Dietary Fat Quality May be More Important Than Fat Quantity in Reducing
Risk of Cardiovascular Deaths in Middle-Aged Men

CHICAGO - The type of dietary fats consumed by middle-aged men,
especially polyunsaturated fats and linoleic acids, may be more
important than total fat intake in reducing the risk of cardiovascular
deaths, according to a study in the January 24 issue of Archives of
Internal Medicine.

According to background information in the article, substitution of
dietary polyunsaturated fat has been recommended for several decades in
the primary prevention of cardiovascular disease (CVD), but few studies
have provided scientific support for the advice. Some metabolic
studies show that polyunsaturated fats lower serum low-density
lipoprotein cholesterol (LDL-C) concentration [the so-called 'bad
cholesterol'], while saturated fat increases LDL-C. Linoleic acid
is a liquid polyunsaturated fatty acid abundant in plant fat and oils
(e.g., flaxseed, linseed oil).

David E. Laaksonen, M.D., Ph.D., from University of Kuopio, Finland,
and colleagues, assessed the dietary linoleic and total polyunsaturated
fatty acid (PUFA) intake with cardiovascular and overall rates of death
in 1,551 middle-aged men living in eastern Finland. The assessments
were made through food records and blood tests for glucose and serum
cholesterol levels.

"During the 15-year follow-up, 78 men died of CVD and 225 of any
cause," the researchers report. "Middle-aged men with proportions
of serum linoleic acid, n-6 (omega-6) fatty acids, and especially PUFA
in the upper third were up to three times less likely to die of CVD
than men with proportions in the lower third. Dietary intake of
linoleic acid and total PUFA as assessed with a 4-day food record was
also inversely associated with CVD, but total fat intake was not."

In conclusion the authors write: "Dietary fat quality thus seems more
important than fat quantity in the reduction of CVD mortality in
middle-aged men. Carrying out recommendations to replace saturated fat
with polyunsaturated fat in the primary prevention of cardiovascular
disease may substantially decrease CVD and to a lesser degree overall
mortality."

(Arch Intern Med. 2005;165: 193-199.

From:	montygram
Subject:	Re: dietary fat & cardio deaths: quality not quantity
Date:	21 Jan 2005 17:13:04 -0800

Typical nonsense "study." Peoples have used coconut oil and palm
kernel oils as dietary staples for thousands of years, and some still
do, and yet, no heart disease. The problem is how unhealthy "red meat"
is, not the saturated fatty acids. It's all about oxidative stress as
the mechanism, and it's the polyunsaturated fatty acids in meat, not
the saturated ones, than can produce oxidative stress, though the iron
content, the oxidized cholesterol, the high tryptophan content, etc.
are also problems. Also, there is the social factor, that is, those
who say they eat less "saturated fat" generally take care of themselves
better than those who say "I just eat what I want, and I love pork
rinds aned greasy burgers." Basically, this kind of "study" is more of
a sociological document than a scientific one.
I've been packing my body with loads of highly saturated fats and
non-oxidized cholesterol for a few years now. These substances should
be dietary staples, not avoided as if they were "disease causing." I'm
the only one in my family (I'm 40, they are old or a few years younger)
who is not obese and does not have a "chronic disease." A recent MRA
showed no signs of atherosclerotic plaque. My cholesterol was 209 with
63 HDL and 129 LDL on the last test, and the glucose was 75. TGs were
in normal range.

