Coconut oil study by Nobel Prize winner Houssay.

[monty1945]

Many people don't know that these older, on-point studies
even exist:

Science 23 May 1947: Vol. 105. no. 2734, pp. 548 - 549 DOI:
10.1126/science.105.2734.548

"Experimental Diabetes and Diet."

B=2E A. HOUSSAY 1 and C. MART=CDNEZ 1

1 Instituto de Biologia y Medicina Experimental, Buenos
Aires, Argentina

In the experiments described the following observations have
been made:

(1) The toxic and diabetogenic action of alloxan increases in
rats fed a low protein diet and even more so in the case
of a high lard or ox fat diet.

(2) The action of these fat diets was corrected by the
addition of methionine, thiouracil, or coconut oil, but
there was no modification either by addition of choline or
sulfonamide or by increase in the protein proportion.

(3) In rats fed other high fat diets (olive oil, butter) the
actions of alloxan were not modified, but there was a
slight diminution when high oleomargarine or corn oil
diets were fed. However, complete protection was observed
when a high coconut oil diet was administered.

(4) The unfavorable effect of the high lard diet was observed
also on the initiation and evolution of diabetes due to
subtotal pancreatectomy. Contrarily, feeding a high
protein diet and especially treatment with thiouracil had
a favorable effect.

(5) Diabetes appeared first in subtotal pancreatectomized rats
which were overfed, then in those which ate ad libitum,
and finally in those which were underfed. Diabetes
appeared in rats fed a single meal before it did in those
eating the same amount of food divided into three meals.

[keystone]

As mentioned several times before, when researchers want to
induce one strain of rats to have diabetes for their research
they feed a standard high fat diet. 60 percent of the diet is
fat and the fat is 100 percent coconut oil.

[monty1945]

Your statement is unclear, unlilke the one from the study
that states:

"...complete protection was observed when a high coconut oil
diet was administered..."

Now if you have a study you think is relevant in this context,
go ahead and cite it, and I will take a close look at it.

[monty1945]

I have been looking for such studies for years, and all I find
are studies that implicate "oxidative stress" and arachidonic
acid metabolites. Coconut oil (assuming it is fresh) resists
oxidative stress much better than other fat sources. AA
metabolites could not be generated in an organism that ate
coconut oil as its only major fat source. I have seen studies
were "saturated fat" is used, but that usually turns out to be
lard, not coconut oil. However, if you refuse to cite one
study, I cannot reconize you as a serious scholar in this
context. It sounds like you want science to be more like a
religion, whereas I examine evidence, and am not interested in
what people claim who cannot cite on-point evidence or
molecular-level mechanisms.

[monty1945]

I will cite a study that you may be thinking of when you made
your claim:

Diabetes Res. 1990 Jan;13(1):43-7. "Glucose turnover in BHE
rats fed EFA deficient hydrogenated coconut oil." Kim MJ, Pan
JS, Berdanier CD. Department of Foods and Nutrition,
University of Georgia, Athens 30602.

The effects of feeding corn or hydrogenated coconut oil on
various parameters of glucose metabolism in prediabetic BHE
rats was studied. Weanling rats were fed a 6% fat-64% sucrose
diet. At seven weeks of age, the rats were weight matched
within diet treatments. Half of the rats were injected with
6(3)H/U14C glucose while their weight matched counterparts
were injected with U14C alanine and 3HOH. Diet had no effect
on glucose mass, glucose space, hepatic glycogen or blood
glucose levels. However, diet did affect other parameters. HCO
fed rats had higher fractional irreversible glucose turnover
rates, fractional glucose carbon recycling, hepatic fatty acid
synthesis rates, adipose fatty acid synthesis rate, lower
muscle glycogen and lower rates of incorporation of glucose
into muscle glycogen than corn oil fed rats. These differences
in glucose flux explain the maintenance of glucose homeostasis
in these prediabetic coconut oil fed rats in the face of
increased fatty acid and glucose synthesis.

What happens in these kinds of experiments is that the animals
have been fed a "normal" diet, which means arachidonic acid
incorporation in the animals' cells. When fed the HCO diet, AA
is released, and for a while there is more oxidative stress
and AA metabolites, unless the diet is supplemented correctly
with antioxidant-rich foods. However, if the diet was done in
a way consistent with the scientific method, there would be 2
more groups, and these would be animals which incorporated the
natural Mead acid instead of AA in the animals' cells. But ask
yourself a very basic question,. which is why do hunans a very
coconut-rich diets have the lowest diabetes rates in the
world? Do a google search for coconut oil diabetes and read
through some of the evidence you find there.

[monty1945]

The person who responded to my original post did not make a
distinction between hydrogenated and fresh coconut oil,
however, I'd like to see an experiment done correctly with
both forms of coconut oil - there might not be much of a
difference. I suspect both are a lot healthier than oils like
corn, fish, soy, safflower, canola, etc., but I would allow
the animals to live normals lives and see which group lives
longer, rather than looking for "markers."

