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Medical Forum / General / Cardiology / August 2006

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Cheese

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Buddha Pest - 24 Aug 2006 21:59 GMT
I've been eating a daily slice of cheddar cheese lately. About 2 x 2 square
slice (inches). I figure this would get my daily allotment of dairy
products. But I am concerned about cholesterol, triglicerydes, etc.? How
does this small amount of cheese affect that? I usually eat or drink no
other dairy products whatsoever until I do the occasional pig-out of ice
cream. Thanks.
William Wagner - 24 Aug 2006 22:20 GMT
> I've been eating a daily slice of cheddar cheese lately. About 2 x 2 square
> slice (inches). I figure this would get my daily allotment of dairy
> products. But I am concerned about cholesterol, triglicerydes, etc.? How
> does this small amount of cheese affect that? I usually eat or drink no
> other dairy products whatsoever until I do the occasional pig-out of ice
> cream. Thanks.

http://www.yourdiseaserisk.harvard.edu/hccpquiz.pl?func=start&quiz=heart

Get blood work that is real then plug in different  numbers.  Want
drugs?  OK but look at what the numbers can mean.

Bon appetite.

Bill who reads carbs good to reduce and ice cream is fat and sugar last
time I looked ;))

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This article is posted under fair use rules in accordance with
Title 17 U.S.C. Section 107, and is strictly for the educational
and informative purposes. This material is distributed without profit.

Susan - 24 Aug 2006 22:23 GMT
> I've been eating a daily slice of cheddar cheese lately. About 2 x 2 square
> slice (inches). I figure this would get my daily allotment of dairy
> products. But I am concerned about cholesterol, triglicerydes, etc.? How
> does this small amount of cheese affect that? I usually eat or drink no
> other dairy products whatsoever until I do the occasional pig-out of ice
> cream. Thanks.

Dairy products don't cause dyslipidemia, especially if it's dairy from
grass fed cows.

Starches and sugar cause dyslipidemia/metabolic syndrome.

Susan
Andrew B. Chung, MD/PhD - 25 Aug 2006 00:58 GMT
> > I've been eating a daily slice of cheddar cheese lately. About 2 x 2 square
> > slice (inches). I figure this would get my daily allotment of dairy
[quoted text clipped - 5 lines]
> Dairy products don't cause dyslipidemia, especially if it's dairy from
> grass fed cows.

Depends on how much is consumed. 3% is fat.  There is also plenty of
sugar (lactose).  Most folks is ASD will attest to dairy products
raising their blood glucose.

> Starches and sugar cause dyslipidemia/metabolic syndrome.

Again, depends how much is being consumed and whether there is any
visceral adiposity.

It is the visceral adipose tissue that is really the cause of metabolic
syndrome (MetS).

May GOD continue to heal your heart, dear neighbor Susan whom I love
unconditionally.

Prayerfully in Christ's amazing love,

Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit

As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).

http://groups.google.com/group/sci.med.cardiology/msg/d3b7b57d0fbf89ed?

> Susan
Buddha Pest - 24 Aug 2006 23:55 GMT
Thanks, Bill and Susan. Thanks for the info.

> I've been eating a daily slice of cheddar cheese lately. About 2 x 2
> square slice (inches). I figure this would get my daily allotment of dairy
> products. But I am concerned about cholesterol, triglicerydes, etc.? How
> does this small amount of cheese affect that? I usually eat or drink no
> other dairy products whatsoever until I do the occasional pig-out of ice
> cream. Thanks.
Joe Doe - 25 Aug 2006 05:07 GMT
> I've been eating a daily slice of cheddar cheese lately. About 2 x 2 square
> slice (inches). I figure this would get my daily allotment of dairy
> products. But I am concerned about cholesterol, triglicerydes, etc.? How
> does this small amount of cheese affect that? I usually eat or drink no
> other dairy products whatsoever until I do the occasional pig-out of ice
> cream. Thanks.

Cheese is very high in saturated fat (about 6 grams in an an oz of
cheese).  A 2x2 square may be about an 1.5 oz.  Saturated fat depresses
LDL receptor levels and consequently raises circulating levels of LDL.  
Ice cream has even higher levels of saturated fat (in the range of 14-24
grams per serving). So both are potentially bad.  Most people feel you
should keep your saturated fat intake to less than 7% of daily calorie
intake (about 14 grams total for a 2000 calorie per day diet).  Eat low
fat yogurt & similar products as a much better source of dairy
(beneficial probiotics + dairy). In general for a heart friendly diet
the best thing you could do is lower your consumption of saturated and
trans fats and increase your consumption of monosaturated and add a
small amounts of omega 3 fats.

For some references on saturated fat mechanism for raising LDL see for
example

Brown and Goldstein's web site (Nobel Laureates in 1985 for discovery of
LDL receptor.

http://www.utsouthwestern.edu/utsw/cda/dept14857/files/114532.html

or this paper

http://www.jlr.org/cgi/content/abstract/38/3/459

Or read pages 481 to 485 and 798 at this link which is a book put out by
the National Academy of Science on Dietary Reference intakes and
summarizes a great deal of data

http://darwin.nap.edu/books/0309085373/html/481.html

This site has some good general info on atherosclerosis:

http://www.baylorhealth.edu/proceedings/13_2/13_2_questions.html

If you are highly motivated you could read Brown and Goldstein's Lecture
on the the LDL receptor that they delivered when they got the Nobel
Prize:

http://nobelprize.org/nobel_prizes/medicine/laureates/1985/brown-goldstei
n-lecture.pdf#search=%22brown%20goldstein%20ldl%22

Roland

Roland
Joe Doe - 25 Aug 2006 05:17 GMT
In general for a heart friendly diet
> the best thing you could do is lower your consumption of saturated and
> trans fats and increase your consumption of monosaturated and add a
> small amounts of omega 3 fats.

I should also add that you should add a great deal of vegetables and
fruits and fiber rich foods like beans.  

Roland
Susan - 25 Aug 2006 13:09 GMT
> Cheese is very high in saturated fat (about 6 grams in an an oz of
> cheese).  A 2x2 square may be about an 1.5 oz.  Saturated fat depresses
> LDL receptor levels and consequently raises circulating levels of LDL.  

No it doesn't.  Find the studies that found this effect from alpine
grass fed cows or grass fed beef anywhere, or from saturated fat in the
absence of significant glycemic load.

Further, higher LDL is not a good CVD risk predictor, as compared to
high TGL, caused by high glycemic load.

> Ice cream has even higher levels of saturated fat (in the range of 14-24
> grams per serving).

Good ice cream does, anyway.  :-)

>> So both are potentially bad.

Actually, that's what makes it so good.

  Most people feel you
> should keep your saturated fat intake to less than 7% of daily calorie
> intake (about 14 grams total for a 2000 calorie per day diet).  Eat low
[quoted text clipped - 6 lines]
> For some references on saturated fat mechanism for raising LDL see for
> example

A recent study involving over 40,000 middle-aged and older American
men over a period of six years found that there was no link between
saturated fat intake and heart disease in men. It also supported the
contention that linolenic acid (a form of fat) is preventive against
heart disease. (Ascherio A et. al. Dietary fat and risk of coronary
heart disease in men: cohort follow up study in the United States.
British Medical Journal, 1996 Jul 13, 313:7049, 84-90.)"

"Several studies have shown that high-carbohydrate low-fat diets lead
to high triglycerides, elevated serum insulin levels, lower HDL
cholesterol levels, and other factors known to raise the risk of
coronary artery disease. (See Liu GC; Coulston AM; Reaven GM. Effect
of high-carbohydrate low-fat diets on plasma glucose, insulin and
lipid responses in hypertriglyceridemic humans. Metabolism, 1983 Aug,
32:8, 750-3. See also Coulston AM; Liu GC; Reaven GM. Plasma glucose,
insulin and lipid responses to high-carbohydrate low-fat diets in
normal humans. Metabolism, 1983 Jan, 32:1, 52-6. See also Olefsky JM;
Crapo P; Reaven GM. Postprandial plasma triglyceride and cholesterol
responses to a low-fat meal. American Journal of Clinical Nutrition,
1976 May, 29:5, 535-9. See also Ginsberg H et. al. Induction of
hypertriglyceridemia by a low-fat diet. Journal of Clin Endocrinol
Metab, 1976 Apr, 42:4, 729-35) "

"The idea that saturated fats cause heart disease is completely wrong,
but the statement has been 'published' so many times over the last
three or more decades that it is very difficult to convince people
otherwise unless they are willing to take the time to read and learn
what...produced the anti-saturated fat agenda." (Dr. Mary Enig,
Consulting Editor to the Journal of the American College of Nutrition,
President of the Maryland Nutritionists Association, and noted lipids
researcher.)

