Literature review of cholesterol (long)

[Guest guest]

A couple people mentioned that they were always on the lookout for

more info about how fat and cholesterol have nothing to do with

coronary heart disease. So here is a literature review I did. Its

still a draft and not fully polished yet. I apologize for its length

and filling people's emails!

Bond

justin_bond@...

The Fat of the Land

Live from the fat of the land. The cream rises to the top. The cream

of the crop. Fallen on lean times. As sickly as skimmed milk. The

goodness of a diet rich in fat permeates our language. As recently as

a couple generations ago parents were advised to feed their children

diets rich in meat, eggs, butter and cream to ensure proper growth

and nourishment. Now we're supposed to avoid those foods because they

raise cholesterol, a substance that makes up 17% of the dry weight of

the brain. Cholesterol is also the precursor to vitamin D and both

male and female sex hormones. It's an essential component of cellular

membranes, as well as the bile acids that are needed to digest and

absorb fat and fat-soluble vitamins. Cholesterol is so important to

life that every single cell in the body except nerve cells can

synthesize it. But supporters of the diet-heart theory would have you

believe that cholesterol, so essential to life in so many ways, is

actually a toxin that is killing us(90, 91). Could this be true? Or

will our obsession with cholesterol someday be regarded in the same

way as other medical wrong turns like bleeding and leeching? A review

of the literature of coronary heart disease (CHD) suggests that it

will.

The Clinical Trials

Lets begin with the clinical trials. They are the only form of

science that can separate correlation from causation, and the central

issue under discussion is whether high blood cholesterol (or

LDL " bad " cholesterol, as cholesterol lowering drugs and low-fat

diets work primarly by lowering LDL) causes coronary heart disease

(CHD), or is merely correlated to it.

Clinical Trials: Dietary Intervention

Over the decades " healthy " diets have been put to the test many

times. Dr. Lee Hooper led a team that did a survey of these diets,

involving over 30,000 patient-years of observation, and found no

reduction in coronary or total mortality (1). Most of these patients

were drawn from very high risk groups for coronary heart disease -

middle-aged men screened for extremely high cholesterol levels and

people who had already suffered from one heart attack. If a low-fat

diet can't help these guys, who can it help?

Clinical Trials: Multiple Risk Factor Intervention

Researchers are aware of the ineffectiveness of a low-fat diet, which

is why there has been much more study of multiple risk factor trials.

These are trials in which many risk factors for CHD are attacked at

once: usually diet, blood-pressure, smoking and obesity. It was hoped

that these trials would succeed whereas diet by itself does not. The

very fact that diet-heart supporters have emphasized multiple risk

factor trials over pure dietary trials when it comes time to design a

clinical trial is telling; its like your sports buddy that trash

talks until you tell him to put his money where his mouth is.

The most famous of these trials is the Multiple Risk Factor

Intervention Trial (MR.FIT). In this study middle-aged men screened

to have the highest 1% of the population's cholesterol level ate a

low-fat diet, lost weight, quit smoking and took medication to lower

high blood pressure. Despite reducing dietary saturated fat intake by

25%, halving dietary cholesterol and increasing polyunsaturated fat

intake by 33% (6) (polyunsaturated fats lower cholesterol(4) and

having a higher rate of quitting smoking than the usual care

(control) group, there were 265 fatalities in the special

intervention group and 260 in the usual care group (7).

MR.FIT may be the most famous of the multiple risk factor trials, but

it is no exception. In a survey of multiple risk factor intervention

trials involving over 900,000 patient-years of observation, no

statistically significant reduction in either coronary or total

mortality was found (10). Keep in mind that these are multiple risk

factor interventions. The authors of the study speculated that

possibly a 10% benefit was being obscured. Considering that the same

groups of people which were eating the low-fat diets were also the

ones that were getting more exercises and quitting smoking, a good

theory would be that the benefits of exercises and quitting smoking

are offset by the harm in eating what was once considered a poverty

diet.

A Dietary Intervention That Does Work

The only dietary intervention that does work involves the addition of

fat to the diet. Omega-3 fatty acids (fish and flax oils) have been

found to have a statistically significant reduction in total mortality

(2). They show an even larger reduction in coronary mortality, but

due to the fact that there have been only a few small-scale studies

involving a total of only 2700 patients, that reduction is not

statistically significant. Omega-3 fatty only lower cholesterol by a

couple percent and aren't considered to work by lowering cholesterol

(2).

