The current surge in diabetes mellitus appears to have begun about 30 years ago; particularly worrying is the increase in juvenile Type 2 diabetes that was almost unheard of 20 years ago (2). At the same time, the incidence of associated factors like obesity and precursors such as metabolic syndrome have also risen. In 1962, juvenile Type 2 diabetes accounted for only two to four percent of diabetes, but by 1994, it accounted for 16% of diagnoses in children, particularly in ethnic minority groups (4,5). This can be attributed to the additional stresses on the body that obesity causes, in combination with an extra need for insulin during adolescence, with diagnoses of Type 2 diabetes in juveniles mirroring the rise in obesity (4). Childhood obesity more than doubled between 1960 and 1994 (5).
While there are many issues related to Type 2 diabetes, the biggest problem is the insensitivity of the cells to insulin. That is, the cell membrane does not want to take any more sugar into the cell. On the one hand, it wants to get the sugar out of the blood to stop causing damage to the blood and, on the other, the cell membrane won't let the sugar in. Diabetes is the inability of sugar to penetrate the cell membrane and to get to where the work needs to be done in the cell. The cell membrane stops 'listening'to the insulin, which is trying to get the sugar out of the blood.
Listen to the wisdom of your cells and your body. That wisdom is telling people with diabetes that the cells literally do not want any more sugar (or fat) to be taken into the cell. They already have enough and don't want any more. It is sending us a message. If we listen to it then we have to change the way we eat and our lifestyle, primarily our level of activity and stress. However, if we ignore it and just take the drugs that force more sugar into the cell, the problem continues to get worse and we require more medication and even serious surgery. The definition causes the disease.
Treating the Definition
Unfortunately, how we define diabetes and how we treat the definition is a major part of the problem. According to the current definition, someone has diabetes when he or she has two fasting glucose measurements above 126 mg/dL (7.0 mmol/L). People with fasting glucose levels from 100 to 125 mg/dL (5.6 to 6.9 mmol/L) are considered to have pre-diabetes. While this may change a little between countries and organisations, the bottom line is when the blood sugar gets to a certain high level, you have diabetes. Pre-diabetes means that your blood sugar level is higher than normal, but it has not yet increased enough to be classified as Type 2 diabetes. However, without intervention, pre-diabetes is likely to become Type 2 diabetes in 10 years or less and the destructive mechanisms associated with insulin resistance may be at work for up to 15 years prior to diagnosis.
It doesn't really matter if a person has impaired glucose tolerance, insulin resistance, pre-diabetes or diabetes, he or she needs to take action now. A better approach would be to recognise any consistent (two or three times in a row) increase in blood fasting sugar as illness and see it as a call to action and not wait around until blood sugar rises above 126 mg/dL. A few years ago, someone I know was told he was okay when his sugar levels were going up because he was not yet a diabetic and, when he got there, then he was told he needed to do something. As soon as elevated sugar occurs, destructive forces are at work and action needs to be taken. Sustained elevated blood sugar at any level - not just when it gets to 126mg/dL - is contributing to damage.
A healthy individual produces around 31 units of insulin per day. The Type 2 diabetic may secrete as much as 114 units per day. Unfortunately, both the increased sugar and insulin in the blood lead to health complications. In addition, high insulin levels (hyperinsulinemia) makes the liver produce very low density lipoproteins (VLDL), raises fibrinogen which increases the risk of clots and raises inflammatory markers such as C-reactive protein. This puts diabetics at increased risk of many forms of chronic illness including cancer, cardiovascular disease and Alzheimer's.
High concentrations of glucose can lead to a cellular accumulation of a byproduct of glucose metabolism, sorbitol, which can lead to tissue damage, as well as glycation (glycosylation) when glucose bonds and damages proteins, producing advanced glycation end products (AGEs). Many of the complications of diabetes come from AGEs. These result when glucose crosslinks with proteins in the body, and are closely associated with the formation of reactive oxygen species (free radicals) (6). AGEs can damage collagens in the skin, arteries and connective tissues, damage eye lens proteins and brain nerve cells, leading to conditions such as skin damage, heart attack, arthritis, blindness and neurodegenerative diseases (7). While this process is not limited to diabetic patients, it occurs much more frequently than in non-diabetics due to higher glucose and free radical levels in the bloodstream.
There is also increasing evidence that low-grade inflammation plays a major role in Type 2 diabetes and associated complications such as abnormal blood fat levels (dyslipidemia) and atherosclerosis. Elevated circulating inflammatory markers such as C-reactive protein and interleukin-6 predict the development of Type 2 diabetes and other features of type 2 diabetes such as fatigue, sleep disturbance and depression (8).
