On another newsgroup, I tried to point out to someone asking about "glycation" that this was a problem only if you have the wrong fatty acids in your body (and not enough antioxidant-rich foods). My first post was:
QUOTE:
Glycation is certainly a big problem, but remember that when it occurs
in your body, to vital biomolecules, you are in trouble once it passes
a certain threshold. What happens to the food before it gets into your
body may just make it undigestible, which is less of a problem. The
evidence suggests that it is the unsaturated fatty acids, especially
the omega 6, arachidonic acid, that causes a great deal of damage
(which is why I only consume trace amounts of polyunsaturated fatty
acids in my diet).
For example, see:
THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 271, No. 17, Issue of April
26, pp. 9982-9986, 1996
© 1996 by The American Society for Biochemistry and Molecular Biology,
Inc. Printed in U.S.A.
"The Advanced Glycation End Product, Ne-(Carboxymethyl)lysine, Is
a Product of both Lipid Peroxidation and Glycoxidation Reactions*"
QUOTE: "CML is also formed during
metal-catalyzed oxidation of polyunsaturated fatty
acids in the presence of protein... We also report that CML, heretofore
described as a gly-coxidation
product, is formed during peroxidation of polyunsat-urated
fatty acids (PUFA) in the presence of ribonuclease A (RNase), a protein
that contains neither enzymatically nor
nonenzymatically attached carbohydrate... oxidation of fatty acid is
clearly a more efficient source of CML, despite the fact that the
glucose is in solution throughout the course of the experiment,
while the PUFA are only progressively solubilized. Further,
after 6 days of incubation, a large fraction of the arachidonate
was oxidized based on its solubilization in the aqueous phase,
while 2% of the glucose is oxidized during this same time
period... The observations described above indicate that CML,
previ-ously
described as a glycoxidation product or AGE, may, in fact,
be derived from PUFA during lipid peroxidation reactions. UNQUOTE.
UNQUOTE.
After this followed several other responses, and basically they ignored my point and kept talking about issues unrelated to the role of fatty acids. I then posted the following:
QUOTE:
Seems like some of you are "seeing ghosts." It is the lipid peroxidation that is causing the glycation problems (in vivo). Here is yet another study that makes this point:
Diabetes, Obesity and Metabolism
Volume 7 Page 448 - July 2005
doi:10.1111/j.1463-1326.2004.00387.x
Volume 7 Issue 4
Short Report
High-fat diet enhances visceral advanced glycation end products, nuclear O-Glc-Nac modification, p38 mitogen-activated protein kinase activation and apoptosis
S.-Y. Li1, Y. Liu1, V. K. Sigmon1, A. McCort1 and J. Ren1*
High-fat diet intake often leads to obesity, insulin resistance and hypertension, which present a common and detrimental health problem. However, precise mechanism underlying tissue damage due to high-fat diet-induced obesity has not been carefully elucidated. The present study was designed to examine the effect of high-fat diet intake on visceral advanced glycation end products (AGEs) formation, nuclear O-Glc-NAc modification and apoptosis in heart, liver and kidney. Adult male Sprague-Dawley weight-matched rats were fed for 12 weeks with a high-fat diet (45% kcal from fat) or an isocaloric low-fat diet (10% kcal from fat). High-fat diet feeding significantly elevated body weight. Blood pressure and heart rate were comparable between the two rat groups. Competitive enzyme-linked immunosorbent assay showed significantly elevated serum AGE levels, visceral AGE formation, caspase-3 activation and cytoplasmic DNA fragmentation in heart and liver but not kidney samples of high-fat diet fed rats compared with those from low-fat diet fed group. Western blot analysis further revealed that high-fat diet feeding induced overt nuclear O-Glc-NAc modification and p38 mitogen-activated protein kinase activation in heart and liver although not in kidney samples of the high-fat diet-fed rats. Collectively, our results indicated that high-fat diet intake is associated with obesity accompanied by elevated serum and visceral AGEs, visceral post-translational nuclear O-Glc-NAcylated modification and apoptosis, which may contribute to high-fat diet-induced tissue damage.
Now, if they were more knowledgable they would do another experiment, this time using fresh coconut oil, and giving the animals a "high fat" diet. What they would find is that this diet is not a problem at all, but because they are assuming that "saturated fat is bad," they apparently don't even consider this possibility, and this is why much "science" today is unscientific. You must control for all possibly relevant factors in order to follow the scientific method.
UNQUOTE. |
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