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498 pages, Kindle Edition
First published January 2, 2024
* damages hemoglobin, to abnormal form A1C. p. 270. High levels of hemoglobin A1C (above 6% of hemoglobin pp. 301, 308) predict severity of diabetes, and risk of heart disease, stroke, and premature death. p. 271. (p. 370 defines 5.7% as prediabetic, 6.5% as diabetic.)
* Damaged proteins such as hemoglobin A1C are "advanced glycation end products (AGEs)," so acronymed as they are effects of age, accelerated by high blood sugar. These damaged proteins can knit together with other proteins, "cross-linking" to cause, for example, loss of elasticity in the skin, and stiffening joints, heart, lungs, and arteries, retinas, nerves, and kidneys. pp. 272-273.
* High blood sugar inside cells that can't regulate penetration of glucose into their interiors, can damage the cell's DNA, which can lead to cancer. p. 273.
* High blood sugar oxidizes the protein and fats of LDL in the blood, leading to plaque deposits in blood-vessel walls. p. 274. Saturated fat becomes LDL, so if you eat saturated fat AND carbohydrate, plaques form in your blood vessels. p. 274.
* damages the pancreas, reducing its ability to make insulin. p. 335.
* signals cells to take in glucose as fuel--which they then do unless they've become insulin resistant. p. 167. Insulin resistance leaves blood glucose high despite high levels of blood insulin. p. 263. Insulin injected to lower blood sugar /all/ goes into the blood circulation, so it all signals cells to take in glucose. Insulin from the pancreas first shuts off glucagon production p. 328, then goes to the liver, which releases only half of it into the bloodstream. p. 326.
* signals muscle and liver to store glucose in glycogen form (includes 3 water molecules per glucose molecule).
* signals the liver and fat cells to turn carbohydrates into fat, in the form of triglycerides. pp. 153, 159, 264.
* signals fat cells to sequester fatty acids. They do this at insulin concentrations so tiny other cells can't detect it. pp. 150, 154, 159-160.
* inhibits excretion of salt in the urine, which also retains water and raises blood pressure. p. 266
* enables fatty plaques to form in the walls of blood vessels, damaging them, harming the heart, kidneys, retinas, lower limbs. p. 183.
* causes weight gain, in part by sequestering fats in the fat cells and inhibiting the body's cells from metabolizing fat. Diabetics on sufficient insulin to control blood sugar to 150 to 200 mg/dl (normal range is 70 to 140 mg/dl p. 319), on the American Diabetes Association recommended diet of 50% carbohydrates, 15% protein, 35% fat, gain, on average, 10 pounds in a year, and keep it on, gaining weight even while eating less. pp. 308-309.
* Insulin injected to lower a diabetic's blood sugar, risks lowering it too much, sometimes to coma and death. p. 309. In health, the pancreas releases the counteracting hormone glucagon to keep blood sugar from going too low. Hypoglycemic coma occurs only by insulin injection. p. 326. Insulin inhibits the pancreas from releasing glucagon, which would have signaled the liver to convert glycogen and amino acids to glucose. p. 328. Coma commonly occurs at blood glucose levels around 45 mg/dl. p. 342. However, people adapted to using ketones instead of glucose as fuel have suffered no ill effects of blood glucose as low as 10 mg/dl. pp. 341, 445. [E.J. Drenick et al., 1972, "Resistance to Symptomatic Insulin Reactions after Fasting," The Journal of Clinical Investigation 51, no. 10 (Oct.): 2757-62.] Blood glucose levels above 180 mg/dl prompt the kidneys to excrete glucose in the urine. p. 342.
* raises blood sugar. If you have high blood sugar, you have high glucagon. Even if insulin is zero, we don't become diabetic unless the pancreas is oversecreting glucagon. p. 328. Injecting the hormone somatostatin reduces glucagon secretion, so lowers blood sugar. p. 328.