Zee wrote:
> Dietary Fat Quality May be More Important Than Fat Quantity in
Reducing
> Risk of Cardiovascular Deaths in Middle-Aged Men
>
>
>
> CHICAGO - The type of dietary fats consumed by middle-aged men,
> especially polyunsaturated fats and linoleic acids, may be more
> important than total fat intake in reducing the risk of
cardiovascular
> deaths, according to a study in the January 24 issue of Archives of
> Internal Medicine.
>
>
>
> According to background information in the article, substitution of
> dietary polyunsaturated fat has been recommended for several decades
in
> the primary prevention of cardiovascular disease (CVD), but few
studies
> have provided scientific support for the advice. Some metabolic
> studies show that polyunsaturated fats lower serum low-density
> lipoprotein cholesterol (LDL-C) concentration [the so-called 'bad
> cholesterol'], while saturated fat increases LDL-C. Linoleic acid
> is a liquid polyunsaturated fatty acid abundant in plant fat and oils
> (e.g., flaxseed, linseed oil).
>
>
>
> David E. Laaksonen, M.D., Ph.D., from University of Kuopio, Finland,
> and colleagues, assessed the dietary linoleic and total
polyunsaturated
> fatty acid (PUFA) intake with cardiovascular and overall rates of
death
> in 1,551 middle-aged men living in eastern Finland. The
assessments
> were made through food records and blood tests for glucose and serum
> cholesterol levels.
>
>
>
> "During the 15-year follow-up, 78 men died of CVD and 225 of any
> cause," the researchers report. "Middle-aged men with proportions
> of serum linoleic acid, n-6 (omega-6) fatty acids, and especially
PUFA
> in the upper third were up to three times less likely to die of CVD
> than men with proportions in the lower third. Dietary intake of
> linoleic acid and total PUFA as assessed with a 4-day food record was
> also inversely associated with CVD, but total fat intake was not."
>
>
>
> In conclusion the authors write: "Dietary fat quality thus seems more
> important than fat quantity in the reduction of CVD mortality in
> middle-aged men. Carrying out recommendations to replace saturated
fat
> with polyunsaturated fat in the primary prevention of cardiovascular
> disease may substantially decrease CVD and to a lesser degree overall
> mortality."
>
> (Arch Intern Med. 2005;165: 193-199.

From:	montygram
Subject:	Re: dietary fat & cardio deaths: quality not quantity
Date:	22 Jan 2005 12:26:27 -0800

Good question, Paul. What happens is that the oxidized cholesterol
gets stuck in the interstitial spaces in your arteries and then a
chronic inflammatory response occurs. It's like digging a hole and
having too much dirt after you fill the hole back in (if you want a
simplistic analogy). Coconut oil does not oxidize cholesterol, whereas
polyunsaturates, in general, do. Do a search on www.pub.med.com and
see for yourself (search for oxysterols and oxidized cholesterol). As
for Zwala, how do you account for generations of people living on diets
with highly saturated fatty acids in their staple foods? These
researchers are "fools" or shills, and I don't cared which.

Regarding the "study:"

The serum issue involves the PUFAs being metabolized into much more
dangerous substances (e.g., isoprostanes), since the differences in
serum PUFAs in most peoples' diets these days is negligible. I used to
post recipes here (that appeared once a week in my local newspaper),
because you could see from them that what most people eat, including
"vegetarian" recipes, contained very similar amounts of saturated fatty
acids (I think Gary Taubes has made this point in his famous articles
on this issue). Only if you use a lot of butter/cream, chocolate,
coconut, or palm kernel oil as base ingredients would you have to worry
about being "above normal" in your saturated fatty acid
consumption.

The other point, about "saturated fat" consumption, really implicates
"red meat" in particular, and again the differences between the
fatty acid composition is negligible. For example, lard at about 39%
saturated fat and chicken/turkey around 30% is nothing compared to
coconut oil at 92%. There are still several large populations using
coconut oil these days (Sri Lanka, Phillipines, etc.), and on that
diet, "heart disease" is very rare (check out WHO statistics). How can
people who consider themselves "scientific experts" and who want to
tell millions of people what to do be totally unaware of the millions
of people who consume huge amounts of saturated fatty acids, and yet
have an incredibly low incidence of heart disease? Don't they feel any
responsibility to at least address this glaring contradiction in their
claims?

