Reflections on diabetes, focus on type 2 diabetes


A year ago I promised a friend I would write about type 2 diabetes (from here on abbreviated as T2D). She has T2D and wanted to know more about it, after being justifiably horrified by the high percentage of amputees and blind people at the diabetes clinic she attends. I started to do my research and discovered that there is an astonishing amount of information about diabetes on the web.

Diabetes affects millions of people worldwide. At the recent United Nations Summit on Non-Communicable Diseases (held in New York in September 2011) the number of people with diabetes world wide was estimated at 366 million, with 4.6 million deaths attributed it in 2011 alone. The number of people diagnosed with and dying of diabetes is rising. The web site of the International Diabetes Federation has plenty more frightening statistics concerning the scope of problem. (

First, an overview -at its simplest, diabetes is uncontrolled high blood glucose levels, a.k.a. hyperglycemia, with two major causes: a lack of insulin, and insulin resistance.

Insulin is a hormone that is made by the islet cells within the pancreas. As levels of sugars and carbohydrates (complex sugars) in the bloodstream rise during digestion, insulin is secreted by the pancreas. Most cells in the body have insulin receptors, and with insulin, these cells are able to absorb the sugars. In the absence of insulin, cells are unable to take the sugars in and the cells starve. In a word, the person with no insulin starves to death at a cellular level.

Type 1 diabetes (T1D) was formerly called juvenile-onset diabetes. The pancreas stops producing insulin. This is normally caused by an autoimmune reaction against the insulin producing cells (beta islet cells) of the pancreas.  It can occur at any age although it usually develops in children or young adults.

Type 2 diabetes is caused by insulin resistance or insufficient insulin production. The insulin is there, but the cells seem unable to recognise it. The biggest risk factors associated with developing T2D are being overweight and sedentary, conditions that are becoming more common everywhere. With obesity comes the added complication of high lipid levels (also known as high cholesterol). So the type 2 diabetic suffers from both high blood sugar levels and high blood lipid levels.

T2D is more common in people over 40 though the age of diagnosis is dropping as more people become overweight earlier. Dean Ornish states in a TED talk that diabetes has increased by 70% in 30 year olds in the past ten years. T2D is no longer a disease of the middle aged. (

High blood sugar levels are poisonous. They wreak havoc by gumming up proteins and causing nerve and blood vessel damage. As an example of how this damages nerves and blood vessels,  I will tell the story of an acquaintance. This man is in his 60’s, moderately overweight and does not exercise. A few years ago he developed a sore on his leg. Maybe he bumped his leg, or maybe he didn’t notice his socks rubbing against his leg creating a small sore. He didn’t notice because he doesn’t feel things as well as he should.  He has nerve damage caused by hyerglycemia. His sore didn’t heal because of reduced blood flow, also a consequence of high blood sugar levels. The sore grew and eventually became infected, gangrene followed. Last year he had to have his leg amputated. Unfortunately his story is all too common.

Circulation problems are a serious complication for diabetics. Hyperglycemia causes peripheral nerve damage (tingling, numbness), reducing sensation, especially in the extremities: feet, lower legs. It also causes vascular damage impairing circulation.. This makes for a deadly combination. People with T2D also have the added complication of high cholesterol levels which cause plaque formation (atherosclerosis)

Almost everything I have written so far is available on any number of web sites devoted to diabetes. For the rest of this blog I am going to focus on T2D. The things I am going to look at are more esoteric: i.e. why people get T2D and what things predispose a person toward T2D.

In spite of all of extensive searches, I was unable to come up with an explanation for why people get T2D. It is as big a mystery to the doctors and scientists researching T2D as it is to me. Gain some weight, lead a sedentary lifestyle, get T2D.

My personal theory is that we did not evolve to carry around this much extra “energy” for extended periods of time (i.e. years). For thousands of years mankind lived in an environment of feast and famine, with famine being more common than feast. In times of plenty it was a good survival strategy to save that excess food as fat. Then during lean times, like famine, war, drought, or illness, the energy stored as fat was there to bridge the gap, to provide sustenance that the environment was not providing.

