Vlassara finally comes clean; High fat diet = High AGE diet

[Guest guest]

Ha, Vlassara has painted herself into a corner now. The chief proponent of the "AGE" or "glycotoxin" pespective on nutrition, she has now determined that a "high fat" diet featuring a lot of fat cooked at 120 degrees celsius for 30 minutes is considerably more toxic to normal rats eating a "high fat" diet than food that does not receive such treatment.

The rats that performed the best in her experiment? The "controls", of course, with a diet featuring all of 5% fat.

Looks like she is now going to start turning into another "low fat" advocate, and I notice that she incorporates more discussion of "ALEs" in her discussion, which are "advanced lipid peroxidation" products.

The one interesting thing from the investigation that needs to be corroborated is the observation that cooking fats, and then feeding massive amounts to normal rats, causes them to "melt down". Are humans this sensitive? Perhaps, and if that is the case, this could have very profound ramifications.

So, is the best way to avoid this effect is to go "Ornish"?

At the very least, it would appear that cold fats are good fats.

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

Related Articles,

Links

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@....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 altered 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]

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http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstract & list_uids=16046296

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