Re: Polyunsaturated Fats now the most Dangerous fat.

[Guest guest]

Hi :

" Maybe that is all we have to worry about for CHD,

just avoid the bad poly fats and high glycemic carbs, which is

probably what everyone on this group does anyway. "

Interesting post. But maybe what we need to do, above all, for CHD,

is maintain a CRON diet (with the types of fat, then, perhaps being a

minor detail?)? .............

........... WUSTL subjects were not required to maintain any specific

fat, or protein, or carb intake. They had each chosen their own way

to implement CRON. Yet they seem to have astonishingly low CHD risk.

Do we know the percentage of CHD deaths in these mediterranean

dieters? I believe the number is 6% in Japan, but a lot higher than

that in France (although, of course, the french rate is much lower

than that of north America.) The japanese do use vegetable oils and

are not especially fussy about the type. They also eat a lot of

(high GI) white rice.

In my opinion, with regard to concern about CHD it might be better to

study what is so effective about the japanese diet, rather than that

of the Mediterranean. I believe that the average caloric intake in

Japan is a lot lower than in north America. Perhaps that is the key

factor in japanese CHD health .......... CR?

Rodney.

>

> sorry, but I just can't help myself going down this road again,

that

> felton study really stuck in my mind (http://www.pubmed.com)

search

> number 7934543. And listed below is a bang-uptodate brand-new study

> which backs up what Felton and others discovered in 1994.

>

> New article is " Dietary fats, carbohydrate, and progression of

> coronary atherosclerosis in postmenopausal women " pubmed:15531663

>

> The conclusion is " Carbohydrate intake was positively associated

> with atherosclerotic progression (P = 0.001), particularly when the

> glycemic index was high. Polyunsaturated fat intake was positively

> associated with progression when replacing other fats (P = 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. " (read this carefully, it really turns

> things on their head)

>

> > this is based on a 20-30% fat diet (but I suspect the same would

> be true even for a higher percentage of fat) but essentially,

> merging felton and this study the sat/mono/poly debate would seem

to

> be suggestive of mono fats being the safest, sat fats being second

> safest (would put them joint first but as they raise LDL it may be

> that they contribute to heart disease in other ways), though I feel

> they probably do not have a big impact and the number one villain

is

> Polyunsaturated fats.

>

> Now we do need some poly fats but when you look at the break down

of

> meat fat which we have been eating for millions of years then we

see

> that monofat is on average the most predominate fat, then saturated

> fat and then a small amount of polyunsaturated fat and looking at

> the recipe links by Tony on Sardinia Centarians my cursory look

> suggest again their fat intake would have been mono first, sats

> second and poly third (same for Mediterranean diet). Nature (as in

> meat)does not like poly fats, our hearts get clogged with poly

fats,

> poly fats are the bad guys, we probably need only small amounts and

> those should be a good percentage of omega3.

>

> BUT, these studies add fuel to the arguments of two very different

> camps, they prove Pritkin/Ornish correct as a very low fat diet

will

> obviously be low in poly fats and they prove the paleo (eat a lot

of

> fat and protein) diets correct as they too will have low

> polyunsaturated fat levels and low carbs. But who gets the worse

> end of the stick, which societies are so stupid as to live off high

> polyunsaturated fats combined with high glycemic foods and which

> societies have high CHD rates - yes, its us, the UK and USA and

> other countries following the Standard American Diet - the culprit

> for clogged arteries seems to be (margarines, fried foods,

partially

> hydrogenated fats and overcooked/rancid vegi oils) tied in with

high

> glycemic carbs. Maybe that is all we have to worry about for CHD,

> just avoid the bad poly fats and high glycemic carbs, which is

> probably what everyone on this group does anyway.

>

> rant now over, ....

[Guest guest]

If my understanding of your post is correct, you are saying what we've been saying.

I say eat all the poly you need - 11 grams of omega six. In soy you'll pick up a little omega 3.

Then if you avocado or a few nuts, you'll end up at a little over 20 % fat as long as you refrain from fatty meats. Eat a little lean meat you still get <30% fat and that's the def of low fat - NOT ORNISH.