Clinical Trails: Drug Interventions

The diet and multiple risk factor trials were a disappointment. The

conventional wisdom was that they didn't lower cholesterol enough. If

you really want to lower cholesterol you need drugs, and over the

years many of these drugs have been created. The major categories

are: estrogen and thyroid hormones, resins - drugs which bind to the

cholesterol containing bile acids and prevent them from being re-

absorbed into the bloodstream, fibrates - which reduce the synthesis

of VLDL in the liver, and statins - which cause the body to reduce

the synthesis of a molecule called melavonate, which is distant

precursor to cholesterol, and niacin - which also reduces the

synthesis of VLDL cholesterol.

Supporters of the diet-heart theory typically point to the trials of

cholesterol lowering drugs as conclusive proof that high cholesterol

causes coronary heart disease. In particular, the statin drugs lower

cholesterol by an average of 22%and have been shown to reduce the

risk of coronary and total mortality (2). The problem with that

theory is glossing over the results of the non-statin cholesterol

lowering drugs. In a survey of 59 cholesterol reducing trials

involving 170,000 subjects, Dr. H.C. Bucher and colleagues found that

only statins reduce coronary or total mortality. None of the other

drugs had a benefit (2).

Statins reduce the rate CHD because they have a beneficial impact on

the process of atherosclerosis, and they do this in ways that are

unrelated to their cholesterol reduction. This is not surprising

because atherosclerosis itself has very little to do with cholesterol.

A Quick `n Dirty Guide to Atherosclerosis

Have you ever wondered why you haven't heard the phrase " clogging

your veins? " After all, there's just as much cholesterol in the blood

that runs through your veins as your arteries. If high cholesterol

caused arteries to become sclerotic then it should do the same to

veins, but veins show very little atherosclerosis(16). If you

surgically replace a section of artery with a section of vein, as in

a venous bypass surgery, the vein will rapidly become sclerotic(19).

It's the location that matters; atherosclerosis only happens in very

specific places. Think of blood as a river and arteries as the river

bank. Atherosclerosis happens at places where the water flows in

swirls and eddys or becomes turbulant. Most of these places are where

the arteries form branches or make sharp turns(16). If

atherosclerosis were caused by circulating cholesterol embedding

itself into arteries, then you would find it all over your arteries

and not in these very specific locations; this was recognized by the

American Heart Association in a report in 1992(25).

The old `cholesterol clogs arteries' theory grew out of thousands of

experiments in which animals, usually rabbits, were fed large amounts

of cholesterol and subsequently developed a condition that is similar

to atherosclerosis. But the old adage about the man who lost his car

keys only looking under the streetlamp because the light was good

applies here. Feeding cholesterol to omnivorous species, including

humans(69), hardly budges the levels of blood cholesterol. But when

you feed cholesterol to a vegetarian species like rabbits, the blood

cholesterol skyrockets(68) to levels much higher than can be found in

humans(129). The rabbits stored this excess cholesterol in special

cells called foam cells which would build up in the arteries. But

foam cells also built up in the liver and spleen(129), which has

nothing to do with atherosclerosis - its evidence of a completely

seperate condition. Furthermore, in humans atherosclerosis is not

primarily a build up of foam cells.

The innermost layer of the inner wall of the arteries is composed of

single layer of cells called the endothelium. Underneath the

endothelium is a layer of supportive connective tissue along with

smooth muscle cells (SMC). Collectively these make up the inner wall

of the artery, called the intima. In humans the first step of

atherosclerosis is a build up of SMCs(16,17,18); this is how the

arteries respond to turbulant blood flow. Cholesterol has nothing to

do with the process. To summarize, the arterial plaque of cholesterol

fed rabbits is a buildup of foam cells, human plaque is a buildup of

SMCs which may or may not accumulate foam cells at a later stage.

They are two separate conditions.

Now lets look at how atherosclerotic plaque can cause heart attacks.

A survey of autopsy studies found that 86% of coronary events are

caused by lesions that block less than 70% of the artery, and that

68% of events are caused by lesions that block less than 50% of the

artery (27). Heart attacks are not caused by arterial plaque blocking

the artery, but by the rupture of arterial plaque(28,29,30,31) which

can release powerful clotting agents into the bloodstream (32). It is

these clotting agents that cause the blockage, not the plaque itself.

