Insulin resistance refers especially to a markedly reduced decrease in circulating glucose concentration by insulin. However, insulin has many functions, and therefore exerts different effects on the various organs carrying the insulin receptor. This compensatory increase in circulating insulin levels is aimed at preventing a disturbance of glucose homeostasis and thus the onset of type 2 diabetes mellitus. The persistence of compensatory hyperinsulinism is responsible for most, if not all, of the abnormalities that pertain to the metabolic syndrome.

Glucose regulation is an ancestral process that has operated in the context of body composition (muscle tissue to adipose tissue ratios) as observed in free-living wild-type animals. However, agriculture and social stratification among humans led to the emergence of elite groups and nobility in whom food acquisition and physical exertion became dissociated. This promoted obesity among the wealthy. More recently, the social impact of industrialization has further increased this fact, which has further altered the proportions of fat and muscle in many humans, rich or not, and also in some of their household pets.

The fat percentage of contemporary wild animals is directly correlated with body size in a range from less than 5% in mice to about 35% in blue whales. Many men and women now have body fat percentages equal to or greater than those of blue whales, even though a blue whale is 1,000 times larger than an average human being.

Recently studied hunter-gatherers constitute the best available analog of humans and useful information about their body composition. Despite its limitations (quite a few), body mass index (BMI) can be used to compare hunter-gatherers with present-day Western individuals.BMI in 2001 averaged 20.9. In the mid-19th century the BMI of college students was similar (21.1) but the BMI of contemporary college students (year 2010) was notably higher (25.8).

Furthermore, comparative tricipital skinfold values (hunter-farmers, 4.7 mm; current 19-year-old North Americans, 15.5 mm) indicate that most of the differences can be attributed to the extra adipose tissue that contemporary humans have. Consequently, it seems likely that in recent years, muscle to fat ratios have deviated from the ancestral pattern of years ago, which leads to abnormal carbohydrate metabolism.

The skeletal remains of pre-agricultural humans indicate that their musculature was comparable to that of contemporary top athletes. For highly trained athletes, the ratio of skeletal muscle to adipose tissue is nearly 5:1 (approximately 50% of body weight as muscle and 10% as fat).

For today’s female athletes, the ratio may be as high as 3:1 (approximately 45% muscle, 15% fat), but because superior female athletes often experience ovulatory dysfunction (which they would have been selected against during evolution) the projected tissue ratios in the past for Stone Age women would be 35% to 40% muscle and 20% to 25% fat.

Today, in the U.S., and increasingly around the world, people with excess fat (men, 25%, women 35%) and less muscle (40% and 30%, respectively) have become commonplace. These individuals have an elevated risk of insulin resistance. For these individuals, the ratio of insulin receptors on adipocytes has increased relative to that on myocytes.

The insulin receptors of myocytes (muscle cells) and adipocytes are essentially identical. Consequently, fat tissue and skeletal muscle compete throughout the body for circulating insulin, i.e., insulin molecules, which are coupled to adipocyte receptors, are not available to muscle insulin receptors and vice versa.

For this reason, the relative proportions of the two tissues play an important role in determining how insulin molecules released during any pancreatic secretory pulse are distributed.

While the insulin receptors of adipocytes and myocytes are structurally identical, the impact of their biochemical properties differs. In humans, an insulin molecule that activates a muscle insulin receptor induces 2- to 3-fold more glucose “clearance” than a molecule that reacts with an adipose tissue receptor. That is, an insulin molecule that couples to an adipocyte insulin receptor results in less glucose “clearance” than if it had coupled to a myocyte insulin receptor. Other factors being equal, it means that lean, muscular, fit individuals exhibit more whole-body insulin sensitivity than sarcopenic, overfat, poorly fit individuals. The latter may be considered to suffer from “systemic” or whole-body insulin resistance.

The obese is not a thin person who has gained extra kilos, nor is it only a question of quantity, but of other factors such as the location of the adipose tissue, its physiological state and the great endocrine capacity that this tissue has, since it is not merely an inert tissue that “stores” energy.

Therefore, although at the beginning obesity is usually accompanied by a NON-proportional increase in muscle tissue, this will be more of a burden than a functional and beneficial tissue. It is assumed that weight gain occurs in both tissues, i.e. muscle and adipose, but not in an adequate proportion, establishing in general (it is very relative) a proportion of 10 to 1, i.e. for every 10 kg of fat mass, 1 kg of muscle mass is gained, which inevitably leads to a disproportion that will cause metabolic havoc and ultimately lead to disease. From a certain point of obesity and with the possible appearance of metabolic alterations, the path towards the loss of muscle tissue itself will begin, above all a notable loss of functionality and quality and ultimately of quantity. At this point it is already possible to relate excess fat tissue in pathological obese people to a state of sarcopenia, dinapenia and osteopenia. In fact, Baumgartner et al. (2004) define the combination of these morbidities as ‘sarcopenic obesity’ of which I speak so much today.

Hence the importance of context. When we blame obesity on carbohydrates or insulin alone, we are being radically simplistic. In fact, insulin is not to blame but insulin resistance, caused by the multiple reasons explained, especially by such altered body composition. TODAY WE HAVE LESS MUSCLE AND MORE FAT THAN EVER IN OUR EVOLUTIONARY HISTORY, due to factors that include a sedentary lifestyle combined with a diet rich in ultra-processed products rich in fats and sugars. But we have not been evolutionarily designed to be seated or to eat products, but real food, so that is the main problem, since the increase of fatty tissue and the loss of muscle tissue observable among the current population will condition us to be resistant to insulin, and this will lead us to the vicious circle of obesity. But today’s athletes DO REPRESENT our evolutionary ancestors, with high rates of physical activity and optimal body composition (muscle tissue and fat tissue), so high consumption of carbohydrates is not a problem for them, in fact they need them, without causing metabolic or health problems, observe the Kitava if not.

In addition, insulin will help to conserve the precious muscle mass, not so much because of its anabolic effect (which is also true in some cases) but above all because of its powerful effect on muscle catabolism. Thus, physical activity, physical exercise and muscle tissue have a lot to say about this problem. In fact, the feared de novo lipogenesis will not be a fact that occurs (at least substantially) in active people and/or athletes. So, apart from all the above, where we mostly go wrong when simplifying this story, it is in the context of the subject.”

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