Re: macro nutrients, sat fats

[Guest guest]

--- In , " Rodney " <perspect1111@y...>

wrote:

> If what you say below is true then why is it that it is only

> saturated and trans fats that are associated with elevated rates of

> CVD?

I wasn't specifically referring to trans-fat. But trans-fat is a

dangerous toxin, not a real food, that gunks up the EFA pathway from

working properly -- the heart muscle has a special affinity for Omega

3's. You don't need to eat a large amount of fat to get EFAs.

As to saturated fat, this quote says it best:

" The more saturated fat one ate, the more cholesterol one ate, the

more calories one ate, the lower peoples' serum cholesterol… we found

that the people who ate the most cholesterol, ate the most saturated

fat, ate the most calories, weighed the least and were the most

physically active. " -- Dr. Castelli, Director of the

prestigious Framingham Study

> All types of fat contain about nine calories per gram. All of

> them, if eaten in excess, have the same identical ability to 'crowd

> out' better nutrition. Why is it that diets high in

> polyunsaturated and monounsaturated fats (that are associated with

> REDUCED rates of CVD) do not crowd out higher nutrient intakes?

What research unequivocally says they do not? Are you essentially

implying that eating large amounts of polys and monos is healthy?!!

Consider that: more fat == more oxidation == more antioxidants

required. There is even a study I cannot recall at the moment

showing that more than 37% of calories from monounsaturated fat

reduces insulin sensitivity, a clear sign of pathology in progress.

Also consider that: excess protein is converted into glucose.

Cconsider that: excess glucose is converted into saturated fat.

Would you then claim that a high, whole-grain carbohydrate diet is

going to cause CVD according to the Lipid Theory due to the excess

saturated fat and/or cholesterol produced internally? Oh boy.

You know, in general, it seems to me that the economic propaganda and

incentives for the Lipid Theory sure makes it exceedingly difficult

to consider that woefully inadequate nutrition may actually be the

real cause of CVD. I think perhaps it's collective denial and an

unwillingness to face self-responsibility. What do people in denial

do? Bury their heads in the sand and take the path of least

resistance. It's more pscyhologically comforting and self-validating.

We probably take it far way too granted in here, but not too long ago

it was " firmly established " that nutrition having ANY influence on

all-cause mortality or disease was considered complete B.S.. A

theory that was invented 60+ years ago is definitely based on that

kind of old school thinking.

Logan

[Guest guest]

Hi Logan:

I understood your argument to be that it is not high blood lipids

that cause CVD, it is inadequate intake of what you consider to be

the appropriate nutrients. You said, I thought, that the reason for

the association between saturated fats and CVD was not that saturated

fats are harmful, but rather that eating fat, because of its high

caloric content, crowds out the good nutrients the consumption of

which, you believe, prevents CVD. Now first of all did I

misunderstand you on this point? If I did then clarification would

be helpful. If not then .............

.............. your point about fat crowding out good nutrients

cannot be applied, selectively, by you, only to saturated fats. You

cannot escape the fact that if your line of reasoning is correct then

ALL FATS (since they all contain lots of calories) should crowd out

healthy nutrients, and thereby, according to you, cause CVD. But

this is not born out by epidemiological studies.

> " There is even a study I cannot recall at the moment

> showing that more than 37% of calories from monounsaturated fat

> reduces insulin sensitivity, a clear sign of pathology in progress.

> "

[Clearly no rational individual, least of all me, suggests that

eating 37% of calories from just one type of fat (mono, you noted) is

advisable. You are talking to someone who, from 1974 to 1998

consumed a diet averaging between 10% and 15% of calories from all

types of fat. And since 1998 between 15% and 20%. And with lipids

numbers in the lowest 5% of the population - although nowhere near as

good as those shown by people here who are established on CRON. So

it is certainly not my view that high overall fat intake is

desirable.]

But you cannot escape the fact that the Nurses' Health Study -

probably the best epidemiological study so far in history - shows

that while trans fats and saturated fats are harmful, monounsaturated

fats are somewhat helpful and polyunsaturated fats quite helpful for

preventing CVD. If your reasoning were correct then the study

results would have shown, instead, that all fats are harmful because

they all, according to you, should crowd out the beneficial nutrients

you believe in. (At the risk of repetition, the Nurses' Health Study

has been going on for thirty years, has followed more than 100,000

individuals and, imo, cannot be ignored just because its results do

not fit with your preconceived view of things). In addition the very

recent (not yet published) huge INTERHEART study shows a very

consistent dose-response relationship between lipids values and

myocardial infarction. Indeed lipids values are the MOST important

of the nine factors they identified.

Also bear in mind that the HEALTHIEST people in the Mediterranean

region, the inhabitants of Crete, consume truly humungous quantities

of olive oil, a lot more than I consider advisable. But it certainly

does them no apparent harm. They live longer than any other group in

the region. Not only do they use it for cooking and in salad

dressings, their biggest source of it is in their preserved foods.

When they eat the preserved foods they also eat the olive oil they

used to preserve it. Why are they so healthy while eating such huge

amounts of fat? Why is this fat not causing CVD, as your line of

reasoning would indicate it ought to, by crowding out the nutrients

you beleive in?

Most of these nutrients, it seems to me based on what you have posted

here, you would like to take in the form of supplements, from sources

obscure enough that most of us could not find them even if we wished

to. Do you have thirty year studies, 100,000 strong to support your

supplement recommendations?

So the issue seems to be: " what do you accept as evidence? " What DO

you accept as evidence of your point of view?

Rodney.

> > All types of fat contain about nine calories per gram. All of

> > them, if eaten in excess, have the same identical ability

to 'crowd

> > out' better nutrition. Why is it that diets high in

> > polyunsaturated and monounsaturated fats (that are associated

with

> > REDUCED rates of CVD) do not crowd out higher nutrient intakes?

> What research unequivocally says they do not? Are you essentially

> implying that eating large amounts of polys and monos is

healthy?!!

> Consider that: more fat == more oxidation == more antioxidants

> required. There is even a study I cannot recall at the moment

> showing that more than 37% of calories from monounsaturated fat

> reduces insulin sensitivity, a clear sign of pathology in progress.

>

> Also consider that: excess protein is converted into glucose.

> Cconsider that: excess glucose is converted into saturated fat.

> Would you then claim that a high, whole-grain carbohydrate diet is

> going to cause CVD according to the Lipid Theory due to the excess

> saturated fat and/or cholesterol produced internally? Oh boy.

>

> You know, in general, it seems to me that the economic propaganda

and

> incentives for the Lipid Theory sure makes it exceedingly difficult

> to consider that woefully inadequate nutrition may actually be the

> real cause of CVD. I think perhaps it's collective denial and an

> unwillingness to face self-responsibility. What do people in

denial

> do? Bury their heads in the sand and take the path of least

> resistance. It's more pscyhologically comforting and self-

validating.

>

> We probably take it far way too granted in here, but not too long

ago

> it was " firmly established " that nutrition having ANY influence on

> all-cause mortality or disease was considered complete B.S.. A

> theory that was invented 60+ years ago is definitely based on that

> kind of old school thinking.

>

> Logan

[Guest guest]

--- In , " Rodney " <perspect1111@y...>

wrote:

> Also bear in mind that the HEALTHIEST people in the Mediterranean

> region, the inhabitants of Crete, consume truly humungous

quantities

> of olive oil, a lot more than I consider advisable. But it

certainly

> does them no apparent harm. They live longer than any other group

in

> the region. Not only do they use it for cooking and in salad

> dressings, their biggest source of it is in their preserved foods.

> When they eat the preserved foods they also eat the olive oil they

> used to preserve it. Why are they so healthy while eating such

huge

> amounts of fat? Why is this fat not causing CVD, as your line of

> reasoning would indicate it ought to, by crowding out the nutrients

> you beleive in?

Hi All,

There was much of interest to me in the pdf-available below full

paper, which is presnted after the media article.

These included:

" Olive oil may not prevent colon cancer because of its

monounsaturated fatty acid (MUFA) content, but

because of its other components such as its anti-oxidants

or phytosterols " .

European Journal of Cancer Prevention June 2004;13(3):219-230

The term 'Mediterranean diet', implying that all Mediterranean people

have

the same diet, is a misnomer. The countries around the

Mediterranean basin have

different diets, religions and cultures. Their diets differ in

the amount of

total fat, olive oil, type of meat, wine, milk, cheese, fruits

and vegetables;

and the rates of coronary heart disease and cancer, with the

lower death rates

and longer life expectancy occurring in Greece. The diet of

Crete represents the

traditional diet of Greece prior to 1960. Analyses of the

dietary pattern of the

diet of Crete shows a number of protective substances, such as

selenium,

glutathione, a balanced ratio of n-6/n-3 essential fatty acids

(EFA), high

amounts of fibre, antioxidants (especially resveratrol from

wine and polyphenols

from olive oil), vitamins E and C, some of which have been

shown to be

associated with lower risk of cancer, including cancer of the

breast. Epidemiological

studies and animal experiments indicate that n-3 fatty acids

exert protective

effects against some common cancers, especially cancers of the

breast, colon and

prostate. Many mechanisms are involved, including suppression

of neoplastic

transformation, cell growth inhibition, and enhanced apoptosis

and anti-angiogenicity,

through the inhibition of eicosanoid production from n-6 fatty

acids; and

suppression of cyclooxygenase 2 (COX-2), interleukin 1 (IL-1)

and IL-6 gene

_expression by n-3 fatty acids. Recent intervention studies in

breast cancer

patients indicate that n-3 fatty acids, and docosahexaenoic

acid (DHA) in

particular, increase the response to chemopreventive agents. In

patients with

colorectal cancer, eicosapentaenoic acid (EPA) and DHA decrease

cell proliferation,

and modulate favourably the balance between colonic cell

proliferation and

apoptosis. These findings should serve as a strong incentive

for the initiation

of intervention trials that will test the effect of specific

dietary patterns in

the prevention and management of patients with cancer.

Giacosa A.

The Mediterranean diet and its protective role against cancer.

Eur J Cancer Prev. 2004 Jun;13(3):155-7. No abstract available.

PMID: 15167212 [PubMed - in process]

The term `the Mediterranean diet' was first popularized

by Ancel Keys in his book How to Eat Well and Stay Well: the

Mediterranean Way, in 1975. This followed the publication

of his studies which showed that Mediterranean countries

have diets associated with low incidence of cardiovascular

disease. Later studies have demonstrated that the

Mediterranean countries also show a low incidence of

cancers of the colon and breast and there is now little

doubt that the Mediterranean countries enjoy a low risk

of many of the diet-related diseases of affluence (Hill and

Giacosa, 1992; Hu, 2003).

The Mediterranean is a large area with many different

diet patterns, but they are all characterized by high

consumption of fruit, vegetables, legumes and dietary

fibre and low intakes of meat and saturated fats. In all of

these respects they agree with the current concepts of a

`healthy diet' and one towards which many countries in

northern Europe are moving (Trichopoulou, 2001).

A further general characteristic of the Mediterranean diet

is the consumption of olive oil, usually in large amounts,

and of fish.

The antioxidant potential of the Mediterranean diet

The Mediterranean diet not only produces favourable

effects on blood lipids but also protects against oxidative

stress. Oxidative damage is thought to represent one of

the mechanisms leading to chronic diseases such as

atherosclerosis and cancer. Many studies suggest that a

link exists between fruit and vegetables or the amounts of

plasma antioxidant vitamins (ascorbic acid, tocopherol

and carotenoids) and risk of death from cancer or coronary

heart diseases. Although emphasis has been given to

different components of the diet, attention has recently

shifted to the diet as a whole. The Mediterranean diet is

able to modulate oxidative stress through complex

mechanisms and not just the high antioxidant compound

content. The preference for fresh fruit and vegetables in

the Mediterranean diet will result in a higher consump-tion

of raw foods, a lower production of cooking-related

oxidants and a consequent decreased waste of nutritional

and endogenous antioxidants. The high intake of anti-

oxidants and fibre helps to scavenge even the small

amount of oxidants or oxidized compounds (Ghiselli et al.,

1997).

Mediterranean diet and DNA adducts

The interaction between environmental carcinogenic

exposures and genetic and acquired susceptibility, such

as polymorphism of metabolizing enzymes and of DNA

repair enzymes, age at starting carcinogen exposure,

gender and ethnicity, may play an important role in most

human cancers (Perera, 1997). Nutritional factors,

including low intake of saturated fat and high consump-tion

of fruit and vegetables, may change an individual's

risk of cancer, particularly of epithelial tumours, in a

favourable direction (Potter and Steinmetz, 1996; La

Vecchia and Tavani, 1998). A general protective effect

against cancer at different sites in the body has been

suggested for a number of fruit and vegetables, including

fresh fruit and vegetables, cruciferous and leek vegetables

(Potter and Steinmetz, 1996).

There are a number of biologically active chemicals in

fruit and vegetables that may potentially reduce the

likelihood of cancer, such as carotenoids, ascorbate,

tocopherols, isothiocyanates, phenols and selenium (Pot-ter

and Steinmetz, 1996) (Table 1), through a number of

mechanisms, including induction and/or inhibition of

enzymes involved in carcinogen metabolism or in DNA

repair, antioxidant effects, increased apoptosis and

decreased cell proliferation (La Vecchia and Tavani,

1998).

