Insuln Response to HiCarb vs LoCarb?

I was under the impression that a high-fat meal would cause a lower
insulin response than a high-carb meal. If so, why does the following
study seem to indicate the opposite?

Meal composition affects insulin secretion in women with type 2
diabetes: a comparison with healthy controls. The Hoorn prandial
study.

BACKGROUND/OBJECTIVE: Early insulin secretion following a meal is
representative for normal physiology and may depend on meal
composition. To compare the effects of a fat-rich and a carbohydrate-
rich mixed meal on insulinogenic index as a measure of early insulin
secretion in normoglycemic women (NGM) and in women with type 2
diabetes mellitus (DM2), and to assess the relationship of
anthropometric and metabolic factors with insulinogenic index.
SUBJECTS/METHODS: Postmenopausal women, 76 with NGM and 64 with DM2,
received a fat-rich meal and a carbohydrate-rich meal on separate
occasions. Early insulin response was estimated as insulinogenic index
( big up tri, Deltainsulin(0-30 min)/ big up tri, Deltaglucose(0-30
min)) for each meal. Associations of fasting and postprandial
triglycerides, body mass index, waist and hip circumference and
alanine aminotransferase with insulinogenic indices were determined.
RESULTS: Women with NGM present with higher insulinogenic index than
women with DM2. The insulinogenic index following the fat-rich meal
( big up tri, DeltaI(30)/ big up tri, DeltaG(30) (fat)) was higher
than the index following the carbohydrate-rich meal (big up tri,
DeltaI(30)/ big up tri, DeltaG(30) (CH)) (P0.05 in women with DM2,
and not significant in women with NGM). In women with DM2, homeostasis
model assessment for insulin resistance was positively associated with
big up tri, DeltaI(30)/ big up tri, DeltaG(30) (CH). In women with
NGM, waist circumference was independently and inversely associated
with big up tri, DeltaI(30)/ big up tri, DeltaG(30) (fat) and with big
up tri, DeltaI(30)/ big up tri, DeltaG(30) (CH); hip circumference was
positively associated with big up tri, DeltaI(30)/ big up tri,
DeltaG(30) (fat). CONCLUSIONS: The insulinogenic index following the
fat-rich meal was higher than following the isocaloric carbohydrate-
rich meal, which might favorably affect postprandial glucose
excursions, especially in women with DM2. The association between a
larger waist circumference and a lower meal-induced insulinogenic
index in women with NGM requires further mechanistic studies. PMID:
17987050

Protein causes the strongest, long lasting insulin release after a meal..
How much protein was in the meals the study subjects ate?

I don't have access to the full study, but I assume the protein in
both meals were the same.

This points to the fact that it's not the total amount of insulin
secreted after a meal that is undesirable, it's sudden and very high
secretion, apparently. *Fat does not stimulate insulin secretion.
Glycemic carbs induce a sharp, sudden increase in insulin secretion.
Protein induces a longer/stronger, and steady secretion.

Which causes a sharper insulin response, carbs or protein?

On second reading of the study, it seems it conclusions are difficult
to interpret because:
1. The abstract doesn't indicate macronutrient breakdown for "fat-
rich" meal. It may be mod-fat, mod-carb meal according to low-carb
proponents.
2. The "Insulinogenic" index incorporate trigs and glucose levels.

-------------
Below study on rabbits say cholesterol, not saturated fats, cause
problems. Why does cholesterol supplementation cause major problems
for rabbits. Don't rabbits have cholesterol in their blood? Is the
cholesterol in this and most such experiments oxidized? Is the
cholesterol in raw egg yolks oxidized? Does it become oxidized when
hard boiled?