My guess is that these "researchers" had their "saturated fat is bad"
idea in mind when they began the study, and only looked at the evidence
in a way that supported this notion, when there is ample evidence to
the contrary. You can't eat foods high in cholesterol and expect to do
anything you want with them. Cooking them at high temperatures while
exposed to air is something I would never do. Using a highly
unsaturated oil as a cooking oil is also really unhealthy, as opposed
to using a tiny amount of tahini (for taste) at low temperatures, which
is something I often do. These "researchers" are basically clueless.
If you don't do some independent thinking and research, these guys
will have you changing your diet every couple of days

From:	zwalanga at yahoo.com
Subject:	Re: dietary fat & cardio deaths: quality not quantity
Date:	21 Jan 2005 17:40:39 -0800

montygram wrote:
> Typical nonsense "study." Peoples have used coconut oil and palm
> kernel oils as dietary staples for thousands of years, and some still
> do, and yet, no heart disease. The problem is how unhealthy "red
meat"
> is, not the saturated fatty acids. It's all about oxidative stress
as
> the mechanism, and it's the polyunsaturated fatty acids in meat, not
> the saturated ones, than can produce oxidative stress, though the
iron
> content, the oxidized cholesterol, the high tryptophan content, etc.
> are also problems. Also, there is the social factor, that is, those
> who say they eat less "saturated fat" generally take care of
themselves
> better than those who say "I just eat what I want, and I love pork
> rinds aned greasy burgers." Basically, this kind of "study" is more
of
> a sociological document than a scientific one.
> I've been packing my body with loads of highly saturated fats and
> non-oxidized cholesterol for a few years now. These substances
should
> be dietary staples, not avoided as if they were "disease causing."
I'm
> the only one in my family (I'm 40, they are old or a few years
younger)
> who is not obese and does not have a "chronic disease." A recent MRA
> showed no signs of atherosclerotic plaque. My cholesterol was 209
with
> 63 HDL and 129 LDL on the last test, and the glucose was 75. TGs
were
> in normal range.
>
> Zee wrote:
> > Dietary Fat Quality May be More Important Than Fat Quantity in
> Reducing
> > Risk of Cardiovascular Deaths in Middle-Aged Men
> >
> >
> >
> > CHICAGO - The type of dietary fats consumed by middle-aged men,
> > especially polyunsaturated fats and linoleic acids, may be more
> > important than total fat intake in reducing the risk of
> cardiovascular
> > deaths, according to a study in the January 24 issue of Archives of
> > Internal Medicine.
> >
> >
> >
> > According to background information in the article, substitution of
> > dietary polyunsaturated fat has been recommended for several
decades
> in
> > the primary prevention of cardiovascular disease (CVD), but few
> studies
> > have provided scientific support for the advice. Some metabolic
> > studies show that polyunsaturated fats lower serum low-density
> > lipoprotein cholesterol (LDL-C) concentration [the so-called 'bad
> > cholesterol'], while saturated fat increases LDL-C. Linoleic
acid
> > is a liquid polyunsaturated fatty acid abundant in plant fat and
oils
> > (e.g., flaxseed, linseed oil).
> >
> >
> >
> > David E. Laaksonen, M.D., Ph.D., from University of Kuopio,
Finland,
> > and colleagues, assessed the dietary linoleic and total
> polyunsaturated
> > fatty acid (PUFA) intake with cardiovascular and overall rates of
> death
> > in 1,551 middle-aged men living in eastern Finland. The
> assessments
> > were made through food records and blood tests for glucose and
serum
> > cholesterol levels.
> >
> >
> >
> > "During the 15-year follow-up, 78 men died of CVD and 225 of any
> > cause," the researchers report. "Middle-aged men with proportions
> > of serum linoleic acid, n-6 (omega-6) fatty acids, and especially
> PUFA
> > in the upper third were up to three times less likely to die of CVD
> > than men with proportions in the lower third. Dietary intake of
> > linoleic acid and total PUFA as assessed with a 4-day food record
was
> > also inversely associated with CVD, but total fat intake was not."
> >
> >
> >
> > In conclusion the authors write: "Dietary fat quality thus seems
more
> > important than fat quantity in the reduction of CVD mortality in
> > middle-aged men. Carrying out recommendations to replace saturated
> fat
> > with polyunsaturated fat in the primary prevention of
cardiovascular
> > disease may substantially decrease CVD and to a lesser degree
overall
> > mortality."
> >
> > (Arch Intern Med. 2005;165: 193-199.