Ornish's low fat is a special case for CAD reversal.

Atkin's is a special case for atkin's patients with metabolic syndrome.

Pritikin is a special case for their patients.

Regards.

----- Original Message -----

From: rwalkerad1970

Sent: Tuesday, November 16, 2004 6:17 AM

Subject: [ ] Polyunsaturated Fats now the most Dangerous fat.

sorry, but I just can't help myself going down this road again, that felton study really stuck in my mind (http://www.pubmed.com) search number 7934543. And listed below is a bang-uptodate brand-new study which backs up what Felton and others discovered in 1994.New article is "Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women" pubmed:15531663The conclusion is "Carbohydrate intake was positively associated with atherosclerotic progression (P = 0.001), particularly when the glycemic index was high. Polyunsaturated fat intake was positively associated with progression when replacing other fats (P = 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." (read this carefully, it really turns things on their head)> this is based on a 20-30% fat diet (but I suspect the same would be true even for a higher percentage of fat) but essentially, merging felton and this study the sat/mono/poly debate would seem to be suggestive of mono fats being the safest, sat fats being second safest (would put them joint first but as they raise LDL it may be that they contribute to heart disease in other ways), though I feel they probably do not have a big impact and the number one villain is Polyunsaturated fats.Now we do need some poly fats but when you look at the break down of meat fat which we have been eating for millions of years then we see that monofat is on average the most predominate fat, then saturated fat and then a small amount of polyunsaturated fat and looking at the recipe links by Tony on Sardinia Centarians my cursory look suggest again their fat intake would have been mono first, sats second and poly third (same for Mediterranean diet). Nature (as in meat)does not like poly fats, our hearts get clogged with poly fats, poly fats are the bad guys, we probably need only small amounts and those should be a good percentage of omega3. BUT, these studies add fuel to the arguments of two very different camps, they prove Pritkin/Ornish correct as a very low fat diet will obviously be low in poly fats and they prove the paleo (eat a lot of fat and protein) diets correct as they too will have low polyunsaturated fat levels and low carbs. But who gets the worse end of the stick, which societies are so stupid as to live off high polyunsaturated fats combined with high glycemic foods and which societies have high CHD rates - yes, its us, the UK and USA and other countries following the Standard American Diet - the culprit for clogged arteries seems to be (margarines, fried foods, partially hydrogenated fats and overcooked/rancid vegi oils) tied in with high glycemic carbs. Maybe that is all we have to worry about for CHD, just avoid the bad poly fats and high glycemic carbs, which is probably what everyone on this group does anyway.rant now over, ....

[Guest guest]

jwwright wrote:

Ornish's low fat is a

special case for CAD reversal.

Atkin's is a special case

for atkin's patients with metabolic syndrome.

Pritikin is a special case

for their patients.

I wonder if you would amplify this a little

Positive Dennis

[Guest guest]

I have a hard time figuring out what "Japanese" eat, but I do have a book on the Okies. And they appear to do low intake. But both are smaller people which would make me think they got less to eat less when young.

EU peoples are harder to figure out. The Mediterranean diet focused on EU descendants, might be more applicable to me.

Ergo, comparing rates of anything between ethnics is not easy. And especially comparing Americans with Japanese is silly because Americans are diverse.

I can tell you that up until about 1970, we weren't using a lot of oil. The SAD has not been around forever. Fats food entered the fried chicken, french fries, fried fish. My first was KFC in 1965. My parents didn't die of fast food (1973-75). So a main contributor has to be just too many calories.

My family and my wife's sibling's/in-laws are slimming down. Her big bro is 165# now at 78yo. The principal reason is less food intake, not any one food, and the knowledge they had to get smart about food intake or die.

Regards.

----- Original Message -----

From: Rodney

Sent: Tuesday, November 16, 2004 8:01 AM

Subject: [ ] Re: Polyunsaturated Fats now the most Dangerous fat.