"The diet-heart hypothesis [which suggests that high intake of
saturated fat and cholesterol causes heart disease] has been
repeatedly shown to be wrong, and yet, for complicated reasons of
pride, profit and prejudice, the hypothesis continues to be exploited
by scientists, fund-raising enterprises, food companies and even
governmental agencies. The public is being deceived by the greatest
health scam of the century." (Dr. George V. Mann, participating
researcher in the Framingham study and author of CORONARY HEART
DISEASE: THE DIETARY SENSE AND NONSENSE, Janus Publishing 1993.)

High intake of fats from the Omega-3 group increase HDL cholesterol,
which is considered protective against heart disease. Obviously it
would be difficult to eat an Omega-3 rich diet while following a
traditional fat reduced diet, especially if one were following one of
the popular American diets that has one eating only 20-30 grams of fat
per day. (Franceschini G. et. al. Omega-3 fatty acids selectively
raise high-density lipoprotein 2 levels in healthy volunteers.
Metabolism, 1991 Dec, 40:12, 1283-6. See also Journal of the American
College of Nutrition 1991:10(6);593-601)

A recent American study showed that low-fat, high-carbohydrate diets
(15% protein, 60% carbohydrate, 25% fat) increase risk of heart
disease in post-menopausal women over a higher fat, lower carbohydrate
diet (15% protein, 40% carbohydrate, 45% fat). (Jeppeson, J., et. al.
Effects of low-fat, high-carbohydrate diets on risk factors for
ischemic heart disease in postmenopausal women. American Journal of
Clinical Nutrition, 1997;65:1027-33)

The largest and most comprehensive study on diet and breast cancer to
date, studying over 5,000 women between 1991 and 1994, showed that
women with the lowest intake of dietary fat had a significantly higher
incidence of breast cancer than the women with the highest intake of
dietary fat. It also found that women with the highest intake of
starch had a significantly higher incidence of breast cancer than the
women with the lowest intake of starch. The study found no evidence
that saturated fat had any effect one way or the other on breast
cancer, and that unsaturated fat had a significantly protective effect
against breast cancer. (Franceschi S et. al. Intake of macronutrients
and risk of breast cancer. Lancet; 347(9012):1351-6 1996)

"The commonly-held belief that the best diet for prevention of
coronary heart disease is a low saturated fat, low cholesterol diet is
not supported by the available evidence from clinical trials. In
primary preventions, such diets do not reduce the risk of myocardial
infarction or coronary or all-cause mortality. Cost-benefit analyses
of extensive primary prevention programmes, which are at present
vigorously supported by governments, health departments, and health
educationalists, are urgently required....Similarly, diets focused
exclusively on reduction of saturated fats and cholesterol are
relatively ineffective for secondary prevention and should be
abandoned. There may be other effective diets for secondary prevention
of coronary heart disease but these are not yet sufficiently well
defined or adequately tested." (European Heart Journal, Volume 18,
January 1997.)

"We found no evidence of a positive association between total dietary
fat intake and the risk of breast cancer. There was no reduction in
risk even among women whose energy intake from fat was less than 20
percent of total energy intake. In the context of the Western
lifestyle, lowering the total intake of fat in midlife is unlikely to
reduce the risk of breast cancer substantially." (Hunter, DJ et. al.
Cohort studies of fat intake and the risk of breast cancer - A pooled
analysis. New England Journal of Medicine, 334: (6) FEB 8 1996)

2) Title: DG-DISPATCH - ENDO 99: Diabetics Improve Health With Very
High-Fat,
Low
Carb Diet
Doctor's Guide
June 15, 1999

By Cameron Johnston
Special to DG News

SAN DIEGO, CA -- June 15, 1999 -- A very high-fat, low-carbohydrate diet
has
been shown to have astounding effects in helping type 2 diabetics lose
weight
and improve their blood lipid profiles.

The results of three studies involving such a diet, which is similar to,
but
has a few key differences from the famous "Dr. Atkins Diet", were
presented
today
at the annual meeting of the Endocrine Society.

Dr. James Hays, an endocrinologist and director of the Limestone Medical
Center in Wilmington, DE, admitted that the concept of a high-fat diet in
people
who are already at higher risk of cardiovascular disease might seem
incongruous.
Nonetheless, this study of 157 men and women with type 2 diabetes showed
an
impressive benefit in body mass index (BMI) triglycerides, HDL, LDL and
HbA1c.

Most people are encouraged to reduce the amount of fat in their diets,
particularly saturated fats, and diabetics in particular are advised to
reduce
their
overall caloric intake, Dr. Hays explained in an interview in San Diego
during
the
conference.

Whereas a normal diet would be in the order of 1800 to 2100 calories,
with 60
percent of calories coming from carbohydrates and 30 percent from fat,
patients

in this diet were restricted to 1800 calories per day and were
encouraged to
get
50 percent of their caloric intake from fat, and just 20 percent from
carbohydrates.
The balance of 30 percent would come from proteins.

A whopping 90 percent of the fat content in their diets was saturated
fat,
compared
with just 10 percent that was monounsaturated fat.

"I think this is at least worth considering for any diabetic," Dr. Hays
said in
an interview.
"The thing many diabetics coming into the office don't realize is that
other
forms of
carbohydrates will increase their sugars, too. Dietitians will point them
toward complex carbohydrates ... oatmeal and whole wheat bread, but we
have to
deliver the message that these are carbohydrates that increase blood
sugars,
too."

Higher-fat diets, on the other hand, seem to make the person feel full
faster
so they eat less; higher-fat diets also tend to reduce postprandial
hypoglycemia so the patients feel better after eating.

"Every diabetic comes home from the doctor with instructions as to what
their
diet should consist of, but they're not getting the information from
dietitians about what complex carbohydrates they should eat,"

Dr. Hays said:
"The important thing here is no ketosis. We absolutely don't want people
to
become
ketotic, and so we said they had to have so many exchanges of fresh
fruits and
vegetables and we specified the ones they could eat."

They were able to eat all the meat and cheese they wanted, but as for
carbohydrates, they are restricted to eating unprocessed foods, mainly
fresh
fruit and vegetables, he added.

Subjects recruited into the study (84 men, 73 women) were all type 2
diabetics
and
were required to undergo a standard American Diabetes Association
modified diet
for
one full year before entry into the trial. Over the course of one year,
the
subjects achieved a mean decline in total cholesterol of between 231 and
190
mg/dl. Triglycerides declined from 229 to 182 mg/dl.

Low-density lipoproteins (LDL cholesterol) fell from 133 to 105 mg/dl,
while
HDL
increased from 44 to 47 mg/dl.

HbA1c, which at the start of the study averaged 3.34 percent above
normal,
declined to the point that at one year, the mean was just 0.96 percent
above
normal.

The average weight loss among subjects in the study was in the order of
40
pounds, Dr. Hays said.

By the end of the one-year study, he added, 90 percent of the patients
had
achieved ADA (American Diabetes Association) targets for HbA1c, HDL,
LDL and triglycerides.

Even among juvenile diabetics, he said, they might not be overweight and
they
might have more or less normal lipid levels, but when they are on this
kind of
diet
it is possible to treat them with lower doses of insulin and make their
lives a
little
safer, he said.

As for the response from cardiologists who see a high-fat diet as
anathema to
what they have been instructing their patients for years now, Dr. Hays
said he
has
three cardiologist patients who are now on the diet.

"If you have a diet that results in weight loss, lower cholesterol, and a
better lipid profile, eventually, everybody will be eating that way.
It's going
to come
whether we like it or not."

The New England Journal of Medicine -- November 20, 1997 -- Vol. 337,
No. 21

Dietary Fat Intake and the Risk of Coronary Heart Disease in Women
Frank B. Hu, Meir J. Stampfer, JoAnn E. Manson, Eric Rimm, Graham A.
Colditz, Bernard A. Rosner, Charles H. Hennekens, Walter C. Willett
-------------------------------------------------------------------------
-------

Abstract
Background. The relation between dietary intake of specific types of
fat, particularly trans unsaturated fat, and the risk of coronary
disease remains unclear. We
therefore studied this relation in women enrolled in the Nurses' Health
Study.