I really have no set ideas here. It seems to me many men have
cardiovascular problems beginning in their 40s no matter how they eat;
eat like you describe, or eat like me--modified Mediterranean. (I
wouldn't dare touch coconut oil or palm oil). I am constantly amazed at
the different ways of eating that seem to work for different
individuals.

Zee

From:	Happy Dog
Subject:	Re: dietary fat & cardio deaths: quality not quantity
Date:	Sat, 22 Jan 2005 04:01:54 -0500

wrote in message news:
>> > (Arch Intern Med. 2005;165: 193-199.
>
>
> I really have no set ideas here. It seems to me many men have
> cardiovascular problems beginning in their 40s no matter how they eat;
> eat like you describe, or eat like me--modified Mediterranean. (I
> wouldn't dare touch coconut oil or palm oil).

Bsed on, exactly, what?

I am constantly amazed at
> the different ways of eating that seem to work for different
> individuals.

"Work"? They lived longer? Felt better? Died of something unexpected for
their peer group? Be specific.

m

From:	Paul E. Lehmann
Subject:	Re: dietary fat & cardio deaths: quality not quantity
Date:	Fri, 21 Jan 2005 21:54:22 -0500

I am curious as to how or if one differentiates between cardiovascular
disease and lesions from age related narrowing of the arteries without
lesions.

I plead ignorance on the subject and am just trying to figure out if
narrowing of the arteries is in itself cardiovascular disease or whether
there has to be a lesion along with the narrowing in order for there to be
a diagnosis of cardiovascular disease.

I can mentally picture water pipes with calcium deposits narrowing with time
because of lime and other mineral deposits. I can also picture water pipes
with a structural defect in the pipe which may eventually fail along with
the mineral deposits.

In such a simplistic picture I can visualize the water pipes without the
structural defect in the pipes continue to cary water for quite some time
(although with a higher velocity because of the narrowing) without actually
bursting. I suppose that the higher velocity caused by the narrowing could
in itself increase the pressure in the pipe and eventually cause a
structural failure in the pipe. Is this how it works? Does anyone really
know?

From:	Sbharris[atsign]ix.netcom.com
Subject:	Re: dietary fat & cardio deaths: quality not quantity
Date:	21 Jan 2005 20:04:39 -0800

COMMENT:

It's way too complicated a subject to discuss fully. The short form
(which I can't do justice, so this is only approximate) is that
vascular aging per se in absense of atherosclerosis can be studied in
animals like the rat that don't get atherosclerosis or hypertension on
standard diets. As they age, you can see standard "successful aging"
which thickens the artery lining "intima" a bit, and causes the main
wall "media" to expand and lose some elasticity. None of these things
is enough to cause increases in pressure. Actually, what typically
happens is diastolic pressure drops and systolic pressure remains the
same, so that pulse pressure (systolic minus diastolic, or upper number
minus lower one) increases a little without any hypertension. This
happens as blood pressure characteristics come to be set by the large
arteries and their characteristics in advanced "healthy" aging, as
opposed to being set by small artery tone.

This is pretty much what happens in humans in the absense of disease,
with aging. It's what is seen in undeveloped countries in people on a
very low fat diet, who never get atherosclerosis or hypertension.
Normal aging is a pulse pressure of 40 at age 40 and about 60 at age
80. Anything above a pulse pressure of around 80 at 80 usually means
there's some artery damage by more than healthy aging.

