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Today one in eleven adults in the world suffers from diabetes, while half of the cases are not even diagnosed. The number of patients has tripled over the past 20 years and could reach 700 million in the coming years.
The reasons why this previously rare non-communicable disease is spreading around the world like a pandemic, according to scientists, should be sought in the distant history of mankind
When we talk about diabetes, the keyword here is insulin, a hormone produced after eating by the beta cells of the pancreas. Its task is to "store" in the cells that came with food to use in the "hungry" time.
In this sense, insulin is a universal anabolic, increasing the synthesis of fat, protein, and glycogen (animal "starch"). But the reverse catabolic functions, including the formation of glucose, it inhibits.
With diabetes, the concentration of "sugar" (glucose) in the blood increases, and the reason lies in a decrease in the level of secretion and/or the effectiveness of insulin.
Type 1 diabetes is an autoimmune disease in which beta cells are attacked by the body's own antibodies, making it impossible to produce insulin.
But in the case of type 2 diabetes, which makes the main contribution to the modern "epidemic", everything is much more complicated: in addition to the dysfunction of beta cells, we meet here with another pathology - a violation of the sensitivity of cells to insulin.
And people with insulin resistance, which at first is accompanied by increased synthesis of this hormone, are much more numerous than official patients with diabetes.
The concept of insulin resistance is the basis of the popular concept of "metabolic syndrome", which refers to a whole cluster of risk factors for the development of diseases that determine the structure of mortality in modern people.
By the way, the external expression of reduced sensitivity to insulin can serve as abdominal obesity, in which fat accumulates in the abdominal cavity. (Mendrick et al., 2017)
The concept of insulin resistance is the basis of the popular concept of "metabolic syndrome", which refers to a whole cluster of risk factors for the development of diseases that determine the structure of mortality in modern people.
By the way, the external expression of reduced sensitivity to insulin can serve as abdominal obesity, in which fat accumulates in the abdominal cavity.
So, where does type 2 diabetes come from?
Genome-wide studies revealed the presence of many genes associated with the development of this disease, but the contribution of each such gene was very small.
So, to predict the development of diabetes in a particular patient, it is much cheaper and easier to measure the waist circumference instead of genetic analysis and find out what his/her parents were ill with.
But with the help of a bioinformatic approach and the study of "gene networks" underlying the pathogenesis of type 2 diabetes, it was possible to find out that it is based on groups of very "ancient" genes that arose at the early stages of evolution.
The stages of progression of type 2 diabetes are accompanied by hyperglycemia, decreased insulin production, and increased cell resistance to this hormone. (DeFronzo, 2004)
The latter fact makes us pay close attention to the situation with energy exchange in the history of the hominin subfamily, which includes modern man and all his distant and close "relatives".
Running through our family tree, from the Australopithecines to the Neanderthals and Sapiens, we can see that there have been major changes in the lifestyle and diet of these primitive people over the course of evolution. Food became more high-calorie, it increased the proportion of animal protein and fat, which was reflected, first of all, in the increase in the size of the brain.
It is believed that this main human organ is able to consume up to 40-45% of all energy produced in the body on an empty stomach! There is a hypothesis that such an energetically imperfect structure could develop and increase in volume precisely due to the very insulin resistance.
For our ancestors, reduced insulin sensitivity in muscle cells, liver, adipose tissue, and other peripheral organs may have been a protective mechanism for survival in extreme situations, such as prolonged starvation.
Indirectly, this assumption is supported by the results of a study of Jamaicans who suffered from marasmus, a state of deep energy deficiency, before birth and in early childhood (Francis-Emmanuel et al., 2014). These people were less sensitive to insulin, they were found to have more disorders of carbohydrate metabolism and cases of diabetes.
Usually, such changes are explained by the fact that when there is a lack of energy substrates, the "bookmark" of beta cells is disrupted. But there is another way to look at it: perhaps these people survived because they were initially less sensitive to insulin, which allowed their brains to develop.
And not so long ago, modern humans discovered a new genetic locus associated with the development of diabetes, which we inherited from Neanderthals.
Radical changes in the way of life and nutrition of humans, which could serve as a prerequisite for the modern epidemic of diabetes, began to occur about 15-10 thousand years ago when hunters, nomads, and gatherers began to move to a settled life.
The most striking difference was a sharp increase in carbohydrate intake, including fast carbohydrates, and an equally sharp reduction in dietary fiber intake. Subsequently, foods that were completely unthinkable for our ancestors began to play an increasingly important role in nutrition: refined carbohydrates, vegetable oils, processed cereals, and dairy products.
These days, their share in the diet reaches 70%, and they all require a rapid and significant release of insulin, which means a large load on the beta cells of the pancreas.
However, until the mid-XX century, the rapid spread of diabetes mellitus was not observed. Most people continued to engage in intensive physical labor, and this activity is associated with increased sensitivity to insulin. In addition, for most of the world's population, the problem was rather the lack of food than the excess.
The industrial revolution brought new changes to the structure of human nutrition, which we know firsthand - from fast food to an increase in the total caloric content of the diet, and motor activity began to decline, including due to the development of transport, the advent of the computer and the Internet.
All this immediately affected the spread of obesity, primarily among the population of the industrialized countries of America and Europe. This is where the epidemic of diabetes began.
One of the striking consequences of the industrial revolution is the widespread prevalence of obesity among adults and children.
By the way, life itself set up an experiment on native Americans - Pima Indians, whose traditional food was based on beans, corn, zucchini, and other crops.
When the Pima from the US state of Arizona were pushed back to the territory where farming became impossible, they actually began to starve.
Later, the US government began to supply food aid to the Indians in the form of flour, sugar, lard and canned food, which in conditions of low physical activity led to the rapid spread of obesity and diabetes.
By the end of the last century, every second adult Indian had diabetes! However, this does not apply in any way to representatives of another Pima population that lives in a remote area of Mexico and has preserved a traditional way of life and nutrition (Schulz et al., 2015).
How to prevent a negative scenario?
The recommendations are banal: a healthy diet (which does not necessarily mean a return to the "stone age diet") and high physical activity.
After all, even in people who are genetically predisposed to developing type 2 diabetes, intensive fitness classes over three years reduced this risk by 60% (Florez et al., 2017).
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