HOME
Insulin Resistance Information
Part 3: What are the symptoms of insulin resistance?
There is only one easily recognised, outward physical sign of insulin resistance: That is the type of obesity known as ?apple shape' obesity ? excess fat around the waist and upper half of the body. Other than that, a glucose tolerance test during which insulin and blood glucose are measured can help determine if someone is insulin resistant. Insulin resistance is characterised by:
- Resistance to insulin-mediated glucose uptake.
- Fat cells releasing a hormone resistin that causes insulin resistance.
- Glucose intolerance
- High blood insulin levels
- Increased levels of low density lipoproteins (LDL)
- Decreased high-density lipoprotein cholesterol (HDL)
- High blood pressure
- Overweight and obesity, particularly around the waist and upper part of the body.
Why are so many people insulin resistant, and some more so than others?
Many millions of years ago, our primate ancestors ate a plant-based diet. The brain and reproductive tissues evolved a specific requirement for glucose as a source of fuel. But the Ice Ages which dominated the last two-and-a-half million years of human evolution changed all that. With little or no plant material around for much of the year, the diet must have changed to one much lower in carbohydrate and high in proteins and fat. This meant that there would be less glucose available directly from carbohydrates. Certain metabolic adaptations would have been necessary to accommodate the lower glucose intake. Studies in both humans and experimental animals indicate that the adaptation that took place is what we now call insulin resistance. As the new low-carbohydrate, carnivorous diet would have disadvantaged reproduction in insulin-sensitive individuals, it would have positively selected for individuals with insulin resistance. Natural selection would therefore result in a high proportion of people with genetically-determined insulin resistance.
Many ethnic populations, such as the American Pima Indians, did not adopt agriculture until approximately 2,000 years ago.[i] Other populations, like the Eskimos and the Australian Aborigines, continued to maintain a hunter-gatherer lifestyle until recently.[ii] Even the traditional carbohydrate foods of these and other ethnic populations have been shown to be low on the glycaemic index (see below), producing relatively small increases in blood glucose and insulin.[iii]
The introduction of food processing which raised the quantity and quality of dietary carbohydrates, reversed the dietary evolution of the last two million years. That this is the cause of modern diseases appears to be the only theory that explains why the prevalence of these diseases is lower in those populations that developed agriculture earlier.[iv]
The current high-glycaemic-index ?Western' nutrition, with large amounts of sugar, refined cereals, potatoes, and white rice is, therefore, a new phenomenon which stresses the beta cells of the pancreas much more than previous carbohydrate-rich diets, and represents a chronic challenge. It is easy to imagine that this massive chronic stimulus may cause the beta cells of the pancreas to malfunction and overproduce, resulting in high blood insulin levels after meals, especially in genetically predisposed subjects.
Epidemiological studies support this theory. High blood insulin levels are a common characteristic of several ethnic groups with a high prevalence of diabetes: Native Americans,[v] Mexican Americans,[vi] and Pacific Islanders.[vii] The reason these populations develop high insulin levels after meals seems due to a limited genetic adaptation to high-carbohydrate nutrition, because they have been subjected to such a diet for a relatively short period of time.
When these populations and Aborigines,[viii] and Native Americans[ix] urbanise and are exposed to high glycaemic-index nutrition, they develop hyperinsulinaemia and very high rates of type-2 diabetes mellitus. In Pima Indians, Nauruans, and Mexican Americans, type-2 diabetes and obesity have reached epidemic proportions. Eskimos, once thought to be resistant, are now developing diabetes in increasing numbers.
Southern Europeans may have a relatively low incidence of diabetes compared with other populations because they were among the first to adopt agriculture, and their diet has been high in carbohydrate for several thousand years. Thus their beta cells have been exposed to high-carbohydrate nutrition for longer than any other group, and are consequently better adapted to such a diet. But even amongst them, the dramatic increase in consumption of high-glycaemic-index food during the last quarter of the Twentieth Century, in part as a result of low-fat, high-carbohydrate ?healthy' diets, together with a progressive increase in sugar consumption, which is now up to 70 kg (150 lb) per head in most Western countries,[x] has stressed the beta cells of even better adapted persons beyond limits. This explains the current epidemic of obesity and of the metabolic syndrome in many Western societies.
Genetic factors of obesity can also be explained by this hypothesis. The fact that obesity runs in families [xi] may be due to a genetically determined higher susceptibility of the beta cells to foods that stimulate insulin production, or it may be because mothers teach their daughters to eat the same way that they do. Either way, these are traits that are passed on to the next generation.
The importance of insulin resistance is that it is accompanied by a progressive deterioration of the small capillaries supplying blood to many tissues, including the skeletal muscles that provide most of the body's insulin mediated glucose disposal. These changes in the blood vessels and circulation may cause a decline in muscle blood flow and increase the severity of the metabolic disorder.[xii]
References
[i]. Szathmary EJE, Ritenbough E, Goodby CM. Dietary changes and plasma glucose levels in an Amerindian population undergoing cultural transition. Soc Sci Med 1987; 24: 791-804.
[ii]. Schraer CD, Lanier AP, Boyko EJ, et al. Prevalence of diabetes in Alaskan Eskimos, Indians and Aleuts. Diabetes Care 1988; 11: 693-700.
[iii]. Brand JC, Snow J, Nabhan GP, et al. Plasma glucose and insulin responses to traditional Pima Indian meals. Am J Clin Nutr 1990; 51: 416-420.
[iv]. Miller JC, Colagiuri S. The carnivore connection: dietary carbohydrate in the evolution of NIDDM. Diabetologia 1994; 37: 1280-6
[v]. Lillioja S, Mott DM, Spraul M, et al. Insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependent diabetes mellitus: Prospective studies of Pima Indians. N Engl J Med 1993; 329: 1988-1992.
[vi]. Haffner SM, Miettinen H, Gasloll SP, et al. Decreased insulin secretion and increased insulin resistance are independently related to the 7-year risk of NIDDM in Mexican Americans. Diabetes 1995; 44: 1386- 1391.
[vii]. Sicree RA, Zimmet P, King HO, et al: Plasma insulin responses among Nauruans: Prediction of deterioration in glucose tolerance over 6 years. Diabetes 1987; 36: 179-186.
[viii]. Wise PH, et al. Diabetes and associated variables in the South Australian Aborigines. Aust NZ Med 1976; 6: 191-196.
[ix]. Lillioja S, Mott DM, Spraul M, et al. op cit
[x]. Putnam JJ, Allshouse JE. Food consumption, prices and expenditures, 1970-97. Economic Research Service, US Department of Agriculture. Stat Bull 1999; 965: 24.
[xi]. Sorensen T. The genetics of obesity. Metabolism 1995; 44: 4-6.
[xii]. Ganrot PO. Insulin resistance syndrome: possible key role of blood flow in resting muscle. Diabetologia 1993; 36: 876-9.
Related Articles