Shorter Life Expectancy
As a result of these processes, diabetics are a lot more fragile and have shorter life expectancies than those without diabetes (9), and diabetics are at high risk for development of eye, kidney, foot, nerve, cardiac, and vascular complications (10). Cardiovascular mortality is three times higher in those with diabetes (11) and diabetics are two to six times more likely to experience a myocardial infarction (heart attack) than the general population (12,13,14).
The major factors in causing Type 2 diabetes appear to be a combination of high levels of fat accumulating inside the cells (IMCL), mitochondria defects and lack or responsiveness of the cell membrane to insulin.
Over many years of poor diet and lack of exercise, the cells in the body accumulate fat, which sends messages to the mitochondria (the cell's powerhouse) DNA to stop burning energy and to the cell's membrane to stop letting in more energy (sugar). The cell has accumulated too much fat and it literally tells the rest of the cell to slow down all functioning.
Due to the lack of nutrients in the cell, it is also likely that it is difficult for the cell to carry out its normal metabolic functions. As a result, through the genes it sends a message to the cell membrane that there is excess sugar and fat in the system and to close off the insulin receptors and sugar transporters on the cell membrane. On the other hand, within the cell, metabolism is sluggish and slow almost as though the cell is being starved of sugar. So it sends messages to the brain to provide more sugar.
The mitochondria are involved in crucial cellular activity such as fatty acid oxidisation, glucose/substrates transport and insulin receptiveness (15). It was found that Type 2 diabetics and, to a lesser extent, obese individuals have around 30% smaller mitochondria than healthy individuals, as well a greatly increased number of fractured and disturbed mitochondria (15,16). In Type 2 diabetes, the problem appears to be too few mitochondria. That is, people with Type 2 diabetes have fewer mitochondria than they need to burn up the accumulating fat.
It appears that after three days, fatty foods not only accumulate quickly as intramyocellular lipids (IMCL) but also turn off the genes that would help burn fat. Your ability to eliminate fat inside your cells seems to be slowed down when you eat fatty foods. It appears that a sudden influx of fat in the muscle cells signals them to turn off the fat-burning mitochondria and save the fat for future needs. This is probably an adaptation in our evolution from the days when we had many food shortages. Fortunately, the fat inside your cells disappears and returns to normal function in the absence of fat in the diet.
A processed diet, along with low nutrient levels, damages the cell membrane. Saturated fats and trans fats replace the healthy fats in the cell membrane to become more rigid and hardened. Free radicals cause oxidation and damage to the cell membrane, which leads to its further inability to transport sugar and nutrients into the cell.
In the past few years, much of what we thought we knew about diabetes has been turned on its head. What is now coming into focus is an understanding of its fundamental causes. Diabetes Type 2 is not a fixed sentence. Just last week I saw a person who explained to me that he used to have diabetes Type 2. He had lost 20 kilograms and had gone on a nutrient-dense, fresh vegetable juice, nutrient supplementation, vegetarian, no carbohydrate diet and changed his attitude to illness and his lifestyle. Almost every week I hear of people reversing their diabetes (Type 2) not to mention the dozen or so new books and DVDs on the topic. Hundreds of studies have shown the effectiveness of diet, exercise and nutritional supplementation in the treatment and prevention of diabetes.
Unfortunately, general recommendations for the management of Type 2 diabetes - including eating five servings of vegetables daily, eating more whole grain bread and cereals, legumes, pulses, fruit, reducing sugar and goods high in sugar, and cutting down on the saturated fat intake by eating moderate quantities of lean meat - do not go anywhere near far enough. In fact, following the general healthy eating guidelines will in most cases lead to a worsening of the disease. Diabetics following the diabetic diets get sicker, simply because it's not enough. To reverse decades of damage, more emphasis needs to be put on a highly nutritious eating program, improved digestion and physical activity. It takes a lot to reverse 20 or 30 years of damage.
Dr Peter Dingle is a researcher, educator and public health advocate.
He has a PhD in the field of environmental toxicology and is not a medical doctor.
Matthew Partridge, Walter Molina
1. Narayan et al. 2000
2. Gerozissis 2008
3. Shaw et al. 2003
4. Joe et al. 1999
5. Carroll et al. 2010
6. Rosen and Toeller 1999
7. Colman and Packer 1999
8. Pickup 2004
9. Kaufnian et al. 1998
10. Strano-Paul 2000
11. Keen 2000
12. Gonzales‑Barranco 1998;
13. Haffher 2006;
14. Henry 1998
15. Ferrell et al. 2005
16. He et al. 2002
Dr Peter Dingle (PhD) has spent the past 30 years as a researcher, educator, author and advocate for a common sense approach to health and wellbeing. He has a PhD in the field of environmental toxicology and is not a medical doctor. He is Australia’s leading motivational health speaker and has 14 books in publication.