Flavonoids and other phenolic compounds have been

detected in grapes, apples, berries, olive, lettuce, onions,

red wine, olive oil and in other components of the

`Mediterranean diet'. Dietary phenolics, mostly of plant

origin, might protect against cancer by affecting the

kinetics of DNA adduct formations, i.e. by modifying the

cytochrome P450-dependent metabolisms, by inducing

the detoxification or DNA repair pathways or by

antioxidant activity (Malaveille et al., 1996; Peluso and

Vineis, 2000). High intake of cruciferous vegetables, such

as broccoli, cabbage and cauliflower has been associated

with lower bladder cancer risk. Combined intake of

tomatoes, tomato sauce, tomato juice and pizza has been

related to lower prostate cancer risk. High consumption

of tomatoes and tomato-based products, including

spaghetti sauce, tomato soup and tomato paste, has been

associated with lower cancer risk for different anatomic

sites (Giovannucci, 1999).

Broccoli, tomatoes and pizza are typical features of the

`Mediterranean diet' and important dietary sources of

isothiocyanates and lycopene, two phytochemicals that

can act as antioxidants or by inducing detoxifying

enzymes (Giovannucci et al., 1995). Therefore, it is

possible that phytochemicals other than flavonoids may

be additionally or complementarily involved in the

reported protective effects of the `Mediterranean diet'

on leukocyte DNA adduct formations.

The antioxidant/anticancer potential of

phenolic compounds isolated from olive oil

High intakes of dietary fats have been implicated in the

development of a number of diseases, including cancer.

Recently, however, the epidemiologic data linking breast

and colon cancer with total fat intake have not been

upheld. In this regard, evidence is emerging that it is not

only the amount but also the type of dietary fat that is

important in the aetiology of some cancers, with

particular regard to olive oil (La Vecchia et al., 1995;

Franceschi et al., 1996, 1997; Braga et al., 1998), and of fish

oil (Simopoulos, 2001).

For this reason, the phenolic and squalene content of a

range of seasoning oils and their antioxidant potential

were quantitated (Owen et al., 2000a).

Recent studies have shown that olive oil, and in particular

extra virgin olive oil, contains an abundance of phenolic

antioxidants including simple phenols (hydroxytyrosol,

tyrosol), aldehydic secoiridoids, flavonoids and lignans

(acetoxypin resinol, pinoresinol). All of these phenolic

substances are potent inhibitors of reactive oxygen

species attack on, for example, salicylic acid and 2-

deoxyguanosine. Currently, there is growing evidence

that reactive oxygen species are involved in the aetiology

of fat-related neoplasms such as cancer of the breast

and colorectum. A plausible mechanism is a high

intake of O-6 polyunsaturated fatty acids which are

especially prone to lipid peroxidation initiated and

propagated by reactive oxygen species, leading to the

formation (via a,b-unsaturated aldehydes such as trans-4-

hydroxy-2-nonenal) of highly promutagenic exocyclic

DNA adducts.

Previous studies have shown that the colonic mucosa of

cancer patients and those suffering from predisposing

inflammatory conditions, such as ulcerative colitis

and Crohn's disease, generates appreciably higher

quantities of reactive oxygen species compared

with normal tissue. Those studies have been extended

by developing accurate high-performance liquid chroma-tography

(HPLC) methods for the quantitation of

reactive oxygen species generated by faecal matrix (Owen

et al., 2000b). The data show that the faecal matrix

supports the generation of reactive oxygen species

in abundance. As yet, there is a dearth of evidence

linking this capacity to actual components of the

diet which may influence the colorectal milieu. However,

using the newly developed methodology we can demon-strate

that the antioxidant phenolic compounds present

in olive oil are potent inhibitors of free radical generation

by the faecal matrix. This indicates that the study of the

inter-relation between reactive oxygen species and diet-ary

antioxidants is an area of great promise for elucidating

mechanisms of colorectal carcinogenesis and possible

future chemopreventive strategies.

Update on fat consumption and cancer risk

A review of the available data on the relationship between

fat consumption and cancer risk emphasizes the pre-ventive

role of the Mediterranean diet.

General considerations

> There is a shortage of well-designed intervention

studies on the relation between diet and cancer risk.

> Laboratory and animal studies give invaluable

information on, for example, mechanisms of

carcinogenesis, but cannot be used to predict the

effect of diet changes on risk of cancer in humans.

> The Mediterranean region provides valuable evidence

of the effect of a particular dietary pattern on health, in

which dietary fat is not harmful, and may even decrease

the risk of cancer at certain sites.

Colon cancer

> There is no evidence that the total fat or saturated fat

intake is related to colon cancer risk in the

Mediterranean context.

> There is evidence that certain types of fat, for example

olive oil and fish oil, may decrease the risk of colon

cancer.

> Olive oil may not prevent colon cancer because of its

monounsaturated fatty acid (MUFA) content, but

because of its other components such as its anti-oxidants

or phytosterols.

> There is disagreement about the strength of the

association between red meat and colon cancer.

Breast cancer

> Evidence concerning the influence of dietary fats on

breast cancer is inconclusive.

> There is some evidence from case–control studies that

high intakes of MUFAs and polyunsaturated fatty acids

(PUFAs) are associated with a decreased risk of breast

cancer.

> Population-based studies have found that total fat

intakes ranging from 20 to 40% of total energy intake

are not related to breast cancer risk.

Prostate cancer

> There is a little evidence of an association between the

intake of saturated fats and the incidence of prostate

cancer.

Priorities for future research

> More well-designed intervention studies of the

effect of diet change on cancer risk in humans are

needed.

> A better understanding of the interaction between

intake of animal products (e.g. red meat) and protective

factors (e.g. fruit, vegetables, wholegrain cereals) in the

diet are needed.

> An improved understanding of the role of lifestyle in

early life on subsequent cancer risk is needed.

> We need to know more about gene–environment

interactions, and the importance of genetic

polymorphism in determining cancer risk.

> The general increase in male life expectancy in western

countries makes it important to improve our

understanding of prostate cancer.

Conclusion

The Mediterranean diet appears to be a healthy diet,

whose benefits are mainly due to its high antioxidant

potential. The preference for fresh fruit and vegetables,

typical of Mediterranean populations, will result in a

higher consumption of raw foods. This involves a reduced

production of cooking-related oxidants, with a conse-quent

decreased waste of nutritional and endogenous

antioxidants.

The abundance of phenolic compounds and other

antioxidants in typical Mediterranean foods (olive oil,

wine, herbs, fruits and vegetables) increases the palat-ability

of foods, and contributes to cooking-derived

carcinogens and peroxides being present at a low level.

Thus the Mediterranean diet is not only non-toxic, but

health promoting as well.

References

Braga C, La Vecchia C, Franceschi S, et al. (1998). Olive oil, other

seasoning

fats, and the risk of colorectal carcinoma. Cancer 82: 448–453.

Franceschi S, Favero A, Decarli A, et al. (1996). Intake of

macronutrients and the

risk of breast cancer. Lancet 347: 1351–1356.

Franceschi S, Favero A, La Vecchia C, et al. (1997). Food groups and

risk of

colorectal cancer in Italy. Int J Cancer 72: 56–61.

Ghiselli A, D'Amicis A, Giacosa A (1997). The antioxidant potential

of the

Mediterranean diet. Eur J Cancer Prev 6 (Suppl 1): S15–S19.

Giovannucci E (1999). Tomatoes, tomato-based products, lycopene and

cancer:

review of the epidemiologic literature. J Natl Cancer Inst 91: 317–

331.

Giovannucci E, Ascherio A, Rimm EB, et al. (1995). Intake of

carotenoids and

retinol in relation to risk of prostate cancer. J Natl Cancer Inst 87:

1767–1776.

Hill MJ, Giacosa A (1992). The Mediterranean diet. Eur J Cancer Prev

1: 339–340.

Hu FB (2003). The Mediterranean diet and mortality – olive oil and

beyond.

N Engl J Med 348: 2595–2596.

Keys, Ancel B (1975). How to eat well and stay well: the

Mediterranean way.

New York: Doubleday.

La Vecchia C, Tavani A (1998). Fruit and vegetables, and human

cancer. Eur J

Cancer Prev 7: 3–8.

La Vecchia C, Negri E, Franceschi S, et al. (1995). Olive oil, other

dietary fats, and

the risk of breast cancer (Italy). Cancer Causes Control 6: 545–550.

Malaveille C, Hautefeuille A, Pignatelli B et al. (1996). Dietary

phenolics as

antimutagens and inhibitors of tobacco related DNA adduction in the

urothelium of smokers. Carcinogenesis 17: 2193–2200.

Owen RW, Mier W, Giacosa A, et al. (2000a). Phenolic compounds and

squalene in olive oils: the concentration and antioxidant potential

of total

phenols, simple phenols, secoiridoids, lignans and squalene. Food Chem

Toxicol 38: 647–659.

Owen RW, Giacosa A, Hull WE, et al. (2000b). The

antioxidant/anticancer

potential of phenolic compounds isolated from olive oil. Eur J Cancer

36:

1235–1247.

Peluso M, Vineis P (2000). `Mediterranean diet' and DNA adducts. Eur

J Cancer

Prev 9: 71–72.

Perera FB (1997). Environment and cancer: who are susceptible?

Science 278:

1068–1073.

Potter JD, Steinmetz K (1996). Vegetables, fruit and phytoestrogens as

preventive agents. In: Steward BW, McGregor D, Kleiheus O (editors):

Principles of Chemoprevention, IARC Publication No. 139. Lyon:

Interna-tional

Agency for Research on Cancer; pp. 61–90.

Simopoulos AP (2001). The Mediterranean diets: what is so special

about the

diet of Greece? The scientific evidence. J Nutr 131: 3065S–3073S.

Trichopoulou A (2001). Mediterranean diet: the past and the present.

Nutr Metab

Cardiovasc Dis 11: 1–4.

Cheers, Alan Pater

[Guest guest]

>

> As to saturated fat, this quote says it best:

>

> " The more saturated fat one ate, the more cholesterol one ate, the

> more calories one ate, the lower peoples' serum cholesterol… we

found

> that the people who ate the most cholesterol, ate the most

saturated

> fat, ate the most calories, weighed the least and were the most

> physically active. " -- Dr. Castelli, Director of the

> prestigious Framingham Study

Hi All,

To quote your Dr. W. Catelli, he in the scientific literature says: " …

Diet intervention trials have shown that a reduction in total

cholesterol and saturated fat consumption produced reduction in CHD

incidence proportionate to the fall in cholesterol. …

PMID: 2220800 [PubMed - indexed for MEDLINE] " .

Therefore, since saturated fats increase cholesterol, your arguments

may be not justified.

Cheers, Al Pater.

[Guest guest]

> " The more saturated fat one ate, the more cholesterol one ate, the more

calories one ate, the lower peoples' serum cholesterol... we

>>found that the people who ate the most cholesterol, ate the most saturated

> fat, ate the most calories, weighed the least and were the most

> physically active. " -- Dr. Castelli, Director of the

> prestigious Framingham Study

This quote is often thrown around the internet and the WWW. However, as shown,

it is direct opposition to published documented quotes from Dr Castelli. I

have also had the opportunity to spend some time with him and speak to him

personally and from my conversations with him, I would say that the above quote

does not represent our conversation and his comments to me.

So, my question is, instead of just re-distributing this " random " quote without

its context, can you put provide the proper context for us by telling us when

and where the quote is from?

Thanks

jeff

[Guest guest]

Thanks for pointing that out, but Catelli published that study that a

full two years before the quote I posted. Here's a more recent

abstract from him:

" Our understanding of coronary artery disease risk and the

atherosclerotic process has changed greatly in recent years. For

example, it is now known that angiographically apparent coronary

artery plaque is not the major cause of myocardial infarction (MI).

Rather, it is unstable, soft plaque that cannot be seen

angiographically that is prone to rupture and result in infarction.

Also important are changes in vascular reactivity resulting from

diet. Cholesterol levels by themselves reveal little about a

patient's coronary artery disease risk. Most infarctions occur in

patients who have normal total cholesterol levels. At-risk patients

can be identified using the ratio of total-to-high-density

lipoprotein (HDL) cholesterol levels. The ratio of triglyceride to

HDL cholesterol levels is also important. Simple steps to assess

patients' risk in practice are outlined. Primary prevention trials

demonstrate that coronary artery disease risk can be lowered

dramatically with diet and drug therapy. " [PMID: 9860378]

Considering the decades Catelli's been involved in research trying to

prove the anarchronistic Lipid Theory, this is a remarkable

admission! Perhaps he just went " soft in the head " in his old age or

maybe he was beginning to realize and accept the futility of the

theory. There's nothing of note published from him thereafter,

except for one study [PMID: 10388480] which actually lends some

support to the modern, competing theory!