Hi :"Maybe that is all we have to worry about for CHD,just avoid the bad poly fats and high glycemic carbs, which isprobably what everyone on this group does anyway."Interesting post. But maybe what we need to do, above all, for CHD, is maintain a CRON diet (with the types of fat, then, perhaps being a minor detail?)? ....................... WUSTL subjects were not required to maintain any specific fat, or protein, or carb intake. They had each chosen their own way to implement CRON. Yet they seem to have astonishingly low CHD risk. Do we know the percentage of CHD deaths in these mediterranean dieters? I believe the number is 6% in Japan, but a lot higher than that in France (although, of course, the french rate is much lower than that of north America.) The japanese do use vegetable oils and are not especially fussy about the type. They also eat a lot of (high GI) white rice.In my opinion, with regard to concern about CHD it might be better to study what is so effective about the japanese diet, rather than that of the Mediterranean. I believe that the average caloric intake in Japan is a lot lower than in north America. Perhaps that is the key factor in japanese CHD health .......... CR?Rodney.

[Guest guest]

These are diets designed for special cases - they are therapeutic diets. Ornish, Pritikin, Atkin's treat patients as did Dr Kempner before them.

If I were "sick", as in metabolic syndrome, I would try atkin's maybe Pritikin. If I had CAD I would do Ornish.

I don't have those. So I search for a food intake that first gets me the RDA's for vit, mins, fatty acids, and amino acids. I can do that with about 8# of romaine with the exception of a few things like selenium. That's about 550 kcals. Then what I need is energy, either from carbos or fatty acids.

I determine my caloric need using the harris-benedict equation. And I add that much energy.

Simply stated but not simple to do. In reality I would have trouble eating 8# of romaine and it's expensive. So an idealized food intake has to be do-able. It has to use available foods, meet budget, and provide variety. I could never stick to eating the same food every day. If I mix the greens, brassica, fruits, grain, I can get all the RDA's and a few more.

The hardest things to get are Ca, fiber, Mg, Se, Zn. Normally I don't have to add any soy oil or other oil. I would do that if I didn't have avocado, walnuts or pesto, eg.

But I don't have a large requirement for protein - I do very well with no meats, at 56 gms using dairy. If I switch some carbs to protein, keeping the calories constant, I will lose weight, indicating I'm burning the protein.

It just happens that the diet I derived for myself, looks a lot like ornish, or pritikin. I arrived at mine in frustration to find something I wasn't "allergic" to. I had never heard of Kempner's rice diet, but that was what I did. Rice, fruit and milk. After stabilizing blood pressure, dropping the betablocker, I got a lot more active and felt a lot better. I never had metabolic syndrome but I think I had a lot of visceral fat. Drop that fat and no more gut problems.

So I have to conclude I did the right thing, but that's FOR ME. Others may be totally different. And in the process I found my diet qualifies for CRAN. I don't know about CRON. Sounds like it may be excess of RDA's for vitamins/minerals. I only do an MV and vit D.

Probably the biggest confusion factor is separating diet from dieting. CR is not dieting. But once you find the minimum you need to maintain your weight, you can drop the calories or add exercise and lose weight when and if you wish and you don't have to call it anything but CR.

As for chemicals extending lifespan, I'm a skeptic.

Regards.

----- Original Message -----

From: Dennis De Jarnette

Sent: Tuesday, November 16, 2004 8:38 AM

Subject: Re: [ ] Polyunsaturated Fats now the most Dangerous fat.

jwwright wrote:

Ornish's low fat is a special case for CAD reversal.

Atkin's is a special case for atkin's patients with metabolic syndrome.

Pritikin is a special case for their patients.I wonder if you would amplify this a littlePositive Dennis

[Guest guest]

Hi All,

For another discussion on the topic, is the below.

It does appear to me to present some considerable loopholes in the

analyses.

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 - in process]

EDITORIAL 1102-1103

It is an article of faith that saturated fat raises LDL

cholesterol

and accelerates coronary artery disease, whereas unsaturated

fatty acids have the opposite effect (1, 2). One of the earliest and

most convincing studies of the better efficacy of unsaturated than

of saturated fat in reducing cholesterol and heart disease is the

Finnish Mental Hospital Study conducted in the 12 y between

1959 and 1971. In this study, the usual high-saturated-fat insti-

tutional

diet was compared with an equally high-fat diet in which

the saturated fat in dairy products was replaced with soybean oil

and soft margarine and polyunsaturated fats were used in cook-ing.

