The ninety-year-old mystery of insulin resistance in type 2 diabetes has finally been solved! Type 2 diabetes is not a disease, but usually the symptom of an eating disorder. The missing link between obesity and type 2 diabetes is identified: glucose resistance. A biopsychosocial model of the so-called type 2 diabetes is presented. Epidemic obesity is described as a cultural failure.

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Excerpts from the book

The Unculture of Internal Medicine


Rolf H. Fricke


History of the treatment of diabetes type 1 and 2

At that time, the discussion began as to whether these disease patterns were related to each other or had a fundamentally different mechanism of origin. In 1926 and 1927, MacLean differentiated between real diabetes and hepatic or simple glycosuria. For him, real diabetes was the insufficiency of the β-cells leading to insulin deficiency and impairment of storage and oxidation of glucose. Other cases of high blood sugar, especially in the elderly, were characterized by hepatic glycosuria. Liver and muscles are probably not able to store glucose in a normal way. This leads to an increase in blood sugar and the glucose is then excreted in the urine. However, this is not diabetes at all; it is rather a hepatic glycosuria in which the storage of glucose, but not oxidation, is defective. Another important distinguishing feature of real diabetes is the presence of ketone bodies due to excessive fat burning [95] [96]. He came close to reality, but unfortunately nobody listened to him.

In 1927, Lawrence used the term “insulin resistance” in a patient who did not respond to insulin as originally hoped [97]. In 1931, Falta and Boller distinguished between insular and insulin-resistant diabetes. With insular diabetes they described the insufficient production of insulin by the β-cells of the pancreas, which is nowadays called type 1 diabetes [98].

First semantic confusion: the symptom diabetes mellitus becomes the diagnosis

To my mind, the theoretical concept of “diabetes” is burdened with several semantic confusions that hinder targeted research and effective treatment of type 2 diabetes. In this section, I will describe three semantic confusions on which the concept of type 2 diabetes is based.

The first semantic confusion, in my opinion, is that symptoms such as large amounts of urine and glucose in the urine are being promoted to a disease. Diabetes mellitus, a lot of sweet urine, is not a disease but a symptom.

Second semantic confusion: insulin resistance versus insulin sensitivity

The second semantic confusion is the concept of insulin resistance. Insulin is a hormone, a messenger substance. The term hormone was coined by Ernest Starling at the beginning of the 20th century from the Greek “horme”, which means to excite and arouse [104]. Hormones are endogenous active substances that are distributed throughout the bloodstream to regulate physiological processes; they are signaling substances. In the organism, no resistance to a signal from a messenger substance is built up. The correct and already used term is insulin sensitivity.

Third semantic confusion: diabetes types 1 and 2

From the first and second semantic confusion follows the third. Because the symptom of glycosuria or diabetes was erroneously classified as a disease that could be suppressed by insulin in a few cases, but in most cases showed contradictory, seemingly inexplicable reactions to insulin, two completely different diseases were thrown into the symptom pot of diabetes…


From insulin resistance to glucose resistance

…and now I will explain why insulin resistance is a phantom. Instead, the essential aspect of type 2 diabetes is glucose resistance, with which the body’s cells defend themselves against the cell toxin glucose. Glucose resistance and insulin sensitivity are two sides of the same coin. When insulin sensitivity decreases, glucose resistance increases and vice versa.

Let’s imagine for a moment that the cells did not reject the messages of the hormone insulin and actually did absorb all the glucose offered in the blood. The cells of the adipose tissue would then convert glucose into fat and the adipose tissue would grow infinitely if it could (we will see later that these are the wet dreams of some scientists). Other body cells have different ways of dealing with a long-term strongly increased glucose supply.

They can pick one of several ways of death.

For example, they could simultaneously burn enormous amounts of fat and glucose by abundantly producing adenosine triphosphate, ATP, the ubiquitous energy currency in the body. The result is the death of the cells [105] [106] [107].

This means that the body’s cells have to protect themselves against an excessively high glucose concentration, because glucose in the cell acts directly or indirectly as a toxin in different ways. The glucose resistance of the cell is perceived if the high blood sugar level does not decrease despite high insulin levels. Glucose resistance is a genetically determined protective mechanism of cells against the cell toxin glucose. Insulin resistance is a phantom. The rejection of the messenger substance insulin is a symptom of the cell’s glucose resistance.

In certain situations, it makes sense for the organism to prefer to burn fat and to block the burning of glucose. The body can excrete the excess glucose in an emergency; you just have to drink a hell of a lot. This is what causes the symptom of sweet urine.