Logan

>

>

> >

> > As to saturated fat, this quote says it best:

> >

> > " The more saturated fat one ate, the more cholesterol one ate,

the

> > more calories one ate, the lower peoples' serum cholesterol… we

> found

> > that the people who ate the most cholesterol, ate the most

> saturated

> > fat, ate the most calories, weighed the least and were the most

> > physically active. " -- Dr. Castelli, Director of the

> > prestigious Framingham Study

>

> Hi All,

>

> To quote your Dr. W. Catelli, he in the scientific literature

says: " …

> Diet intervention trials have shown that a reduction in total

> cholesterol and saturated fat consumption produced reduction in CHD

> incidence proportionate to the fall in cholesterol. …

> PMID: 2220800 [PubMed - indexed for MEDLINE] " .

>

> Therefore, since saturated fats increase cholesterol, your

arguments

> may be not justified.

>

> Cheers, Al Pater.

[Guest guest]

--- In , " Rodney " <perspect1111@y...>

> I understood your argument to be that it is not high blood lipids

> that cause CVD, it is inadequate intake of what you consider to be

> the appropriate nutrients. You said, I thought, that the reason

That's correct.

> fats are harmful, but rather that eating fat, because of its high

> caloric content, crowds out the good nutrients the consumption of

> which, you believe, prevents CVD. Now first of all did I

> misunderstand you on this point? If I did then clarification would

No, you didn't, except that I specifically said saturated fat and

cholesterol are not a causation of CVD. I haven't seen specific-

enough research to unequivocally say that saturated fats per se are

unharmful; there may be negative characteristics INDEPENDENT of

nutrition that hasn't been uncovered yet. e.g. suppose someone

proved that the high saturated fat intake alone that our Paleolithic

ancestors ate was responsible for their short maximum lifespan.

> ............. your point about fat crowding out good nutrients

> cannot be applied, selectively, by you, only to saturated fats.

>You

> cannot escape the fact that if your line of reasoning is correct

then

> ALL FATS (since they all contain lots of calories) should crowd out

> healthy nutrients, and thereby, according to you, cause CVD. But

> this is not born out by epidemiological studies.

You implied that unlimited amounts of poly and mono were healthy

which I threw back to you as rhetorical question designed to get you

to think about how ridiculous that line of reasoning was, but let me

be direct.

High intakes of ANY fat will provide inadequate nutrition and/or

crowd out existing nutrition. Now why this is so with saturated fat

is easy to explain. There's relatively very little, if any,

beneficial nutrition in saturated fat to begin with!!! Compare that

to polys and monos. The monos have the powerful antioxidants, the

polys contain or can produce the EFA's. That doesn't mean saturated

fat directly causes CVD, does it? As someone else recently

said, " absence of proof is not proof of absence " .

> But you cannot escape the fact that the Nurses' Health Study -

> probably the best epidemiological study so far in history - shows

> that while trans fats and saturated fats are harmful,

> monounsaturated fats are somewhat helpful and polyunsaturated fats

> quite helpful for preventing CVD. If your reasoning were correct

> then the study results would have shown, instead, that all fats are

> harmful because they all, according to you, should crowd out the

> beneficial nutrients you believe in. (At the risk of repetition,

Someone could attempt to feed these Nurses monos without antoxidants

and polys without EFA's or which contain trans-fat and I'll wager

you'll have exactly the same situation as with saturated fats. Would

that make any of them a direct cause of CVD? Remember, I'm not

concerned with the correlating risk factors of which there are

aplenty, but actual causes. The Lipid Theory has been demoted to

correlation by decades of subsequent research, as opposed to it's

initial claims of causation.

> recent (not yet published) huge INTERHEART study shows a very

> consistent dose-response relationship between lipids values and

> myocardial infarction. Indeed lipids values are the MOST important

> of the nine factors they identified.

I'm not ignoring anything. Correlation is not causation. I trust

that you don't lack the critical thinking skills necessary to know

the difference between the two meanings. Reducing risk is not the

same as eradication. Reminder: Half of all heart attack victims have

normal or low cholesterol levels, one of the two foundations of the

Lipid Theory.

> used to preserve it. Why are they so healthy while eating such

> amounts of fat? Why is this fat not causing CVD, as your line of

> reasoning would indicate it ought to, by crowding out the nutrients

> you beleive in?

Because monos actually contain highly-active nutrition, specifically

polyphenols and antioxidants! The rest of their diet is very

nutrition-dense as well.

> to. Do you have thirty year studies, 100,000 strong to support

> your supplement recommendations?

I think you can find plenty of mounting evidence for nutritional

supplementation on PubMed. But supplementation being necessary is an

artifact of depleted soils and modern factory farming, as I'm sure

you well know. In an ideal world, we wouldn't need to supplement.

> So the issue seems to be: " what do you accept as evidence? " What

> DO you accept as evidence of your point of view?

It's not a question of evidence, it is a question of causation.

Surely, you're wise enough by now to know that what is commonly held

as beliefs en masse is almost always uncommonly wrong. E-mail me and

I'll send you " my point of view " . It is too long to post here.

Logan

[Guest guest]

No, Thank you.

First, the quote is from 1998. Which means if it was published in Nov 1998, it

was written much earlier in the year or even the year before as publication can

often take months.

However, the next year , towards the end of 1999 at the national cholesterol

summit meeting, Dr. Castelli was asked what he would do to reverse the

coronary artery disease epidemic if he were omnipotent. His answer: " Have the

public eat the diet of the rural Chinese as described by Dr. T. Colin , "

author of the Cornell China study ( Castelli, Sept. 2-3, 1999).

My communication with him was towards the end of 1998 and he said virtually the

exact same thing and in addition, while eating our lunch, he said to me, " you

know, we would all be better off if we could get everyone to eat a more whole

food vegetarian or at least near vegetarian diet. "

Second, his quote isnt in oppostion to anything I said in anyway, nor does it

support the contention you were making.

I dont know if you have read the full article or the full supplement which was

dedicated to this topic. If not, I will try and post it tommorrow from work.

So, placed in time and in context, his statements in no way support any

" anarchronistic lipid theory " nor support to a competing theory, but a futher

understanding and development of the lipid theory and the proper diet to reduce

the risk of CVD.

So, again, can you show me any study or reference (other than a misrepresented

quote) that proves or documents that the cholesterol theory is outdated and this

so called compteting theory has any merit?

thanks

jeff

[Guest guest]

>> e.g. suppose someone proved that the high saturated fat intake alone that our

Paleolithic ancestors ate was responsible for their short maximum lifespan.

Which Paleolithic ancestors are you talking about exactly?

While there are definetly differing views on what our ancestors ate, even the

ones that beleive the fat content may have been higher than what is commonly

recommended, they all seem to agree that is was very low in saturated fat with

the magority of the fat coming from MUFAs and PUFAs, with more Omega 3s and a

better ratio.

The paradoxical nature of hunter-gatherer diets: meat-based, yet

non-atherogenic.

Eur J Clin Nutr. 2002 Mar;56 Suppl 1:S42-52 Cordain L, Eaton SB, JB, Mann

N, Hill KAlthough fat intake (28-58% energy) would have been similar to or

higher than that found in Western diets, it is likely that important qualitative

differences in fat intake, including relatively high levels of MUFA and PUFA and

a lower omega-6/omega-3 fatty acid ratio, would have served to inhibit the

development of CVD.

Cardiovascular disease resulting from a diet and lifestyle at odds with our

Paleolithic genome: how to become a 21st-century hunter-gatherer.Mayo Clin Proc.

2004 Jan;79(1):101-8.O'Keefe JH Jr, Cordain L.

Until 500 generations ago, all humans consumed only wild and unprocessed food

foraged and hunted from their environment. These circumstances provided a diet

high in lean protein, polyunsaturated fats (especially omega-3 [omega-3] fatty

acids), monounsaturated fats, fiber, vitamins, minerals, antioxidants, and other

beneficial phytochemicals.

Dietary lean red meat and human evolution.

Eur J Nutr. 2000 Apr;39(2):71-9.Mann N.

A study of human and pre-human diet history shows that for a period of at least

2 million years the human ancestral line had been consuming increasing

quantities of meat. During that time, evolutionary selection was in action,

adapting our genetic make up and hence our physiological features to a diet high

in lean meat. This meat was wild game meat, low in total and saturated fat and

relatively rich in polyunsaturated fatty acids (PUFA).

[Guest guest]

This one is older, but still relevant to the discussion of the high SFA content

of the ancestreal diet.

Animal foods in traditional Australian aboriginal diets: polyunsaturated and low

in fat.

Lipids. 1986 Nov;21(11):684-90.

Naughton JM, O'Dea K, Sinclair AJ.

Australian Aborigines develop high frequencies of diabetes and cardiovascular

diseases when they make the transition to an urban lifestyle. The composition of

the traditional diet, particularly its lipid components, is a most important

aspect of the hunter-gatherer lifestyle that would bear on the risk of these

diseases. We have examined the fat content and fatty acid composition of a

variety of animal foods eaten traditionally by Aborigines from different regions

of Australia. The muscle samples of the wild animals from all over Australia

were uniformly low in fat (less than 2.6% wet weight) with a high proportion of

polyunsaturated fatty acids (greater than or equal to 20% PUFA). Liver samples

had a higher range of fat content (5-10% wet weight) but were also rich in PUFA

(33-42%). Depot fat samples varied widely in their PUFA content (5-40%). In

terms of their PUFA composition the foods tended to fall into three groups: (i)

those rich in both n-3 and n-6 PUFA, which included land-based, coastal and

freshwater animals; (ii) those rich in n-3 PUFA, i.e., marine species; (iii)

those rich in n-6 PUFA, mainly land-based species. The results of these analyses

suggest that even when the traditional Aboriginal diet contained a high

proportion of animal foods it would have been low in fat with a high proportion

of PUFA and thereby could have protected Aborigines against cardiovascular

diseases and related conditions through a combination of factors: low energy

density, low saturated fat and relatively high PUFA content.

[Guest guest]

--- In , " Jeff Novick " <jnovick@p...>

> However, the next year , towards the end of 1999 at the national

> cholesterol summit meeting, Dr. Castelli was asked what he

> would do to reverse the coronary artery disease epidemic if he were

> omnipotent. His answer: " Have the public eat the diet of the rural

> Chinese as described by Dr. T. Colin , " author of the

> Cornell China study ( Castelli, Sept. 2-3, 1999).

Why didn't he specifically say to take statins, lower cholesterol or

lower saturated fat intake? Could it be the nutrient-dense, largely

vegetarian diet of the rural Chinese provides adequate or even

optimal nutrition to ward off coronary artery disease? What another

amazing revelation from this guy! I wouldn't say that diet is

optimally healthy though; they do have higher incidences of other

disease (prostate cancer, I believe) because of soil defenciencies.

> Second, his quote isnt in oppostion to anything I said in anyway,

> nor does it support the contention you were making.

I'm going to chalk this down to a matter of interpretation. Where

you see fat and cholesterol being " bad " , I see a nutritional vacuum.

> I dont know if you have read the full article or the full

> supplement which was dedicated to this topic. If not, I will try

> and post it tommorrow from work.

If it has any relevance to the cause of CVD mortality as opposed to

risk factors of CVD mortality, I'm interested. Notice what I'm

saying.... causation NOT correlation. We've all been bombarded with

correlation as causation propaganda for eons.

> So, placed in time and in context, his statements in no way support

> any " anarchronistic lipid theory " nor support to a competing

> theory, but a futher understanding and development of the lipid

> theory and the proper diet to reduce the risk of CVD.

Ah ha! " A further understanding and development " . It has now been

over 60 years. At what point do you stop twisting yourself into a

pretzel and consider that the Lipid Theory is not the cause of CVD?

The real world proves the Lipid Theory is B.S. as far as its original

claims of causation go. Normally, when a theory hasn't lived up to

its claims, you start looking to formulate a better theory, which is

what happened.

> So, again, can you show me any study or reference (other than a

> misrepresented quote) that proves or documents that the cholesterol

> theory is outdated and this so called compteting theory has any

> merit?

I'm not aware of any studies meeting those specific requirements.

But since you seem to have an " in " with Catelli and he appears to be

making different statements now than 10 or 20 years ago, why don't

you motivate him to do the research comparing the two theories? It

would settle the issue once and for all and we won't have to spend

the next generation debating it.

Logan

[Guest guest]

Logan, Jeff, Al,

It seems that the debate about fats keeps going on without getting

anywhere. Let us take a different approach.

In Message 14314 I reviewed the Perlman patent for Smart Balance

margarine, [u.S. Patent 5,382,442 Perlman , et al., January 17, 1995

(http://tinyurl.com/4xdrc) ], and found that it is based on work

originally done by Hegsted, et al.:

Quantitative effects of dietary fat on serum cholesterol in man.

Hegsted DM, McGandy RB, Myers ML, Stare FJ. Am J Clin Nutr. 1965

Nov;17(5):281-95. PMID: 5846902 [PubMed - indexed for MEDLINE]

The patent by Perlman reviews Hegsted's work and scrutinizes the

" Hegsted equation " which can be used to predict the changes in serum

cholesterol based on the caloric percentages of specific fatty acids

in the diet. The Hegsted equation is:

Delta SC =

+ 8.45 Delta C14:0

+ 2.12 Delta C16:0

- 1.87 Delta C18:2

+ 0.056 Delta DietaryCholesterol

- 6.24

Where Delta SC is the change in serum cholesterol, C14:0 is myristic

acid, C16:0 is palmitic acid, and C18:2 is linoleic acid.

