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Type 1 Diabetes - A New Discovery

In about December of 2006 I heard about surprising new research published in Cell out of the University of Toronto which suggested that the cause of Type 1 Diabetes may actually be inflammation to the sensory neurons that innervate the islet cells of the pancreas.  Previous to this research it was believed that Type 1 Diabetes was an autoimmune problem where the T cells killed the pancreatic β cells causing an inability to manufacture insulin.  However, when the inflamed neurons were removed using capsaicin, an anti-oxidative and anti-inflammatory peptide found in hot chili peppers, Type 1 Diabetes in mice was reversed, despite the persistent pools of T-cells.  According to this research, it seems that the inflamed neurons (TRPV1  primary afferent neurons) are responsible for the proliferation of T-cells and the islet cell stress, and therefore, Type 1 diabetes, so the disease is neurological in nature as opposed to an endocrine or autoimmune problem as previously believed. Talk about a revolution in how to view this disease!  The question now becomes, "why are those nerves inflamed"?  If science can answer that question, perhaps we will uncover the root cause of the problem.  Although it is far too early to talk about a cure for Type 1 diabetes any time soon, one can be hopeful that progress is being made to that end, as the researchers were able to cure mice of the disease.  The association between capsaicin and reducing blood sugar was first noticed in a study done in dogs in 2001, where the researchers found that capsaicin seemed to increase insulin sensitivity.

Diabetes is a disease that results in elevated blood-sugar levels, although the reason for the poor blood-sugar control is different in Type 1 versus Type 2.  Insulin is the hormone that aids in the transport of sugar into the cells to be used as fuel. In Type 2 Diabetes, the pancreas manufactures insulin, but the insulin receptors on the surfaces of the cells of the body become resistant, effectively closing the door to insulin thereby preventing sugar from leaving the bloodstream and entering the cells. Currently the most effective way to manage Type 2 diabetes is to reduce the consumption of sugar, flour products, fruit juices, and high glycemic fruit and starchy vegetables, as having excessive sugar in the blood creates and environment where glycation (a sugar molecule haphazardly binding to a protein or lipid) is more likely to occur, which damages the arterial walls and increases the risk of heart disease.  In Type 1 Diabetes, the pancreas is unable to manufacture insulin, so the diabetic must inject insulin in order to manage the disease. Type 1 diabetics spend their life doing a careful dance between the timing of insulin injections, the timing of eating, and choosing the right foods in order to try to keep their blood sugar from swinging from high to low and back again.  Diabetic or not, maintaining even blood-sugar levels is one of the most important elements to maintaining good health.

The above research does not suggest that consuming high amounts of hot chili peppers will help control diabetes.  I did a very cursory search for epidemiological data regarding ethnicity and diabetes and found nothing to support the notion that people from countries that are more likely to eat more hot chili peppers have less diabetes. It makes more sense to suggest that at least with regard to Type 2 Diabetes, individual differences in personal biochemistry make some people much more susceptible to the disease, and those that are particularly sensitive to sugar such as fast oxidizers for example, need to be very careful with respect to the kinds of food they consume in order to mitigate their risk.

Related tips:
Blood-sugar regulation
Sugar - The disease generator
How hormones, neurotransmitters and steroids work

Rasavi, R et al. TRPV1+ Sensory Neurons Control β Cell Stress and Islet Inflammation in Autoimmune Diabetes Cell Vol 127, 1123-1135, 15 December 2006.
Phytotherapy Research August 15:391-394; 2001
Basta G et al. Advanced glycation end products and vascular inflammation: implications for accelerated atherosclerosis in diabetes Cardiovasc Res. 2004 Sep 1;63(4):582-92.
Pamplona, R., et al. Mechanisms of Glycation in Atherogenesis Medical Hypotheses, 40(3)174-181, 1993
Vaccaro O., Ruth, K. J. and Stamler J. Relationship of Postload Plasma Glucose to Mortality with 19 yr Follow up Diabetes Care Oct. 15, 10:328-334, 1992.
Tominaga, M., et al, Impaired Glucose Tolerance Is a Risk Factor for Cardiovascular Disease, but Not Fasting Glucose Diabetes Care 2(6):920-924, 1992

Copyright 2007 Vreni Gurd