Methods. We prospectively studied 80,082 women who were 34 to 59 years
of age and had no known coronary disease, stroke, cancer,
hypercholesterolemia, or
diabetes in 1980. Information on diet was obtained at base line and
updated during follow-up by means of validated questionnaires. During 14
years of follow-up, we
documented 939 cases of nonfatal myocardial infarction or death from
coronary heart disease. Multivariate analyses included age, smoking
status, total energy intake,
dietary cholesterol intake, percentages of energy obtained from protein
and specific types of fat, and other risk factors.

Results. Each increase of 5 percent of energy intake from saturated fat,
as compared with equivalent energy intake from carbohydrates, was
associated with a 17
percent increase in the risk of coronary disease (relative risk, 1.17;
95 percent confidence interval, 0.97 to 1.41; P = 0.10). As compared
with equivalent energy from
carbohydrates, the relative risk for a 2 percent increment in energy
intake from trans unsaturated fat was 1.93 (95 percent confidence
interval, 1.43 to 2.61;
P<0.001); that for a 5 percent increment in energy from monounsaturated
fat was 0.81 (95 percent confidence interval, 0.65 to 1.00; P = 0.05);
and that for a 5
percent increment in energy from polyunsaturated fat was 0.62 (95
percent confidence interval, 0.46 to 0.85; P = 0.003). Total fat intake
was not significantly
related to the risk of coronary disease (for a 5 percent increase in
energy from fat, the relative risk was 1.02; 95 percent confidence
interval, 0.97 to 1.07; P = 0.55).
We estimated that the replacement of 5 percent of energy from saturated
fat with energy from unsaturated fats would reduce risk by 42 percent
(95 percent confidence
interval, 23 to 56; P<0.001) and that the replacement of 2 percent of
energy from trans fat with energy from unhydrogenated, unsaturated fats
would reduce risk by
53 percent (95 percent confidence interval, 34 to 67; P<0.001).

Conclusions. Our findings suggest that replacing saturated and trans
unsaturated fats with unhydrogenated monounsaturated and polyunsaturated
fats is more effective
in preventing coronary heart disease in women than reducing overall fat
intake. (N Engl J Med 1997;337:1491-9.)

Source Information
>From the Departments of Nutrition (F.B.H., M.J.S., E.R., W.C.W.),
Epidemiology (M.J.S., J.E.M., E.R., B.A.R., W.C.W.), and Biostatistics
(B.A.R.),
Harvard School of Public Health; and the Channing Laboratory (M.J.S.,
J.E.M., E.R., G.A.C., B.A.R., C.H.H., W.C.W.) and the Division of
Preventive
Medicine (J.E.M., C.H.H.), Department of Medicine, Brigham and Women's
Hospital and Harvard Medical School -- all in Boston. Address reprint
requests to Dr.
Hu at the Department of Nutrition, Harvard School of Public Health, 665
Huntington Ave., Boston, MA 02115.

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

Susan
Jim Chinnis - 25 Aug 2006 17:15 GMT
Joe Doe <None@mail.utexas.edu> wrote in part:

>Cheese is very high in saturated fat

I've been amassing the full text versions of papers cited as linking
saturated fat to morbidity or mortality and am coming up with nothing
credible.

I'm not finished, but I have pursued  a few lists of references cited in
major journal articles. If anyone has a good cite, please pass it to me!
--
Jim Chinnis   Warrenton, Virginia, USA
William Wagner - 25 Aug 2006 17:48 GMT
> Joe Doe <None@mail.utexas.edu> wrote in part:
>
[quoted text clipped - 8 lines]
> --
> Jim Chinnis   Warrenton, Virginia, USA

Hi Jim.

http://www.obesityonline.org/slides/slide01.cfm?q=CHD

Hurts my little brain!

Bill

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This article is posted under fair use rules in accordance with
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Susan - 25 Aug 2006 18:02 GMT
> Hi Jim.
>
> http://www.obesityonline.org/slides/slide01.cfm?q=CHD
>
> Hurts my little brain!

 Yabbut, can you find a single paper that has good objective evidence
of a role for saturated fat in causing CVD?  That would require
controlling for the powerful hormonal.inflammatory/atherogenic effects
of carbohydrate in the diet.  A good study would examine the role of fat
in the absence of significant glycecmic load.

Otherwise, it's pure crapola.

Susan
William Wagner - 25 Aug 2006 18:42 GMT
> x-no-archive: yes
>
[quoted text clipped - 13 lines]
>
> Susan

Susan what you want is a study designed by you.  I'd like to be able to
do that too.  Seems my questions when I find an answer do not apply to
folks that speak of CABG in the past tense.

Found this  too Jim.

http://www.theses.ulaval.ca/2004/22151/ch01.html#d0e751

Perhaps more crapola. :))

Bill

Signature

S Jersey USA Zone 5 Shade
This article is posted under fair use rules in accordance with
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and informative purposes. This material is distributed without profit.

William Wagner - 25 Aug 2006 18:47 GMT
In article
<not-to-here-williamwag-F91E9C.13424925082006@sn-indi.vsrv-sjc.supernews
.net>,

> > x-no-archive: yes
> >
[quoted text clipped - 25 lines]
>
> Bill

Should have highlighted this from the above URL.

"Indeed, physical inactivity combined with an atherogenic diet (rich in
saturated fat, trans fatty acids and refined sugars) constitute the
perfect combination giving rise to the metabolic syndrome. These
lifestyle variables, acting either through obesity or insulin
sensitivity, disturb the metabolic homeostasis and lead to the multiplex
risk factors."

Sorry!

Bill

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S Jersey USA Zone 5 Shade
This article is posted under fair use rules in accordance with
Title 17 U.S.C. Section 107, and is strictly for the educational
and informative purposes. This material is distributed without profit.

Susan - 25 Aug 2006 19:28 GMT
>  Should have highlighted this from the above URL.
>
> "Indeed, physical inactivity combined with an atherogenic diet (rich in
> saturated fat, trans fatty acids and refined sugars) constitute the
> perfect combination giving rise to the metabolic syndrome.

But the comment is untrue, for saturated fat, and in limiting the advice
about carbs to refined sugars.  They're no worse than wheat, hardly.

 These
> lifestyle variables, acting either through obesity or insulin
> sensitivity, disturb the metabolic homeostasis and lead to the multiplex
> risk factors."

This is an example of the kind of either/or black/white/no greys not
ever sh.t that pisses me off.  IR leads to obesity, then the fat cells
signal to the body in a way to sustain the obesity, and contribute to
IR.  It's not one or the other; it's BOTH.

Susan
William Wagner - 25 Aug 2006 19:43 GMT
> x-no-archive: yes
>
[quoted text clipped - 18 lines]
>
> Susan

Sort of like Yin/Yang.  Can't have one without the other.   When we
dissect  to understand it is real easy to forget the whole.

Bill who saves all of Susan's posts!

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Susan - 25 Aug 2006 19:50 GMT
>  Sort of like Yin/Yang.  Can't have one without the other.   When we
> dissect  to understand it is real easy to forget the whole.

But that's untrue; at the onset of my very worst symptoms of IR I was
thin.  Now I'm type 2 DM and just as thin.

Susan
Susan - 25 Aug 2006 19:25 GMT
>  Susan what you want is a study designed by you.

Not at all!  I'm not a scientist.  I just want studies designed and
interpreted in an objective, controlled, analytical fashion that makes
no assumptions, accepts complexity and nuance,  and takes all variables
into account.

Isn't that what the folks who keep producing these crap studies and
conclusions are paid to do?

  I'd like to be able to
> do that too.  Seems my questions when I find an answer do not apply to
> folks that speak of CABG in the past tense.

Seems to me that it makes no diff.  You want to do that which reduces
CVD risk and atherogenesis, oxidation of lipids, right?

Susan
William Wagner - 25 Aug 2006 19:36 GMT
> x-no-archive: yes
>
[quoted text clipped - 16 lines]
>
> Susan

YUP.  

"CVD risk and atherogenesis, oxidation of lipids"
=   "CVD_raol"  study   perhaps in time .

Maybe that Bill from Microsoft  could fund a few % that way.

Bill

Bill

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Susan - 25 Aug 2006 19:49 GMT
> YUP.  
>
> "CVD risk and atherogenesis, oxidation of lipids"
> =   "CVD_raol"  study   perhaps in time .
>
> Maybe that Bill from Microsoft  could fund a few % that way.

Til he does, the most important thing you can do is eat and exercise in
a way that keeps your blood glucose between 85-105 at all times.

Susan
Jim Chinnis - 25 Aug 2006 22:20 GMT
William Wagner <not-to-here-williamwag@gmail.com> wrote in part:

> Found this  too Jim.
>
>http://www.theses.ulaval.ca/2004/22151/ch01.html#d0e751
>
>Perhaps more crapola. :))

No, but it's a plan for research if my skimming is right. Not really what I
mean. I'm talking about a single study that shows that consuming more
saturated fat rather than (preferably) a number of other things causes the
rate of disease and death to rise.