Perlman concludes that palmitic acid and dietary cholesterol do not

influence serum cholesterol significantly and can be ignored because

myristic acid and linoleic acid alone can explain 85.4% of the

variation in serum cholesterol. It seems that only myristic acid is

cholesteremic of the three major saturated fatty acids in beef tallow

and lard (myristic C14:0 ~3%, palmitic C16:0 ~25%, and stearic C18:0

~17%), but this can be counteracted by the anti-cholesteremic effect

of linoleic acid.

THEREFORE, if all the research by Hegsted and Perlman is valid, we

cannot say " saturated fats increase cholesterol " because not all

saturated fats are metabolized equally. It may be better to say that

*myristic acid* which comprises ~3% of tallow and lard is responsible

for raising cholesterol levels (and presumably altering lipid

profiles).

MOREOVER, from the equation, we can even calculate how much our serum

cholesterol can decrease by adding linoleic acid to the diet. The

logical conclusion is that by using oils high in linoleic acid, such

as safflower oil, grape seed oil, or sunflower oil, we can decrease

our serum cholesterol level without drugs like Lipitor, etc. The

additional oil will increase calories that will have to be compensated

by reducing the calories from other fats.

It seems to me that eating natural saturated fats (meats) will not

have any detrimental effects on lipid profiles when consumed along

with sources of linoleic acids (e.g. sunflower seeds) to balance

cholesterimic and anti-cholesteremic effects of the fats.

Does anybody have any evidence to contradict the Hegsted equation or

Perlman's work?

Tony

>>>

From: " old542000 " <apater@m...>

Date: Mon Sep 6, 2004 4:32 pm

Subject: Re: macro nutrients, sat fats

To quote your Dr. W. Catelli, he in the scientific literature says:

" …

Diet intervention trials have shown that a reduction in total

cholesterol and saturated fat consumption produced reduction in CHD

incidence proportionate to the fall in cholesterol. …

PMID: 2220800 [PubMed - indexed for MEDLINE] " .

Therefore, since saturated fats increase cholesterol, your arguments

may be not justified.

Cheers, Al Pater.

>>>>

[Guest guest]

Thanks for that ref crediting Ancel Keys. The same guy that did "Human Starvation"

Also, the DASH diet is centered around the medit diet, FWIW.

Nothing hard. As I recall none use humungus quantities except those seen in tv ads. Think about it olive oil is not cheap and most of those people are lower income.

Regards.

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

From: old542000

Sent: Monday, September 06, 2004 3:17 PM

Subject: [ ] Re: macro nutrients, sat fats

> Also bear in mind that the HEALTHIEST people in the Mediterranean > region, the inhabitants of Crete, consume truly humungous quantities > of olive oil, a lot more than I consider advisable. But it certainly > does them no apparent harm. They live longer than any other group in > the region. Not only do they use it for cooking and in salad > dressings, their biggest source of it is in their preserved foods. > When they eat the preserved foods they also eat the olive oil they > used to preserve it. Why are they so healthy while eating such huge > amounts of fat? Why is this fat not causing CVD, as your line of > reasoning would indicate it ought to, by crowding out the nutrients > you beleive in? Hi All,There was much of interest to me in the pdf-available below full paper, which is presnted after the media article.These included:"Olive oil may not prevent colon cancer because of itsmonounsaturated fatty acid (MUFA) content, butbecause of its other components such as its anti-oxidantsor phytosterols".European Journal of Cancer Prevention June 2004;13(3):219-230The term 'Mediterranean diet', implying that all Mediterranean people have the same diet, is a misnomer. The countries around the Mediterranean basin have different diets, religions and cultures. Their diets differ in the amount of total fat, olive oil, type of meat, wine, milk, cheese, fruits and vegetables; and the rates of coronary heart disease and cancer, with the lower death rates and longer life expectancy occurring in Greece. The diet of Crete represents the traditional diet of Greece prior to 1960. Analyses of the dietary pattern of the diet of Crete shows a number of protective substances, such as selenium, glutathione, a balanced ratio of n-6/n-3 essential fatty acids (EFA), high amounts of fibre, antioxidants (especially resveratrol from wine and polyphenols from olive oil), vitamins E and C, some of which have been shown to be associated with lower risk of cancer, including cancer of the breast. Epidemiological studies and animal experiments indicate that n-3 fatty acids exert protective effects against some common cancers, especially cancers of the breast, colon and prostate. Many mechanisms are involved, including suppression of neoplastic transformation, cell growth inhibition, and enhanced apoptosis and anti-angiogenicity, through the inhibition of eicosanoid production from n-6 fatty acids; and suppression of cyclooxygenase 2 (COX-2), interleukin 1 (IL-1) and IL-6 gene _expression by n-3 fatty acids. Recent intervention studies in breast cancer patients indicate that n-3 fatty acids, and docosahexaenoic acid (DHA) in particular, increase the response to chemopreventive agents. In patients with colorectal cancer, eicosapentaenoic acid (EPA) and DHA decrease cell proliferation, and modulate favourably the balance between colonic cell proliferation and apoptosis. These findings should serve as a strong incentive for the initiation of intervention trials that will test the effect of specific dietary patterns in the prevention and management of patients with cancer. Giacosa A. The Mediterranean diet and its protective role against cancer.Eur J Cancer Prev. 2004 Jun;13(3):155-7. No abstract available. PMID: 15167212 [PubMed - in process] The term `the Mediterranean diet' was first popularizedby Ancel Keys in his book How to Eat Well and Stay Well: theMediterranean Way, in 1975. This followed the publicationof his studies which showed that Mediterranean countrieshave diets associated with low incidence of cardiovasculardisease. Later studies have demonstrated that theMediterranean countries also show a low incidence ofcancers of the colon and breast and there is now littledoubt that the Mediterranean countries enjoy a low riskof many of the diet-related diseases of affluence (Hill andGiacosa, 1992; Hu, 2003).The Mediterranean is a large area with many differentdiet patterns, but they are all characterized by highconsumption of fruit, vegetables, legumes and dietaryfibre and low intakes of meat and saturated fats. In all ofthese respects they agree with the current concepts of a`healthy diet' and one towards which many countries innorthern Europe are moving (Trichopoulou, 2001).A further general characteristic of the Mediterranean dietis the consumption of olive oil, usually in large amounts,and of fish. The antioxidant potential of the Mediterranean dietThe Mediterranean diet not only produces favourableeffects on blood lipids but also protects against oxidativestress. Oxidative damage is thought to represent one ofthe mechanisms leading to chronic diseases such asatherosclerosis and cancer. Many studies suggest that alink exists between fruit and vegetables or the amounts ofplasma antioxidant vitamins (ascorbic acid, tocopheroland carotenoids) and risk of death from cancer or coronaryheart diseases. Although emphasis has been given todifferent components of the diet, attention has recentlyshifted to the diet as a whole. The Mediterranean diet isable to modulate oxidative stress through complexmechanisms and not just the high antioxidant compoundcontent. The preference for fresh fruit and vegetables inthe Mediterranean diet will result in a higher consump-tionof raw foods, a lower production of cooking-relatedoxidants and a consequent decreased waste of nutritionaland endogenous antioxidants. The high intake of anti-oxidants and fibre helps to scavenge even the smallamount of oxidants or oxidized compounds (Ghiselli et al.,1997). Mediterranean diet and DNA adductsThe interaction between environmental carcinogenicexposures and genetic and acquired susceptibility, suchas polymorphism of metabolizing enzymes and of DNArepair enzymes, age at starting carcinogen exposure,gender and ethnicity, may play an important role in mosthuman cancers (Perera, 1997). Nutritional factors,including low intake of saturated fat and high consump-tionof fruit and vegetables, may change an individual'srisk of cancer, particularly of epithelial tumours, in afavourable direction (Potter and Steinmetz, 1996; LaVecchia and Tavani, 1998). A general protective effectagainst cancer at different sites in the body has beensuggested for a number of fruit and vegetables, includingfresh fruit and vegetables, cruciferous and leek vegetables(Potter and Steinmetz, 1996).There are a number of biologically active chemicals infruit and vegetables that may potentially reduce thelikelihood of cancer, such as carotenoids, ascorbate,tocopherols, isothiocyanates, phenols and selenium (Pot-terand Steinmetz, 1996) (Table 1), through a number ofmechanisms, including induction and/or inhibition ofenzymes involved in carcinogen metabolism or in DNArepair, antioxidant effects, increased apoptosis anddecreased cell proliferation (La Vecchia and Tavani,1998).Flavonoids and other phenolic compounds have beendetected in grapes, apples, berries, olive, lettuce, onions,red wine, olive oil and in other components of the`Mediterranean diet'. Dietary phenolics, mostly of plantorigin, might protect against cancer by affecting thekinetics of DNA adduct formations, i.e. by modifying thecytochrome P450-dependent metabolisms, by inducingthe detoxification or DNA repair pathways or byantioxidant activity (Malaveille et al., 1996; Peluso andVineis, 2000). High intake of cruciferous vegetables, suchas broccoli, cabbage and cauliflower has been associatedwith lower bladder cancer risk. Combined intake oftomatoes, tomato sauce, tomato juice and pizza has beenrelated to lower prostate cancer risk. High consumptionof tomatoes and tomato-based products, includingspaghetti sauce, tomato soup and tomato paste, has beenassociated with lower cancer risk for different anatomicsites (Giovannucci, 1999).Broccoli, tomatoes and pizza are typical features of the`Mediterranean diet' and important dietary sources ofisothiocyanates and lycopene, two phytochemicals thatcan act as antioxidants or by inducing detoxifyingenzymes (Giovannucci et al., 1995). Therefore, it ispossible that phytochemicals other than flavonoids maybe additionally or complementarily involved in thereported protective effects of the `Mediterranean diet'on leukocyte DNA adduct formations. The antioxidant/anticancer potential of phenolic compounds isolated from olive oilHigh intakes of dietary fats have been implicated in thedevelopment of a number of diseases, including cancer.Recently, however, the epidemiologic data linking breastand colon cancer with total fat intake have not beenupheld. In this regard, evidence is emerging that it is notonly the amount but also the type of dietary fat that isimportant in the aetiology of some cancers, withparticular regard to olive oil (La Vecchia et al., 1995;Franceschi et al., 1996, 1997; Braga et al., 1998), and of fishoil (Simopoulos, 2001).For this reason, the phenolic and squalene content of arange of seasoning oils and their antioxidant potentialwere quantitated (Owen et al., 2000a).Recent studies have shown that olive oil, and in particularextra virgin olive oil, contains an abundance of phenolicantioxidants including simple phenols (hydroxytyrosol,tyrosol), aldehydic secoiridoids, flavonoids and lignans(acetoxypin resinol, pinoresinol). All of these phenolicsubstances are potent inhibitors of reactive oxygenspecies attack on, for example, salicylic acid and 2-deoxyguanosine. Currently, there is growing evidencethat reactive oxygen species are involved in the aetiologyof fat-related neoplasms such as cancer of the breastand colorectum. A plausible mechanism is a highintake of O-6 polyunsaturated fatty acids which areespecially prone to lipid peroxidation initiated andpropagated by reactive oxygen species, leading to theformation (via a,b-unsaturated aldehydes such as trans-4-hydroxy-2-nonenal) of highly promutagenic exocyclicDNA adducts.Previous studies have shown that the colonic mucosa ofcancer patients and those suffering from predisposinginflammatory conditions, such as ulcerative colitisand Crohn's disease, generates appreciably higherquantities of reactive oxygen species comparedwith normal tissue. Those studies have been extendedby developing accurate high-performance liquid chroma-tography(HPLC) methods for the quantitation ofreactive oxygen species generated by faecal matrix (Owenet al., 2000b). The data show that the faecal matrixsupports the generation of reactive oxygen speciesin abundance. As yet, there is a dearth of evidencelinking this capacity to actual components of thediet which may influence the colorectal milieu. However,using the newly developed methodology we can demon-stratethat the antioxidant phenolic compounds presentin olive oil are potent inhibitors of free radical generationby the faecal matrix. This indicates that the study of theinter-relation between reactive oxygen species and diet-aryantioxidants is an area of great promise for elucidatingmechanisms of colorectal carcinogenesis and possiblefuture chemopreventive strategies. Update on fat consumption and cancer risk A review of the available data on the relationship between fat consumption and cancer risk emphasizes the pre-ventive role of the Mediterranean diet. General considerations> There is a shortage of well-designed interventionstudies on the relation between diet and cancer risk.> Laboratory and animal studies give invaluableinformation on, for example, mechanisms ofcarcinogenesis, but cannot be used to predict theeffect of diet changes on risk of cancer in humans.> The Mediterranean region provides valuable evidenceof the effect of a particular dietary pattern on health, inwhich dietary fat is not harmful, and may even decreasethe risk of cancer at certain sites. Colon cancer> There is no evidence that the total fat or saturated fatintake is related to colon cancer risk in theMediterranean context.> There is evidence that certain types of fat, for exampleolive oil and fish oil, may decrease the risk of coloncancer.> Olive oil may not prevent colon cancer because of itsmonounsaturated fatty acid (MUFA) content, butbecause of its other components such as its anti-oxidantsor phytosterols.> There is disagreement about the strength of theassociation between red meat and colon cancer.Breast cancer> Evidence concerning the influence of dietary fats onbreast cancer is inconclusive.> There is some evidence from case–control studies thathigh intakes of MUFAs and polyunsaturated fatty acids(PUFAs) are associated with a decreased risk of breastcancer.> Population-based studies have found that total fatintakes ranging from 20 to 40% of total energy intakeare not related to breast cancer risk. Prostate cancer> There is a little evidence of an association between theintake of saturated fats and the incidence of prostatecancer. Priorities for future research> More well-designed intervention studies of theeffect of diet change on cancer risk in humans areneeded.> A better understanding of the interaction betweenintake of animal products (e.g. red meat) and protectivefactors (e.g. fruit, vegetables, wholegrain cereals) in thediet are needed.> An improved understanding of the role of lifestyle inearly life on subsequent cancer risk is needed.> We need to know more about gene–environmentinteractions, and the importance of geneticpolymorphism in determining cancer risk.> The general increase in male life expectancy in westerncountries makes it important to improve ourunderstanding of prostate cancer. ConclusionThe Mediterranean diet appears to be a healthy diet,whose benefits are mainly due to its high antioxidantpotential. The preference for fresh fruit and vegetables,typical of Mediterranean populations, will result in ahigher consumption of raw foods. This involves a reducedproduction of cooking-related oxidants, with a conse-quentdecreased waste of nutritional and endogenousantioxidants.The abundance of phenolic compounds and otherantioxidants in typical Mediterranean foods (olive oil,wine, herbs, fruits and vegetables) increases the palat-abilityof foods, and contributes to cooking-derivedcarcinogens and peroxides being present at a low level.Thus the Mediterranean diet is not only non-toxic, buthealth promoting as well. ReferencesBraga C, La Vecchia C, Franceschi S, et al. (1998). Olive oil, other seasoningfats, and the risk of colorectal carcinoma. Cancer 82: 448–453.Franceschi S, Favero A, Decarli A, et al. (1996). Intake of macronutrients and therisk of breast cancer. Lancet 347: 1351–1356.Franceschi S, Favero A, La Vecchia C, et al. (1997). Food groups and risk ofcolorectal cancer in Italy. Int J Cancer 72: 56–61.Ghiselli A, D'Amicis A, Giacosa A (1997). The antioxidant potential of theMediterranean diet. Eur J Cancer Prev 6 (Suppl 1): S15–S19.Giovannucci E (1999). Tomatoes, tomato-based products, lycopene and cancer:review of the epidemiologic literature. J Natl Cancer Inst 91: 317–331.Giovannucci E, Ascherio A, Rimm EB, et al. (1995). Intake of carotenoids andretinol in relation to risk of prostate cancer. J Natl Cancer Inst 87:1767–1776.Hill MJ, Giacosa A (1992). The Mediterranean diet. Eur J Cancer Prev 1: 339–340.Hu FB (2003). The Mediterranean diet and mortality – olive oil and beyond.N Engl J Med 348: 2595–2596.Keys, Ancel B (1975). How to eat well and stay well: the Mediterranean way.New York: Doubleday.La Vecchia C, Tavani A (1998). Fruit and vegetables, and human cancer. Eur JCancer Prev 7: 3–8.La Vecchia C, Negri E, Franceschi S, et al. (1995). Olive oil, other dietary fats, andthe risk of breast cancer (Italy). Cancer Causes Control 6: 545–550.Malaveille C, Hautefeuille A, Pignatelli B et al. (1996). Dietary phenolics asantimutagens and inhibitors of tobacco related DNA adduction in theurothelium of smokers. Carcinogenesis 17: 2193–2200.Owen RW, Mier W, Giacosa A, et al. (2000a). Phenolic compounds andsqualene in olive oils: the concentration and antioxidant potential of totalphenols, simple phenols, secoiridoids, lignans and squalene. Food ChemToxicol 38: 647–659.Owen RW, Giacosa A, Hull WE, et al. (2000b). The antioxidant/anticancerpotential of phenolic compounds isolated from olive oil. Eur J Cancer 36:1235–1247.Peluso M, Vineis P (2000). `Mediterranean diet' and DNA adducts. Eur J CancerPrev 9: 71–72.Perera FB (1997). Environment and cancer: who are susceptible? Science 278:1068–1073.Potter JD, Steinmetz K (1996). Vegetables, fruit and phytoestrogens aspreventive agents. In: Steward BW, McGregor D, Kleiheus O (editors):Principles of Chemoprevention, IARC Publication No. 139. Lyon: Interna-tionalAgency for Research on Cancer; pp. 61–90.Simopoulos AP (2001). The Mediterranean diets: what is so special about thediet of Greece? The scientific evidence. J Nutr 131: 3065S–3073S.Trichopoulou A (2001). Mediterranean diet: the past and the present. Nutr MetabCardiovasc Dis 11: 1–4.Cheers, Alan Pater