By what? Well, hypertension itself, and diabetes, both cause worse
intimal thickening and worse elasticity, so it looks like aging
changes, but worse.

Atherosclerosis, a local fatty-tumor-like injury disease disease in
blood vessels, has many causes, but starts with injury to the intima
due to flexion or hypertension or chemical causes. You see it where
arteries flex a lot, like the neck, the groin or knee, or in the
bouncing heart. It starts with infiltration of the intima with foamy
lessions, which eventually coalese into plaques.These are generally
non-concentric and bulge into the artery from one side. This does NOT
in an of itself increase the pressure. If blood can't go through, it
just doesn't. Systemic pressure increases per se (systolic and
diastolic increases) are due to disease mechanisms of other types,
occuring in the smaller arteries, NOT due to disease like
atherosclerosis in larger arteries. These pressure increases in turn
cause damage (intimal thickening and loss of elasticity) in larger
arteriies, as above, but cause and effect are in the direction
indicated. The pressure increases cause the thickening in large vessels
but not the reverse (the thickening and elasticity loss per se causes
increased pulse pressure, but NOT hypertension). Similarly,
hypertension also causes atherosclerosis, but NOT the other way around
(with the exception occasionally of lessions in kidney arteries which
directly cut off the kidney blood pressure sensing mechanisms, and can
result in high blood pressure that way-- but this is rare and generally
isn't the way it happens).

SBH

From:	Zee
Subject:	Re: dietary fat & cardio deaths: quality not quantity
Date:	22 Jan 2005 13:05:24 -0800

I simply do not know. I'm learning...!

See the last line in the second citation below (Sat Fats) which says:

"Therefore, the influence of varying saturated fatty acid intakes
against a background of different individual lifestyles and genetic
backgrounds should also be considered.

The first citation below (Dietary Fats) also very interesting,
particularly for women. Thanks for your research montygram.

~~~~~~~~~~~~~~~~~~~~~~~~

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=3DRetrieve&db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15531663
Am J Clin Nutr. 2004 Nov;80(5):1175-84.
* Am J Clin Nutr. 2004 Nov;80(5):1102-3.

Dietary fats, carbohydrate, and progression of coronary atherosclerosis
in postmenopausal women.

Mozaffarian D, Rimm EB, Herrington DM.

Channing Laboratory, Department of Medicine, Brigham and Women's
Hospital and Harvard Medical School, Harvard School of Public Health,
Boston, Massachusetts, USA. dmozaffa@hsph.harvard.edu

BACKGROUND: The influence of diet on atherosclerotic progression is not
well established, particularly in postmenopausal women, in whom risk
factors for progression may differ from those for men. OBJECTIVE: The
objective was to investigate associations between dietary
macronutrients and progression of coronary atherosclerosis among
postmenopausal women. DESIGN: Quantitative coronary angiography was
performed at baseline and after a mean follow-up of 3.1 y in 2243
coronary segments in 235 postmenopausal women with established coronary
heart disease. Usual dietary intake was assessed at baseline. RESULTS:
The mean (+/-SD) total fat intake was 25 +/- 6% of energy. In
multivariate analyses, a higher saturated fat intake was associated
with a smaller decline in mean minimal coronary diameter (P =3D 0.001)
and less progression of coronary stenosis (P =3D 0.002) during follow-up.
Compared with a 0.22-mm decline in the lowest quartile of intake, there
was a 0.10-mm decline in the second quartile (P =3D 0.002), a 0.07-mm
decline in the third quartile (P =3D 0.002), and no decline in the fourth
quartile (P < 0.001); P for trend =3D 0.001. This inverse association was
more pronounced among women with lower monounsaturated fat (P for
interaction =3D 0.04) and higher carbohydrate (P for interaction =3D 0.004)
intakes and possibly lower total fat intake (P for interaction =3D 0.09).
Carbohydrate intake was positively associated with atherosclerotic
progression (P =3D 0.001), particularly when the glycemic index was high.
Polyunsaturated fat intake was positively associated with progression
when replacing other fats (P =3D 0.04) but not when replacing
carbohydrate or protein. Monounsaturated and total fat intakes were not
associated with progression. 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.

PMID: 15531663 [PubMed - indexed for MEDLINE]