So in order to understand what causes heart attacks we needto

understand how plaque can become ruptured. And that's where foam

cells come into the picture, or more specifically, a precursor to

foam cells called macrophages.

The SMCs cannot produce this protective fibrous matrix without growth

factors which are provided by the endothelium or macrophages(17).

Ideally, the macrophages help the SMCs produce a strong fibrous

matrix of connective tissue to support the artery. But all tissue,

including plaque, is in a constant state of turnover as cells die and

are replaced. This process of tissue remodeling is what drives the

creation of plaque, and it can go awry. The number of macrophages (as

well as T-cells and mast cells) increases and the number of SMC's

decrease(33,34). The macrophage secretes an enzyme that degrades the

fibrous cap at a faster rate than the remaining SMC's can repair it

(32). The plaque becomes inflamed. A lipid rich core (only 15% of

which is saturated(35)) from dead macrophages and SMC's is created

which can be occupy up to 40% of the size of theplaque(33). Now the

cap is only attached to the artery along the edges of this lipid

core, which is where the macrophages are concentrated. The cap has

lost much of its strength and is now vulnerable to being ruptured

through mechanical forces(28, 29, 30). Once the plaque ruptures the

macrophages are released into the bloodstream and they produce a

powerful blood coagulant called tissue factor. The lipid core also

contains clotting factors and taken together these may cause a heart

attack. The body's last line of defense is the endothelium, which

regulates blood flow. It will release substances to both thin the

blood and widen the artery, making it less likely that a clot will

completely block the artery. If a clot does block the artery, a heart

attack will result. And it just so happens that statins play many

protective roles in this process.

What Makes Statins Special?

Here we are at the crux of the debate. Statins reduce the risk of

coronary and total mortality. Other cholesterol lowering drugs do

not. However, statins also lower cholesterol by a lot more than other

cholesterol lowering drugs. Lets look at some of the special

properties of statins that don't involve lowering cholesterol.

* Statins reduce the rate of strokes(36,37); non-statins do not(2).

High blood cholesterol is not a risk factor for stroke according to a

survey of 45 different prospective studies with over 450,000 people

and 7.3 million patient-years of observation(38).

* Like aspirin, statins are anti-inflammatory. They lower the blood

levels of C-Reactive Protein(CRP) (45,46), a marker for inflammation

of the arteries. High blood levels of CRP have been shown through

meta-analysis of both prospective epidemiological and clinical

studies to be an independent risk factor for CHD(47, 48).

Furthermore, CRP may play a causal role in atherosclerosis(49). For

example, it's found in atherosclerotic plaques and causes macrophages

to increase the production of tissue factor(50), a powerful clotting

substance. CRP also activates complement(50) (a category of

proteins), and activated complement breaks down tissue so CRP may

make plaques unstable. It's worth noting that omega-3 fatty acids

also lower CRP(51). The effects of other types of fat on CRP have yet

to be studied.

* High cholesterol is not a risk factor for the elderly (79,80,81),

but statins reduce the rate of CHD for the elderly(128). This means

that statins reduce the rate of CHD in a way that has nothing to do

with lowering cholesterol. What's more likely: that cholesterol

causes heart disease in the middle-aged while something other than

cholesterol causes it in the eldery and statins help both conditions,

or that something other than cholesterol, perhaps inflammation,

causes heart disease in all people?

* Recall the basic tenet of the diet-heart theory: cholesterol

gradually builds up in the arteries until they become blocked. Taking

a cholesterol reducing drug should slow down this process, and after

a few years your arteries will be a lot less blocked than they would

be. Your arteries would not be any less blocked 5 minutes after

taking a cholesterol reducing drug. Yet the survival rate for people

taking statins begins to improve relative to the control group

immediately after taking the drugs (39).

* There is no relationship between the degree of cholesterol

reduction by people taking statins and mortality rates (2, 40, 41,

42, 43, 44). Dose-response should be observed in a causal agent.

* Statins slow down the progress of atherosclerosis by reducing

hypertension(52), which has been shown clinically to reduce the risk

of coronary heart disease(26).