[Guest guest]

Hi Tony:

So you feel that a thirty-nine year old research paper represents the

leading edge in dietary fats/lipids/CVD science?

Very interesting if it really does. Some of it - that

polyunsaturated fats have beneficial effects on CVD risk - has been

confirmed by the Nurses' Health Study, as has often been noted here.

But what about the rest of it?

Rodney.

> Logan, Jeff, Al,

>

> It seems that the debate about fats keeps going on without getting

> anywhere. Let us take a different approach.

>

> In Message 14314 I reviewed the Perlman patent for Smart Balance

> margarine, [u.S. Patent 5,382,442 Perlman , et al., January 17, 1995

> (http://tinyurl.com/4xdrc) ], and found that it is based on work

> originally done by Hegsted, et al.:

>

> Quantitative effects of dietary fat on serum cholesterol in man.

> Hegsted DM, McGandy RB, Myers ML, Stare FJ. Am J Clin Nutr. 1965

> Nov;17(5):281-95. PMID: 5846902 [PubMed - indexed for MEDLINE]

>

> The patent by Perlman reviews Hegsted's work and scrutinizes the

> " Hegsted equation " which can be used to predict the changes in serum

> cholesterol based on the caloric percentages of specific fatty acids

> in the diet. The Hegsted equation is:

>

> Delta SC =

> + 8.45 Delta C14:0

> + 2.12 Delta C16:0

> - 1.87 Delta C18:2

> + 0.056 Delta DietaryCholesterol

> - 6.24

>

> Where Delta SC is the change in serum cholesterol, C14:0 is myristic

> acid, C16:0 is palmitic acid, and C18:2 is linoleic acid.

>

> Perlman concludes that palmitic acid and dietary cholesterol do not

> influence serum cholesterol significantly and can be ignored because

> myristic acid and linoleic acid alone can explain 85.4% of the

> variation in serum cholesterol. It seems that only myristic acid is

> cholesteremic of the three major saturated fatty acids in beef

tallow

> and lard (myristic C14:0 ~3%, palmitic C16:0 ~25%, and stearic C18:0

> ~17%), but this can be counteracted by the anti-cholesteremic effect

> of linoleic acid.

>

> THEREFORE, if all the research by Hegsted and Perlman is valid, we

> cannot say " saturated fats increase cholesterol " because not all

> saturated fats are metabolized equally. It may be better to say

that

> *myristic acid* which comprises ~3% of tallow and lard is

responsible

> for raising cholesterol levels (and presumably altering lipid

> profiles).

>

> MOREOVER, from the equation, we can even calculate how much our

serum

> cholesterol can decrease by adding linoleic acid to the diet. The

> logical conclusion is that by using oils high in linoleic acid, such

> as safflower oil, grape seed oil, or sunflower oil, we can decrease

> our serum cholesterol level without drugs like Lipitor, etc. The

> additional oil will increase calories that will have to be

compensated

> by reducing the calories from other fats.

>

> It seems to me that eating natural saturated fats (meats) will not

> have any detrimental effects on lipid profiles when consumed along

> with sources of linoleic acids (e.g. sunflower seeds) to balance

> cholesterimic and anti-cholesteremic effects of the fats.

>

> Does anybody have any evidence to contradict the Hegsted equation or

> Perlman's work?

>

> Tony

>

> >>>

> From: " old542000 " <apater@m...>

> Date: Mon Sep 6, 2004 4:32 pm

> Subject: Re: macro nutrients, sat fats

> To quote your Dr. W. Catelli, he in the scientific literature says:

> " …

> Diet intervention trials have shown that a reduction in total

> cholesterol and saturated fat consumption produced reduction in CHD

> incidence proportionate to the fall in cholesterol. …

> PMID: 2220800 [PubMed - indexed for MEDLINE] " .

>

> Therefore, since saturated fats increase cholesterol, your arguments

> may be not justified.

>

> Cheers, Al Pater.

> >>>>

[Guest guest]

Hi JW:

It is their own local oil. It is not expensive in Crete. The number

I was told via email from one of the Crete study investigators was an

average of 375 ml per person per day. The original article that

prompted my enquiries about what was going on in Crete, and supplied

the contact info there, was in Wine Spectator magazine, probably four

or five years ago.

Rodney.

>

> > Also bear in mind that the HEALTHIEST people in the

Mediterranean

> > region, the inhabitants of Crete, consume truly humungous

> quantities

> > of olive oil, a lot more than I consider advisable. But it

> certainly

> > does them no apparent harm. They live longer than any other

group

> in

> > the region. Not only do they use it for cooking and in salad

> > dressings, their biggest source of it is in their preserved

foods.

> > When they eat the preserved foods they also eat the olive oil

they

> > used to preserve it. Why are they so healthy while eating such

> huge

> > amounts of fat? Why is this fat not causing CVD, as your line

of

> > reasoning would indicate it ought to, by crowding out the

nutrients

> > you beleive in?

>

> Hi All,

>

> There was much of interest to me in the pdf-available below full

> paper, which is presnted after the media article.

>

> These included:

>

> " Olive oil may not prevent colon cancer because of its

> monounsaturated fatty acid (MUFA) content, but

> because of its other components such as its anti-oxidants

> or phytosterols " .

>

> European Journal of Cancer Prevention June 2004;13(3):219-230

>

> The term 'Mediterranean diet', implying that all Mediterranean

people

> have

> the same diet, is a misnomer. The countries around the

> Mediterranean basin have

> different diets, religions and cultures. Their diets differ

in

> the amount of

> total fat, olive oil, type of meat, wine, milk, cheese,

fruits

> and vegetables;

> and the rates of coronary heart disease and cancer, with

the

> lower death rates

> and longer life expectancy occurring in Greece. The diet of

> Crete represents the

> traditional diet of Greece prior to 1960. Analyses of the

> dietary pattern of the

> diet of Crete shows a number of protective substances, such

as

> selenium,

> glutathione, a balanced ratio of n-6/n-3 essential fatty

acids

> (EFA), high

> amounts of fibre, antioxidants (especially resveratrol from

> wine and polyphenols

> from olive oil), vitamins E and C, some of which have been

> shown to be

> associated with lower risk of cancer, including cancer of

the

> breast. Epidemiological

> studies and animal experiments indicate that n-3 fatty

acids

> exert protective

> effects against some common cancers, especially cancers of

the

> breast, colon and

> prostate. Many mechanisms are involved, including

suppression

> of neoplastic

> transformation, cell growth inhibition, and enhanced

apoptosis

> and anti-angiogenicity,

> through the inhibition of eicosanoid production from n-6

fatty

> acids; and

> suppression of cyclooxygenase 2 (COX-2), interleukin 1 (IL-

1)

> and IL-6 gene

> _expression by n-3 fatty acids. Recent intervention studies

in

> breast cancer

> patients indicate that n-3 fatty acids, and docosahexaenoic

> acid (DHA) in

> particular, increase the response to chemopreventive

agents. In

> patients with

> colorectal cancer, eicosapentaenoic acid (EPA) and DHA

decrease

> cell proliferation,

> and modulate favourably the balance between colonic cell

> proliferation and

> apoptosis. These findings should serve as a strong

incentive

> for the initiation

> of intervention trials that will test the effect of

specific

> dietary patterns in

> the prevention and management of patients with cancer.

>

> Giacosa A.

> The Mediterranean diet and its protective role against cancer.

> Eur J Cancer Prev. 2004 Jun;13(3):155-7. No abstract available.

> PMID: 15167212 [PubMed - in process]

>

> The term `the Mediterranean diet' was first popularized

> by Ancel Keys in his book How to Eat Well and Stay Well: the

> Mediterranean Way, in 1975. This followed the publication

> of his studies which showed that Mediterranean countries

> have diets associated with low incidence of cardiovascular

> disease. Later studies have demonstrated that the

> Mediterranean countries also show a low incidence of

> cancers of the colon and breast and there is now little

> doubt that the Mediterranean countries enjoy a low risk

> of many of the diet-related diseases of affluence (Hill and

> Giacosa, 1992; Hu, 2003).

> The Mediterranean is a large area with many different

> diet patterns, but they are all characterized by high

> consumption of fruit, vegetables, legumes and dietary

> fibre and low intakes of meat and saturated fats. In all of

> these respects they agree with the current concepts of a

> `healthy diet' and one towards which many countries in

> northern Europe are moving (Trichopoulou, 2001).