~~~~~~~~~~~~~~~~~~~~~~~~

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=3DRetrieve&db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15531663

American Journal of Clinical Nutrition, Vol. 80, No. 3, 550-559,
September 2004
=A9 2004 American Society for Clinical Nutrition

COMMENTARY

Saturated fats: what dietary intake?1,2,3
J Bruce German and Cora J Dillard

1 From the Department of Food Science and Technology, University of
California, Davis (JBG and CJD), and the Nestle Research Center,
Lausanne, Switzerland (JBG) Saturated fats: what dietary intake?
Conclusions:

Twenty years ago, government guidelines recommended that all persons
consume a low-fat diet, with the advice being to "avoid too much fat,
saturated fat, and cholesterol" (121). Consumption of a low-fat diet
(defined as one containing 20% of energy from fat) was subsequently
shown to induce atherogenic dyslipidemia (122, 123). On the basis of
government guidelines, the food industry was obliged to change the
formulation of foods to a preponderance of low-fat and nonfat products,
with calories from carbohydrates being substituted for fat. It is now
known that a high-carbohydrate diet can lead to the lipoprotein pattern
(124) that characterizes atherogenic dyslipidemia. At the time the 1980
guidelines were established, there was no solid basis for understanding
what the consequences of such overall dietary changes would be for most
persons. The recommendation to lower saturated fat intake was based on
a single marker of health outcome-a correlation between dietary
saturated fat and the incidence of CAD, with blood cholesterol being
the indicator of potential disease. Now, the most recent published
recommendations are for all persons to reduce the saturated fat content
of their diet (10% of total calories), although it was stated in the
Dietary Guidelines Advisory Committee report (2) that "...no lower
limit of saturated fat intake has been identified." The summary report
by the Institute of Medicine (60) takes this recommendation one step
further by clearly stating that "...there is no intake level of
saturated fatty acids...at which there is no adverse effect." This
nutritional rhetoric is driving the food industry to respond to
governmental and public demands to decrease the amounts of all
saturated fats from the food supply. The agricultural enterprise will
continue to lower saturated fatty acids by every means possible.

Public health recommendations for the consumption of total fat and the
composition of fat in the diet are being reevaluated, and this
reevaluation is projected to be finished in 2004. To meet the body's
daily energy and nutritional needs while minimizing the risk of chronic
disease, the newest report on recommendations for healthy eating from
the National Academies' Institute of Medicine is that adults should
get 45-65% of their calories from carbohydrates, 20-35% from fat,
and 10-35% from protein. It was recently pointed out that reducing
the proportion of energy from fat below 30% is not supported by
experimental evidence and that advice to decrease total fat intake has
failed to have any effect on the prevalence of obesity, diabetes, and
cardiovascular disease (125). The recent conference summary from the
Nutrition Committee of the American Heart Association emphasized that
studies with cardiovascular endpoints that go beyond the measurements
of plasma lipids and lipoproteins are needed to evaluate the effects of
individual fatty acids in humans (126).

