7 Responses to “Red meat & diabetes?”

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  1. avatar sue says:

    Bit late reading your article and all the comments. My husband’s type 2 diabetes is fully controlled by diet. A lot of red meat and ‘bad’ processed red meat, ie ham, bacon, sausage and so on. Plenty of green vegetables and also some cheese and full fat milk. Limited carbs. No more than 50 or 60 gramms a day.

    The optician finds no signs of diabetes in his eyes, at all and NO signs of the alleged retinal bleed about nine months ago. Was this a hoax by the NHS retinal screening unit. He has highish cholesterol as statins made him very ill indeed. May have contributed to the onset of T2D. However his bloods and liver tests, all of it, are spot on. He is 71 years of age.

  2. avatar Duffy Pratt says:

    “Diabetes is a condition related to blood glucose levels and insulin – either the body’s failure to release insulin to respond to a rise in blood glucose levels (type 1) or because cells are unresponsive (resistant) to insulin released (type 2). The macro nutrient most relevant to diabetes therefore is carbohydrate. Fat has no relevance and the relevance of protein is debatable, but negligible compared to that of carbohydrate.”

    This is almost exactly parallel to saying that cholesterol is a kind of fat, and that therefore, consumption of carbohydrates is irrelevant. Type 2 Diabetes comes from insulin resistance. It’s not clear what causes insulin resistance. But there is at least some evidence that elevated free fatty acids has an impact on it, and also on the functioning of the pancreas. And even that says nothing about diet, because there is not any necessary relationship between free fatty acids and the consumption of fat.

    People have been misinformed for years about the relationship between dietary fat and cholesterol. Assuming that there is no relationship between diabetes and the consumption of fat, simply because fat doesn’t trigger the production of insulin, may be exactly the same sort of mistake. Body chemistry may be more complicated and surprising than you think.

  3. avatar PigeonOrStatue says:

    There is an excellent article by Dr Jack Kruse (a neurosurgeon) linking magnesium deficiency to obesity and diabetes:
    http://jackkruse.com/gnolls-com-opens-the-door-to-obesity-fight

    “Low intracellular Magnesium (Mg) levels that causes the genesis of insulin resistance peripherally. And we have known it for a long time but have done little in clinical medicine to treat it. This is why so few people know about it. Peripheral leptin and insulin resistance (at muscles and fat cells) occurs first for this to happen but the depletion of Mg always predates insulin resistance. So when blood insulin rises, you lose intracellular Mg and this feedback loop makes the peripheral cells even more insulin resistant because we can’t make insulin or let it act properly on target cells. Simultaneously, arteries constrict decreasing blood flow and glucose and insulin to the target tissues. This worsens the Mg deficits going forward. This feedback loop continues daily in all diabetics until the brain becomes leptin resistant (LR) at the hypocretin neurons. Once this occurs, epigenetic switches are thrown in the hypocretin neurons for leptin and insulin signaling at the brain level…….again this occurs because of the poor Mg concentration at these cells and our DNA/RNA then become “hard wired” for a diabetic metabolism at the brain level. This allows for the human brain to become exquisitely sensitive to the dopamine reward of foods. The reward of foods are important when the brain is already LR because this is an outflow only tract of the hypocretin neurons in the hypothalamus. … The real issue is what is happening to the main nucleus in the brain that controls all energy balance as insulin wrecks the periphery and the liver. That nucleus is the hypocretin neurons. … Obesity is a brain disorder. It also fully explains why no macronutrient is the major cause of obesity. And it ironically, shows why carbs appear to be the major macronutient that causes obesity. Its because of insulin’s affect on Mg directly. I fully understand why we have the Kitavins and the Taubian view of obesity. Its called an incomplete out of context story that can be fully understood by biochemistry.

    There are other ways to obesity and LR too……see the omega six pathway with a heavy preponderance of trans- omega six fats.”

  4. avatar PigeonOrStatue says:

    There are too many confounding factors in this observational study for it to of any use.

    BTW 204,157 people studied, of which 13,759 developed T2D is 6.74%. The person-years of follow-up is not relevant. The population is the people not the person years.

  5. avatar Jean says:

    Just a week ago the Daily Mail ran with this article
    http://www.dailymail.co.uk/health/article-2023882/Could-Atkins-diet-help-diabetes-bay.html
    telling us that the Atkins diet would keep diabetes at bay!

  6. avatar fredt says:

    Another self reporting study that shows maybe a change, yet on self reporting engineering studys we know that they are out by 40 to 50% when scaled to a measurable parameter, ie total products sold, so the any self reporting study is somewhere between useless and dangerous. Traffic studies are real fun to analysis, and then project into the future and spend millions on roads based on those projections. Oh well, that is the real world.

    I often see the 30% under reporting of consumption around in food studies, but I think that is lite. We cannot measure the calories in actual food to 20%, so now we guess at weight of portions, especially at home.

    I used a scales for a while, as an ex-obese person, and I suggest the self reporting error is plus 100% some of the time. Atwater said approximate, and we are now better today, in terms of meaningful measurement. The computer generates two decimals points in tests that are plus/minus 20%. OK. And then compare 1.19 and 1.51 % as different risks. Caca el toro.

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