> A further general characteristic of the Mediterranean diet

> is the consumption of olive oil, usually in large amounts,

> and of fish.

> The antioxidant potential of the Mediterranean diet

> The Mediterranean diet not only produces favourable

> effects on blood lipids but also protects against oxidative

> stress. Oxidative damage is thought to represent one of

> the mechanisms leading to chronic diseases such as

> atherosclerosis and cancer. Many studies suggest that a

> link exists between fruit and vegetables or the amounts of

> plasma antioxidant vitamins (ascorbic acid, tocopherol

> and carotenoids) and risk of death from cancer or coronary

> heart diseases. Although emphasis has been given to

> different components of the diet, attention has recently

> shifted to the diet as a whole. The Mediterranean diet is

> able to modulate oxidative stress through complex

> mechanisms and not just the high antioxidant compound

> content. The preference for fresh fruit and vegetables in

> the Mediterranean diet will result in a higher consump-tion

> of raw foods, a lower production of cooking-related

> oxidants and a consequent decreased waste of nutritional

> and endogenous antioxidants. The high intake of anti-

> oxidants and fibre helps to scavenge even the small

> amount of oxidants or oxidized compounds (Ghiselli et al.,

> 1997).

> Mediterranean diet and DNA adducts

> The interaction between environmental carcinogenic

> exposures and genetic and acquired susceptibility, such

> as polymorphism of metabolizing enzymes and of DNA

> repair enzymes, age at starting carcinogen exposure,

> gender and ethnicity, may play an important role in most

> human cancers (Perera, 1997). Nutritional factors,

> including low intake of saturated fat and high consump-tion

> of fruit and vegetables, may change an individual's

> risk of cancer, particularly of epithelial tumours, in a

> favourable direction (Potter and Steinmetz, 1996; La

> Vecchia and Tavani, 1998). A general protective effect

> against cancer at different sites in the body has been

> suggested for a number of fruit and vegetables, including

> fresh fruit and vegetables, cruciferous and leek vegetables

> (Potter and Steinmetz, 1996).

> There are a number of biologically active chemicals in

> fruit and vegetables that may potentially reduce the

> likelihood of cancer, such as carotenoids, ascorbate,

> tocopherols, isothiocyanates, phenols and selenium (Pot-ter

> and Steinmetz, 1996) (Table 1), through a number of

> mechanisms, including induction and/or inhibition of

> enzymes involved in carcinogen metabolism or in DNA

> repair, antioxidant effects, increased apoptosis and

> decreased cell proliferation (La Vecchia and Tavani,

> 1998).

> Flavonoids and other phenolic compounds have been

> detected in grapes, apples, berries, olive, lettuce, onions,

> red wine, olive oil and in other components of the

> `Mediterranean diet'. Dietary phenolics, mostly of plant

> origin, might protect against cancer by affecting the

> kinetics of DNA adduct formations, i.e. by modifying the

> cytochrome P450-dependent metabolisms, by inducing

> the detoxification or DNA repair pathways or by

> antioxidant activity (Malaveille et al., 1996; Peluso and

> Vineis, 2000). High intake of cruciferous vegetables, such

> as broccoli, cabbage and cauliflower has been associated

> with lower bladder cancer risk. Combined intake of

> tomatoes, tomato sauce, tomato juice and pizza has been

> related to lower prostate cancer risk. High consumption

> of tomatoes and tomato-based products, including

> spaghetti sauce, tomato soup and tomato paste, has been

> associated with lower cancer risk for different anatomic

> sites (Giovannucci, 1999).

> Broccoli, tomatoes and pizza are typical features of the

> `Mediterranean diet' and important dietary sources of

> isothiocyanates and lycopene, two phytochemicals that

> can act as antioxidants or by inducing detoxifying

> enzymes (Giovannucci et al., 1995). Therefore, it is

> possible that phytochemicals other than flavonoids may

> be additionally or complementarily involved in the

> reported protective effects of the `Mediterranean diet'

> on leukocyte DNA adduct formations.

> The antioxidant/anticancer potential of

> phenolic compounds isolated from olive oil

> High intakes of dietary fats have been implicated in the

> development of a number of diseases, including cancer.

> Recently, however, the epidemiologic data linking breast

> and colon cancer with total fat intake have not been

> upheld. In this regard, evidence is emerging that it is not

> only the amount but also the type of dietary fat that is

> important in the aetiology of some cancers, with

> particular regard to olive oil (La Vecchia et al., 1995;

> Franceschi et al., 1996, 1997; Braga et al., 1998), and of fish

> oil (Simopoulos, 2001).

> For this reason, the phenolic and squalene content of a

> range of seasoning oils and their antioxidant potential

> were quantitated (Owen et al., 2000a).

> Recent studies have shown that olive oil, and in particular

> extra virgin olive oil, contains an abundance of phenolic

> antioxidants including simple phenols (hydroxytyrosol,

> tyrosol), aldehydic secoiridoids, flavonoids and lignans

> (acetoxypin resinol, pinoresinol). All of these phenolic

> substances are potent inhibitors of reactive oxygen

> species attack on, for example, salicylic acid and 2-

> deoxyguanosine. Currently, there is growing evidence

> that reactive oxygen species are involved in the aetiology

> of fat-related neoplasms such as cancer of the breast

> and colorectum. A plausible mechanism is a high

> intake of O-6 polyunsaturated fatty acids which are

> especially prone to lipid peroxidation initiated and

> propagated by reactive oxygen species, leading to the

> formation (via a,b-unsaturated aldehydes such as trans-4-

> hydroxy-2-nonenal) of highly promutagenic exocyclic

> DNA adducts.

> Previous studies have shown that the colonic mucosa of

> cancer patients and those suffering from predisposing

> inflammatory conditions, such as ulcerative colitis

> and Crohn's disease, generates appreciably higher

> quantities of reactive oxygen species compared

> with normal tissue. Those studies have been extended

> by developing accurate high-performance liquid chroma-tography

> (HPLC) methods for the quantitation of

> reactive oxygen species generated by faecal matrix (Owen

> et al., 2000b). The data show that the faecal matrix

> supports the generation of reactive oxygen species

> in abundance. As yet, there is a dearth of evidence

> linking this capacity to actual components of the

> diet which may influence the colorectal milieu. However,

> using the newly developed methodology we can demon-strate

> that the antioxidant phenolic compounds present

> in olive oil are potent inhibitors of free radical generation

> by the faecal matrix. This indicates that the study of the

> inter-relation between reactive oxygen species and diet-ary

> antioxidants is an area of great promise for elucidating

> mechanisms of colorectal carcinogenesis and possible

> future chemopreventive strategies.

> Update on fat consumption and cancer risk

> A review of the available data on the relationship between

> fat consumption and cancer risk emphasizes the pre-ventive

> role of the Mediterranean diet.

> General considerations

> > There is a shortage of well-designed intervention

> studies on the relation between diet and cancer risk.

> > Laboratory and animal studies give invaluable

> information on, for example, mechanisms of

> carcinogenesis, but cannot be used to predict the

> effect of diet changes on risk of cancer in humans.

> > The Mediterranean region provides valuable evidence

> of the effect of a particular dietary pattern on health, in

> which dietary fat is not harmful, and may even decrease

> the risk of cancer at certain sites.

> Colon cancer

> > There is no evidence that the total fat or saturated fat

> intake is related to colon cancer risk in the

> Mediterranean context.

> > There is evidence that certain types of fat, for example

> olive oil and fish oil, may decrease the risk of colon

> cancer.

> > Olive oil may not prevent colon cancer because of its

> monounsaturated fatty acid (MUFA) content, but

> because of its other components such as its anti-oxidants

> or phytosterols.

> > There is disagreement about the strength of the

> association between red meat and colon cancer.

> Breast cancer

> > Evidence concerning the influence of dietary fats on

> breast cancer is inconclusive.

> > There is some evidence from case-control studies that

> high intakes of MUFAs and polyunsaturated fatty acids

> (PUFAs) are associated with a decreased risk of breast

> cancer.

> > Population-based studies have found that total fat

> intakes ranging from 20 to 40% of total energy intake

> are not related to breast cancer risk.

> Prostate cancer

> > There is a little evidence of an association between the

> intake of saturated fats and the incidence of prostate

> cancer.

> Priorities for future research

> > More well-designed intervention studies of the

> effect of diet change on cancer risk in humans are

> needed.

> > A better understanding of the interaction between

> intake of animal products (e.g. red meat) and protective

> factors (e.g. fruit, vegetables, wholegrain cereals) in the

> diet are needed.

> > An improved understanding of the role of lifestyle in

> early life on subsequent cancer risk is needed.

> > We need to know more about gene-environment

> interactions, and the importance of genetic

> polymorphism in determining cancer risk.

> > The general increase in male life expectancy in western

> countries makes it important to improve our

> understanding of prostate cancer.

> Conclusion

> The Mediterranean diet appears to be a healthy diet,

> whose benefits are mainly due to its high antioxidant

> potential. The preference for fresh fruit and vegetables,

> typical of Mediterranean populations, will result in a

> higher consumption of raw foods. This involves a reduced

> production of cooking-related oxidants, with a conse-quent

> decreased waste of nutritional and endogenous

> antioxidants.

> The abundance of phenolic compounds and other

> antioxidants in typical Mediterranean foods (olive oil,

> wine, herbs, fruits and vegetables) increases the palat-ability

> of foods, and contributes to cooking-derived

> carcinogens and peroxides being present at a low level.

> Thus the Mediterranean diet is not only non-toxic, but

> health promoting as well.

> References

> Braga C, La Vecchia C, Franceschi S, et al. (1998). Olive oil,

other

> seasoning

> fats, and the risk of colorectal carcinoma. Cancer 82: 448-453.

> Franceschi S, Favero A, Decarli A, et al. (1996). Intake of

> macronutrients and the

> risk of breast cancer. Lancet 347: 1351-1356.

> Franceschi S, Favero A, La Vecchia C, et al. (1997). Food groups

and

> risk of

> colorectal cancer in Italy. Int J Cancer 72: 56-61.

> Ghiselli A, D'Amicis A, Giacosa A (1997). The antioxidant

potential

> of the

> Mediterranean diet. Eur J Cancer Prev 6 (Suppl 1): S15-S19.

> Giovannucci E (1999). Tomatoes, tomato-based products, lycopene

and

> cancer:

> review of the epidemiologic literature. J Natl Cancer Inst 91:

317-

> 331.

> Giovannucci E, Ascherio A, Rimm EB, et al. (1995). Intake of

> carotenoids and

> retinol in relation to risk of prostate cancer. J Natl Cancer

Inst 87:

> 1767-1776.

> Hill MJ, Giacosa A (1992). The Mediterranean diet. Eur J Cancer

Prev

> 1: 339-340.

> Hu FB (2003). The Mediterranean diet and mortality - olive oil

and

> beyond.

> N Engl J Med 348: 2595-2596.

> Keys, Ancel B (1975). How to eat well and stay well: the

> Mediterranean way.

> New York: Doubleday.

> La Vecchia C, Tavani A (1998). Fruit and vegetables, and human

> cancer. Eur J

> Cancer Prev 7: 3-8.

> La Vecchia C, Negri E, Franceschi S, et al. (1995). Olive oil,

other

> dietary fats, and

> the risk of breast cancer (Italy). Cancer Causes Control 6: 545-

550.

> Malaveille C, Hautefeuille A, Pignatelli B et al. (1996). Dietary

> phenolics as

> antimutagens and inhibitors of tobacco related DNA adduction in

the

> urothelium of smokers. Carcinogenesis 17: 2193-2200.

> Owen RW, Mier W, Giacosa A, et al. (2000a). Phenolic compounds and

> squalene in olive oils: the concentration and antioxidant

potential

> of total

> phenols, simple phenols, secoiridoids, lignans and squalene. Food

Chem

> Toxicol 38: 647-659.

> Owen RW, Giacosa A, Hull WE, et al. (2000b). The

> antioxidant/anticancer

> potential of phenolic compounds isolated from olive oil. Eur J

Cancer

> 36:

> 1235-1247.

> Peluso M, Vineis P (2000). `Mediterranean diet' and DNA adducts.

Eur

> J Cancer

> Prev 9: 71-72.

> Perera FB (1997). Environment and cancer: who are susceptible?

> Science 278:

> 1068-1073.

> Potter JD, Steinmetz K (1996). Vegetables, fruit and

phytoestrogens as

> preventive agents. In: Steward BW, McGregor D, Kleiheus O

(editors):

> Principles of Chemoprevention, IARC Publication No. 139. Lyon:

> Interna-tional

> Agency for Research on Cancer; pp. 61-90.

> Simopoulos AP (2001). The Mediterranean diets: what is so special

> about the

> diet of Greece? The scientific evidence. J Nutr 131: 3065S-3073S.

> Trichopoulou A (2001). Mediterranean diet: the past and the

present.

> Nutr Metab

> Cardiovasc Dis 11: 1-4.

>

> Cheers, Alan Pater

>

>

>

[Guest guest]

tracking it down, I found this:

http://www.vegsource.com/talk/science/messages/833.html

FWIW.

maybe someone knows the book?

regards.