Much of the older work I've read so far was done without understanding of
the effects of trans-fats. Usually, studies decreased saturated fat while
decreasing trans-fat and then attributed the reduced disease to reduction of
the sat-fat.

I don't have a firm opinion on the truth of the matter, BTW. That's why I'm
interested in finding any good studies that speak directly to the issue.
--
Jim Chinnis   Warrenton, Virginia, USA
Susan - 25 Aug 2006 23:50 GMT
> William Wagner <not-to-here-williamwag@gmail.com> wrote in part:
>
[quoted text clipped - 13 lines]
> decreasing trans-fat and then attributed the reduced disease to reduction of
> the sat-fat.

I think you meant they increased the trans fats?

Susan
Jim Chinnis - 27 Aug 2006 01:43 GMT
Susan <nevermind@nomail.com> wrote in part:

>x-no-archive: yes
>
[quoted text clipped - 19 lines]
>
>Susan

No.

The study that seems to have convinced researchers that saturated fat was
implicated in raising overall mortality and coronary artery disease in
particular was reported in 1972 in Finland. It was a large well-done study
IMO in nearly all respects. The study was done in two mental hospitals. The
patients in one were placed on a modified diet designed to reduce serum
cholesterol. After six years the hospital diets were switched. The
investigators looked at the morbidity and mortality data. They also studied
the fatty acid content of the patients' fat.

The diet was very effective in lowering heart disease and heart disease and
overall mortality.

The diet consisted of the normal diet, but with a few substitutions.
Ordinary milk was replaced by an emulsion of soybean oil in skim milk, and
butter and stick margarine were replaced with a soft margarine high in
polyunsaturates.

So....there were several changes. The cholesterol-lowering diet reduced
saturated fats, reduced trans-fats, and increased a broad range of
polyunsaturates (including short-chain omega-3).

One obviously can debate whether the benefit was due to sat fat reduction,
trans-fat reduction, or supplementing with ALA. Yet this large randomized
study seems to me to be the primary argument for an observed link between
sat fat and morbidity and mortality. At the time the study was reported, the
Lyon study was more than 20 years away, and knowledge of effects of trans
fats was negligible.
--
Jim Chinnis   Warrenton, Virginia, USA
Jim Chinnis - 27 Aug 2006 01:47 GMT
Sorry, I forget to give the reference to the Finnish study:

Lancet. 1972 Dec 30;2(7792):1418-9.
Cholesterol-lowering diet and mortality from coronary
heart-disease.Miettinen M, Turpeinen O, Karvonen MJ, Elosuo R, Paavilainen
E.
PMID: 4118706
--
Jim Chinnis   Warrenton, Virginia, USA
Susan - 27 Aug 2006 01:50 GMT
> No.
>
[quoted text clipped - 18 lines]
> saturated fats, reduced trans-fats, and increased a broad range of
> polyunsaturates (including short-chain omega-3).

Oh, okay!

> One obviously can debate whether the benefit was due to sat fat reduction,
> trans-fat reduction, or supplementing with ALA. Yet this large randomized
> study seems to me to be the primary argument for an observed link between
> sat fat and morbidity and mortality. At the time the study was reported, the
> Lyon study was more than 20 years away, and knowledge of effects of trans
> fats was negligible.

Interesting.  One potential confounder is the significant role that
psychiatric meds play in food cravings and obesity, too.

Susan
Juhana Harju - 26 Aug 2006 06:18 GMT
: William Wagner <not-to-here-williamwag@gmail.com> wrote in part:
:
[quoted text clipped - 8 lines]
: consuming more saturated fat rather than (preferably) a number of
: other things causes the rate of disease and death to rise.

Nowadays there are ethical reasons why such trial can not be done. It would
be unethical to put any patient on a saturated fat diet as it is considered
to be atherogenic based on a large body of evidence.

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

Susan - 26 Aug 2006 14:14 GMT
> Nowadays there are ethical reasons why such trial can not be done. It would
> be unethical to put any patient on a saturated fat diet as it is considered
> to be atherogenic based on a large body of evidence.

 What's unethical is for the AHA and the ADA to keep promoting the high
glycemic diet that is now proven to promote heart disease and diabetes.

Since low fat diets raise TGL, HbA1C and lower HDL, they are the
unethical choices:

SusanLipids 1995 Nov;30(11):969-76 Related Articles, Links

Low-fat diets do not lower plasma cholesterol levels in healthy men
compared to high-fat diets with similar fatty acid composition at
constant caloric intake.

Nelson GJ, Schmidt PC, Kelley DS.

Western Human Nutrition Research Center, USDA, ARS, Presidio of San
Francisco, California 94129, USA.

In most studies reporting the effects of high-fat (HF) and low-fat (LF)
diets on human plasma fatty acids (FA) and lipoprotein levels, the
design involved adding to the diet an oil that had an FA composition
(FAC) very different from the FAC of the control diet. Thus, it is
difficult to determine if simply reducing the fat content of the diet
without changing the dietary FAC changes the tissue FAC or alters plasma
lipid levels. In this study, we fed diets that contained either 22 or
39% of calories from fat, but had no differences in their FAC, for 50 d
to a group (n = 11) of healthy men (20-35 y). Thus, the
polyunsaturated/saturated ratios (1.0) of the diets were identical as
were the n-3/n-6 ratio and the monounsaturated-to-total fat ratios. The
diets contained (wt% of total fat) approximately 28% saturated FA, 33%
monounsaturated cis-FA, 6% monounsaturated trans-FA, 22% n-6
polyunsaturated FA, and 7% n-3 polyunsaturated FA, and 4% other minor
FA. The diets consisted of natural foods and were formulated to contain
16 en% protein, either 45 or 62 en% carbohydrate (CHO) and at least the
recommended daily allowance for all micronutrients. Both diets contained
360 mg of cholesterol per day. All subjects were given the HF diet for
20 d, and then six were placed on the LF and the other five remained on
the HF diet for 50 d. The two groups were crossed-over for the remaining
50 d of the study. The subjects' baseline total cholesterol level was
173 mg/dl, after 50 d on the HF diet it was 177 mg/dl and after 50 d on
the LF diet, 173 mg/dl. The differences were not significant, and there
were no significant changes in either the LDL or HDL cholesterol levels
with either diet. Triglyceride levels, and consequently very low density
lipoprotein levels, rose significantly on the LF, higher CHO diet
compared to the levels found in the subjects on the HF diet (91.5 and
66.4 mg/dl respectively, P < 0.002). The linoleic acid content of the
plasma, platelets, and red blood cells was significantly (P < 0.05)
reduced in the LF diet compared to HF diet, without any obvious
physiological effects. Hence, many earlier observations indicating
reductions in plasma lipid levels when people are on LF diets may be due
to changes in the FAC of the diet, not the reduction in fat calories.

PMID: 8569436 [PubMed - indexed for MEDLINE]
Juhana Harju - 26 Aug 2006 15:03 GMT
: x-no-archive: yes
:
[quoted text clipped - 8 lines]
: Since low fat diets raise TGL, HbA1C and lower HDL, they are the
: unethical choices:

I am not promoting low fat diets, but Mediterranean type of diets containing
mainly monounsaturated fats.

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

Susan - 26 Aug 2006 16:20 GMT
> I am not promoting low fat diets, but Mediterranean type of diets containing
> mainly monounsaturated fats.

I hope you're referring specifically to the Cretan diet?

Still, your statement about saturated fat has not one single controlled
variable study to support it, and it's unethicalf for you to keep saying
it without being able to produce one.

Susan
Jim Chinnis - 26 Aug 2006 17:28 GMT
"Juhana Harju" <shantigiriorama@gmail.com> wrote in part:

>: William Wagner <not-to-here-williamwag@gmail.com> wrote in part:
>:
[quoted text clipped - 12 lines]
>be unethical to put any patient on a saturated fat diet as it is considered
>to be atherogenic based on a large body of evidence.

Sometimes we discover that what we knew to be true was wrong. A number of
well-established medical/surgical procedures have been abandoned because
randomized trials showed them to be worthless or worse.

But I agree that the current mindset (and evidence) would make a sat-fat
randomized trial difficult. I just wonder about the hundreds of millions of
people who avoid sat fat to improve their health. Suppose they are making it
worse? Surely letting that possibly go on is unethical also?
--
Jim Chinnis   Warrenton, Virginia, USA
Juhana Harju - 26 Aug 2006 19:43 GMT
: "Juhana Harju" <shantigiriorama@gmail.com> wrote in part:
:
[quoted text clipped - 24 lines]
: of millions of people who avoid sat fat to improve their health.
: Suppose they are making it worse?

