Here's a post I did to another newsgroup, with a main point being that it is getting some press coverage, despite the flaws:
For example: "Low-carb Diet Reduces Inflammation And Blood Saturated
Fat In Metabolic Syndrome."
Source:http://www.sciencedaily.com/releases/2007/12/071203091236.htm
But when you look at the actual study (or, in this case, the
abstract), you find that the "low fat" diet was 24% fat ! The "low
fat" group also ate much less protein (28% vs. 20%). And we are not
told (in the abstract) what the sources of fat were, which can make
all the difference, since inflammatory molecules are made from fatty
acids, not carbohydrates.
One off the researchers is quoted as saying:
"The real importance of diets that lower carbohydrate content is that
they are grounded in mechanism -- carbohydrates stimulate insulin
secretion which biases fat metabolism towards storage rather than
oxidation. The inflammation results open a new aspect of the
problem..."
First of all, the diet was fed for 12 weeks, so if that's all you want
to live, then fine, but otherwise, it's obviously too short a term for
humans to worry about, whatever the results were. On a diet of 5% or
less fat, coming from fresh coconut oil mostly, the results would be
totally different (though it would have to be much longer than a 12
week study, due to the changeover from AA to Mead acid, which takes at
least approximately 2 years). Secondly, in general, if you have a
great deal of fatty acid oxidation, you are going to have more free
radical damage to vital biomolecules, but again, it would take a lot
more than 12 weeks to see the effects of such damage. Thirdly, there
is an obvious non sequitur in this statement; the person seems to
think there is a necessary connection between insulin secretion and
"inflammation" (leaving aside the fact that chronic inflammation of
unknown origin is only possible with AA in your cells).
Calorie-restriction researcher Dr. Spindler found, for instance, that
his CR animals experience an intense an beneficial insulin spike
during meals. The insulin "comes and goes" quickly, not doing any
damage, not becoming "resistant," and apparently doing an excellent
job of recycling vital biomolecules. What does "inflammation" (what
they actually mean are "markers" of "inflammation") have to do with
this? Note that in their own abstract they state clearly: "Both diets
significantly decreased the concentration of several serum
inflammatory markers..." And what were the subjects' diets like
before the study? All we are told in the abstract is that these
people were: "Overweight men and women with atherogenic
dyslipidemia." Thus, they choose people with obvious dietary issues
and fed them low calorie diets (1504 or 1478 kcal).
I would characterize this "study" as a near total "mess," and more of
a study of calorie restriction (many of the subjects were likely
consuming at least 3000 kcal per day before the study) than anything
else, but again, the time period studied is too short term to know
what the long term effects would be from either of these "CR" diets.
The abstract of the study is:
Abnormal distribution of plasma fatty acids and increased inflammation
are prominent features of metabolic syndrome. We tested whether these
components of metabolic syndrome, like dyslipidemia and glycemia, are
responsive to carbohydrate restriction. Overweight men and women with
atherogenic dyslipidemia consumed ad libitum diets very low in
carbohydrate (VLCKD) (1504 kcal:%CHO:fat:protein = 12:59:28) or low in
fat (LFD) (1478 kcal:%CHO:fat:protein = 56:24:20) for 12 weeks. In
comparison to the LFD, the VLCKD resulted in an increased proportion
of serum total n-6 PUFA, mainly attributed to a marked increase in
arachidonate (20:4n-6), while its biosynthetic metabolic intermediates
were decreased. The n-6/n-3 and arachidonic/eicosapentaenoic acid
ratio also increased sharply. Total saturated fatty acids and 16:1n-7
were consistently decreased following the VLCKD. Both diets
significantly decreased the concentration of several serum
inflammatory markers, but there was an overall greater anti-
inflammatory effect associated with the VLCKD, as evidenced by greater
decreases in TNF-alpha, IL-6, IL-8, MCP-1, E-selectin, I-CAM, and
PAI-1. Increased 20:4n-6 and the ratios of 20:4n-6/20:5n-3 and n-6/n-3
are commonly viewed as pro-inflammatory, but unexpectedly were
consistently inversely associated with responses in inflammatory
proteins. In summary, a very low carbohydrate diet resulted in
profound alterations in fatty acid composition and reduced
inflammation compared to a low fat diet.
Lipids. 2007 Nov 29 [Epub ahead of print].
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView... |
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