Type 2 diabetes appeared in the beginning of the 20th century, when sugar ceased to be a rare commodity to come and grace every kitchen table. Before that, the Old World relied on honey or beet sugar for sweetening. And, as the near lack of sweet recipes in the great culinary treaties of the Middles Ages shows, desserts as we know them scarcely existed, whereas today they take up at least a quarter of the cookbooks’ pages, and sometimes whole books.

The colonization of the West Indies and the subsequent development of sugarcane production set up a new deal. Ever since then, we have enjoyed a Faustian relationship with sugar. On one hand, sugar’s glucose is the organism’s major fuel source, but for this very reason, our metabolism is designed to also be able to make it from the proteins and fat in our diet. For millenniums, this ability was a great asset as the vast majority of Mankind was chronically underfed, but it became irrelevant a little more than a century ago, when the dietary needs of Western people started to be routinely met. As our organism has not yet adapted and continues in his old ways, endeavoring to transform ‘everything’ into glucose without taking into account the sugar that we eat (in excess) and which takes a metabolic shortcut and avoids the normal circuit of breaking down of the proteins, lipids and complex carbohydrates into simple carbohydrates that the body is able to use. Trouble began, and the health problems linked to our growing love of sugar. One might say it is poetic justice for the sugarcane plantations’ slaves…

In addition, this formerly rare commodity is associated to wealth and joy in many cultures: who would imagine a festive menu without a dessert? From the traditional wedding cakes to Christmas pudding, Stollen, Panettone and other holidays specialties, from Middle Eastern baklavas to Australian pavlova, and even Easter eggs, that initially symbolized renewal (the egg holds a life in germ) and are now chocolate presents, sugar is everywhere. Some sweet recipes even hold a traditional place in religious rituals: the quince jelly eaten to break the Yom Kippur fast, and the dates nibbled before the evening meals during the month of Ramadan.

When those traditions came into being, sugar was rare and expensive – during Queen Victoria’s reign, a pound of sugar cost as much as a pound of gold! – therefore, the risk of addiction long remained rather theoretical.

Times have changed and the number of sugar addicts increase every year, with tragic consequences in terms of public health. By gorging on sweets and foods rich in hidden carbohydrates, we disrupt our metabolism and fuel the type 2 diabetes pandemic.

The good news: it is a slowly developing chronic disease, so one doesn’t become diabetic in a day, or even in a year. Before that, there is always a phase of prediabetes that can last from two to twenty-five years. During this phase, it is still possible to arrest the evolution towards type 2 diabetes.

Where does this acute sensitivity to sugar come from? Eating too much sugary foods, soft white bread, or instant noodles triggers much too often the processes that allow for the metabolism of glucose by our body. Normally, a surge in blood glucose triggers the release of insulin by the pancreas, so as to bring the glycemia (blood glucose concentration) back to a normal level. When overworked, these regulating mechanisms become dulled and the liver and the other tissues involved develop a resistance to insulin: this is called impaired glucose tolerance (IGT).

The liver, the muscles, the adipocytes and all the cells that absorb the glucose from the blood respond less and less adequately to insulin; they lose their ability to use efficiently the glucose “fuel”. The liver regulates less quickly and well its own production of glucose (hepatic gluconeogenesis) in response to insulin.

And, while it is so busy dealing with sugar, the liver is less available to transform dietary fats, which therefore accumulate within it, thus promoting hepatic steatosis (fatty liver) as well as muscular steatosis (fatty deposits in muscles), and insulin resistance. As a result, the person’s body produces larger quantities of insulin to maintain normal levels of glucose in the blood. Insulin resistance is the best predictive factor for type 2 diabetes. And the fat content of our muscles is the most reliable indication of insulin resistance. It seems that these improperly transformed fats influence the Glut 4 receptors which control the way glucose enters our cells. Studies on animals have shown that an increase in the lipid concentration in an organ or tissue increases the insulin resistance of the said organ or tissue.

At this point, one may talk of prediabetes, an intermediate state between normal glucose regulation and established type 2 diabetes. It is defined as follows:

– A moderate fasting hyperglycemia (high blood sugar concentration), i.e., according to WHO criteria, over 1.10 gram/liter but under 1.26 g/l (the normal fasting glycemia range is 0.7 to 1.05 g/l);

– Or impaired glucose tolerance (IGT), i.e. a glycemia between 1.40 and 2 g/l two hours after the oral ingestion of 75 grams of glucose;

– Or a glycated hemoglobin level between 5.7 and 6.4%. Glycated hemoglobin measures the hemoglobin molecules (the molecules that convey oxygen in the blood flow) altered by the fixation of glucose. It normally accounts for 4 to 5.6% of the circulating hemoglobin.

Whereas the type 2 diabetes risk is 0.7% per year in normal subjects, it rises to 5 to 10% per year in patients displaying at least one of these anomalies (and a near-certainty if they do no change their habits…).

At this stage, another major organ of the ‘metabolic’ body requires our attention: the pancreas. First, the insulin-producing beta cells of the pancreas (islets of Langerhans) shall produce more insulin in order to bring the glycemia (blood glucose concentration) back to a normal level. But in time, the overworked pancreas tires out and there comes a degeneration followed by the destruction (apoptosis) of the beta cells, hastened by the toxic effect of the excess glucose in the blood vessels. When the pancreas is no longer able to balance the impaired insulin sensitivity of the cells, type 2 diabetes (fasting glycemia over 1.27 g/l) appears.

Once this point of no return is crossed, the situation is, in the present state of medical knowledge, irreversible: once diabetic, one is diabetic for life, without any hope of a cure. One can only, through diet and hygiene changes, and/or a medical treatment, endeavour to prevent the occurring of cardiovascular or neurologic complications.

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