I found another study that is interesting in the context of
this thread:

QUOTE: 2. Rats were divided into three groups: (i) a
control group fed standard rat laboratory chow; (ii) a lard
group fed a high-fat diet containing 20% lard; and (iii) a
fish oil group fed a high-fat diet containing 20% fish oil
for 14 weeks.

3=2E Systolic blood pressure and fasting blood glucose were
markedly increased in the lard group, whereas in the fish oil
group they were only transiently increased at the beginning
and decreased to levels seen in the control group.

4=2E Intraperitoneal glucose tolerance test demonstrated that
fish oil reversed the impairment of glucose disposal found in
the lard group. However, plasma insulin levels were raised
transiently at 30 min in the fish oil group compared with the
control group.

5=2E Insulin secretion from pancreatic islets stimulated with
glucose in vitro was also enhanced by fish oil.

6=2E These results lead us to conclude that fish oil improves
glucose tolerance by enhancing insulin secretion from
pancreatic =CE=B2-cells. UNQUOTE.

SOURCE: Clinical and Experimental Pharmacology and Physiology
Volume 27 Issue 5-6 Page 412 - May/June 2000

On the internet:
http://www.blackwell-synergy.com/doi/abs/10.1046/j.1440-1=
681.2000.03244.x?cookieSet=3D1&journalCode=3Dcep

Note that they used lard for one group, even though it is only
about 40% saturated, unlike coconut, which is about 92%
saturated, and so it's not clear why they did this, though
they don't say here what the control diet was, exactly.

[Pramesh Ru]

monty1945@lycos.com wrote:
> I will cite a study that you may be thinking of when you
> made your claim:
>
> Diabetes Res. 1990 Jan;13(1):43-7. "Glucose turnover in BHE
> rats fed EFA deficient hydrogenated coconut oil." Kim MJ,
> Pan JS, Berdanier CD. Department of Foods and Nutrition,
> University of Georgia, Athens 30602.

How could there be any benefit whatsoever from "hydrogenated"
coconut oil? Go for the virgin stuff.

> The effects of feeding corn or hydrogenated coconut oil on
> various parameters of glucose metabolism in prediabetic BHE
> rats was studied. Weanling rats were fed a 6% fat-64%
> sucrose diet. At seven weeks of age, the rats were weight
> matched within diet treatments. Half of the rats were
> injected with 6(3)H/U14C glucose while their weight matched
> counterparts were injected with U14C alanine and 3HOH. Diet
> had no effect on glucose mass, glucose space, hepatic
> glycogen or blood glucose levels. However, diet did affect
> other parameters. HCO fed rats had higher fractional
> irreversible glucose turnover rates, fractional glucose
> carbon recycling, hepatic fatty acid synthesis rates,
> adipose fatty acid synthesis rate, lower muscle glycogen and
> lower rates of incorporation of glucose into muscle glycogen
> than corn oil fed rats. These differences in glucose flux
> explain the maintenance of glucose homeostasis in these
> prediabetic coconut oil fed rats in the face of increased
> fatty acid and glucose synthesis.
>
>
> What happens in these kinds of experiments is that the
> animals have been fed a "normal" diet, which means
> arachidonic acid incorporation in the animals' cells. When
> fed the HCO diet, AA is released, and for a while there is
> more oxidative stress and AA metabolites, unless the diet is
> supplemented correctly with antioxidant-rich foods. However,
> if the diet was done in a way consistent with the scientific
> method, there would be 2 more groups, and these would be
> animals which incorporated the natural Mead acid instead of
> AA in the animals' cells. But ask yourself a very basic
> question,. which is why do hunans a very coconut-rich diets
> have the lowest diabetes rates in the world? Do a google
> search for coconut oil diabetes and read through some of the
> evidence you find there.
>
>

--

Pramesh Rutajit - p297tongue6221@newsguy.com - Remove
tongue to reply.

[Mattlb]

On May 8, 10:31 pm, monty1...@lycos.com wrote:
> Many people don't know that these older, on-point studies
> even exist:

What "point" is it "on"? It's a study in which a toxic
oxidizing agent (alloxan) is injected into rats to destroy
their pancreatic beta cells and give them diabetes.

> Science 23 May 1947: Vol. 105. no. 2734, pp. 548 - 549 DOI:
> 10.1126/science.105.2734.548

> (2) The action of these fat diets was corrected by the
> addition of methionine, thiouracil, or coconut oil,

So several things help reduce death in the week following
diabetes induction and no mechanisms are suggested. Also,
you've picked a study which highlights why rodents aren't
always good models as alloxan isn't toxic to beta cells
in humans.

In conclusion, therefore, in rats which have been made
diabetic by a chemical treatment coconut oil helps survival,
but it may or may not be due to the presence of something in
the coconut oil, or the absence of something present in
other oils.