You have such suspicions, I don't. There are numerous ways saturated fats
are harmful to body. They raise LDL cholesterol and promote atherosclerosis
and thrombosis, worsen endothelial function and make arteries more
dense(postprandial effect) and cell membranes more stiff - to name just few
of the effects.

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

Susan - 26 Aug 2006 19:58 GMT
> You have such suspicions, I don't. There are numerous ways saturated fats
> are harmful to body.

You keep saying it even though not one single scintilla of controlled
scientific evidence has demonstrated it yet.  If it had, I'm sure you'd
cite it, but you never have.

 They raise LDL cholesterol and promote atherosclerosis
> and thrombosis, worsen endothelial function and make arteries more
> dense(postprandial effect) and cell membranes more stiff - to name just few
> of the effects.

None of the above has ever been found true in a properly controlled study.

That's your religious belief, not a scientifically established fact.

Susan
Juhana Harju - 26 Aug 2006 20:03 GMT
: x-no-archive: yes
:
:: You have such suspicions, I don't. There are numerous ways saturated
:: fats are harmful to body.

:: They raise LDL cholesterol and promote atherosclerosis
:: and thrombosis, worsen endothelial function and make arteries more
[quoted text clipped - 3 lines]
: None of the above has ever been found true in a properly controlled
: study.

In my posting below there is one recent study of the mechanisms saturated
fat has adverse effect on vascular function.

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

Susan - 26 Aug 2006 20:20 GMT
> In my posting below there is one recent study of the mechanisms saturated
> fat has adverse effect on vascular function.

That's not true; it wasn't eaten alone, it was eaten as part of a meal
that had profound hormonal effects.

Find a study that demonstrates that saturated fats, in the absence of
glycemic load, are causative of *any* health risks.

If not, stop making unethical claims to support your belief system.

Susan
Juhana Harju - 26 Aug 2006 20:23 GMT
: x-no-archive: yes
:
:: In my posting below there is one recent study of the mechanisms
:: saturated fat has adverse effect on vascular function.
::
: That's not true; it wasn't eaten alone,

LOL You are really funny. How do you plan a trial where fat only is eaten?

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

Susan - 26 Aug 2006 20:50 GMT
> LOL You are really funny. How do you plan a trial where fat only is eaten?

You are dense beyond belief.  Numerous studies are conducted in which
the % of calories from fat is very high, including saturated fat, and
the% of calories from carbohydrate very low.  Your lack of intellectual
rigor and paucity analytic acumen is astounding.

I've provided you with many citations to support my assertions; you've
yet to provide a single one for yours.

Susan
Juhana Harju - 26 Aug 2006 19:59 GMT
:: "Juhana Harju" <shantigiriorama@gmail.com> wrote in part:
:::: William Wagner <not-to-here-williamwag@gmail.com> wrote in part:
[quoted text clipped - 31 lines]
: arteries more dense(postprandial effect) and cell membranes more
: stiff - to name just few of the effects.

Here is one recent study:

J Am Coll Cardiol. 2006 Aug 15;48(4):715-20.
Consumption of saturated fat impairs the anti-inflammatory properties of
high-density lipoproteins and endothelial function.
Nicholls SJ, Lundman P, Harmer JA, Cutri B, Griffiths KA, Rye KA, Barter PJ,
Celermajer DS.
The Heart Research Institute, Sydney, Australia; Department of Medicine,
University of Adelaide, Adelaide, Australia.

OBJECTIVES: The purpose of this study was to investigate the influence of
dietary fatty acids on the anti-inflammatory properties of high-density
lipoproteins (HDL) and vascular function. BACKGROUND: The effect of dietary
fatty acids on atherogenesis remains uncertain. METHODS: Fourteen adults
consumed an isocaloric meal containing either a polyunsaturated or a
saturated fat on 2 occasions. The effects of post-prandial HDL on
endothelial cell expression of intercellular adhesion molecule-1 (ICAM-1)
and vascular cell adhesion molecule-1 (VCAM-1) were determined.
Flow-mediated dilation (FMD) and microvascular reactivity were assessed
before and 3 and 6 h after the meal. RESULTS: Plasma triglycerides, insulin,
and nonesterified fatty acids rose after the meals. The HDL collected 6 h
after the saturated meal were less effective than HDL isolated from fasting
plasma in terms of their ability to inhibit expression of ICAM-1 and VCAM-1,
whereas HDL collected 6 h after the polyunsaturated meal had an inhibitory
activity that was greater than that of HDL collected from fasting plasma (p
< 0.004 and p = 0.01 for comparison of effect of meals on ICAM-1 and VCAM-1,
respectively). Post-hyperemic microvascular flow significantly increased at
3 h after the polyunsaturated meal by 45 +/- 14% and by 21 +/- 11% after the
saturated meal. The FMD decreased 3 h after the saturated meal by 2.2 +/-
0.9% (p< 0.05 compared with baseline) and by 0.9 +/- 1% after the
polyunsaturated meal. CONCLUSIONS: Consumption of a saturated fat reduces
the anti-inflammatory potential of HDL and impairs arterial endothelial
function. In contrast, the anti-inflammatory activity of HDL improves after
consumption of polyunsaturated fat. These findings highlight novel
mechanisms by which different dietary fatty acids may influence key
atherogenic processes. PMID: 16904539

http://tinyurl.com/fh3jl

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

Jim Chinnis - 26 Aug 2006 20:09 GMT
The problem is that disease and mortality are caused by a complex chain.
Certain nutrients may have some documented "bad" effects (such as increased
LDL) yet improve health and longevity on the whole.

We don't know as much as you think we do when it comes to actual morbidity
and mortality.
--
Jim Chinnis   Warrenton, Virginia, USA
Juhana Harju - 26 Aug 2006 20:20 GMT
: The problem is that disease and mortality are caused by a complex
: chain. Certain nutrients may have some documented "bad" effects (such
: as increased LDL) yet improve health and longevity on the whole.
:
: We don't know as much as you think we do when it comes to actual
: morbidity and mortality.

I understand you reasoning. As there are _numerous_ metabolic ways saturated
fats have been found to be harmful it is very likely that the overall effect
is also detrimental. In addition, there is the epidemiological evidence and
many feeding studies.

However, I am willing to admit that there is an possibility that for some
subgroups increasing saturated fats _might_ be beneficial, e.g. some elderly
people, as high serum cholesterol is protecting in very old age.

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

Susan - 26 Aug 2006 20:46 GMT
> I understand you reasoning. As there are _numerous_ metabolic ways saturated
> fats have been found to be harmful it is very likely that the overall effect
> is also detrimental.

You haven't yet cited a single one that's well controlled for variables.
 Your assertion is, therefore, unethical and a lie.

 In addition, there is the epidemiological evidence and
> many feeding studies.

See above.  In the Framingham nurse's study, the highest fat eaters had
the least CVD and breast cancer; the highest starch eaters had the most.
 Some researchers spun it the other way.

> However, I am willing to admit that there is an possibility that for some
> subgroups increasing saturated fats _might_ be beneficial, e.g. some elderly
> people, as high serum cholesterol is protecting in very old age.

You have yet to cite a single credible study finding a causative role
for saturated fat in any health risk.

Susan
Juhana Harju - 26 Aug 2006 21:47 GMT
: x-no-archive: yes
:
[quoted text clipped - 8 lines]
: had the least CVD and breast cancer; the highest starch eaters had
: the most. Some researchers spun it the other way.

You deviate from the subject. I am not comparing saturated fat to carbs but
to unsaturated fats.

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

Susan - 26 Aug 2006 22:44 GMT
> You deviate from the subject. I am not comparing saturated fat to carbs but
> to unsaturated fats.

I didn't veer, you failed to comprehend.

I wasn't *comparing* them, I was saying that the carbohydrate, which has
profound metabolic hormonal effects, has not been controlled for in a
single study finding fault with saturated fat.

Knowing that, it is completely dishonest to propose that saturated fat
is causative.

Susan
Juhana Harju - 27 Aug 2006 09:28 GMT
:: The problem is that disease and mortality are caused by a complex
:: chain. Certain nutrients may have some documented "bad" effects (such
[quoted text clipped - 12 lines]
: some elderly people, as high serum cholesterol is protecting in very
: old age.

Even in old age higher monounsaturated fat intake is associated with
increased survival.