Each diet was provided for 6 y and then the alternate diet was

provided for the next 6 y (3). After a comparison of the effects of

the 2 diets in both men and women, the incidence of coronary

artery disease was lower by 50% and 65% after the consumption

of polyunsaturated fat in the 2 hospitals.

In this issue of the Journal, Mozaffarian et al (4) report the

opposite association. They found that a higher saturated fat in-take

is associated with less progression of coronary artery disease

according to quantitative angiography. How can this paradox be

explained? In food-frequency questionnaires, saturated fat in-take

is more precisely estimated than is total fat. If saturated fat

is more precisely estimated, it will associate more strongly in

statistical analyses with the outcome variable, even though other

variables—such as total fat or carbohydrate— could be more

relevant physiologically. We believe that these possibilities de-serve

a closer look.

Unlike the diet used in the Finnish Mental Hospital Study, the

diet described by Mozaffarian et al was low in fat, averaging 25%

of energy. The study subjects were women with coronary artery

disease: most were hypertensive, many had diabetes (19 –31%),

their body mass index (kg/m^2 ) ranged from 29 to 30, and their

lipid profile indicated combined hyperlipidemia (triacylglycerol

concentration: 200 mg/dL; HDL-cholesterol concentration:

40–50 mg/dL; above-average LDL concentration: 135–141 mg/

dL); these characteristics are consistent with the metabolic syn-

drome.

In addition, two-thirds of these women were taking sex

hormones. The importance of each of these points is addressed

below.

What are the effects of a low-fat, high-carbohydrate diet in

comparison with those of a higher-fat, lower-carbohydrate diet?

The response differs by the 2 main types of hyperlipidemia:

simple hypercholesterolemia and combined hyperlipidemia. In

our studies of simple hypercholesterolemia in men, a fat intake

<25% of energy and a carbohydrate intake >60% of energy was

associated with a sustained increase in triacylglycerol of 40%, a

decrease in HDL cholesterol of 3.5%, and no further decrease in

LDL in comparison with higher fat intakes (5). In contrast, a

low-fat diet in persons with combined hyperlipidemia caused no

worsening of triacylglycerol or HDL, but intakes of fat 40% of

energy and of carbohydrate 45% of energy for 2 y were asso-ciated

with a lower triacylglycerol concentration at a stable

weight (6). In the subjects of Mozaffarian et al, a greater saturated

fat intake paralleled a total fat intake, which ranged from 18% to

32% of energy in the first to fourth quartiles. Modest favorable

trends in triacylglycerol and HDL-cholesterol concentrations

were observed with higher fat intakes.

Triacylglycerol and HDL-cholesterol concentrations are

stronger predictors of coronary artery disease in women, whereas

the LDL-cholesterol concentration is a stronger predictor in men

(7). Because VLDL triacylglycerol secretion and removal rates

in healthy women are double those of men (8), conditions im-pairing

lipoprotein removal would be expected to exaggerate the

hyperlipidemic response in women as compared with that in men

(9). This sex difference is seen with the development of diabetes.

The increment in lipids is greater in women than in men and is

associated with a greater increment in coronary artery disease

risk in women than in men (9). Similarly, the development of

insulin resistance and obesity is associated with a greater lipopro-

tein

increment in women than in men (10). The exaggerated

decreases in HDL- and HDL2 -cholesterol concentrations ob-served

with the consumption of a low-fat Step II diet in women

but not in men appear to be another facet of this effect (11).

The failure of female sex hormones to prevent coronary artery

disease has been a great disappointment (9). This effect might

also be due to an estrogen-induced increase in lipoprotein entry

against a fixed or impaired rate of lipoprotein removal, as might

be expected in women with the metabolic syndrome and coro-nary

artery disease.

Would saturated fat still be bad for anyone? Not necessarily.