Note as well that they didn't try fish oil.

Again, what was the point you were so pleased about?

MattLB

[keystone]

>I have been looking for such studies for years, and all I
>find are studies that implicate "oxidative stress" and
>arachidonic acid metabolites. Coconut oil (assuming it is
>fresh) resists oxidative stress much better than other fat
>sources. AA metabolites could not be generated in an organism
>that ate coconut oil as its only major fat source. I have
>seen studies were "saturated fat" is used, but that usually
>turns out to be lard, not coconut oil. However, if you refuse
>to cite one study, I cannot reconize you as a serious scholar
>in this context. It sounds like you want science to be more
>like a religion, whereas I examine evidence, and am not
>interested in what people claim who cannot cite on-point
>evidence or molecular-level mechanisms.

You must read carefully, we are talking about a standard
accepted research practice. When one wants to study some
question in diabetes using rodents as the model then one must
first make them diabetic before starting the research. There
are a number of ways used to do this. One is the high fat
approach which creates rodents with diabetes very much like
type 2 human diabetes.

One rodent chow company has a standard diet with 60 percent
fat which some researchers use to create the diabetes. That 60
percent fat is 100 percent coconut oil. Others use lard as in
one example also in this thread.

That is the reality of the situation in rodent diabetes
research models. Any conclusions drawn from that reality as to
coconut oil or any saturated fat is left to the reader's own
imagination. In diabetes research in general saturated fat is
implicated in the onset of diabetes for those with the genetic
disposition. Some have described diabetes as a disordr of fat
metabolism.

Thus I'm not mentioning any studies but a standard practice
where coconut oil is the only fat source.

[Mattlb]

On May 10, 5:07 am, monty1...@lycos.com wrote:
> I found another study that is interesting in the context of
> this thread:
>
> QUOTE: 2. Rats were divided into three groups: (i) a
> control group fed standard rat laboratory chow; (ii) a lard
> group fed a high-fat diet containing 20% lard; and (iii) a
> fish oil group fed a high-fat diet containing 20% fish oil
> for 14 weeks.

> 6. These results lead us to conclude that fish oil improves
> glucose tolerance by enhancing insulin secretion from
> pancreatic =CE=B2-cells. UNQUOTE.

So you're quoting a study that says fish oil is good. Are you
feeling alright?

> Note that they used lard for one group, even though it is
> only about 40% saturated, unlike coconut, which is about 92%
> saturated, and so it's not clear why they did this,

Because it's a non-fish animal fat. The exact composition is
not so important as the fact that it's not rich in EPA/DHA
like fish oil is (plus, the taste of coconut oil is known to
put some animals off).

> though they don't say here what the control diet was,
> exactly.

Standard rat pellets, that contain less than 20% fat.

MattLB

[Pramesh Ru]

keystone@mark.com wrote:
>> I have been looking for such studies for years, and all I
>> find are studies that implicate "oxidative stress" and
>> arachidonic acid metabolites. Coconut oil (assuming it is
>> fresh) resists oxidative stress much better than other fat
>> sources. AA metabolites could not be generated in an
>> organism that ate coconut oil as its only major fat source.
>> I have seen studies were "saturated fat" is used, but that
>> usually turns out to be lard, not coconut oil. However, if
>> you refuse to cite one study, I cannot reconize you as a
>> serious scholar in this context. It sounds like you want
>> science to be more like a religion, whereas I examine
>> evidence, and am not interested in what people claim who
>> cannot cite on-point evidence or molecular-level
>> mechanisms.
>
> You must read carefully, we are talking about a standard
> accepted research practice. When one wants to study some
> question in diabetes using rodents as the model then one
> must first make them diabetic before starting the research.
> There are a number of ways used to do this. One is the high
> fat approach which creates rodents with diabetes very much
> like type 2 human diabetes.
>
> One rodent chow company has a standard diet with 60 percent
> fat which some researchers use to create the diabetes. That
> 60 percent fat is 100 percent coconut oil. Others use lard
> as in one example also in this thread.
>
> That is the reality of the situation in rodent diabetes
> research models. Any conclusions drawn from that reality as
> to coconut oil or any saturated fat is left to the reader's
> own imagination. In diabetes research in general saturated
> fat is implicated in the onset of diabetes for those with
> the genetic disposition. Some have described diabetes as a
> disordr of fat metabolism.
>
> Thus I'm not mentioning any studies but a standard practice
> where coconut oil is the only fat source.

The problem here is such statements are deceptive since most
of these fats have been hydrogenated to create trans-fats.
Most coconut oil studies in the past that I have seen are
always hydrogenated, a practice that is certain to increase
disease states. From what I have been able to gather,
non-hydrogenated coconut oil - virgin coconut oil - is a
healthy choice and saturated fats that have not be
hydrogenated are healthy as well.

--

Pramesh Rutajit - p297tongue6221@newsguy.com - Remove
tongue to reply.