The body can’t excrete fat like that, fat can only be burnt. When the fat stores are no longer able to absorb fat, the excess floats freely in the blood or is stored elsewhere. And then there is the beginning of a metabolic syndrome with fat deposits on the heart, in the blood vessels, cardiovascular diseases, high blood pressure, obesity, etc. The human body becomes a dump.

Glucose as a toxin: Glycation

In the following four chapters, I will cover a selection of scientific publications regarding the aforementioned toxic effects of glucose.

Glycation is the uncontrolled addition of glucose to proteins and thus their destruction or restriction of function. The reaction products are called Advanced Glycation Endproduct (AGE).

In people with an elevated blood sugar level, there is a greater risk of spontaneous aggregation of glucose to functional proteins [120]. The effects of high blood glucose levels can be measured, for example, in hemoglobin. Hemoglobin is a protein in the red blood cells that absorb oxygen in the lungs and release it back into the tissue. The red blood cells have no glucose transporters, and glucose can penetrate directly through the cell wall into the interior of the cells and adhere to the hemoglobin. Red blood cells do not have a cell nucleus and they live for an average of 120 days. As a result, glucose has less toxic effects in red blood cells than in normal body cells.

Hemoglobin with attached glucose is called glycohemoglobin, abbreviated HbA1c. The normal range of HbA1c in healthy individuals is between four and six percent of total hemoglobin. A major objective of diabetes treatment is to maintain the HbA1c level below 7-8% [121]. The glycated hemoglobin differs from normal hemoglobin in that it releases the absorbed oxygen more slowly, which results in a lack of oxygen in the tissue. This impairs the system’s performance [122] [123].

The medical database contains almost 39,000 publications on this subject dating from the beginning of research on HbA1c in the late 1970s [127] [128].


Fats as a toxin

This chapter covers some publications which illustrate the toxic effects of fats in a chronic overload of the organism with high calorific food. The term insulin resistance is used here because it is the standard term in medicine.

The 16th-century physician Paracelsus became a figure of contemporary history because he recognized an important principle: “All things are poison, and nothing is without poison, the dosage alone makes it so a thing is not a poison.” It is exactly the same with glucose or fat; in moderate quantities, they are indispensable for the body’s energy supply, and in excess, they have various direct or indirect toxic effects.

According to Joost, it is generally accepted that type 2 diabetes is caused by the combination of insulin resistance and progressive insufficiency of pancreatic β-cells. In a plausible scenario, insulin resistance would occur when fat cells have reached a critical size and the fat tissue stores are limited. Ectopic triglycerides and fatty acids induce insulin resistance in the liver and muscles. In addition, a chronic inflammatory condition probably contributes to insulin resistance. This inflammation would be triggered by an infiltration of immune cells into the fat tissue in obesity. Ectopic fats also appear to affect the ‘lipotoxicity’ of cells, probably in combination with the exposure of cells to high concentrations of glucose (‘glucotoxicity’) [155].

Metabolic syndrome

Roberts et al. stated in 2013: “Although attempts have been made to engineer drugs to improve insulin sensitivity and ameliorate MS (note: Metabolic Syndrome) phenotypes, due to the myriad of beneficial effects that exercise and physical activity provide, virtually the entire population will benefit from increased physical activity levels. Although for select individuals physically unable to perform physical activity, drug mimetics for exercise might have credence for selected phenotypes; no drug therapies will be able to mimic the array of adaptations that occur with regular physical activity in the context of MS and its related causes and complications (emphasis by the author). Even if a polypill for many of these adaptations was possible, it is likely that, as discussed below, many would not even take it” [161].

Fat people should become fatter

“What causes the insulin resistance underlying obesity?” asked Hardy, Czecha, and Corvera in their review of 2012 [170]. This text, published in a scientific journal, is extensively appreciated for its particularly absurd conclusions. Nevertheless, it has been quoted more than 150 times…


Bariatric Surgery

Surgeons noticed the connection between severe obesity and addiction quite quickly. After obesity surgery was launched about 20 years ago, some of the patients who had undergone surgery suddenly became alcohol dependent. It’s called addiction shift. Therefore, the surgeons have carried out research together with psychiatrists, psychologists and other colleagues [175] [176] [177]. Since it is now clear in the context of obesity surgery that eating serves purely psychological needs beyond energy intake, one must begin to assess the use of addiction therapies in obese patients [178]. Finally, one starts to realize that the obese patients must be addicted if they have been operated on in surgery [179].