Effect of High Fat Diet Without Cholesterol Supplementation on
Oxidative Stress and Lipid Peroxidation in New Zealand White Rabbits.
Aim: Dietary fats may affect coronary artery disease risk by
influencing factors other than serum cho-lesterol. The effect of diets
containing coconut oil and sunflower oil without cholesterol
supplementation on oxidative stress and lipid peroxidation were
studied in male New Zealand White rabbits.Methods: Animals assigned to
four groups (control, cholesterol-fed, coconut oil-fed and sunflower
oil-fed), given an isocaloric diet and studied for 6 months. The lipid
profile, reduced glutathione, glutathione peroxidase, superoxide
dismutase, vitamin C and lipid peroxidation were evaluated at the
beginning of the study, at the third month and at the end of the study
period. Results: Serum lipid values did not show significant variation
between animals fed coconut oil and sunflower oil, but total
cholesterol, triglycerides and LDL-cholesterol were significantly
higher and HDL-cholesterol was reduced in cholesterol-fed animals.
Lipid peroxidation was higher in cholesterol-fed and sunflower oil-fed
rabbits compared to controls and coconut oil-fed rabbits. Though other
parameters such as reduced glutathione, glutathione peroxidase,
superoxide dismutase and ascorbate did not vary between the two oil-
fed rabbit groups, cholesterol-fed rabbits showed severe oxidative
stress.Conclusion: We conclude that in the absence of cholesterol
supplementation, coconut oil intake up to 30% of daily energy supply
did not cause hypercholesterolemia or oxidative stress in rabbits.
PMID: 20032571

Jarod wrote:
Susan wrote:

A recent meta analysis indicates that saturated fat has no causal
relationship to CVD.

Do you probably have a link which points me directly to this analysis?
(I have full access to nearly all the public medical databases).

Thanks!


Here is an older one from 2000. Claims a WEAK association between fat
and heart disease. Actually there was a "trend" to decreased fat being
protective, but it was not statistically significant.

The data opposing the classic strong link between fat and heart disease
is almost 10 years old, but the contrary "expert medical opinion" has
been so deeply ingrained by millions of repetitions that it will take a
long time to die out.

The classic masters of propaganda knew that repeating a lie often enough
would make it "true".


http://www.ncbi.nlm.nih.gov/pubmed/1...&ordinalpos=10

Cochrane Database Syst Rev. 2000;(2):CD002137.
Reduced or modified dietary fat for prevention of cardiovascular disease.

Hooper L, Summerbell CD, Higgins JP, Thompson RL, Clements G, Capps N,
Davey Smith G, Riemersma RA, Ebrahim S.

The Cochrane Suite, MANDEC, University Dental Hospital of Manchester,
Higher Cambridge Street, Manchester, UK, M15 6FH.

Update in:

* Cochrane Database Syst Rev. 2001;(3):CD002137.

BACKGROUND: Reduction or modification of dietary fat can improve total
cholesterol levels, but may also have a variety of effects, both
positive and negative, on other cardiovascular risk factors. OBJECTIVES:
The aim of this systematic review was to assess the effect of reduction
or modification of dietary fats on total and cardiovascular mortality
and cardiovascular morbidity over at least 6 months, using all available
randomized clinical trials. SEARCH STRATEGY: The Cochrane Library,
MEDLINE, EMBASE, CAB Abstracts, CVRCT registry and related Cochrane
Groups' trial registers were searched through spring 1998, SIGLE to
January 1999. Trials known to experts in the field and biographies were
included through May 1999. SELECTION CRITERIA: Trials fulfilled the
following criteria: 1) randomized with appropriate control group, 2)
intention to reduce or modify fat or cholesterol intake (excluding
exclusively omega-3 fat interventions), 3) not multi factorial, 4)
healthy adult humans, 5) intervention at least six months, 6) mortality
or cardiovascular morbidity data available. Inclusion decisions were
duplicated, disagreement resolved by discussion or a third party. DATA
COLLECTION AND ANALYSIS: Rate data were extracted by two independent
reviewers and meta-analysis performed using random effects methodology.
Meta-regression and funnel plots were used. MAIN RESULTS: Twenty seven
studies were included (40 intervention arms, 30,901 person-years). There
was no significant effect on total mortality (rate ratio 0.98, 95% CI
0.86 to 1.12), a trend towards protection form cardiovascular mortality
(rate ratio 0.91, 95% CI 0. 77 to 1.07), and significant protection from
cardiovascular events (rate ratio 0.84, 95% CI 0.72 to 0.99). The latter
became non-significant on sensitivity analysis. Trials where
participants were involved for more than 2 years showed significant
reductions in the rate of cardiovascular events and a suggestion of
protection from total mortality. The degree of protection from
cardiovascular events appeared similar in high and low risk groups, but
was statistically significant only in the former. REVIEWER'S
CONCLUSIONS: The findings are suggestive of a small but potentially
important reduction in cardiovascular risk in trials longer than two
years. Lifestyle advice to all those at high risk of cardiovascular
disease (especially where statins are unavailable or rationed), and to
lower risk population groups, should continue to include permanent
reduction of dietary saturated fat and partial replacement by unsaturates.

