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.

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?

In general for a heart friendly diet

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

Roland

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.

Good ice cream does, anyway.  :-)

Actually, that's what makes it so good.

  Most people feel you

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

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

Joe Doe <None@mail.utexas.edu> wrote in part:

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

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>