Exp Gerontol. 2005 Apr;40(4):335-43.
Unsaturated fatty acids intake and all-causes mortality: a 8.5-year
follow-up of the Italian Longitudinal Study on Aging.
Solfrizzi V, D'Introno A, Colacicco AM, Capurso C, Palasciano R, Capurso S,
Torres F, Capurso A, Panza F.
Department of Geriatrics, Center for Lipoprotein Metabolism, University of
Bari Policlinico, Piazza G. Cesare, 11-70124 Bari, Italy.

Recent evidence suggested a protective role of dietary monounsaturated fatty
acids (MUFA) and polyunsaturated fatty acids (PUFA) intakes against several
chronic diseases and, therefore, an increased human longevity. After a
median follow-up of 8.5 years, we investigated the possible role of MUFA,
PUFA, and other selected food groups in protecting against all-causes
mortality in a population-based, prospective study, conducted in one of the
eight centers of the Italian Longitudinal Study on Aging (ILSA),
Casamassima, Bari, Italy. Out of 704 elderly subjects (65-84 years), 278
nondemented persons agreed to participate at the first survey (1992-1993).
During the follow-up, there were 91 deaths. A semi-quantitative food
frequency questionnaire evaluating macronutrient daily intakes were
performed at the first survey. Higher MUFA intake was associated with an
increase of survival (hazard ratio 0.81, 95% CI 0.66-0.99), a higher
unsaturated fatty acids (UFA) to SFA ratio (hazard ratio 1.20, 95% CI
0.99-1.45) increased total mortality only marginally, while no effect about
other selected food groups were found. In conclusion, in this prospective
study on older nondemented subjects with a typical Mediterranean diet, a
higher MUFA intake increased survival, while a higher UFA/SFA ratio
increased total mortality, but only marginally. PMID: 15820615

http://tinyurl.com/loa8c

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

Matti Narkia - 28 Aug 2006 00:52 GMT
>: The problem is that disease and mortality are caused by a complex
>: chain. Certain nutrients may have some documented "bad" effects (such
[quoted text clipped - 7 lines]
>is also detrimental. In addition, there is the epidemiological evidence and
>many feeding studies.

But see what Serge Renaud, the originator and one of the authors of
the Lyon Diet Heart Study, and D Lanzmann-Petithory write in the
abstract of the review article

Renaud S, Lanzmann-Petithory D.
Coronary heart disease: dietary links and pathogenesis.
Public Health Nutr. 2001 Apr;4(2B):459-74. Review.
PMID: 11683541 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra
ctPlus&list_uids=11683541
>:

   "For decades it has been postulated that the main environmental
   factor for coronary heart disease (CHD) was the intake of
   saturated fatty acids (SFA). Nevertheless, confirmation of the
   role of SFA in CHD through intervention trials has been
   disappointing. ..."

Signature

Matti Narkia

Matti Narkia - 28 Aug 2006 01:45 GMT
>: The problem is that disease and mortality are caused by a complex
>: chain. Certain nutrients may have some documented "bad" effects (such
[quoted text clipped - 11 lines]
>subgroups increasing saturated fats _might_ be beneficial, e.g. some elderly
>people, as high serum cholesterol is protecting in very old age.

Indeed. See for example

Mozaffarian D, Rimm EB, Herrington DM.
Dietary fats, carbohydrate, and progression of coronary
atherosclerosis in postmenopausal women.
Am J Clin Nutr. 2004 Nov;80(5):1175-84. Erratum in: Am J Clin Nutr.
2005
Jan;81(1):199.
PMID: 15531663 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/80/5/1175>

  "Conclusions: In postmenopausal women with relatively low total fat
   intake, a greater saturated fat intake is associated with less
   progression of coronary atherosclerosis, whereas carbohydrate
   intake is associated with a greater progression."

Comment in the editorial of the same issue of AJCN:

Knopp RH, Retzlaff BM.
Saturated fat prevents coronary artery disease? An American paradox.
Am J Clin Nutr. 2004 Nov;80(5):1102-3. No abstract available.
PMID: 15531654 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/80/5/1102>

Signature

Matti Narkia

Juhana Harju - 28 Aug 2006 06:10 GMT
::: The problem is that disease and mortality are caused by a complex
::: chain. Certain nutrients may have some documented "bad" effects
[quoted text clipped - 29 lines]
:    progression of coronary atherosclerosis, whereas carbohydrate
:    intake is associated with a greater progression."

Consider the fact the in the American diet carbs are very refined whereas is
Finland, where we live, they are not so often. Also, if I can draw proper
conclusions, the epidemiological evidence shows that saturated fats are more
harmful in Finland as there are fewer protective features in the local diet
e.g. too little antioxidants and too little liquid vegetable oils (the
intake of vegetable oils has increased during last decades).

See
Artaud-Wild SM, Connor SL, Sexton G, Connor WE.
Differences in coronary mortality can be explained by differences in
cholesterol and saturated fat intakes in 40 countries but not in France and
Finland. A paradox.
Circulation. 1993 Dec;88(6):2771-9.

Abstract:
http://tinyurl.com/fbofa

Full text as a pdf-file:
http://circ.ahajournals.org/cgi/reprint/88/6/2771

Figure 2 A shows clearly that saturated fat is associated with heart disease
even more clearly in Finland.

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

Matti Narkia - 28 Aug 2006 02:05 GMT
>: William Wagner <not-to-here-williamwag@gmail.com> wrote in part:
>:
[quoted text clipped - 12 lines]
>be unethical to put any patient on a saturated fat diet as it is considered
>to be atherogenic based on a large body of evidence.

That's a rather strange view considering that at least for some
subpopulations saturated fat may be associated with¨less
progression of coronary atherosclerosis, see

Mozaffarian D, Rimm EB, Herrington DM.
Dietary fats, carbohydrate, and progression of coronary
atherosclerosis in postmenopausal women.
Am J Clin Nutr. 2004 Nov;80(5):1175-84. Erratum in: Am J Clin Nutr.
2005
Jan;81(1):199.
PMID: 15531663 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/80/5/1175>

  "Conclusions: In postmenopausal women with relatively low total fat
   intake, a greater saturated fat intake is associated with less
   progression of coronary atherosclerosis, whereas carbohydrate
   intake is associated with a greater progression."

Signature

Matti Narkia

Juhana Harju - 28 Aug 2006 06:11 GMT
::: William Wagner <not-to-here-williamwag@gmail.com> wrote in part:
:::
[quoted text clipped - 30 lines]
:    progression of coronary atherosclerosis, whereas carbohydrate
:    intake is associated with a greater progression."

There are always exceptions to be found. That is the way low carbers draw
their conclusions.

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

Matti Narkia - 28 Aug 2006 21:53 GMT
>::: William Wagner <not-to-here-williamwag@gmail.com> wrote in part:
>:::
[quoted text clipped - 33 lines]
>There are always exceptions to be found. That is the way low carbers draw
>their conclusions.

Is it really? My bias-dectector went berserk from your last sentence.

Remember also that earlier you wrote:

  "Nowadays there are ethical reasons why such trial can not be done.
   It would be unethical to put any patient on a saturated fat diet
   as it is considered to be atherogenic based on a large body of
   evidence"

Do you still think that "It would be unethical to put any patient on a
saturated fat diet"?

Signature

Matti Narkia

Jim Chinnis - 25 Aug 2006 22:13 GMT
Susan <nevermind@nomail.com> wrote in part:

>x-no-archive: yes
>
[quoted text clipped - 13 lines]
>
>Susan

Agree.
--
Jim Chinnis   Warrenton, Virginia, USA
Joe Doe - 27 Aug 2006 03:23 GMT
> I've been amassing the full text versions of papers cited as linking
> saturated fat to morbidity or mortality and am coming up with nothing
> credible.

> Jim Chinnis   Warrenton, Virginia, USA

I do not know if a study will every satisfy you. In the meantime for
somebody with CAD this is a real time experiment - they can choose to
act based on the best available evidence or choose to wait to be
convinced while the disease progresses.

The reality is you can use surrogate endpoints like LDL reduction to
argue for limiting saturated fat consumption.  For example replacing  25
gram of saturated fat with monounsaturated fat is expected to decrease
LDL by 15 mg/dL based on regression equation from several metanalysis.  
This corresponds to a 10% reduction in cardiac events over 5 years for a
person starting with an initial LDL of around 150.  The reality is
somebody with established CAD needs very aggressive treatment if they
hope to prevent the disease from advancing based on physical measurement
of progression of the disease as several IVUS based studies have shown.
The seemingly modest reduction in LDL may be quite important in helping
people meet aggressive lipid lowering targets - assume a target of 60
mg/dL or less for LDL.  This may need multiple drugs or the aid of
prudent dietary measures to help meet the goal.  

