Wed, 15 Oct 2003 22:51:50 -0400 in article <[email hidden]>
Dr. Andrew B. Chung said:Jim Chinnis said:"Dr. Andrew B. Chung, MD/PhD" <[email hidden]> wrote in part:
Quoted message said:Matti Narkia wrote:
Quoted message said:> With all due respect, I'm afraid that you won't qualify for my purposes.
>
>
Then why are you here hanging out in a cardiology newsgroup?
Providing us with great, detailed information and a willingness to put the
science first?
I greatly appreciate Matti Narkia's contributions. They fit well in this
science newsgroup.
Then you'd better advise Matti to believe that ketones are bad rather than find
out from drinking a bottle of it.
Hmmm ... Let's find out how bad a ketogenic diet really is by reading a couple
of citations from the study:
Sharman MJ, Kraemer WJ, Love DM, Avery NG, Gomez AL, Scheett TP, Volek JS.
A ketogenic diet favorably affects serum biomarkers for cardiovascular disease
in normal-weight men.
J Nutr. 2002 Jul;132(7):1879-85.
PMID: 12097663 [PubMed - indexed for MEDLINE]
http://www.nutrition.org/cgi/content/full/132/7/1879 (full text)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12097663&dopt=Abstract
"... There were significant decreases in fasting serum TAG (-33%),
postprandial lipemia after a fat-rich meal (-29%), and fasting serum
insulin concentrations (-34%) after men consumed the ketogenic diet.
Fasting serum total and LDL cholesterol and oxidized LDL were
unaffected and HDL cholesterol tended to increase with the ketogenic
diet (+11.5%; P = 0.066). In subjects with a predominance of small
LDL particles pattern B, there were significant increases in mean and
peak LDL particle diameter and the percentage of LDL-1 after the
ketogenic diet. There were no significant changes in blood lipids in
the control group. To our knowledge this is the first study to
document the effects of a ketogenic diet on fasting and postprandial
CVD biomarkers independent of weight loss. The results suggest that a
short-term ketogenic diet does not have a deleterious effect on CVD
risk profile and may improve the lipid disorders characteristic of
atherogenic dyslipidemia.
[...]
There were changes in the distribution of the LDL subfractions that
would be considered favorable in terms of CVD. We observed general
increases in the mean and peak LDL particle sizes during the
ketogenic diet, which were more pronounced in subjects that exhibited
a pattern B distribution at the start of the study. Individuals with
pattern B exhibit a predominance of small dense lipoproteins and this
distribution is associated with increased risk of CVD (13 ,14 ) and
was recently shown to be the best discriminate factor for the
presence of CVD even when adjusting for other risk factors (21 ).
Although the characterization of pattern B is likely to have a
genetic origin (22 ), changes in diet are known to influence the
distribution of LDL subclasses. For example, switching to a fat-rich
diet (46% vs. 24% of total energy) was shown to increase mean
particle diameter and large LDL-1 mass and decrease small dense LDL-
III cholesterol (28 ), while reductions in dietary fat have the
opposite effect (6 ,7 ). Despite the changes in LDL size, we did not
observe any significant changes in oxidized LDL concentrations.
Collectively these studies indicate that when dietary fat is reduced,
the distribution of LDL moves toward a smaller more dense particle
and when dietary fat is increased the distribution of LDL moves
toward a larger less dense particle. The reason some individuals are
more stable in their LDL subclass distribution in response to changes
in diet is unknown but is likely to reflect complex interactions
between metabolic and genetic traits that are influenced to varying
extents depending on the level of dietary fat (1 ,7 ).
We observed a significant decrease in fasting and postprandial
insulin responses after the ketogenic diet. Decreases in resting
insulin concentrations have been reported in response to 3–4 d of a
low-carbohydrate diet high in fat (34 –38 ). The mechanism for such a
response probably resides in the greater reliance on fat oxidation
induced by dietary carbohydrate restriction (39 ) and subsequent
reduced requirement for insulin to assist in glucose uptake. To our
knowledge, the reduced postprandial insulin response to a fat-rich
meal observed after a ketogenic diet has not been reported in the
literature. According to our estimate of insulin resistance using
fasting levels of glucose and insulin, subjects in this study were
not insulin resistant and there was no adverse effect of the
ketogenic diet on insulin sensitivity. This is in agreement with
other studies showing no adverse effects on glucose metabolism or
insulin resistance after ketogenic diets using the insulin clamp
technique (40 ,41 ).
Numerous studies now suggest that high-carbohydrate diets can raise
TAG levels, create small, dense LDL particles, and reduce HDL
cholesterol (i.e., atherogenic dyslipidemia)—a combination along with
insulin resistance, that has been termed syndrome X (42 ,43 ).
Syndrome X is postulated to be resistance to insulin-mediated glucose
disposal by muscle (44 ), 30% of adult males and 10% to 15% of
postmenopausal women have this particular syndrome X profile, which
is associated with several-fold increase in heart disease risk.
Replacing saturated fat with carbohydrate appears to accentuate
insulin concentrations and the atherogenic dyslipidemia associated
with syndrome X (44 ,45 ). The ketogenic diet in this study resulted
in favorable responses in fasting TAG, postprandial lipemia, HDL-C,
LDL particle size, and insulin levels in healthy normolipidemic men.
Although the duration of the diet was short (6 wk), these data
suggest that a ketogenic diet does not have an adverse effect on
accepted biochemical risk factors for CVD and improves those
associated with syndrome X."
As for high-carbohydrate diets I repeat the following quote from above:
"Numerous studies now suggest that high-carbohydrate diets can raise
TAG levels, create small, dense LDL particles, and reduce HDL
cholesterol (i.e., atherogenic dyslipidemia)—a combination along with
insulin resistance, that has been termed syndrome X (42 ,43 )"
Doesn't sound too good?
See also
Ketogenic Diet Reduces Seizures In Many Children, Hopkins Researchers Find
http://www.sciencedaily.com/releases/2001/10/011001071818.htm
Hemingway C, Freeman JM, Pillas DJ, Pyzik PL.
The ketogenic diet: a 3- to 6-year follow-up of 150 children enrolled
prospectively.
Pediatrics. 2001 Oct;108(4):898-905.
PMID: 11581442 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11581442&dopt=Abstract
"... CONCLUSION: Three to 6 years after initiation, the ketogenic
diet had proven to be effective in the control of difficult-to-
control seizures in children. The diet often allows decrease or
discontinuation of medication. It is more effective than many of the
newer anticonvulsants and is well-tolerated when it is effective."
--
Matti Narkia
