Autoimmune Thyroid Disease

An Unfortunate and Lengthy Adventure in Misdiagnosis

GI blues

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This article by Barry Groves is quite a good summary of the problems with the GI diet. Like Groves, I get extremely annoyed by those women’s magazines (Healthy magazine is one of the worst offenders) written by airheads who perpetuate misinformation about the GI/GL of foods and how GI and fat/protein consumption interact. I laugh at people who eat commercial brown bread for the sake of GI. And if I see full-fat dairy products and red meat in the “high GI” list of one more magazine, I think I will do violence. FAT AND PROTEIN HAVE NO GI. THEY LOWER THE GI OF ANY MEAL! For God’s sake.

If you want to lose weight you need to reduce your calories below the minimum daily threshold of those you can burn. The only way to reduce hunger comfortably is on a moderate to low carbohydrate diet.

Dietary fat in and of itself does not cause weight gain independently of calorie consumption. Calorie for calorie, it is the most satiating macronutrient. Carbohydrate is the least satiating macronutrient because it stimulates insulin production. Even fibre stimulates insulin production because the sensation of fullness stimulates the vagus nerve and encourages the release of more insulin.

The classic GI/GL diets slow the thyroid down by encouraging the consumption of fibre, whole grains, beans, and nuts, all of which contain an array of anti-thyroid substances. This means you have to reduce calories even more than normal in order to see lasting results.

All high carbohydrate diets encourage insulin production. A genuine low-GI diet, one which includes fat and protein to slow down the digestion of carbohydrates, encourages less insulin production than a non-genuine low-GI diet based around those tiresome indigestible ‘complex carbohydrates’. Even high protein diets encourage insulin production. Only dietary fat does not cause insulin release.

Excess dietary carbohydrate is converted in the liver into triglycerides (fats). Unlike dietary fat, which enters the bloodstream slowly, the triglycerides created in the liver surge into the bloodstream all at once. High triglycerides are considered a crude marker for CHD, though this is probably because they correlate with high insulin levels.

The main fatty acid found in adipose tissue is the monounsaturated fat oleic acid, the main constituent of olive oil. Animal fats are roughly 50/50 saturated and monounsaturated, and oleic acid is the main constituent of the monounsaturated component. Saturated fats make necessary building materials in the body. Monounsaturated fats are not quite as useful chemically, and this is why the body prefers to store them in adipose tissue instead of converting them into saturates, which uses up energy.

Fats and carbohydrates enter cells with the aide of insulin. Once inside the cells, short chain fatty acids enter the mitochondria by passive diffusion. Longer chain fatty acids like oleic acid and stearic acid require l-carnitine, an amino acid, in order to enter the mitochondria. L-carnitine is manufactured in the liver. High insulin levels block the production of l-carnitine. High insulin levels combined with excess energy from both carbohydrates and fats mean that longer chain fats are stored in the cells instead of burned for energy in the mitochondria. If insulin levels are low enough that not enough energy can be pushed into the cells (such as during an overnight fast, at the start of a low carbohydrate diet, or in the case of type I diabetes), then ketones are produced.

All this means that insulin is the fat storage hormone. Only small amounts of insulin are required to build muscle. Largely, insulin builds fat. In particular it builds fat around the stomach area, distorting the figure. This results in what is commonly known as a beer belly – because alcohol encourages insulin release too. The adipose fat in this area is of a dysfunctional nature. Fat cells are not passive, they release hormones like leptin, which regulate hunger. Fat cells around the midriff are particularly resistant to insulin and leptin levels, yet because they require energy, they require additional insulin, which the body duly provides. Even more insulin encourages even more fat storage around the midriff.

Insulin also increases the sex hormones above normal. Oestrogen and testosterone are increased in both sexes, and oestrogen is another fat storage hormone. Testosterone is a muscle builder, but only builds muscle in the presence of protein. So you may well be built like a brick sh*t-house, but you will have a beer belly to be proud of (think Germans). This is the reason why so many men and women have distorted figures these days. We know from epidemiological data from the 1950s that our shapes have changed. Women have broader shoulders, wider waists and less feminine curves than they used to have. Men are doughy and chubby where they should be visibly muscular. This is because everyone’s sex hormones are too high. Yet conversely our fertility is lower.

If, on the other hand, you want to gain muscle weight, you need to increase your calories above your maximum daily threshold. Some, but not all of these extra calories should come from protein. Spare energy is required to build muscle, and protein is not energy. Protein shakes are largely useless (and dangerous) sources of protein, being deficient in the body-building micronutrients found in meat and eggs. The muscles must also be challenged in order to grow. Insulin helps to build muscle, but it is very rare that one does not have quite enough already. In order to prevent fat gain you need to remain in a state of glycogen depletion (without running on empty tanks), because after the glycogen stores are filled a metabolic switch is triggered that encourages fat storage. Glycogen depletion can be encouraged with heavy exercise, or spells of carbohydrate reduction. Too much glycogen depletion results in weight loss. This is why a zig-zagging or cyclical approach is extremely useful.

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Written by alienrobotgirl

9 April, 2006 at 9:30 am

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