The modest LDL reduction would be even more beneficial for somebody who
adopts this kind of strategy very young because it is clear that modest
reductions for long periods of time are much more beneficial over long
periods of time (See for example Brown and Godstein's opinion piece in
Science 311, 1721-1723 - Lowering LDL - Not only how Low but how Long ?).

Similar arguments could be made for effects on endothelial function etc.
 
I personally love cheese but certainly limit my intake and I am mindful
of all saturated fat I consume. I do not think the entire scientific
community is deluding themselves in thinking it is a bad player in  CAD.  
For example, scientists had no problem showing very low fat diets did
shift LDL patterns to more atherogenic forms etc.  I.e. they are not as
wedded to "dogma" as Susan seems to suggest from her posts.  

Roland
Jim Chinnis - 27 Aug 2006 05:12 GMT
Joe Doe <None@mail.utexas.edu> wrote in part:

>I do not know if a study will every satisfy you. In the meantime for
>somebody with CAD this is a real time experiment - they can choose to
>act based on the best available evidence or choose to wait to be
>convinced while the disease progresses.

Roland, you may be misunderstanding my point. I do reduce my intake of
saturated fat based on what we know.

All the same, it seems to me that a good trial that relates sat fat to
endpoints would be nice to have. That's why I've been reviewing the old
literature that is always cited as evidence.

So far without success.
--
Jim Chinnis   Warrenton, Virginia, USA
David Rind - 27 Aug 2006 12:43 GMT
> The reality is you can use surrogate endpoints like LDL reduction to
> argue for limiting saturated fat consumption.  

I'm willing to grant that that is probably true for cardiac mortality,
but not for overall mortality. We have relatively little evidence that
interventions (other than statins) that reduce LDL lead to a reduction
in all-cause mortality in people without known CHD. And even in people
with known CHD, high-intensity statin regimens lower LDL more and reduce
CHD events more than low-intensity statin regimens, but have no
important effect on all-cause mortality.

So I'd be cautious about using LDL reduction as a surrogate for overall
improved mortality outcomes. For instance, I'd really like to see a
randomized trial showing that ezetimibe has some important benefit for a
clinical endpoint rather than a chemical endpoint.

Signature

David Rind
drind@caregroup.harvard.edu

Jim Chinnis - 28 Aug 2006 22:08 GMT
Joe Doe <None@mail.utexas.edu> wrote in part:

>I personally love cheese but certainly limit my intake and I am mindful
>of all saturated fat I consume. I do not think the entire scientific
>community is deluding themselves in thinking it is a bad player in  CAD.

I believe that one day our studies of saturated fat vs unsaturated etc. will
be laughed at. I think the "Nutrition labels" in the US with their careful
counting of grams of saturated fat will be laughed at.

I think we might as well have chosen to classify foods by whether the food
has a low or high ratio of width to length.
--
Jim Chinnis   Warrenton, Virginia, USA
Juhana Harju - 28 Aug 2006 22:27 GMT
: Joe Doe <None@mail.utexas.edu> wrote in part:
:
[quoted text clipped - 10 lines]
: I think we might as well have chosen to classify foods by whether the
: food has a low or high ratio of width to length.

:-D You forgot height.

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

Jim Chinnis - 28 Aug 2006 22:49 GMT
"Juhana Harju" <shantigiriorama@gmail.com> wrote in part:

>: Joe Doe <None@mail.utexas.edu> wrote in part:
>:
[quoted text clipped - 12 lines]
>
>:-D You forgot height.

I was thinking long dimension to the smallest perpendicular... Maybe they
should include BMI on nutrition labels. Green beans would do well. Rice less
so. Grapes awful. Eel would be better than shrimp.

I suspect that classification may turn out to make as much sense as
saturated vs monounsaturated vs polyunsaturated fat.
--
Jim Chinnis   Warrenton, Virginia, USA
William Wagner - 28 Aug 2006 23:23 GMT
> "Juhana Harju" <shantigiriorama@gmail.com> wrote in part:
>
[quoted text clipped - 23 lines]
> --
> Jim Chinnis   Warrenton, Virginia, USA

Na waist to hip on string beans or grapes etc.

:))

Bill

http://www.bmi-calculator.net/waist-to-hip-ratio-calculator/

Signature

S Jersey USA Zone 5 Shade
This article is posted under fair use rules in accordance with
Title 17 U.S.C. Section 107, and is strictly for the educational
and informative purposes. This material is distributed without profit.

Juhana Harju - 29 Aug 2006 04:49 GMT
:: "Juhana Harju" <shantigiriorama@gmail.com> wrote in part:
:::: Joe Doe <None@mail.utexas.edu> wrote in part:
[quoted text clipped - 22 lines]
:
: Na waist to hip on string beans or grapes etc.

Some day nutritionists will realize that round shape (or lack of it) of food
reveals its healthiness. Round foods are healthy i.e. oranges, pomegranates,
blueberries. Even broccoli, onions and carrots are round when looked from
above. Foods lacking round shape promote illness, like meat, milk and
bananas. BTW, many cheeses are round by their shapes and that is why they
don't promote illness. Always remember to buy round shaped cheeses only!

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

Matti Narkia - 27 Aug 2006 15:47 GMT
>> I've been eating a daily slice of cheddar cheese lately. About 2 x 2 square
>> slice (inches). I figure this would get my daily allotment of dairy
[quoted text clipped - 5 lines]
>Cheese is very high in saturated fat (about 6 grams in an an oz of
>cheese).  A 2x2 square may be about an 1.5 oz.  Saturated fat depresses

If we believe Serge Renaud, the originator and one of the authors of
the Lyon Diet Heart Study, and why wouldn't we, cheese has never been
associated with CHD:

Bruno Simini.
Serge Renaud: from French paradox to Cretan miracle
Lancet, Volume 355, Number 9197, 01 January 2000  
<http://www.thelancet.com/journals/lancet/article/PIIS0140673605719905/fulltext>

   Renaud's answer is simple. The participants in the Lyon
   study ate like Cretans: no butter, cream, or milk; lots
   of vegetables, fruit, bread, and cereals; and little
   meat. For the study, Renaud designed a margarine similar
   in composition to olive oil, but enriched in a-linolenic
   acid. Patients ate cheese (“a 9000 year old invention not
   linked to coronary disease”) and, of course, drank wine.

Cheese does not seem to affect serum lipis unfavorably:

Colquhoun DM, Somerset S, Irish K, Leontjew LM.
Cheese added to a low fat diet does not affect serum lipids.
Asia Pac J Clin Nutr. 2003;12 Suppl:S65.
PMID: 15023695 [PubMed - in process]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra
ctPlus&list_uids=15023695
&>

   "Background - Dietary fat is the major macronutrient that
   modifies lipids and lipoproteins. Saturated fat increases LDL,
   HDL with minimal effect on triglycerides. Part of the French
   Paradox is high intake of cheeses and low rates of CHD. The
   effect of cheeses on serum lipids has not been investigated.
   Method - 20 patients had baseline cholesterol, 4 week low fat
   (LF) diet (< 25% of calories as fat) followed by 4 week cheese
   diet (100g of camembert daily, 32-35% of calories of fat).
   Plasma Lipids were measured at baseline, after LF, and after
   cheese diet. Patients had dietary counseling at LF and cheese.
   Food intake was assessed by 3 day dietary diaries at the end of
   each diet period. Results - During LF compared to baseline,
   Total cholesterol, HDL and LDL (Friedewald calculation) dropped
   significantly (P=0.001, P=0.0001 and P=0.008). No other changes
   were detected. Conclusions - On the background of a LF diet,
   including cheese is not associated with adverse effects on
   serum lipids. Fermentation presumably is responsible for these
   favorable effects."

Nestel PJ, Chronopulos A, Cehun M.
Dairy fat in cheese raises LDL cholesterol less than that in butter in
mildly hypercholesterolaemic subjects.
Eur J Clin Nutr. 2005 Sep;59(9):1059-63.
PMID: 16015270 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=16015270
>

   "... CONCLUSION: A total of 40 g dairy fat eaten daily for 4 weeks
   as  butter, but not as cheese, raised total and LDL cholesterol
   significantly compared with a diet containing significantly less
   saturated fat. Dietary advice regarding cheese consumption may
   require modification."

