According to the National Diabetes Informational Clearinghouse which is a part of the NIH’s NIDDK branch. Type II diabetes is most prevalent in ethic populations with historic diets that were rich in complex starches and vegetable proteins in including Hispanic, African and most Native American populations, with the highest rates being Native Americans form the South and Southwest. The lowest rates are seen in Americans of European decent whose historic diet in some cases was high in animal proteins and fats. Most tellingly the exception to the very high rate of Type II diabetes in Native Americans is Alaskan Natives which had historic diet so rich in animal fat even Northern Europeans could not adapt to it, and a rate of NIDDM that is lower than even Americans of Northern European decent.
After Native Americans, Pacific Islanders have the highest levels of Type II diabetes. Similarly these people ate a diet high was vegetable proteins and complex starches, but they had greater access to fats from palm related oils. They also naturally have high levels of body fat, since their life style and the isolation left them vulnerable to famine caused by crop failure. Like Native Americans they Westernized quickly, and with their already high BMI they saw a rapid spike in Type II diabetes.
Interestingly Northern Europe with the exception of Finland and Russia, still have low-ish rates of NIDDM despite urbanization. The population Finland and Russia are the exception for a variety of reasons, including their differing genetic background from the rest of Northern Europe, a strong reliance on grain for their diet and the economic woes caused by the fall of the USSR.
Asia is too ethnically mixed for one number to summarize the population, but the NIDDK indicates that type II diabetes is on the rise in worldwide, with the biggest spikes seen away from the coasts, and in warm climates. The same is true for India, but without deconvoluting the results to account for the religious dietary restrictions the data cannot be accurately used to draw conclusions. Similarly, by lumping Caucasians into a single group they are missing the ethnic diversity, and suppressing the any patterns that might be hidden in the data. This is a data mining exercise and after reading the relevant reports there are several obvious trends with susceptibility to type II diabetes, but the only three that hold up world wide are certain ethnic backgrounds, increased age and increased body fat. (Plus were you put this weight is as risk factor for many diseases, since well distributed fat doesn’t carry the same risk as belly fat. Fat distribution is a genetic trait, since belly fat is storage and distributed fat is insulation.)
Given this information I believe that my theory about that NIDDM is an environmentally induced control failure of normal metabolic processes. Your body puts up a no vacancy sign for glucose and lipids but you keep eating and not exercising, and eventually the metabolic feed back leads to insulin resistance, or significant reduction in insulin production, since the body doesn’t know what else to do. It also explains why there is no ketoacidosis, since the body isn’t worried about starving, but insulin resistance slows the reaccumulation of intramusclar glycogen.
The strongest evidence I have to support my theory is that NIDDM is clearly an epigenetic disease, and epigenetic diseases with incomplete penetrance and strong environmental component are often caused by feedback loops being ignored long enough that the system breaks.
If I was designing the experiments to look at the epigenetic mechanism I would look at the protein faction, DNA methylation and condensation state of the genes in the insulin receptor pathways and plus their promoters in the muscle and adipose tissues of obese people with and conclusively without NIDDM. Then I would follow up with similar studies of the Beta cells form people whose NIDDM caused a reduction in insulin production, vs. just insulin resistance. The issue is that clearly different ethnic groups have different responses to the feedback stimulus, so you aren’t looking for one gene one disease. NIDDM is many diseases with a common group of causes and a common group of symptoms.
The odd thing about epigenetic diseases is the treatment/cure is often nothing more than resetting the system, or moving the conditions back with in spec so the system resets its self. This can be done slowly with diet and exercise or quickly with gastric surgery. The use of selective cold treatment would not cure NIDDM, but it could reduce the symptoms, by forcing the body to raise the metabolic rate and thus clear glucose faster, without completely depleting the stores of glycogen. Heck being bored at work and fidgeting versus being engaged and completely still could have the same effect. Other simple things can help, use a bathroom that is further away (if possible on another floor and use the stairs), walk 5 minutes of every hour even if it is just to grab a glass of water. In an 8 hour day you’ll walk 40 minutes. It is discontinuous, so it’s not as good as taking one 40 minute walk, but every little bit helps.
NIDDM is a disease that takes years to “get”, and without radical treatment it should take years to go away, but a greater level of control can be achieved relatively quickly by doing things that clear glucose and lipids.
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