tunderbar

Interesting study:

http://www.ajcn.org/cgi/content/full...f108ef31aa5b16

Current trends in health promotion emphasize the importance of
reducing dietary fat intake. However, as dietary fat is reduced, the
dietary carbohydrate content typically rises and the desired reduction
in plasma cholesterol concentrations is frequently accompanied by an
elevation of plasma triacylglycerol. We review the phenomenon of
carbohydrate-induced hypertriacylglycerolemia, the health effects of
which are among the most controversial and important issues in public
health nutrition today. We first focus on how seminal observations
made in the late 1950s and early 1960s became the basis for subsequent
important research questions and areas of scientific study. The second
focus of this paper is on the current knowledge of biological
mechanisms that contribute to carbohydrate-induced
hypertriacylglycerolemia. The clinical rationale behind mechanistic
studies is this: if carbohydrate-induced hypertriacylglycerolemia
shares a metabolic basis with endogenous hypertriacylglycerolemia
(that observed in subjects consuming high-fat diets), then a similar
atherogenic risk may be more likely than if the underlying metabolic
mechanisms differ. The third focus of the paper is on both the
positive metabolic changes that occur when high-carbohydrate diets are
consumed and the potentially negative health effects of such diets.
The review concludes with a summary of some important research
questions that remain to be addressed. These issues include the level
of dietary carbohydrate that induces carbohydrate-induced
hypertriacylglycerolemia, whether the phenomenon is transient or can
be avoided, whether de novo lipogenesis contributes to the phenomenon,
and what magnitude of triacylglycerol elevation represents an increase
in disease risk.

nicholas

"tcomeau" <tunderbar@hotmail.com> ha scritto nel messaggio
news:b550f406.0310241523.77ca6453@posting.google.c om...

http://www.ajcn.org/cgi/content/full...dd2ac896d0e975
e1f108ef31aa5b16

Ciculation 106; 2530-2532 2002
Circulation 1995; 92, 194-204
Am J Cardiol. 1992 Feb 15;69(5):440-4.
Diabetes Care. 1983 May-Jun;6(3):268-73.
Diabetes Care. 1982 Jul-Aug;5(4):370-4.
Diabetes Care 17(12):1-4,'94
New England Journal of Medicine 323:1921, 1990
Arch Int Med 1991, 151: 1389
Am J Med. 1985 Jan;78(1):23-7.
Jounal Of American College Nutrition 2003; 41, 263-272
Journal of Cardiopulmonary Rehabilitation 12:194-201,'92
Preventive Cardiology 53) 110-118 2002
Preventive Cardiology 2:159-163, 1999
Engl J Med. 2002 Feb 7;346(6):393-403
J Clin Nutr 1994May;59(5):980-4
Obes Res. 2002 Feb;10(2):78-82.
Journal of American College Nutrition 2002 21: 268-274
American Journal of Cardiology 79:1112, 1997, 93

We review the phenomenon of

tunderbar

also:

http://www.lbl.gov/Science-Articles/...-patternb.html

"an extreme low fat/high carbohydrate diet can, for some individuals,
actually increase the risk of heart disease, says a scientist with the
U.S. Department of Energy’s Lawrence Berkeley National
Laboratory (Berkeley Lab)."

moosh!

On 24 Oct 2003 16:23:31 -0700, tunderbar@hotmail.com (tcomeau) posted:


So many uncertainties.

What is the form of the carb intake?

Perhaps the wholefood/refined dichotomy is more important than the
fat/carb dichotomy.

What is the exercise regime of the subjects? What is the calorie
balance and weight status of the subjects?

In other words, it is likely heathiest to eat a high-carb, wholefood,
eucaloric diet with regular moderate exercise.

Any deviations from this will give a slight to moderate downside, that
may also bring a benefit that tips it to be of net benefit..

Such things as eating higher-fat, eucaloric diets in some folk may
give hunger-reducing benefits that outweigh the small disadvantages of
the higher fat consumption.

moosh!

On 25 Oct 2003 10:48:12 -0700, tunderbar@hotmail.com (tcomeau) posted:

The first half dozen words are:

"Because of certain inherited genetic traits...."

You *are* grasping at straw dust now.

doug freese

It goes on to say:
"reported on the recent findings of his research group in which it
was shown that in genetically susceptible individuals, an extreme
low-fat/high-carbohydrate diet can produce metabolic reactions that
cause a change in the cholesterol profile of their blood.

Further along:
"Tests for these genetically susceptible traits are not widely
available."

