Re: Coconut Oil And Tumor Growth
- From: Mark Thorson <nospam@xxxxxxxxx>
- Date: Thu, 06 Sep 2007 16:13:18 -0700
monty1945@xxxxxxxxx wrote:
"I've posted abstracts to several studies by
scientists that find horrible effects on
coconut oil diets."
Oh, really? Where is this study?
Here they are:
This study blames the MUCH higher rate of
cardiovascular mortality in Singapore as compared
to Hong Kong on consumption of saturated fats
including coconut oil.
Eur J Epidemiol. 2001;17(5):469-77.
Differences in all-cause, cardiovascular and
cancer mortality between Hong Kong and Singapore:
role of nutrition.
Zhang J, Kesteloot H.
Department of Epidemiology, School of Public
Health, Catholic University of Leuven, Belgium.
BACKGROUND: The majority of inhabitants in Hong Kong
and Singapore are ethnic Chinese, but all-cause and
cardiovascular mortality rates in these two regions
are markedly different. This study describes
differences in the magnitude and trends in mortality
and attempts to explain these differences.
METHODS: Data of mortality rates in 1963-1965 and
1993-1995 in the age class of 45-74 years, dietary
habits and other factors were compared between
Hong Kong and Singapore using Japan, Spain and the USA
as reference countries. Mortality and food consumption
data were obtained from WHO and FAO, respectively.
RESULTS: Large differences in all-cause and cardiovascular
mortality exist between Hong Kong and Singapore. The
difference in total cancer mortality was less consistent
and smaller. The most pronounced finding was that ischemic
heart disease mortality in 1993-1995 was 2.98 and 3.14 times
higher in Singapore than in Hong Kong in men and women,
respectively. Of the five countries considered, Singapore
has the highest all-cause mortality in both sexes in the
period of 1960-1995. The ratio of animal to vegetal fat
was higher in Singapore (2.24) than in Hong Kong (1.08).
Singapore had higher serum concentrations of total
cholesterol and low-density lipoprotein cholesterol
than Hong Kong, but the opposite result was observed
for high-density lipoprotein cholesterol.
CONCLUSIONS: There are striking differences in all-cause
and cardiovascular mortality between Hong Kong and
Singapore. These differences can be most reasonably and
plausibly explained by their differences in dietary
habits, for example, a higher consumption of coconut and
palm oil, mainly containing saturated fat, in Singapore.
Coconut oil raises cholesterol more than
beef fat!
Am J Clin Nutr. 1985 Aug;42(2):190-7.
Plasma lipid and lipoprotein response of humans
to beef fat, coconut oil and safflower oil.
Reiser R, Probstfield JL, Silvers A, Scott LW,
Shorney ML, Wood RD, O'Brien BC, Gotto AM Jr,
Insull W Jr.
This study's purpose was to evaluate the fasting
human plasma lipid and lipoprotein responses to
dietary beef fat (BF) by comparison with coconut
oil (CO) and safflower oil (SO), fats customarily
classified as saturated and polyunsaturated.
Nineteen free-living normolipidemic men aged
25.6 +/- 3.5 yr consumed centrally-prepared
lunches and dinners of common foods having 35%
fat calories, 60% of which was the test fat.
The test fats were isocalorically substituted,
and each fed for five weeks in random sequences
with intervening five weeks of habitual diets.
Plasma total cholesterol (TC), high-density
lipoprotein cholesterol (HDL-C), and low-density
lipoprotein cholesterol (LDL-C) concentrations
among individuals follows the same relative rank
regardless of diet. Triglycerides (TG)
concentrations among individuals also maintain
their relative rank regardless of diet but in
a different order from that of the cholesterols.
Plasma TC, HDL-C, and LDL-C responses to BF were
significantly lower and TG higher than to CO.
As compared to SO, BF produced equivalent levels
of TG, HDL-C, and LDL-C and marginally higher TC.
Thus, the customary consideration of BF as
"saturated" and grouping it with CO appears
unwarranted.
This study in a rat model for myocardial
infarction (induced with a synthetic hormone)
found omega-3 fatty acids to be protective
against lipid peroxidation and cardiovascular
death, while coconut oil raised indicators of
damage to the heart muscle.
J Nutr Biochem. 1999 Jun;10(6):338-44.
Effect of saturated, omega-3 and omega-6
polyunsaturated fatty acids on myocardial
infarction.
Nageswari K, Banerjee R, Menon VP.
School of Biomedical Engineering, Indian
Institute of Technology, Bombay, India.
Dietary fatty acids have cholesterol lowering,
antiatherogenic, and antiarrhythmic properties
that decrease the risk of myocardial infarction (MI).