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

From: Jeff Novick

Sent: Monday, September 06, 2004 7:29 PM

Subject: RE: [ ] Re: macro nutrients, sat fats

> "The more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower peoples' serum cholesterol... we>>found that the people who ate the most cholesterol, ate the most saturated> fat, ate the most calories, weighed the least and were the most> physically active." -- Dr. Castelli, Director of the> prestigious Framingham StudyThis quote is often thrown around the internet and the WWW. However, as shown, it is direct opposition to published documented quotes from Dr Castelli. I have also had the opportunity to spend some time with him and speak to him personally and from my conversations with him, I would say that the above quote does not represent our conversation and his comments to me. So, my question is, instead of just re-distributing this "random" quote without its context, can you put provide the proper context for us by telling us when and where the quote is from?Thanksjeff

[Guest guest]

> Hi JW:

>

> It is their own local oil. It is not expensive in Crete. The number

> I was told via email from one of the Crete study investigators was an

> average of 375 ml per person per day.

375 ml * (1liter/1000ml) * (34 oz/liter) * (28gr/oz) * (884/100 cal/gr)

3155.88 calories

Those guys REALLY must like oo.

Aequalsz

[Guest guest]

Ever see someone swig olive oil? I *love* spending my summers in Greece...

The feta is bad for CR, though the fresh vegetables and general climate of

care about one's food is a refreshing change from the North American

perspective.

I'd be remiss if I didn't point out that there's a host of social factors

that may come into play as well, not the least of which is an active

lifestyle with a lot of ambulatory time. A " traditional " diet would also be

influenced by the religious calendar, and the olive itself occupies a very

special role: it provides oil that one cooks with and consumes straight, its

flesh *is* food, its oil lights your home with lamps (or the church), it

gives shade in the summer, its wood is used for the fire to warm a home and

the various woodworked domestic items, and you make soap from its oil as

well...

Olives are the perfect fruit and can creep into every nook & cranny of daily

life.

Best,

> -----Original Message-----

> From: aequalsz [mailto:aequalsz@...]

> Sent: Tuesday, September 07, 2004 10:11 AM

>

> Subject: [ ] Re: macro nutrients, sat fats

>

>

>

> > Hi JW:

> >

> > It is their own local oil. It is not expensive in Crete. The number

> > I was told via email from one of the Crete study investigators was an

> > average of 375 ml per person per day.

>

> 375 ml * (1liter/1000ml) * (34 oz/liter) * (28gr/oz) * (884/100 cal/gr)

>

> 3155.88 calories

>

> Those guys REALLY must like oo.

>

> Aequalsz

>

>

>

>

>

>

[Guest guest]

--- In , " Gifford " <gifford3@t...>

wrote:

> Ever see someone swig olive oil? I *love* spending my summers in

Greece...

Hello,

Would it be possible to get your opinion about the safety of US

citizens in Greece at the present time? I was there briefly during my

army tour in Germany about 35 years ago but have heard the political

climate has worsened since. Also read about a terrorist bombing in

May of this year if I remember correctly. The reason I'm wondering is

because I have a few extra days of my European vacation open and

wanted to see Greece again. Thanks in advance.

Aequalsz

[Guest guest]

Hi Aequalsz:

That is a good point. It makes me wonder whether I got the

denominator right (per person? or was it perhaps per family? It was

a long time ago. Perhaps it included the oil burned for light?).

But whatever the denominator, the amount calculated at the time was

very large. Yet they live a long time, and without high tech

medicine. Because they don't need it.

Rodney.

--- In , " aequalsz " <aequalsz@y...>

wrote:

> --- In , " Rodney " <perspect1111@y...>

wrote:

> > Hi JW:

> >

> > It is their own local oil. It is not expensive in Crete. The

number

> > I was told via email from one of the Crete study investigators

was an

> > average of 375 ml per person per day.

>

> 375 ml * (1liter/1000ml) * (34 oz/liter) * (28gr/oz) * (884/100

cal/gr)

>

> 3155.88 calories

>

> Those guys REALLY must like oo.

>

> Aequalsz

[Guest guest]

Looking at Castelli's book at amazon: (not taking sides, I didn't find that silly quote) folks can search this til content, better yet buy the book (10$) or used 0.39$.

The New Good Fat, Bad Fat: Lower Your Cholesterol and Reduce Your Odds of a Heart Attackby P. Castelli, Glen C. Perseus Publishing null May, 1997

What he said or meant is probably in this book.

But what I've read makes a good case for low fat, IMO.

1.

on Page 1:

"... and misinformation make it hard for anyone to know what to believe. "A professor says on the Internet that the cholesterol campaign is a myth and we should all eat more fat."' "If you're a senior citizen with coronary-artery disease, don't ..."

2.

on Page 2:

"... do our best to come up with the best information we can possi- bly get. Almost everyone knows too much cholesterol is a principle cause of heart attacks. Not everyone knows that when they eat saturated fat their bodies make cholesterol. ..."

3.

on Page 13:

"... butter and other things loaded with fat. And keep in mind that as this fat goes in, your body makes cholesterol and triglycerides. Little by little these add to deposits in your coronary arteries that may cause a lot of grief. ..."

1.

on Page 14:

"... rarely. 2. According to Oski, M.D., the editor-in-chief of The Yearbook of Pediatrics. 3. The student was P. Castelli. 4. Because hormonal replacement therapy markedly reduces the risk of these devas- tating causes in women who are no longer ..."

2.

on Page 19:

"... rise in cholesterol increases the chance of coronary artery disease by 2% in both men and women. Co-author P. Castelli was the Medical Director of the Framingham Heart Study of The National Heart, Lung and Blood Institute from 1979 until ..."

3.

on Page 22:

"... the seri- ousness of high triglycerides. Figure G shows a definite relationship between high triglyceride levels and coronary-artery disease. Dr. Castelli tracked triglyceride data carefully over many years in the Framingham Heart Study and the evidence leaves no doubt. The higher ..."

4.

on Page 25:

"... RISK W 11 3X AVER. CHO RISK M 23J4 0 5 10 15 20 25 RELATIVE RISK MEN & WOMEN CASTELLI WP: CAN J CARDIOL 1988 Figure H 25 ..."

5.

on Page 27:

"... 150 100 50 CORONARY HEART DISEASE & HDL CHOLESTEROL 0 <25 25-34 35-44 45-54 55-64 65-74 75+ HDL CHOLESTEROL Gordon, Castelli, et al: A J Med, 1977 Figure I TOTAL CHOLESTEROL / HDL FRAMINGHAM HEART STUDY-NATIONAL HEART, LUNG, AND BLOOD INSTITUTE ..."

6.

on Page 40:

"... of your bad- fat budget. By the way, is your bad-fat budget 10 or 20 grams a day? NorEs 1. Castelli, WP and , G. "A Simple Strategy to Limit Saturated Fat after Cholesterol Screening;" Postgraduate Medicine, vol. 84, September 1, ..."

7.

from Index:

"... Soup 122 Carrots, Honey-Glazed 179 Casseroles Baked-Zucchini 180 Chicken-Almond 205 Chili Mac 214 Hearty Chicken & Rice 205 Tuna 193 Castelli, P. v-vi Cauliflower-Curry Soup 126 Celery 128 Cerivastatin 99 Charts 18, 22, 23, 25, 27 Cheese 58 Cheese Crepes ..."

8.

from Back Cover:

"... count to 10, you can follow a simple plan to reduce the risk of heart attacks in your family. Drs. Castelli and have filled this book with helpful tips and encouraging advice that will help you make the change to ..."

9.

from Front Cover:

"... Y. Castelli, M.D. Glen C. GriffiD, M.D. Lower your cholesterol & reduce your odds of a heart attack "This is simply the ..."

10.

from Front Matter:

"... is so helpful and easy to follow, it's going to save my life." ine Torgersen "Kudos to Drs. and Castelli for the clearest advice on preventing heart attacks. This book helped save my life. It can do the same for ..."

11.

from Front Matter:

"... can count to 10 What's fact and what isn't? Answers about antioxidants Recipes and tips for enjoyable eating P Castelli, MD & Glen C. , MD ..."

12.

from Copyright:

"... America. Library of Congress Cataloging-in-Publication Data Castellie, P Good fat, bad fat: reduce your heart-attack odds / P. Castelli, Glen C. . p. cm. Includes bibliographical references and index. ISBN 1-55561-117-6 1. Hypercholesteremia-Prevention. 2. Myocardial infarction-Prevention. 3. Lowfat diet-Recipes. ..."

13.

from Front Matter:

"... About the Authors ABOUT THE AUTHORS P Castelli, M.D. Doctors everywhere know Bill Castelli as the soft-spoken expert who crusades all over the world teaching about the dangers ..."

14.

from Front Matter:

"... recognized that high triglycerides, low HDL levels and cholesterol/HDL ratios over 4 are major risk factors for heart disease, Dr. Castelli warned us about them. In his clear, deliberate way, Castelli continues to unravel difficult problems and to patiently explain the ..."

15.

from Front Matter:

"... Now he takes every opportunity to teach people the simple system of cutting down on bad fat that he and Castelli created to replace the complicated instructions patients are usually given. On his first day of medical school, Glen set ..."

regards.

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

From: Jeff Novick

Sent: Monday, September 06, 2004 8:42 PM

Subject: RE: [ ] Re: macro nutrients, sat fats

No, Thank you.First, the quote is from 1998. Which means if it was published in Nov 1998, it was written much earlier in the year or even the year before as publication can often take months. However, the next year , towards the end of 1999 at the national cholesterol summit meeting, Dr. Castelli was asked what he would do to reverse the coronary artery disease epidemic if he were omnipotent. His answer: "Have the public eat the diet of the rural Chinese as described by Dr. T. Colin ," author of the Cornell China study ( Castelli, Sept. 2-3, 1999). My communication with him was towards the end of 1998 and he said virtually the exact same thing and in addition, while eating our lunch, he said to me, "you know, we would all be better off if we could get everyone to eat a more whole food vegetarian or at least near vegetarian diet."Second, his quote isnt in oppostion to anything I said in anyway, nor does it support the contention you were making. I dont know if you have read the full article or the full supplement which was dedicated to this topic. If not, I will try and post it tommorrow from work.So, placed in time and in context, his statements in no way support any "anarchronistic lipid theory" nor support to a competing theory, but a futher understanding and development of the lipid theory and the proper diet to reduce the risk of CVD.So, again, can you show me any study or reference (other than a misrepresented quote) that proves or documents that the cholesterol theory is outdated and this so called compteting theory has any merit?thanksjeff

[Guest guest]

Its NOT the olive oil.

http://my.webmd.com/content/article/67/80070.htm?lastselectedguid={5FE84E90-BC77-4056-A91C-9531713CA348}

Adherence to a Mediterranean Diet and Survival in a Greek PopulationAntonia Trichopoulou, M.D., Tina Costacou, Ph.D., Bamia, Ph.D., and Dimitrios Trichopoulos, M.D.NEJM Volume 348:2599-2608 June 26, 2003 Number 26 ABSTRACTBackground Adherence to a Mediterranean diet may improve longevity, but relevant data are limited.Methods We conducted a population-based, prospective investigation involving 22,043 adults in Greece who completed an extensive, validated, food-frequency questionnaire at base line. Adherence to the traditional Mediterranean diet was assessed by a 10-point Mediterranean-diet scale that incorporated the salient characteristics of this diet (range of scores, 0 to 9, with higher scores indicating greater adherence). We used proportional-hazards regression to assess the relation between adherence to the Mediterranean diet and total mortality, as well as mortality due to coronary heart disease and mortality due to cancer, with adjustment for age, sex, body-mass index, physical-activity level, and other potential confounders.Results During a median of 44 months of follow-up, there were 275 deaths. A higher degree of adherence to the Mediterranean diet was associated with a reduction in total mortality (adjusted hazard ratio for death associated with a two-point increment in the Mediterranean-diet score, 0.75 [95 percent confidence interval, 0.64 to 0.87]). An inverse association with greater adherence to this diet was evident for both death due to coronary heart disease (adjusted hazard ratio, 0.67 [95 percent confidence interval, 0.47 to 0.94]) and death due to cancer (adjusted hazard ratio, 0.76 [95 percent confidence interval, 0.59 to 0.98]). Associations between individual food groups contributing to the Mediterranean-diet score and total mortality were generally not significant.Conclusions Greater adherence to the traditional Mediterranean diet is associated with a significant reduction in total mortality.

