monty1945
Sat, Nov-03-07, 17:16
Did you hear about it on CNN TV news today? I did. The claim
is that if you eat less sugar, your skin will age well. First
of all, is there any evidence that this is accurate in the
context of a diet that the vast majority of people would be
willing to eat? And then there is the molecular level
evidence. Firstly, let's take a look at this notion in the
words of a "scientist:"
QUOTE: Protein degradation and malfunction is a major cause of
ageing and can be the result of attacks on proteins by other
molecules.
One of these processes, called glycation, involves the
spontaneous attack by sugars on proteins... UNQUOTE.
So here we have an explicit statement of this claim (and
anything you hear today is "old news").
Source:
http://www.sciencedaily.com/releases/2007/04/070402102354.htm
The problem, as is so often the case, is that this claim is
not consistent with the molecular level evidence, for example:
THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 271, No. 17, Issue of
April 26, pp. 9982-9986, 1996 =A9 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.
My great grandparents, on a low PUFA diet, had very healthy,
tight skin, even in their 90s. This is not true of subsequent
generations, which consume a PUFA-rich diet. Once again, a
substance (sugar) that even many "primitive peoples" on a
"healthy, traditional" diet enjoyed (such as the Okinawans
love of sugar cane) is being demonized instead of the one
substance that is clearly to blame. In fact, in the recent CNN
special, "America's Killer Diet," a chart was shown that
illustrated how PUFA consumption has increased dramatically
since the early 1960s. The experiment I am doing now (on
myself) is to eat various kinds of "junk food," but only items
that are very low in fat or very low in unsaturated fat (and
all containing no or very small amounts of cholesterol, due to
the possibly high oxidized cholesterol content). So far, there
are no problems of any kind to report, despite the very high
sugar content of my present diet (I am still the only one
among my "blood" relatives who is not overweight, and I am not
afflicted with any "chronic" disease).
is that if you eat less sugar, your skin will age well. First
of all, is there any evidence that this is accurate in the
context of a diet that the vast majority of people would be
willing to eat? And then there is the molecular level
evidence. Firstly, let's take a look at this notion in the
words of a "scientist:"
QUOTE: Protein degradation and malfunction is a major cause of
ageing and can be the result of attacks on proteins by other
molecules.
One of these processes, called glycation, involves the
spontaneous attack by sugars on proteins... UNQUOTE.
So here we have an explicit statement of this claim (and
anything you hear today is "old news").
Source:
http://www.sciencedaily.com/releases/2007/04/070402102354.htm
The problem, as is so often the case, is that this claim is
not consistent with the molecular level evidence, for example:
THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 271, No. 17, Issue of
April 26, pp. 9982-9986, 1996 =A9 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.
My great grandparents, on a low PUFA diet, had very healthy,
tight skin, even in their 90s. This is not true of subsequent
generations, which consume a PUFA-rich diet. Once again, a
substance (sugar) that even many "primitive peoples" on a
"healthy, traditional" diet enjoyed (such as the Okinawans
love of sugar cane) is being demonized instead of the one
substance that is clearly to blame. In fact, in the recent CNN
special, "America's Killer Diet," a chart was shown that
illustrated how PUFA consumption has increased dramatically
since the early 1960s. The experiment I am doing now (on
myself) is to eat various kinds of "junk food," but only items
that are very low in fat or very low in unsaturated fat (and
all containing no or very small amounts of cholesterol, due to
the possibly high oxidized cholesterol content). So far, there
are no problems of any kind to report, despite the very high
sugar content of my present diet (I am still the only one
among my "blood" relatives who is not overweight, and I am not
afflicted with any "chronic" disease).