The Relationship Between Toxicity and Insulin Resistance, Diabetes and ObesityNicholas LeRoy, DC, MS
There is growing acknowledgement in the scientific community that toxins are associated with numerous chronic illnesses. For most of us, an association between toxic chemicals and cancer, for example, does not require any stretch of the imagination. However, research has been demonstrating that environmental chemicals as well as endotoxins (toxins produced within the body) are correlated with the development of insulin resistance, type 2 diabetes and obesity.
The toxins to which the average person is exposed are numerous and include the following:
- Persistent Organic Pollutants
- Endocrine Disruptors
- PPAR modulators
- Inorganic Metals
- GGT: >40 units/L
- hsCRP: >0.7 mg/L
- Magnesium: <2 meq/dL
- ANA titre: >1:125
- Uric Acid: >8 mg/dL
- Hemoglobin A1c: >5.5%
- Vitamin D3: <30 ng/mL
- Body Mass Index: >27
- Body Composition: >30% body fat
Insulin resistance, the predecessor to type 2 diabetes, occurs when the cells of the body become increasingly unresponsive to the action of insulin. Insulin is the hormone produced by the pancreas that functions to assist with the proper uptake of sugar into all cells of the body. As the cells become unresponsive, they can no longer use sugar effectively and sugar levels will elevate in the blood, resulting in chronic damage to small blood vessels. Although researchers have known for a long time that central obesity (i.e. belly fat) is strongly correlated with insulin resistance, it is only recently that we understand the role toxins and inflammation play in the genesis of insulin resistance and diabetes.
Elevation of hsCRP, uric acid and the liver enzyme GGT, has been correlated with insulin resistance (1). These are several of the blood markers that suggest toxemia as noted above. GGT is a particularly useful measurement since it will elevate when the body is attempting to produce more glutathione as a result of chemical exposure. Glutathione is a very powerful antioxidant and chemical neutralizer produced by nearly every cell in the body. It is found in especially high abundance in the liver and its production will be increased when faced with high levels of chemicals and free radicals, thus causing an elevation in GGT.
Some chemicals interfere with mitochondrial function to cause a cellular energy deficit with resulting production of free radicals and oxidative stress. Mitochondria are found within cells and are responsible for creating energy. If energy production is hampered, such as by toxic chemicals, cells are no longer able to properly repair themselves, nor are they able to efficiently neutralize toxins. Chronic exposure to the herbicide, atrazine, has been shown to cause mitochondrial dysfunction and insulin resistance (2). On a side note, mitochondrial dysfunction has also been strongly correlated with fibromyalgia and chronic fatigue.
Another group of chemicals to which we are exposed have been termed Persistent Organic Pollutants (POPs). A 2007 study in Diabetes Care found that "POPs may be associated with type 2 diabetes by increasing insulin resistance, and POPs may interact with obesity to increase the risk to type 2 diabetes" (3). Another study found that "there were striking dose-response relations between serum concentrations of six selected POPs and the prevalence of type 2 diabetes" (4).
Bisphenol A (BPA) is another type of Persistent Organic Pollutant most commonly found in many plastics including water bottles. There are many studies indicating the hazards of BPA including research in JAMA that indicated a "strong relationship between urine concentrations of Bisphenol A and the incidence of cardiovascular disease, type 2 diabetes, and liver-enzyme abnormalities in a representative sample of the adult US population" (5). BPA has also been shown to cause the proliferation of milk ducts in the breast and is thus correlated with breast cancer.
Obesogens are a new classification of chemical pollutants that promote obesity. They accomplish this by altering metabolic set-points, disrupting appetite controls and modifying fat homeostasis to promote fat cell growth and hyperplasia. Also falling into the category of obesogens are "endocrine disruptors", chemicals known to alter cortisol, estrogen and testosterone levels. Bisphenol A, one of the Persistent Organic Pollutants indicated above, is likewise an obesogen and endocrine disruptor.
In 2010 research was conducted to study the correlation between several pesticides (PCB, DDE, and hexachlorocyclohexane). The results demonstrated a strong correlation between these pesticides, insulin resistance and increased body mass index (6).
There are many studies that have identified the role of environmental chemicals in causing obesity, as well as the worrisome fact that extremely small amounts of these chemicals can alter the physiology of humansómuch smaller amounts than are necessary to cause cancer. This fact is disturbing considering that chemicals are routinely tested to determine their capacity for causing cancer and death, not for their ability to adversely impact metabolism and physiology.
At this point in this discussion all of the chemicals to which I have referred are known as "exotoxins". Exotoxins are chemicals to which humans are exposed that originate from the environment, or externally. However, there are chemicals to which we are exposed that originate within the body, or internally. These chemicals are termed "endotoxins" and have their origin in the gut.
Intestinal microflora, the bacteria that inhabit our intestines, far outnumber the cells of the human body. Intestinal microfloral composition is almost entirely dependent upon the composition of our diets and the use of medications that can alter the numbers of various bacterial residents. When it comes to intestinal health, it is all about the balance between the various bacteria, some of which are good for us, and some of which are bad. When the balance is compromised, termed dysbiosis, bacterial production of harmful chemicals can result that damage the intestinal lining causing a "Leaky Gut Syndrome". These bacterial waste products will also increase the total toxic load to which we are faced, further burdening detoxification pathways, making it more challenging to effectively cope with externally-derived chemicals and pollutants.
It may seem far-fetched that bacteria in our intestines can contribute to diabetes and obesity, yet this is exactly what research has been demonstrating.
In research published in the American Journal of Clinical Nutrition, researchers asserted that their "work provides evidence of an elevation of serum endotoxin after eating a high fat meal by people that are presumed to be 'normal, healthy volunteers'" (7). Additional research has demonstrated that not only do the types of bacteria in the gut contribute to increased toxins, but that bacteria can actually cause obesity: "Existing evidence warrants further investigation of the microbial ecology of the human gut and points to the modification of the gut microbiota as one means to treat people who are overweight or obese" (8). Furthermore, "Animal models of obesity connect an altered microbiota composition to the development of obesity, insulin resistance and diabetes" (9).
There is an abundance of research correlating insulin resistance, diabetes and obesity with toxic chemical exposure. In fact, the expansion of the information contained in this brief article would result in a book. Suffice it to say that this information is giving us a very different perspective on these chronic illnesses.
My suggestion is to have blood work performed, including the specific tests at the beginning of this article, and undergo a detoxification program with the long-term goal of making lifestyle modifications. These modifications should include avoidance of environmental toxins, treatment of microbial imbalances in the gut, as well as dietary changes to limit chemical exposure while facilitating healthy detoxification.
- Nagoya J Med Sci 2008; 70:1.
- PlosOne 2009; 4:1186-90.
- Diabetes Care 2007; 30:622-28.
- Diabetes Care 2006; 29:1638-43.
- JAMA 2008; 300:1353-54.
- Obesity 2010; Jun 17.
- Am J Clin Nutr 2007; 86:1257-58.
- Mayo Clin Proc 2008; 83:460-69.
- Diabetes Care 2010; 33:2277-84.