The effect of saturated fat and cholesterol ingestion in the form

of 4 eggs/d for 1 mo in obese, insulin-resistant subjects is 33%

of that seen in lean, insulin-sensitive subjects, likely because of

diminished cholesterol absorption (12). Thus, the classic effects

of saturated fat as compared with those of unsaturated fat seen in

the Finnish Mental Hospital Study are likely blunted in the sub-jects

of Mozaffarian et al, whereas the effects of low fat and high

carbohydrate intakes on triacylglycerol and HDL-cholesterol

concentrations appear to be exaggerated by the interactions of

female sex, exogenous sex hormones, and the metabolic syn-drome.

A major effect on cardiovascular disease risk would be

the result of hypertriglyceridemia and low HDL-cholesterol con-

centrations,

which are attenuated by an increase in saturated fat

intake itself or in total fat intake, for which saturated fat is a

more

statistically stable surrogate (4).

In conclusion, the hypothesis-generating report of Mozaffar-ian

et al draws attention to the different effects of diet on lipopro-tein

physiology and cardiovascular disease risk. These effects

include the paradox that a high-fat, high–saturated fat diet is

associated with diminished coronary artery disease progression

in women with the metabolic syndrome, a condition that is epi-demic

in the United States. This paradox presents a challenge to

differentiate the effects of dietary fat on lipoproteins and cardio-

vascular

disease risk in men and women, in the different lipid

disorders, and in the metabolic syndrome.

REFERENCES

1. Kinsell LW, s GD, Cochrane GC, Partridge JW, Jahn JP, Balch

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lipopro-teins.

J Lipid Res 1990;31:1149 –72.

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Effect of cholesterol-lowering diet on mortality from coronary heart-

disease

and other causes. Atwelve-year clinical trial in men and women.

Lancet 1972;2:835– 8.

4. Mozaffarian D, Rimm EB, Herrington DM. Dietary fats, carbohydrate,

and progression of coronary atherosclerosis in postmenopausal women.

Am J Clin Nutr 2004;80:1175– 84.

5. Knopp RH, Walden CE, Retzlaff BM, et al. Long-term cholesterol-

lowering

effects of 4 fat-restricted diets in hypercholesterolemic and

combined hyperlipidemic men. The Dietary Alternatives Study. JAMA

1997;278:1509 –15.

6. Retzlaff BM, Walden CE, Dowdy AA, McCann BS, KV,

Knopp RH. Changes in plasma triacylglycerol concentrations among

free-living hyperlipidemic men adopting different carbohydrate in-

takes

over 2 y: the Dietary Alternatives Study. Am J Clin Nutr 1995;62:

988–95.

7. Knopp RH, Zhu X, Bonet B. Effects of estrogens on lipoprotein

metab-olism

and cardiovascular disease in women. Atherosclerosis 1994;

110(suppl):S83–91.

8. Mittendorfer B, BW,Klein S. Effect of sex and obesity on

basal

VLDL-triacylglycerol kinetics. Am J Clin Nutr 2003;77:573–9.

9. Barrett-Connor E, Giardina EG, Gitt AK, Gudat U, Steinberg HO,

Tschoepe D. Women and heart disease: the role of diabetes and hyper-

glycemia.

Arch Intern Med 2004;164:934 –42.

10. Aikawa K, Retzlaff B, Fish B, et al. Dyslipidemia of insulin

resistance

and obesity: gender differences. Circulation 2002;106(suppl 2):II-75

(abstr 377).

11. Walden CE, Retzlaff BM, Buck BL, Wallick S, McCann BS, Knopp RH.

Differential effect of the National Cholesterol Education Program

(NCEP) Step II diet on HDLcholesterol, its subfractions, and

apoprotein

A-I levels in hypercholesterolemic women and men after 1 year: the

beFIT Study. Arterioscler Thromb Vasc Biol 2000;20:1580 –7.

12. Knopp RH, Retzlaff B, Fish B, et al. Effects of insulin

resistance and

obesity on lipoproteins and sensitivity to egg feeding. Arterioscler

Thromb Vasc Biol 2003;23:1437– 43.