Note the words "in genetically susceptible individuals"

What this says, in some set of people that can not be quantified
have reacted in a certain manner. So, is two or 12 people as someone
posted last week?

Now your being the good propagandist and would like to generalize
this across the entire population. Piss poor strawman. You are
grasping at smoke to prove your case.


--
Doug Freese
"Caveat Lector"
dfreeseS@NOBShvc.rr.com

sufein

x-no-archive: yes


In article <mAVmb.46305$pT1.11510@twister.nyc.rr.com>, Doug Freese
<dfreese@NOBShvc.rr.com> writes:

Reaven of Stanford Univ., and others estimate the prevalence of insulin
resistance at 25 - 30% of the population. Further, research indicates that
risk of CVD rises all along the spectrum of normal glucose levels and HbA1c,
so it's logical to assume that the entire population would benefit from a
lifestyle/diet that would lower these. Low carbing is the only diet to lower
HbA1c and blood glucose levels.

Ann Intern Med 1998 Apr 1;128(7):524-33

Metabolic risk factors worsen continuously across the spectrum of nondiabetic
glucose tolerance. The Framingham Offspring Study.

Meigs JB, Nathan DM, Wilson PW, Cupples LA, Singer DE
Massachusetts General Hospital, Harvard Medical School, Boston University
School of Public Health, 02114, USA. jmeigs@sol.mgh.harvard.edu

BACKGROUND: Categorical definitions for glucose intolerance imply that risk
thresholds exist, but metabolic risk for type 2 diabetes mellitus or
cardiovascular disease may increase continuously as glucose intolerance
increases. OBJECTIVE: To examine the distributions of the following metabolic
risk factors across the spectrum of glucose tolerance: overall and central
obesity, hypertension, low levels of high-density lipoprotein cholesterol, and
increased triglyceride and insulin levels. DESIGN: Cross-sectional analysis.
SETTING: The community-based Framingham Offspring Study. PARTICIPANTS: 2583
adults without previously diagnosed diabetes. MEASUREMENTS: Clinical data;
fasting glucose, insulin, and lipid levels; and glucose and insulin levels
taken 2 hours after oral challenge were collected from 1991 to 1993. Glucose
tolerance was determined by 1980 World Health Organization criteria. Patients
with normal glucose tolerance were categorized into quintiles of fasting
glucose. The distributions of each metabolic risk factor and the metabolic sum
of the six risk factors were assessed across seven categories from the lowest
quintile of normal fasting glucose level through impaired glucose tolerance and
previously undiagnosed diabetes. RESULTS: The mean age of patients was 54 years
(range, 26 to 82 years); 52.7% of patients were women. Glucose tolerance
testing found that 12.7% of patients had impaired glucose tolerance and 4.8%
had previously undiagnosed diabetes. Multivariable-adjusted mean measures of
risk factors and odds ratios for obesity, elevated waist-to-hip ratio,
hypertension, low levels of high-density lipoprotein cholesterol, elevated
triglyceride levels, and hyperinsulinemia showed continuous increases across
the spectrum of nondiabetic glucose tolerance. Although a threshold effect near
the upper range of nondiabetic glucose tolerance could not be ruled out for
triglyceride levels in men and for insulin levels 2 hours after oral challenge
in men and women, no other metabolic risk factors showed clear evidence of
thresholds for increased risk. CONCLUSIONS: Metabolic risk factors for type 2
diabetes mellitus and for cardiovascular disease worsen continuously across the
spectrum of glucose tolerance categories, beginning in the lowest quintiles of
normal fasting glucose level.

PMID: 9518396, UI: 98175274

Blood Glucose Concentration Linked to>Cardiovascular Risk in Nondiabetic Men>
----------------------------------------------------------------------------

WESTPORT,>CT (Reuters Health) Jan 04 - Increased glycated hemoglobin
(HbA1c)>concentrations are predictive of cardiovascular mortality among
all men,>not only those with diabetes, according to a report in the
British>Medical Journal for January 6.

Dr. Kay-Tee Khaw and colleagues, from>the University of Cambridge
School of Clinical Medicine, UK, collected>data on all-cause mortality
and cardiovascular mortality in 4662 men, 45>to 79 years of age, who
participated in the Norfolk UK cohort of the>European Prospective
Investigation into Cancer and Nutrition>(EPIC-Norfolk). At baseline,
from 1995 to 1997, HbA1c was measured and>the subjects were followed
until December 1999.