At this time, research on how specific saturated fatty acids contribute
to CAD and on the role each specific saturated fatty acid plays in
other health outcomes is not sufficient to make global recommendations
for all persons to remove saturated fats from their diet. No randomized
clinical trials of low-fat diets (105) or low-saturated fat diets of
sufficient duration have been carried out; thus, there is a lack of
knowledge of how low saturated fat intake can be without the risk of
potentially deleterious health outcomes. Although the removal of
particular foods from the diet can be accomplished quickly, the removal
of all saturated fats or particular saturated fatty acids from foods
cannot be accomplished quickly by the agricultural community. This will
require modification of existing foods and changes in policies to
improve health, which in turn will require integration of nutrition
needs with economic growth and development; agriculture and food
production, processing, and marketing; health care and education; and
changing of lifestyles and food choices by individual consumers. It
requires years to change the course of commodity manipulation and to
make drastic changes in the food supply. Before such implementation can
be achieved, all food sources of specific saturated fatty acids must be
accurately identified and quantified, the core commodities will need to
be changed at the level of production, agricultural processes will
require new approaches and procedures, and food formulations will need
to be changed. The question remains, What is an appropriate amount to
which saturated fatty acids in the diet can be lowered for optimal
health? Before recommendations are made to further lower the content of
these components in the food supply, should we not wait until
scientific evidence clearly shows that this is the healthiest direction
to take?

Because of the paucity of scientific understanding of the role of
specific fatty acids in humans beyond the effects on total and LDL
cholesterol, research on the effects of specific fatty acids in a
broader health context should be viewed as a clear research priority.
Given the varying health status of much of the developed world, it
would also be appropriate to explore these effects in a range of human
metabolic phenotypes, including persons with various body mass index
values, persons with insulin resistance, and persons with chronic
inflammation. Finally, the scientific community not only is recognizing
the interindividual variation in dietary response and health but is
also building the tools to measure it. Therefore, the influence of
varying saturated fatty acid intakes against a background of different
individual lifestyles and genetic backgrounds should also be
considered.

~~~~~~

From:	Jim Chinnis
Subject:	Re: dietary fat & cardio deaths: quality not quantity
Date:	Sat, 22 Jan 2005 23:00:36 GMT

Another interesting paper is

Mensink RP, Zock PL, Kester AD, Katan MB.

Effects of dietary fatty acids and carbohydrates on the ratio of serum total
to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of
60 controlled trials.

Am J Clin Nutr. 2003 May;77(5):1146-55.

BACKGROUND: The effects of dietary fats on the risk of coronary artery disease
(CAD) have traditionally been estimated from their effects on LDL cholesterol.
Fats, however, also affect HDL cholesterol, and the ratio of total to HDL
cholesterol is a more specific marker of CAD than is LDL cholesterol.
OBJECTIVE: The objective was to evaluate the effects of individual fatty acids
on the ratis of total to HDL cholesterol and on serum lipoproteins. DESIGN: We
performed a meta-analysis of 60 selected trials and calculated the effects of
the amount and type of fat on total:HDL cholesterol and on other lipids.
RESULTS: The ratio did not change if carbohydrates replaced saturated fatty
acids, but it decreased if cis unsaturated fatty acids replaced saturated
fatty acids. The effect on total:HDL cholesterol of replacing trans fatty
acids with a mix of carbohydrates and cis unsaturated fatty acids was almost
twice as large as that of replacing saturated fatty acids. Lauric acid greatly
increased total cholesterol, but much of its effect was on HDL cholesterol.
Consequently, oils rich in lauric acid decreased the ratio of total to HDL
cholesterol. Myristic and palmitic acids had little effect on the ratio, and
stearic acid reduced the ratio slightly. Replacing fats with carbohydrates
increased fasting triacylglycerol concentrations. CONCLUSIONS: The effects of
dietary fats on total:HDL cholesterol may differ markedly from their effects
on LDL. The effects of fats on these risk markers should not in themselves be
considered to reflect changes in risk but should be confirmed by prospective
observational studies or clinical trials. By that standard, risk is reduced
most effectively when trans fatty acids and saturated fatty acids are replaced
with cis unsaturated fatty acids. The effects of carbohydrates and of lauric
acid-rich fats on CAD risk remain uncertain.

Full-text is at:
http://www.ajcn.org/cgi/content/full/77/5/1146

See the figure at
http://www.ajcn.org/cgi/content/full/77/5/1146/F1
--
Jim Chinnis Warrenton, Virginia, USA jchinnis@alum.mit.edu