From: gts (gts_2000@yahoo.com)
Date: Tue May 13 2003 - 12:45:40 MDT
This is the abstract of the research article that Brian mentioned in the
thread called "eating glycotoxins." This research is strong evidence that
humans are not yet adapted to the glycoproteins (AGE's) that are formed when
meat is cooked.
It is also good indirect evidence that humans are not yet adapted to
non-paleolithic foods in general: if we are not yet adapted to AGE's from
cooked meats even after ~50 to ~100 thousand years of camp barbecues then
it's difficult to see how we could be adapted to eating foods that appeared
in the diet only ~12,000 years ago.
ABSTRACT:
Inflammatory mediators are induced by dietary glycotoxins, a major risk
factor for diabetic angiopathy
Helen Vlassara*,, Weijing Cai*, Jill Crandall*,, Teresia Goldberg*, Robert
Oberstein, Veronique Dardaine*, Melpomeni Peppa*, and Elliot J. Rayfield
* Division of Experimental Diabetes and Aging, Department of Geriatrics, and
Division of Endocrinology, Department of Medicine, Mount Sinai School of
Medicine, New York, NY 10029
Edited by Jan L. Breslow, The Rockefeller University, New York, NY, and
approved October 7, 2002 (received for review July 8, 2002)
Diet is a major environmental source of proinflammatory AGEs (heat-generated
advanced glycation end products); its impact in humans remains unclear. We
explored the effects of two equivalent diets, one regular (high AGE, H-AGE)
and the other with 5-fold lower AGE (L-AGE) content on inflammatory
mediators of 24 diabetic subjects: 11 in a 2-week crossover and 13 in a
6-week study. After 2 weeks on H-AGE, serum AGEs increased by 64.5% (P =
0.02) and on L-AGE decreased by 30% (P = 0.02). The mononuclear cell tumor
necrosis factor-/-actin mRNA ratio was 1.4 ± 0.5 on H-AGE and 0.9 ± 0.5 on
L-AGE (P = 0.05), whereas serum vascular adhesion molecule-1 was 1,108 ± 429
and 698 ± 347 ng/ml (P = 0.01) on L- and H-AGE, respectively. After 6 weeks,
peripheral blood mononuclear cell tumor necrosis factor- rose by 86.3% (P =
0.006) and declined by 20% (P, not significant) on H- or L-AGE diet,
respectively; C-reactive protein increased by 35% on H-AGE and decreased by
20% on L-AGE (P = 0.014), and vascular adhesion molecule-1 declined by 20%
on L-AGE (P < 0.01) and increased by 4% on H-AGE. Serum AGEs were increased
by 28.2% on H-AGE (P = 0.06) and reduced by 40% on L-AGE (P = 0.02), whereas
AGE low density lipoprotein was increased by 32% on H-AGE and reduced by 33%
on L-AGE diet (P < 0.05). Thus in diabetes, environmental (dietary) AGEs
promote inflammatory mediators, leading to tissue injury. Restriction of
dietary AGEs suppresses these effects.
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