[Guest guest]

AND:

Morbidity mortality paradox of 1st generation Greek Australians.Kouris-Blazos A - Asia Pac J Clin Nutr - 01-JAN-2002; 11 Suppl 3: S569-75

NLM Citation ID:12492649 (PubMed)Full Source Title:Asia Pacific Journal of Clinical Nutrition

Author Affiliation: Asia Pacific Health and Nutrition Centre, Monash Asia Institute, Monash University, Clayton, Australia. antigone.kourisadm (DOT) monash.edu.au

Authors: Kouris-Blazos A

Abstract:There is evidence in Australia that 1st generation Greek Australians (GA), despite their high prevalence of cardiovascular disease (CVD) risk factors (e.g. obesity, diabetes, hyperlipidaemia, smoking, hypertension, sedentary lifestyles) continue to display more than 35% lower mortality from CVD and overall mortality compared with the Australian-born after at least 30 years in Australia. This has been called a 'morbidity mortality paradox' or 'Greek-migrant paradox'. Retrospective data from elderly Greek migrants participating in the International Union of Nutrition Sciences Food Habits in Later Life (FHILL) study suggests that diets changed on migration due to the: (i) lack of familiar foods in the new environment; (ii) abundant and cheap animal foods (iii) memories of hunger before migration; and (iv) status ascribed to energy dense foods (animal foods, white bread and sweets) and 'plumpness' as a sign of affluence and plant foods (legumes, vegetable dishes, grainy bread) and 'thinness' as a sign of poverty. This apparently resulted in traditional foods (e.g. olive oil) being replaced with 'new' foods (e.g. butter), 'traditional' plant dishes being made more energy dense, larger serves of animal foods, sweets and fats being consumed, and increased frequency of celebratory feasts. This shift in food pattern contributed to significant weight gain in GA. Despite these potentially adverse changes, data from Greece in the 1960s (seven countries study) and from Australia in the 1990s (FHILL study) has shown that Greek migrants have continued to eat large serves of putatively protective foods (leafy vegetables, onions, garlic, tomatoes, capsicum, lemon juice, herbs, legumes, fish) prepared according to Greek cuisine (e.g. vegetables stewed in oil). Furthermore, GA were found to return to the traditional Greek food pattern with advancing years. We suspect that these factors may explain why GA have recently been found to have over double the circulating concentrations of antioxidant carotenoids, especially lutein, compared with Australians of Anglo-Celtic ancestry. This in turn may have helped to make the CVD risk factors 'benign' and reduce the risk of death. This raises the question whether specific dietary guidelines need to be developed for recent migrants to Australia, encouraging them to retain the best of their traditional cultures and include the best of the mainstream culture.

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

From: Jeff Novick

Sent: Tuesday, September 07, 2004 12:25 PM

Subject: RE: [ ] Re: macro nutrients, sat fats

Its NOT the olive oil.

http://my.webmd.com/content/article/67/80070.htm?lastselectedguid={5FE84E90-BC77-4056-A91C-9531713CA348}

Adherence to a Mediterranean Diet and Survival in a Greek PopulationAntonia Trichopoulou, M.D., Tina Costacou, Ph.D., Bamia, Ph.D., and Dimitrios Trichopoulos, M.D.NEJM Volume 348:2599-2608 June 26, 2003 Number 26 ABSTRACTBackground Adherence to a Mediterranean diet may improve longevity, but relevant data are limited.Methods We conducted a population-based, prospective investigation involving 22,043 adults in Greece who completed an extensive, validated, food-frequency questionnaire at base line. Adherence to the traditional Mediterranean diet was assessed by a 10-point Mediterranean-diet scale that incorporated the salient characteristics of this diet (range of scores, 0 to 9, with higher scores indicating greater adherence). We used proportional-hazards regression to assess the relation between adherence to the Mediterranean diet and total mortality, as well as mortality due to coronary heart disease and mortality due to cancer, with adjustment for age, sex, body-mass index, physical-activity level, and other potential confounders.Results During a median of 44 months of follow-up, there were 275 deaths. A higher degree of adherence to the Mediterranean diet was associated with a reduction in total mortality (adjusted hazard ratio for death associated with a two-point increment in the Mediterranean-diet score, 0.75 [95 percent confidence interval, 0.64 to 0.87]). An inverse association with greater adherence to this diet was evident for both death due to coronary heart disease (adjusted hazard ratio, 0.67 [95 percent confidence interval, 0.47 to 0.94]) and death due to cancer (adjusted hazard ratio, 0.76 [95 percent confidence interval, 0.59 to 0.98]). Associations between individual food groups contributing to the Mediterranean-diet score and total mortality were generally not significant.Conclusions Greater adherence to the traditional Mediterranean diet is associated with a significant reduction in total mortality.

[Guest guest]

What I like about the Hegsted equation and U.S. Patent 5,382,442

(1995) by Perlman, et al. is that they characterize the *quantitative*

effect of *specific* fatty acids on serum cholesterol. Perlman

concludes that

Delta SC =

+ 9.10 Delta C14:0 (myristic acid)

- 1.78 Delta C18:2 (linoleic acid)

- 10.15

and has a very nice chart showing a linear relationship between the

predicted and observed serum cholesterol (Fig. 19). Perlman's 1995

patent validates the results of the " thirty-nine year old research

paper " , and brings it closer to " leading edge " .

Perlman's equation is basically telling us that a ratio of ~4:1

linoleic acid to myristic acid will essentially have NO effect on

serum cholesterol because the effect of linoleic acid cancels the

effect of myristic acid.

Now, talking about the Mediterranean diet and olive oil, the reference

given by Jeff states:

>>>

" Olive oil plays a central role, but it is not alone, " says Dimitrios

Trichopoulos, MD, PhD, of Harvard School of Public Health.

" It's among the divine mix of several factors that, when used in

combination, help provide strong evidence of something that is very

important -- eating the proper diet can significantly reduce your risk

of early death. "

>>>

Consider the percentages by weight of linoleic acid (C18:2) in several

oils: Olive oil (10%), canola oil (22%), sunflower oil (68%),

safflower oil (78%).

It takes 8 times more olive oil than safflower oil to achieve the 4:1

ratio of linoleic/myristic acid to get a ratio that is not

cholesteremic.

Fatty acids other than myristic (in meats) and linoleic (in vegetable

oils) are just a source of calories and do not influence cholesterol.

A lof of research looks only at saturated/monounsaturated ratios and

forgets about the polyunsaturated component of vegetable oils. For

this reason you get statements like " the researchers note a

significant reduction in death rates from a higher overall ratio of

monounsaturated fats to saturated fats " . However, Perlman's equation

makes it clear that the monounsaturated fats are just a source of

calories. It is the linoleic acid in the vegetable oils that is

having the beneficial effect, but the researchers do not recognize

this effect because they are not monitoring *specific* fatty acid

compositions.

This is why I prefer detailed quantitative data. You can eliminate

spurious correlations.

I would like to repeat my question from Message 14624:

Does anybody have any evidence to contradict the Hegsted equation or

Perlman's work?

Tony

>>>

From: " Rodney " <perspect1111@y...>

Date: Tue Sep 7, 2004 11:45 am

Subject: Re: macro nutrients, sat fats

Hi Tony:

So you feel that a thirty-nine year old research paper represents the

leading edge in dietary fats/lipids/CVD science?

Very interesting if it really does. Some of it - that

polyunsaturated fats have beneficial effects on CVD risk - has been

confirmed by the Nurses' Health Study, as has often been noted here.

But what about the rest of it?

Rodney.

===

From: " Jeff Novick " <jnovick@p...>

Date: Tue Sep 7, 2004 1:25 pm

Subject: RE: [ ] Re: macro nutrients, sat fats

Its NOT the olive oil.

>>>

http://my.webmd.com/content/article/67/80070.htm?l

astselectedguid={5FE84E90-BC77-4056-A91C-9531713CA348}

Adherence to a Mediterranean Diet and Survival in a Greek Population

Antonia Trichopoulou, M.D., Tina Costacou, Ph.D., Bamia,

Ph.D., and Dimitrios Trichopoulos, M.D.

NEJM Volume 348:2599-2608 June 26, 2003 Number 26

" Olive oil plays a central role, but it is not alone, " says Dimitrios

Trichopoulos, MD, PhD, of Harvard School of Public Health.

" It's among the divine mix of several factors that, when used in

combination, help provide strong evidence of something that is very

important -- eating the proper diet can significantly reduce your risk

of early death. "

While olive oil itself showed little benefit, the researchers note a

significant reduction in death rates from a higher overall ratio of

monounsaturated fats to saturated fats. Olive oil is among the best

sources of monounsaturated fats -- and happens to be the main cooking

oil in most Mediterranean countries -- but other oils frequently

consumed by Greeks and others surrounding the Mediterranean Sea also

contain these healthy fats.

[Guest guest]

Hi Tony:

The idea that olive oil is relatively neutral in its effects, and

polys quite beneficial (according to Hegsted that is because of the

linoleic) is not new. It fits in with the Nurses' Health Study

findings very well indeed. But if the dangers of saturated fats are

accounted for by only one fat component, and even more impressive, by

one which makes up only a small proportion of the saturated fats we

eat, then that is very remarkable, if true. And it is certainly news

to me.

I wonder why this has not been pursued with enthusiasm by the science

community and cattle engineered to have a much lower proportion of

myristic acid. (After all we do now have what they call omega-3

eggs).

Perhaps I will do a search for myristic acid and cholesterol, or CVD,

or CHD or whatever. If I find some good results I will post.

Rodney.

> What I like about the Hegsted equation and U.S. Patent 5,382,442

> (1995) by Perlman, et al. is that they characterize the

*quantitative*

> effect of *specific* fatty acids on serum cholesterol. Perlman

> concludes that

>

> Delta SC =

> + 9.10 Delta C14:0 (myristic acid)

> - 1.78 Delta C18:2 (linoleic acid)

> - 10.15

>

> and has a very nice chart showing a linear relationship between the

> predicted and observed serum cholesterol (Fig. 19). Perlman's 1995

> patent validates the results of the " thirty-nine year old research

> paper " , and brings it closer to " leading edge " .

>

> Perlman's equation is basically telling us that a ratio of ~4:1

> linoleic acid to myristic acid will essentially have NO effect on

> serum cholesterol because the effect of linoleic acid cancels the

> effect of myristic acid.

>

> Now, talking about the Mediterranean diet and olive oil, the

reference

> given by Jeff states:

> >>>

> " Olive oil plays a central role, but it is not alone, " says

Dimitrios

> Trichopoulos, MD, PhD, of Harvard School of Public Health.

> " It's among the divine mix of several factors that, when used in

> combination, help provide strong evidence of something that is very

> important -- eating the proper diet can significantly reduce your

risk

> of early death. "

> >>>

>

>

> Consider the percentages by weight of linoleic acid (C18:2) in

several

> oils: Olive oil (10%), canola oil (22%), sunflower oil (68%),

> safflower oil (78%).

>

> It takes 8 times more olive oil than safflower oil to achieve the

4:1

> ratio of linoleic/myristic acid to get a ratio that is not

> cholesteremic.

>

> Fatty acids other than myristic (in meats) and linoleic (in

vegetable

> oils) are just a source of calories and do not influence

cholesterol.

> A lof of research looks only at saturated/monounsaturated ratios

and

> forgets about the polyunsaturated component of vegetable oils. For

> this reason you get statements like " the researchers note a

> significant reduction in death rates from a higher overall ratio of

> monounsaturated fats to saturated fats " . However, Perlman's

equation

> makes it clear that the monounsaturated fats are just a source of

> calories. It is the linoleic acid in the vegetable oils that is

> having the beneficial effect, but the researchers do not recognize

> this effect because they are not monitoring *specific* fatty acid

> compositions.

>

> This is why I prefer detailed quantitative data. You can eliminate

> spurious correlations.

>

> I would like to repeat my question from Message 14624:

> Does anybody have any evidence to contradict the Hegsted equation or

> Perlman's work?

>

> Tony

>

> >>>

> From: " Rodney " <perspect1111@y...>

> Date: Tue Sep 7, 2004 11:45 am

> Subject: Re: macro nutrients, sat fats

> Hi Tony:

> So you feel that a thirty-nine year old research paper represents

the

> leading edge in dietary fats/lipids/CVD science?

>

> Very interesting if it really does. Some of it - that

> polyunsaturated fats have beneficial effects on CVD risk - has been

> confirmed by the Nurses' Health Study, as has often been noted here.

> But what about the rest of it?

> Rodney.

> ===

> From: " Jeff Novick " <jnovick@p...>

> Date: Tue Sep 7, 2004 1:25 pm

> Subject: RE: [ ] Re: macro nutrients, sat fats

>

> Its NOT the olive oil.

> >>>

>

>

> http://my.webmd.com/content/article/67/80070.htm?l

> astselectedguid={5FE84E90-BC77-4056-A91C-9531713CA348}

>

> Adherence to a Mediterranean Diet and Survival in a Greek Population

> Antonia Trichopoulou, M.D., Tina Costacou, Ph.D., Bamia,

> Ph.D., and Dimitrios Trichopoulos, M.D.

> NEJM Volume 348:2599-2608 June 26, 2003 Number 26

>

> " Olive oil plays a central role, but it is not alone, " says

Dimitrios

> Trichopoulos, MD, PhD, of Harvard School of Public Health.

>

> " It's among the divine mix of several factors that, when used in

> combination, help provide strong evidence of something that is very

> important -- eating the proper diet can significantly reduce your

risk

> of early death. "

>

> While olive oil itself showed little benefit, the researchers note a

> significant reduction in death rates from a higher overall ratio of

> monounsaturated fats to saturated fats. Olive oil is among the best

> sources of monounsaturated fats -- and happens to be the main

cooking

> oil in most Mediterranean countries -- but other oils frequently

> consumed by Greeks and others surrounding the Mediterranean Sea also

> contain these healthy fats.