As expected, Dr.>Khaw's group found that diabetic men had increased
mortality for all>causes, cardiovascular disease and ischemic disease.
They also noted that>HbA1c concentrations were "continuously related to
subsequent all-cause,>cardiovascular, and ischemic mortality through
the whole population." The>lowest mortality rates were associated with
HbA1c concentrations below>5%.

Further, the group noted that a 1% increase in HbA1c was>associated
with a 28% increased risk of death, which was independent of>age, blood
pressure, cholesterol, body mass index and>smoking.

"Eighteen percent of the population excess mortality risk>associated
with a HbA1c concentration of 5% or more occurred in men with>diabetes,
but 82% occurred in men with concentrations of 5% to 6.9% (the>majority
of the population)," Dr. Khaw and colleagues point>out.

The researchers propose that an elevated concentrations of>HbA1c is a
marker for greater absolute risk among all men, and>"preventive
treatment with blood pressure- or cholesterol-lowering drugs>should be
considered in such patients."

They point out that if>the population of nondiabetic men was able to
lower its HbA1c>concentration by 0.1%, total mortality could be reduced
by 5%, and if the>concentration could be lowered by 0.2%, then total
mortality could be>reduced by 10% in this population.
--

Susan

tunderbar

Could the inherited genetic traits have something to do with the fact
that we evolved millions of years with very small amounts or no
amouints at all of refined carbs in our diets? Now we are faced with a
diet that is very high in refined carbs and what happens? Huge
inceases in incidences of obesity, diabetes, CVDs, etc.

I hardly call this grasping. It falls perfectly in line with what I've
been saying here for a couple of years now.

TC

nicholas

"Susan " <sufein@aol.comnospam> ha scritto nel messaggio
news:20031026160213.21232.00001583@mb-m13.aol.com...


that

HbA1c,


lower


This is an idiocy
High-unrefined-carb diet lower both insulin, fasting glucose levels and
hemoglobin A 1c more than low-carb diet expecially more than zone diet
Thsi has been reported many times in the more than 70 studies on the
Pritikin diet, on new studies confronting Pritikin diet with Zone diet
Sear himself admitted that his only study on zone diet didn't show lowered
insulin level
Know I hope people on this ng are smarter than thinking that only
carbohydrates cause on insulin response
Both proteins and carbohydrates cause insulin to be secreted
Fat enhances the amount on insulin secreted at the insulin response of
carohydrates and proteins
High unrefined carbohydrates foods and high in fiber have a lower insulin
response than high fat or protein foods
Both beef and fish make the body secrete more insulin than pasta
Both protein + carbohydrates and protein + fats result in a higher insulin
response as well as carbohydrates + proteins and carbohydrates + fat
So, NO insulin is not secreted only when you eat carbohydrates and by eating
pasta get lower insulin level than by eating a beef steak
The problem with insulin is not actually high-levels caused by
high-proteins, high-fats and high-refined sugars foods, but high sustained
levels caused by high level of lipemia due to low-carb and high fat diets
Within 40 years more than 70.000 subjects in more than 70 studies have
showed that high-unrefined-carbs diet ad libitum lower insulin, glucose,
cholesterol, lipemia, triglyceride, free radicals levels
There are many long term studies showing that low-carb diet ad libitum lower
glucose, insulin and hemoglobin A 1c levels
Read the literature

Diabetes Care. 1983 May-Jun;6(3):268-73.
Diabetes Care. 1982 Jul-Aug;5(4):370-4.
Diabetes Care 17(12):1-4,'94
- - - - - - - - - - - - - - - - - - - - - - - - -
Ciculation 106; 2530-2532 2002
Circulation 1995; 92, 194-204
Am J Cardiol. 1992 Feb 15;69(5):440-4.
New England Journal of Medicine 323:1921, 1990
Arch Int Med 1991, 151: 1389
Am J Med. 1985 Jan;78(1):23-7.
Jounal Of American College Nutrition 2003; 41, 263-272
Journal of Cardiopulmonary Rehabilitation 12:194-201,'92
Preventive Cardiology 53) 110-118 2002
Preventive Cardiology 2:159-163, 1999
Engl J Med. 2002 Feb 7;346(6):393-403
J Clin Nutr 1994May;59(5):980-4
Obes Res. 2002 Feb;10(2):78-82.
Journal of American College Nutrition 2002 21: 268-274
American Journal of Cardiology 79:1112, 1997, 93

sufein

x-no-archive: yes


In article <6yXmb.13865$uv4.4599@news.edisontel.com>, "Nicholas"
<chip_n_dale@email.it> writes:


You're right. Every word that followed the four above was idiocy.

Thanks for the warning.

Susan