This study was designed to study the effects of
various oils rich in either polyunsaturated
(omega-3 or omega-6) fatty acids (PUFA) or
saturated fatty acids (SFA) on the severity of
experimentally induced MI. Male albino Sprague-Dawley
rats (100-150 g; n = 20) were fed diets enriched with
fish oil (omega-3 PUFA), peanut oil (omega-6 PUFA),
or coconut oil (SFA) for 60 days. Experimental MI was
induced with isoproterenol. Mortality rates; serum
enzymes aspartate amino transferase; alanine amino
transferase; creatine phosphokinase (CPK); lipid
profiles in serum, myocardium, and aorta; peroxide
levels in heart and aorta; activities of catalase and
superoxide dismutase; and levels of glutathione were
measured. The results demonstrated that mortality rate,
CPK levels, myocardial lipid peroxides, and glutathione
levels were decreased in the omega-3 PUFA treated group.
Maximum increase in parameters indicative of myocardial
damage was seen in the coconut oil group. These findings
suggest that dietary omega-3 PUFA offers maximum
protection in experimentally induced MI in comparison
to omega-6 PUFA and SFA enriched diets. SFA was found
to have the least protective effect.
And what about the low incidence of disease amongst
peoples who eat huge amounts of coconut?
That's not true. See this:
http://cat.inist.fr/?aModele=afficheN&cpsidt=15328753
The recent estimates for mortality from cardio and
cerebrovascular diseases (CVD) for Sri Lanka-524
deaths per 100 000-is higher than that observed in
many Western economies. However, neither an excessive
total fat intake nor an increase in the more traditional
plasma lipid markers, total and LDL cholesterol (LDL-c)
levels may fully explain the increased vulnerability to
CVD in this population. The average total fat intake of
Sri Lankans is 25 percent of total energy (en%) and the
reported total and LDL-c values are 4.9 and 2.5 mmol/l,
respectively. With regard to the type of dietary fatty
acids, the ratio of saturated/polyunsaturated fatty
acids (PUFAs) in the average Sri Lankan diet is 9/l as
compared with the current recommended ratio of <1/1.
In spite of an adequate total fat intake (25 en%), the
relatively low intake of PUFAs in association with a
high carbohydrate diet (65 en%), appear to be resulting
in similar metabolic outcomes to those of very low fat
diets (VLFD, < 15 en% from fat), as reflected by high
triglycerides and low HDL levels. Metabolic abnormalities
including elevated postprandial hyperlipidemia, more
atherogenic lipoprotein particles, hyperglycemia with
resultant hyperinsulinemia and increased oxidative stress
are likely to be more relevant in such settings. The
application of novel biomarkers for example, lipoprotein
measurements in the postprandial state. LDL particle
size, estimates of endothelial dysfunction, soluble
markers of inflammation and coagulability status may
provide further insight into cardiovascular disease
states in populations where the dietary matrix
represents high intakes of highly digestible
carbohydrates and saturated fat.
And why I am in great health after years on a diet
that I purposely designed to be very rich in dietary
SFAs and very low in PUFAs?
How do you know that? You could have significant
occlusion of your arteries and not know it, until
your first heart attack.
How did I go from being on the verge of death,
at less than 100 pounds (standing at 5'9" tall),
with severe osteoporosis and all kinds of other
problems, on such a tremendously dangerous diet?
Coconut oil will certainly put some fat on you.
I don't see why it would be related to osteoporosis.
Maybe your previous diet was even more preposterous
than the one you're on now. Was it macrobiotic?
Now it's time for you to take the red nose off
and look at the actual evidence.
When you're asked to provide data and you can't
do it, you resort to insults. That is so typical
of people like you, who peddle fringe nutritional
theories.
There is plenty on my site and I explain exactly
what it means, down to the molecular level.
If you are too lazy to read it, that is your
problem.
Go ahead and post your data here, if you have any.
If you just wave your hands and say there's data
behind the curtain, don't expect anybody to
believe you.
Could you please post the abstract for the best
experimental study in animals or humans that
shows a benefit for coconut oil over unsaturated
fats? I've asked you before, but for some
obscure reason you haven't done it. Is it
because you have no such data?
And why are you not taking me up on my
experimental offer?
Because it's totally bogus. Your "experimental
design" is laughable. You don't propose any
kind of pathological examination, and you don't
propose an analytical methodology for reaching
conclusions from the data. Strictly speaking,
what you are proposing is not an experiment.
It is a stunt. And you are using this proposed
stunt to avoid posting any data which would back
up your absurd nutritional theory.
It is directly on point and will demonstrate
clearly that you are correct, if in fact you
are.
No, it wouldn't. A sound experimental design
could do that, but you haven't proposed one.
.
- References:
- Coconut Oil And Tumor Growth
- From: Mark Thorson
- Re: Coconut Oil And Tumor Growth
- From: monty1945
- Re: Coconut Oil And Tumor Growth
- From: Mark Thorson
- Re: Coconut Oil And Tumor Growth
- From: monty1945
- Re: Coconut Oil And Tumor Growth
- From: Mark Thorson
- Re: Coconut Oil And Tumor Growth
- From: monty1945
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