Traditional lifestyles and overweight

The Tsimane are physically inactive only 10% of the day, whereas populations in industrialized nations sit 54% of their waking time. To survive, the Tsimane must be physically active throughout their lives. They also have a limited intake of food and very few are overweight, which protects against heart disease. Their diet consists of 72% carbohydrates, 14% protein and only 14% fat. In the Tsimane population, 85% had no risk of heart disease, compared to only 14% of the US population. Moreover, in the Tsimane population, heart rate, blood pressure, cholesterol and blood glucose was very low compared to the US population [180].

In subsistence farming societies, calorie intake was around 2000 kcal/d. Approximately 70% of the food consisted of carbohydrates and 15% was protein as well as 15% fat. In contrast, in industrial societies, calorie intake (with averages of up to 3800 kcal/d) and the proportion of processed carbohydrates (sugar) and fats rose sharply, while the proportion of dietary fiber-rich food drastically decreased.

Obesity and the brain

In young adults, the volume of the gray matter (nerve cells) in the middle frontal lobe and hippocampus is reduced in cases of childhood maltreatment. These findings are associated with increased anxiety as a personality trait [185]. The volume of gray matter in the middle frontal lobe of the brain is also decreased with high BMI and increased genetic risk of obesity [186].

In children with obesity aged 8–13 years, brain examinations revealed significant brain dysfunction and an increase in impulsivity associated with obesity [187]. Obesity is associated with poorer memory performance and corresponding functional disorders in the brain [188]. In adolescents, in certain brain regions, the density of the gray matter was lower among those with higher BMI, which means that they have fewer nerve cells in the brain [189].

Slim individuals show higher levels of brain activity than obese individuals in brain areas that are important for processing emotional stimuli. A correlation between anxiety processing in the amygdala and obesity was observed. With reduced activity in the amygdala, body weight was higher [191].

In animal experiments, food with a high fat and sugar content was found to cause a change in the neurotransmitters in the brain. The withdrawal of very palatable food leads to a stress-like response. Access to this food weakens the physical effects of acute stress in early life (separation from the mother). Food with a high sugar and fat content weakens the memory and leads to an inflammatory reaction in the hippocampus, a region critical for memory [192].

Obese individuals have significantly fewer dopamine 2 receptors in certain brain regions than lean individuals. A low number of dopamine 2 receptors have also been found in people with cocaine, alcohol and opiate addiction [193].

A review from 2014 cites evidence from animal experiments and human studies to support the hypothesis that in obesity, brain systems are affected similarly to those of cocaine and alcohol addiction. The concept of the reward deficit syndrome is explained in detail. These are said to be genetic and epigenetic phenomena that lead to a disruption of the reward system in the brain and lead to sub-functioning of the dopamine system. A particular gene variant is said to lead to the formation of fewer dopamine 2 receptors, which would cause increased addictive behavior. Systems modulated by dopamine would play the largest role in addictive eating habits [204].

If at the age of 14 insulin is needed because children are so overweight and their blood sugar is so high, prevention should start in kindergarten or the early school years, preferably with the mothers of unborn children. The administration of blood glucose lowering drugs such as metformin or insulin in obese patients with elevated blood sugar levels is a psychological disaster. Because the administration of insulin distracts from the fact that the person himself is responsible for reducing calorie intake and thus lowering blood sugar. If the blood sugar level in obesity does not decrease with the administration of insulin, the phantom insulin resistance is held responsible and the person can apparently relinquish his responsibility. Thus, the theoretical concept of genetic insulin resistance provides a justification for the denial of the eating addiction.

Physical activity and the brain

Physical exercise increases the synthesis of dopamine in the brain [209], increases the number of dopamine 2 receptors in mice with Parkinson’s disease [210], and improves the binding potential of dopamine 2 receptors in animal experiments [211].

New concepts for diagnosis of diabetes and metabolic syndrome

1. There is no insulin resistance. Insulin is not a toxin against which a cell would have to build up resistance. The correct term is insulin sensitivity; the insulin signal is more or less strongly received.

There is a glucose resistance. The body as a whole and individual cells of the body must protect themselves against various toxic effects of glucose. Glucose is already toxic in low concentrations. For example, even at low concentrations of glucose in the blood, parts of the hemoglobin in the red blood cells become ineffective due to the addition of glucose. This is known as glycation. Glycated hemoglobin is called glycohemoglobin, abbreviated HbA1c. A maximum of 6% HbA1c is considered healthy. Other toxic effects of glucose include the formation of oxygen radicals, methylglyoxal formation and apoptosis.

