BARRY'S BOOKS


New book in Dutch

Eet vet word slank

Eet vet word slank gepubliceerd januari 2013

In dit boek lees je o.a.: * heel veel informatie ter bevordering van je gezondheid; * hoe je door de juiste vetten te eten en te drinken kan afvallen; * hoe de overheid en de voedingsindustrie ons, uit financieel belang, verkeerd voorlichten; * dat je van bewerkte vetten ziek kan worden.


Trick and Treat:
How 'healthy eating' is making us ill
Trick and Treat cover

"A great book that shatters so many of the nutritional fantasies and fads of the last twenty years. Read it and prolong your life."
Clarissa Dickson Wright


Natural Health & Weight Loss cover

"NH&WL may be the best non-technical book on diet ever written"
Joel Kauffman, PhD, Professor Emeritus, University of the Sciences, Philadelphia, PA



Insulin Resistance Information




Part 2: Sequence of events

You may be told that being overweight causes insulin resistance but insulin resistance has been shown to exist in a significant proportion of the normal weight population.[i] It really is a ?chicken and egg' situation because increases in body weight and insulin resistance occur at the same time. In simple lay terms the sequence of events is this:

  1. You eat small amounts of carbs and use the resultant glucose up. No problem.
  2. Then you start to eat a little more — 5 portions of fruit, et cetera'.
  3. Now you start to get higher levels of glucose for which the body has no immediate use, and these trigger higher levels of insulin to reduce them.
  4. This starts the process of fat deposition and you start to put on weight.
  5. So you go on a low-fat, carb-based diet. This continues the cycle, increasing levels of glucose and insulin in the blood.
  6. Eventually, your body cells, both muscle cells and adipocytes get to the point where they really don't want to know. Muscle cells refuse to take more glucose; fat cells release a hormone, resistin, and they too lose some of their insulin receptors. At this stage you are insulin resistant.
  7. As the excess glucose now has nowhere to go, this leads to uncontrolled increases in blood glucose and the onset of type-2 diabetes. And, of course, associated complications.

This balancing act which is necessary with a carb-based diet, doesn't happen if you eat a low-carb, high-fat diet.
There are three ways to decrease the blood glucose level and, thus, fat storage: you can exercise — but to accomplish the reduction in glucose needed you would need to run some 3 marathons a week, as a short run or aerobics class is quite useless; you can starve, which is what low-calorie dieting is; or you keep your carbohydrate intake to less than 100g per day and make sure you aren't hungry by eating more fats. It's your choice!

But back to our story:

In 1976 Drs. Kahn and Flier described two syndromes of severe insulin resistance, and research at the time began to focus on the newly described insulin receptor as the cause of insulin resistance.[ii] Further studies, however, showed that the insulin receptor is usually not the cause of insulin resistance.[iii]

Diseases of insulin resistance, particularly diabetes, occur with greater frequency in populations that have recently changed dietary habits from hunter-gatherer to Western cereal grain-based regimes, compared to those with long histories of such diets. This is why obesity and diabetes is so much more common among peoples of African and Asian origin than among those whose ancestry is European. It has been suggested that insulin resistance in hunter-gatherer populations may be an asset, as it would facilitate consumption of high-animal-based diets. The down side of this is that when high-carbohydrate, grain-based diets replace traditional hunter-gatherer diets, insulin resistance becomes a liability and promotes type-2 diabetes.[iv]

Several recent studies have measured insulin levels in populations.[v] These noted higher insulin levels in people with high blood pressure and other vascular disease. For this reason, insulin resistance is now also considered a risk factor for heart disease. These studies have added a great deal of confusion to the field because many individuals with insulin resistance do not have diabetes.

People who are insulin resistant typically have an imbalance in their blood fats (lipids); they have an increased level of triglycerides, a type of fat which increases the risk of heart attacks and decreases the level of HDL.


Because insulin resistance is now such a common condition, it has been suggested that the various facets of syndrome X are involved to a substantial degree in the cause and clinical course of the major diseases of Western civilisation.[vi] There is an enormous amount of evidence that this is the case. In the past two years emerging evidence suggests that the range and variety of diseases and abnormalities associated with insulin resistance may extend far beyond the common maladies that are frequently found in patients. Apart from those already mentioned above, such diverse abnormalities and illnesses as acne, myopia, reduced age of puberty and a trend for increased growth are all linked to insulin resistance by interactions with hormones.

References

[i]. McLaughlin T, Allison G, Abbasi F, et al. Prevalence of insulin resistance and associated cardiovascular disease risk factors among normal weight, overweight, and obese individuals. Metabolism 2004; 53: 495?499.

[ii]. Kahn CR, Flier JS, Bar RS, et al. The syndromes of insulin resistance and acanthosis nigricans: insulin receptor disorders in man. N Engl J Med 1976; 294: 739-745

[iii]. Krook A, O'Rahilly S. Mutant insulin receptors in syndromes of insulin resistance. Bailliers Clin Endocrinol Metab 1996; 10: 97-122.

[iv]. Brand-Miller JC, Colagiuri S. The carnivore connection: dietary carbohydrate in the evolution of NIDDM. Diabetologia, 1994; 37: 1280-1286.

[v]. Despres JP, Lamarche B, Mauriege P, et al. Hyperinsulinemia as an independent risk factor for ischemic heart disease. N Engl J Med 1996; 334: 952-957.

[vi]. Cordain L. Syndrome X: Just the tip of the hyperinsulinemia iceberg. Medikament 2001; 6: 46-51.




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