In another forum, Laurie Masters, the editor of "The 80/10/10 Diet", sent out a bunch of information about the relationship between fat and diabetes. For those of you suffering from candida, diabetes is the eventual outcome of candida if the source of the candida is not removed.

High-fat diet's causal role in blood-sugar metabolic disorders

Bryan,

Thanks for that great article.

Cherimoya

Love Peace and Happiness

Cool!

Gosia


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I believe it. I've noted high fat in the diet of diabetics I know, that could be a reaction to the decrease in the sugar in their diet. They need to get their calories from somewhere and their sugar intake is limited so they get their calories from fat.

I wish that the article had compared the different kinds of fats, surely not all fats have an equal effect.

No, it's sugar. Sugar and starchy carbohydrates.

Medical people tend to look for fat as the culprit because A) diabetics tend to be overweight, and the association between diabetes and heart disease..... but heart disease, again, is from sugar and starchy carbohydrates, not fat.

I'll read the study now, see what they did.... because diabetes has also been shown to be reversible with a high-fat, low-carb diet.



Edited 1 time(s). Last edit at 01/12/2007 04:12PM by sunshine79.

Raw fat is better than cooked fat but lower raw fat is best of all. In this experiment, the rats on 5% fat did better than the ones on low AGE 35% fat, which did better than the rats of 35% high AGE fat. AGEs = glycotoxins, the more you cook your fats, the more AGEs you get.

Regarding P values in the parentheses below, by convention, if P < 0.05 the result is probably not due to chance. If it's 0.01 or less, it's very unlikely to be due to chance.

You can raise insulin through too much of all three of the macronutrients:

too much carbohydrate -> higher insulin and IGPF-1 reduction
too much fat -> higher insulin/leptin
too much protein -> higher insulin/IGF-1

But cooked fat is the worst in terms of glycotoxins and this represents an added potential disease vector.

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Diabetes. 2005 Aug;54(8):2314-9.

Insulin resistance and type 2 diabetes in high-fat-fed mice are linked to high glycotoxin intake.

Sandu O, Song K, Cai W, Zheng F, Uribarri J, Vlassara H.

Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, One Gustave Levy Place, Box 1640, New York, NY 10029. helen.vlassara@mssm.edu.

Dietary advanced glycosylation end products (AGEs) have been linked to insulin resistance in db/db((++)) mice. To test whether dietary AGEs play a role in the progression of insulin resistance in normal mice fed high-fat diets, normal C57/BL6 mice were randomly assigned to

high-fat diets (35% g fat), either high (HAGE-HF group; 995.4 units/mg AGE) or low (by 2.4-fold LAGE-HF group; 329.6 units/mg AGE) in AGE content for 6 months.

Age-matched C57/BL6 and db/db((++)) mice fed regular diet (5% g fat, 117.4 units/mg AGE) served as controls.

After 6 months, 75% of HAGE-HF mice were diabetic and exhibited higher body weight (P < 0.001), fasting glucose (P < 0.001), insulin (P < 0.001), and serum AGEs (P < 0.01) than control mice,

while none of the LAGE-HF mice were diabetic despite a similar rise in body weight and plasma lipids.

The HAGE-HF group displayed markedly impaired glucose and insulin responses during glucose tolerance tests and euglycemic and hyperglycemic clamps and alt ered pancreatic islet structure and function compared with those of LAGE-HF mice, in which findings resembled those of control mice.

The HAGE-HF group had more visceral fat (by two- and fourfold) and more AGE-modified fat (by two- and fivefold) than LAGE-HF and control mice, respectively.

In the HAGE-HF group, plasma 8-isoprostane was higher (P < 0.01) and adiponectin lower (P < 0.001) than control mice, while in the LAGE-HF group, these were more modestly affected (P < 0.05).

These results demonstrate that the development of insulin resistance and type 2 diabetes during prolonged high-fat feeding are linked to the excess AGEs/advanced lipoxidation end products inherent in fatty diets.

PMID: 16046296 [PubMed - in process]