In the body’s cells, there are sophisticated transport and detoxification systems to protect against the cell toxin glucose. In the case of an oversupply of fats and glucose, insulin receptors and glucose transporters are reduced in order to prevent a too high concentration of glucose in the cell. An oversupply of glucose in the cell leads to an overload of the internal protective mechanisms against glucose.

2. Type 1 and 2 diabetes are two completely independent categories. The term diabetes is to be discontinued.

3. Type 1 diabetes is to be known as β-cell insufficiency, which is mostly a result of autoimmune disease. The treatment consists mainly of the administration of insulin and an individually adapted diet.

4. Two new diagnoses are being made of type 2 diabetes:

a) habitual eating disorder with chronic glucose poisoning.

The diagnosis is based on the eating behavior and the toxic effects of having high blood glucose levels for an extended period of time.

The basic metabolic rate of a person is the highest between the ages of 15 and 19 years; after the age of 19, it decreases steadily [219]. However, eating habits are usually maintained, which often leads to an oversupply of calories with reduced physical exertion. Overweight can but does not have to, occur. The treatment is mainly carried out through education and motivational training, adapted calorie intake, and increased physical activity.

b) eating addiction with chronic glucose poisoning.

The diagnosis is based on the eating behavior and the toxic effects of having high blood glucose levels for an extended period of time.

Eating addiction with a chronically increased calorie intake is the main cause of this disease. Essential symptoms are obesity and glucose resistance or decreased insulin sensitivity. This disease is possible at any age, but more probably before the age of 50. The treatment consists mainly of long-term addiction therapy. The treatment is complicated by a variety of concomitant symptoms of obesity such as chronic inflammation, lack of oxygen, impairment of perception and thinking due to brain changes and chronic lack of exercise with the corresponding physical consequences.

5. The diagnosis of metabolic syndrome is replaced by eating disorder or eating addiction with chronic glucose and fat poisoning.

These syndromes are primarily a cultural or psychological problem that should be treated in collaboration with Internal Medicine.

The Unculture of Internal Medicine

The global obesity epidemic is a cultural failure. Since 1980, the number of obese people in the world has more than doubled. Is this a predominantly genetic problem? Epigenetics may have a significant influence. In the uterus the metabolism of the child is adjusted to the mother’s metabolism before birth. In 2016, 40% of adults worldwide were overweight. In the United States, more than 70% of adults were overweight in 2014, while in Germany 59% of men and 37% of women were overweight in 2016 [240] [241].
As early as 1567, Pieter Bruegel showed the consequences with his painting “Land of Cockaigne” of getting the double whopper in your car and having the pizza brought by the delivery man, which you have ordered online, to enjoy with the six-pack of beer while watching TV. Man is not genetically constructed for this type of life. He becomes fat and sluggish, and he degenerates.

Our genetics is set up in such a way that, for example, the cartilage disintegrates if we do not move. The cartilage does not have its own blood vessels. It is supplied by releasing the waste under pressure, like a sponge, and absorbing new nutrients when relieved. This only works if the joint in which the cartilage is located is moved. The brain also needs physical activity in order to develop in a healthy way. Furthermore, human closeness is indispensable for the brain; without it we seek consolation for our loneliness in eating. Food is a cheap, legal addictive drug available everywhere. The sugar in food provides quick satisfaction for the brain.

Thank you for reading all the way to the end. There is even more in the book (personal experiences with doctor-patient communication, in medicine hitherto unknown problems in the treatment of invasive fungal diseases, gentle scientifically based therapy options in cancer treatment, and of course why there is an unculture of internal medicine), the part on diabetes type 2 and obesity takes up almost 40 pages.

The book is available as an e-book (PC, iMac, tablet, smartphone) at for the lowest price of currently 7,47 € (I guess Google doesn’t make any profit with this price, please contact me if Google should change the price). This is a freaking bargain for the solution of the 90-year-old mystery of insulin resistance.

The book is also available at BoD. De (208 pages, 16,90 €, free shipping to most European countries incl. UK*, Ireland, e-book 10,99 € for PC, iMac, tablet) as well as at,,,,

and many other online shops as well as at local booksellers (currency converter).

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The Unculture of Internal Medicine, translation of ‘Die Unkultur der Inneren Medizin’,  Rolf H. Fricke, BoD – Books on Demand, Norderstedt, 2017

ISBN: 9783746017402

©November 2017 Rolf. H. Fricke, last updated February 14, 2018