum levels of an enzyme called GGTP.  Bear with me for a moment, I'm going to get a little technical here, but I promise it is worth it!  GGTP is an enzyme made by the liver.  Its job is to help synthesize glutathione, one of the major chemicals we use to modulate oxidation and to get rid of toxins via phase 2 detoxification.  The take away message here?  People have elevated GGTP levels when their livers are working hard to deal with oxidative stress and detoxification.  

The researchers in the Clinical Chemistry study found that people with GGTP levels in the high normal range and an elevated BMI had a greater risk of developing type 2 diabetes.  High normal--not even out of normal range. Whoa!  In fact, those with GGTP levels in the highest quintile of the normal range and elevated BMI had several times the risk of developing diabetes than those people with the same BMI and normal or low-normal GGTP. 

Now, people can get elevated GGTP levels from a number of sources.  Perhaps they are eating a lot of foods which are inflammatory for them, increasing their demand for modulation of oxidative stress and thus their demand for GGTP.  Perhaps they are drinking lots of alcohol and/or taking lots of prescription or non-prescription drugs, all of which increase the demand on their phase 2 detoxification system and thus their demand for GGTP.  These would be issues which still fall more or less squarely within the realm of individual responsibility.  But other studies indicate that environmental toxins may well play a role in increasing diabetes risk, shifting the locus of responsibility substantially away from the individual and toward the collective.

Two studies published in Diabetes Care during the past two years demonstrate a link between persistent organic pollutants (POP's) and insulin resistance (the dysfunctional precursor to the pathology of type 2 diabetes), as well as a linkage between higher serum concentrations of six selected POP's and the prevalence of type 2 diabetes.  "These finding suggests that persistent organic pollutants...maybe associated with type 2 diabetes risk by increasing insulin resistance, and POP's may interact with obesity to increase the risk to type 2 diabetes."  (Lee, Duk-Hee, et. al.  "Association Between Serum Concentrations of Persistent Organic Pollutants and Insulin Resistance Among Non-Diabetic Adults: Results from the National Health and Examination Survey 1999-2002, " Diabetes CAre 2007; 30:622-28)

Does this mean that we should all feel free to snarf down as much high fructose corn syrup as suits our fancy, and then blame pollution if we end up with diabetes?  Obviously not.   What it does mean is that the pollutants we are pouring into our environment are likely affecting our health in a much broader range of ways than we have previously recognized, and in ways that standard toxicological testing (pathetically inadequate as it is anyway) for pesticides, fertilizers, flame-retardants, food additives, etc. will never reveal.  The interactions between our individual bodies, with all their variations, and the environment are of immense multiplicity, whereas scientific research has historically been fixated on reducing complexity.  Researchers like to reduce causality to one-cause, one-effect--but that model is utterly obsolete when it comes to understanding the effects of chemicals on human health.  These studies are just one more piece of evidence suggesting that we need to abandon the standard of proof that has so far dominated our approach to polluting industries (as well as to global climate change), a standard of proof that demands that we conclusively demonstrate that a single product or process--in isolation--causes harm before regulating industrial activities.  Instead, we need to move to a standard of proof that demands that we demonstrate that products and processes--in their complex interactions with the environment we already have--are NOT harmful before marketing or implementing them.

These studies also suggest that we need to develop a more robust understanding of and response to environmental pollution as a public health problem.  Americans have historically been loathe to put much energy into public health; our pitiful funding of public health endeavors in general testifies to our absurd attachment to an individualistic paradigm that nature is constantly proving wrong.  And our cultural devotion to an utterly mythical "free market" means that we tend to put profit first, and then blame individuals when they are sickened by profiteering polluters.   But the cost of caring for Americans with diabetes is already staggering.  If we fail to intervene in ways that succeed in reducing the prevalence of this disease, it could well have a disastrous effect on our health care system and on our already-tottering economy as a whole.   As if we needed another wake-up call! 

On an immediate, individual level, these studies suggest that we should stop subtly blaming and shaming overweight people who are diabetic.  We have an ingrained habit of blaming obesity on the bad habits of individuals and an erroneous belief that obesity alone creates diabetes--these two factors combine to incline us to blame victims of diabetes for their disease.  This is rude, cowardly (because we are just trying to pretend that if we do everything "right" we won't get sick), and distracts us from the real problem.  Furthermore, it doesn't work!  Shaming people for their disease does not give them the courage and strength to do what they can and need to do to improve their health.