Today people have a greater abundance of food available to them than any other time in history. Our bodies don’t know what to make of it. T2D is a message that the extra energy stores are FULL, there is no more room! Consequently, the sugars in the blood are unable to enter these “full” cells because those cells have stopped recognizing insulin. Unfortunately the message that one’s cells are full does not seem register with the appetite centers, or people would stop feeling hungry and stop eating when their cells were full.

Which brings up the question of why some people more likely to get T2D than others? My cousin has it but her husband doesn’t. A few things that influence your susceptibility to T2D are genetics, epigenetics, mysterious environmental factors, and diet.

Genetics you should be familiar with. We speak of getting our curly hair from our dad, or our eyes from our mom, and so we did. The program for making those traits is in your genes, one half of which you got from your mother and half from your father. We also inherit the propensity to get certain diseases from our parents. If a relative has T2D, you are more likely to get T2D. The closer that person is related to you –parents, siblings, aunts and uncles, grandparents- the more overlap there is in your genetic code, the greater the likelihood of you getting the same diseases.

Epigenetics is harder to define. It is one of the ways that the environment alters how the genetic code is read, and this modification is passed from parent to child. You inherit genes from your parents, epigenetic changes to the genetic code alters how those genes are expressed.

Some examples: if a woman was malnourished during her pregnancy her children have a higher probability of being overweight, getting T2D and schizophrenia. (Prenatal Famine and Adult Health, Annual Review of Public Health, Vol. 32: 237-62 (Volume publication date April 2011) and (

What happens to a man prior to puberty has epigenetic consequences for his male children. Using birth records and records of crop production in northern Sweden, the Avon Longitudinal Study of Parents and Children (ALSPAC) has discovered some surprising links between fathers and sons. If food was scarce (crop failure resulting in famine) prior to the male child’s puberty, his sons have a lower risk of getting cardiovascular disease. But the boys who experienced years of really good crops (feast) before puberty have sons and grandsons with an increased mortality to T2D. (

Studies done in the UK have shown that if a man starts smoking before he goes through puberty his sons will have a higher body mass index, i.e. be overweight, which increases the risk of getting T2D. (

In essence, the environment our parents and grandparents grew up in alters our risk of getting certain diseases, including T2D. And what we do and have done has epigenetic consequences for our children. A sobering thought.

Being overweight or obese is the single biggest risk factor for T2D. In the USA, almost one third of the adult population is obese! It is an epidemic. And it isn’t just people who are getting fatter, animals are also getting fatter. In a study headed by David Allison the weight of 20,000 animals from 24 populations (feral as well as domestic) living with or around people in North America were analysed. Weights of animal groups from 50 years ago were compared to weights from the present. The surprising results were that feral rats got fatter as did house pets and laboratory animals (whose diet has presumably not changed).  It appears that there is something in the environment (a pollutant?) that is also making us gain weight. Or maybe the feral animals are eating our leftovers? ( and

What we eat has changed over time. Fast food and processed food is far more available today than it was in the past. In a recent paper by Jenny P-Y Ting, macrophages (a component of the immune system) were exposed to palmitate, an unsaturated fat found in many processed foods. The macrophages released interleukin-1 beta, a substance released during inflammation. Interleukin-1 beta reduces insulin signalling in liver, fat and muscle cells. Put another way, the inflammation caused by palmitate “blinds” these tissues to the action of insulin. ( Being blind to insulin is the same as being insulin resistant. So one’s diet, specifically the fats in one’s diet, can lead to insulin resistance.

In the end, the best we can do is follow the advice given to us.  Exercise more, eat less, eat fewer processed foods and more fruits and vegetables, and keep our weight under control. The importance of exercise in the control of T2D cannot be understated. Get up and move your muscles! Exercise has decided health benefits, and if you have T2D it is especially true ( Not only were we not meant to carry around fat for prolonged periods, we were not designed to be so sedentary either.

Additionally do not fall for the stereotype that only really fat people get T2D. I am constantly surprised at how little overweight one needs to be to get T2D. It could happen to any of us.

Here are some very good websites about diabetes:

The website of the International Diabetes Federation. The statistics are frightening.

Dean Ornish’s TED talk. It is only 3 ½ minutes long, so watch it!

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