Biong AS, Muller H, Seljeflot I, Veierod MB, Pedersen JI.
A comparison of the effects of cheese and butter on serum lipids,
haemostatic variables and homocysteine.
Br J Nutr. 2004 Nov;92(5):791-7.
PMID: 15533268 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=15533268
>

   "... Total cholesterol was significantly lower after the CH diet
   than after the BC diet (-0.27 mmol/l; P=0.03), while the
   difference in LDL-cholesterol was found to be below
   significance level (-0.22 mmol/l; P=0.06). There were no
   significant differences in HDL-cholesterol, triacylglycerols,
   apo A-I, apo B or lipoprotein (a), haemostatic variables and
   homocysteine between the diets. The results indicate that, at
   equal fat content, cheese may be less cholesterol increasing
   than butter. ..."

Tholstrup T, Hoy CE, Andersen LN, Christensen RD, Sandstrom B.
Does fat in milk, butter and cheese affect blood lipids and
cholesterol differently?
J Am Coll Nutr. 2004 Apr;23(2):169-76.
PMID: 15047684 [PubMed - in process]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=15047684
>

   "... RESULTS: Fasting LDL cholesterol concentration was
   significantly higher after butter than cheese diet (p = 0.037),
   with a borderline significant difference in total cholesterol
   (p = 0.054) after the experimental periods of three weeks.
   Postprandial glucose showed a higher response after cheese diet
   than after milk diet (p = 0.010, diet x time interaction).
   CONCLUSIONS: A different effect of fat in milk and butter could
   not be confirmed in this study. The moderately lower LDL
   cholesterol after cheese diet compared to butter diet should be
   investigated further..."

Hauswirth CB, Scheeder MR, Beer JH.
High {omega}-3 Fatty Acid Content in Alpine Cheese. The Basis for an
Alpine Paradox.
Circulation. 2004 Jan 6;109(1):103-7. Epub 2003 Dec 15.   
PMID: 14676141 [PubMed - as supplied by publisher]
<http://circ.ahajournals.org/cgi/content/full/109/1/103>
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1
4676141&dopt=Abstract
>

Segall JJ.
Why is cheese safe for the coronary arteries?
Int J Cardiol. 1992 May;35(2):281-3. No abstract available.
PMID: 1572753 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=1572753
>

Signature

Matti Narkia

Juhana Harju - 27 Aug 2006 16:37 GMT
::: I've been eating a daily slice of cheddar cheese lately. About 2 x
::: 2 square slice (inches). I figure this would get my daily allotment
[quoted text clipped - 11 lines]
: associated with CHD:
: [...]

In the Oxford vegetarian study consumption of eggs and cheese were both
positively associated with ischemic heart disease mortality (P for trend, <
0.01 for both foods).

http://www.ajcn.org/cgi/content/full/70/3/525S

: Cheese does not seem to affect serum lipis unfavorably:
:
: Colquhoun DM - -
: Cheese added to a low fat diet does not affect serum lipids.
: Asia Pac J Clin Nutr. 2003;12 Suppl:S65.
: PMID: 15023695 [PubMed - in process]

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra
ctPlus&list_uids=15023695
&>

:    [...] Fermentation presumably is responsible for these
:    favorable effects."

I just read some other study where calcium was found to reduce the
absorption of saturated fat. That might be one attenuating factor in
addition to fermentation.

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

Jim Chinnis - 27 Aug 2006 17:52 GMT
"Juhana Harju" <shantigiriorama@gmail.com> wrote in part:

>In the Oxford vegetarian study consumption of eggs and cheese were both
>positively associated with ischemic heart disease mortality (P for trend, <
>0.01 for both foods).

That's an interesting study. It's hard to assess the potential effects of
self-selection of the vegetarians and having the vegetarians pick the
meat-eaters, though.
--
Jim Chinnis   Warrenton, Virginia, USA
Jim Chinnis - 27 Aug 2006 18:02 GMT
Jim Chinnis <jchinnis@SPAMalum.mit.edu> wrote in part:

>"Juhana Harju" <shantigiriorama@gmail.com> wrote in part:
>
[quoted text clipped - 5 lines]
>self-selection of the vegetarians and having the vegetarians pick the
>meat-eaters, though.

(Hit send before I'd finished!)

Similarly, the vegetarians/vegans picked friends or associates in order to
eliminate social/economic biases. But still...I doubt that vegans eat out as
much. I suspect they make more of their meals from scratch. Being a
"meat-eater" may well mean in large measure eating fish-and-chips, greasy
factory-produced hamburger, washed down with colas.

I'm a passable statistician, but no amount of statistical expertise can sort
out those kinds of things in a non-randomized study.
--
Jim Chinnis   Warrenton, Virginia, USA
Matti Narkia - 27 Aug 2006 19:50 GMT
>::: I've been eating a daily slice of cheddar cheese lately. About 2 x
>::: 2 square slice (inches). I figure this would get my daily allotment
[quoted text clipped - 17 lines]
>
>http://www.ajcn.org/cgi/content/full/70/3/525S

This is an epidemiological study, and apparently one with a flawed
design. A citation:

   "... All subjects were volunteers. The vegetarian subjects were
   recruited through the Vegetarian Society of the United Kingdom,
   publicity in the national and local media, and word of mouth
   via subjects already recruited. Nonvegetarian subjects were
   recruited by the vegetarian subjects, who were asked to
   nominate friends and relatives of similar lifestyle and social
   class but who ate meat, fish, or both. ..."

Also, the death rate ratios for cheese were not statistically
significant, although the trend was. Another peculiarity of this
study: green vegetables were associated with non-significant increase
in IHD mortality. I wonder whether refined grain products, potatoes or
some other high glycemic foods would have been associated with
significant increase in IHD mortality, if they had been researched.
However, for some strange reason they were not investigated.

BTW, you convieniently chose to leave out the following part of my
message when citing my comment:

 "Bruno Simini.
 Serge Renaud: from French paradox to Cretan miracle
 Lancet, Volume 355, Number 9197, 01 January 2000  

<http://www.thelancet.com/journals/lancet/article/PIIS0140673605719905/fulltext>

     Renaud's answer is simple. The participants in the Lyon
     study ate like Cretans: no butter, cream, or milk; lots
     of vegetables, fruit, bread, and cereals; and little
     meat. For the study, Renaud designed a margarine similar
     in composition to olive oil, but enriched in a-linolenic
     acid. Patients ate cheese (“a 9000 year old invention not
     linked to coronary disease”) and, of course, drank wine."

Eating cheese didn't seem to affect very unfavorably the participants
of the Lyon Diet Heart Study: despite eating cheese their CHD event
and mortality was reduced 70% in relation to control group.

>: Cheese does not seem to affect serum lipis unfavorably:
>:
[quoted text clipped - 11 lines]
>absorption of saturated fat. That might be one attenuating factor in
>addition to fermentation.

Can your above comment be interpreted as an agreement with that cheese
does not seem to affect serum lipids unfavorably?

Signature

Matti Narkia

Juhana Harju - 27 Aug 2006 20:16 GMT
:::: In article
:::: <uqoHg.13446$xp2.12977@newsread1.news.pas.earthlink.net>, "Buddha
[quoted text clipped - 36 lines]
: Also, the death rate ratios for cheese were not statistically
: significant, although the trend was.

P for trend < 0.01 is statistically significant.

: Another peculiarity of this
: study: green vegetables were associated with non-significant increase
: in IHD mortality.

I agree. There are other peculiarities as well: nut consumption was not
associated with reduced risk of IHD contrary to some other, well designed
studies.

: I wonder whether refined grain products, potatoes or
: some other high glycemic foods would have been associated with
[quoted text clipped - 3 lines]
: BTW, you convieniently chose to leave out the following part of my
: message when citing my comment:

I left out something else as well; I don't understand your complaints.
Normally people complain because postings are not edited enough.

:  "Bruno Simini.
:  Serge Renaud: from French paradox to Cretan miracle
:  Lancet, Volume 355, Number 9197, 01 January 2000

<http://www.thelancet.com/journals/lancet/article/PIIS0140673605719905/fulltext>

:      Renaud's answer is simple. The participants in the Lyon
:      study ate like Cretans: no butter, cream, or milk; lots
[quoted text clipped - 14 lines]
::: Asia Pac J Clin Nutr. 2003;12 Suppl:S65.
::: PMID: 15023695 [PubMed - in process]

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra
ctPlus&list_uids=15023695
&>

:::    [...] Fermentation presumably is responsible for these
:::    favorable effects."
[quoted text clipped - 5 lines]
: Can your above comment be interpreted as an agreement with that cheese
: does not seem to affect serum lipids unfavorably?

At least I think that it is not so harmful as butter.