In article ,
pamela wrote:

Jarod wrote:
Susan wrote:

A recent meta analysis indicates that saturated fat has no causal
relationship to CVD.

Do you probably have a link which points me directly to this analysis?
(I have full access to nearly all the public medical databases).

Thanks!


Here is an older one from 2000. Claims a WEAK association between fat
and heart disease. Actually there was a "trend" to decreased fat being
protective, but it was not statistically significant.

The data opposing the classic strong link between fat and heart disease
is almost 10 years old, but the contrary "expert medical opinion" has
been so deeply ingrained by millions of repetitions that it will take a
long time to die out.

One point is how weak the supposed effect is. The statin pushers have to
hide the fact that the alleged gains are miniscule for any individual.

It doesn't make sense for any individual, but it's supposed to make up
for it by reducing the number of cardio vascular events in large
populations.

Oh, and side effects are *notoriously* under reported. A little muscle
weakness, a little cognitive decline etcetera (or a lot actually), may
not be reported and if it is will be brushed off with "You're getting
older." Sexual "side effect" are even more notoriously likely to not be
reported or taken seriously.

Meanwhile I have taken off like 70-80 pounds, just by carb restriction,
I am not sure because I didn't want to weigh myself before the weight
started coming off.

--
A computer without Microsoft is like a chocolate cake without mustard.

Walter Bushell wrote:
In article ,
pamela wrote:

Jarod wrote:
Susan wrote:

A recent meta analysis indicates that saturated fat has no causal
relationship to CVD.
Do you probably have a link which points me directly to this analysis?
(I have full access to nearly all the public medical databases).

Thanks!

Here is an older one from 2000. Claims a WEAK association between fat
and heart disease. Actually there was a "trend" to decreased fat being
protective, but it was not statistically significant.

The data opposing the classic strong link between fat and heart disease
is almost 10 years old, but the contrary "expert medical opinion" has
been so deeply ingrained by millions of repetitions that it will take a
long time to die out.

One point is how weak the supposed effect is. The statin pushers have to
hide the fact that the alleged gains are miniscule for any individual.

It doesn't make sense for any individual, but it's supposed to make up
for it by reducing the number of cardio vascular events in large
populations.

Oh, and side effects are *notoriously* under reported. A little muscle
weakness, a little cognitive decline etcetera (or a lot actually), may
not be reported and if it is will be brushed off with "You're getting
older." Sexual "side effect" are even more notoriously likely to not be
reported or taken seriously.


I foolishly let myself be given statins, as a trial. There was an
immediate reduction of LDL to down just below 100, but because of other
"risk factors" they wanted to go even lower. Again, I foolishly went
along, as a trial.

Within 2 weeks, myalgia (muscle weakness) set in. I had to reduce the
weights on exercise weight machines by generally 20 percent. My walking
time on the inclined treadmill went down from nearly 60 minutes to about
8 minutes with fatigue and claudication.

I stopped the statins immediately.

Research on Pubmed.gov on the subject showed that myalgia was considered
common and underreported or dismissed by the clinician as unrelated to
the statin. I found one paper claiming that exercisers were especially
prone to myalgia from statins, claiming that up to 20 percent of such
patients would have weakness/pain problems.

I found out that no one is clear on what the cause of statin induced
myalgia is, and there is no clear or "official" information on what is
best to do to recover from it - except stop the statins. Evidently, not
all myalgia symptoms are easily eliminated, and may be permanent.

Because the National Cholesterol Education Panel is heading towards
getting everybody to seek ever lower levels of cholesterol, the current
drugs are inadequate. One drug company reported on the existing programs
to create strong statins with less tendency to induce myalgia because
without such drugs, the widespread application of them will be nearly
impossible.