*Impaired endothelial function, the inabilityof the endothelium to

regulate the width of the artery and the thickness of the blood, is a

marker for atherosclerosis(53). Statins help to restore endothelial

function in a manner very similar to exercise(54,55).

* Statins stabilize the plaque that does form (56,57) by inhibiting

the ability of macrophages to weaken the cap of the plaque.

* Statins are an anti-oxidant(58,59)

* When plaques do rupture, statins can reduce the risk of a heart

attack because they have anti-clotting effects(60,61,62)

* Long-term use of statins lowers lp(a)(63), which is a form

of " extra-bad " LDL cholesterol. Lp(a) is also lowered by dietary

saturated fat(64).

To summarize, statins have powerful effects beyond simply lowering

cholesterol. They effects reduce the incidence of stroke, and the

incidence of CHD in the elderly. What do you think is lowering the

risk of CHD in the middle-aged? If its cholesterol reduction, then 30

clinical studies of non-statins have failed to demonstrate it. How

many clinical trials have to fail before you revise your hypothesis?

50? 100? More? At what point does a hypothesis become non-

falsifiable? How about when the hypothetical benefits of a treatment

are so slight that even decades of clinical studies don't to show a

benefit? By comparison, omega-3 fatty acids have shown a real benefit

with only one percent of the patient-years of observation(2).

A word of caution before you say 'Statins sound great, where do I

sign up?' There are serious concerns about the long-term health of

statins. One statin drug, Baycol, has already been pulled from the

market because its caused more than 50 deaths(65). Statins also cause

cancer in laboratory animals(66). I know what you're thinking:

everything causes cancer in lab animals if you feed them enough of

it. But while the dosages were higher than what humans are taking,

the animals don't absorb the drugs as efficiently. Blood levels were

comparable to those in humans taking the drug(66). While no increase

in cancer rates have yet been found in humans, the clinical trials

only run for 5 to 7 years. Cancer would not be expected to develop so

quickly, for example there is a 25 year lag period between taking up

smoking and the onset of lung cancer.

Epidemiology

Epidemiology is the study of how diseases spread. It cannot establish

causality, but it does allow you develop hypothesis's for clinical

testing. The most important fact about the epidemiology of CHD is

that we're still doing it 25 years after the first clinical trial on

CHD. We don't do epidemiology on, say, tuberculosis because we

actually know the cause. The challenge of epidemiology is to look for

strong and consistent correlations, or " risk factors " for a disease.

Then those correlations can be tested clinically to see if they're

causal. High cholesterol is neither a strong, nor consistent risk

factor for coronary heart disease:

*In a review of 18 prospective epidemiological studies(98), it was

found that high cholesterol was a risk factor for CHD in 13 and had

no effect in the other 5. Why the overall trend cannot be ignored,

high cholesterol does not have the consistent predictive power

expected of a causal factor. Furthermore, cholesterol was not found

to be a risk factor for total mortality.

*Women have a lower risk of heart attacks than men at equivalent

cholesterol levels(99).

*High blood cholesterol is not a risk factor for the elderly

(79,80,81), even though they are the ones most likely to have heart

attack. (It should be noted that low HDL " good " cholesterol may have

some predictive power(100), but bear in mind that saturated fat

raises HDL compared to unsaturated fat and carbohydrates(4)). This

fact has been recognized in the American College of Physicians recent

guidelines in which they do not recommend screening the elderly for

high cholesterol(101). How can something that causes a disease not be

a risk factor for the people most likely to suffer from it? This

would be like finding that the people most likely to get malaria have

never been bitten by mosquitoes!

*The famous Framingham study found cholesterol to be a significant

risk factor, but of 17 risk factors surveyed, cholesterol came in

dead last and the second to last risk factor was stronger by a factor

of 10!(102)

*Poor cholesterol profiles are correlated to several factors that are

a sign of poor health: obesity(84), smoking(85), lack of exercise

(86,87) and high blood pressure(88). And while studies can and do

adjust for these factors, they can't adjust for everything.

*Most heart attacks happen in people who don't have high cholesterol

levels, as was acknowledged by Castelli, a prominent

supporter of the diet-heart theory(89). Can you imagine saying: most

cases of Tuberculosis occur in people who are not infected with TB?

If high cholesterol causes CHD then it must be elevated in all cases.

Diet-heart supporters have minimized this by focusing on finding more

and more complicated equations that incorporate more and more risk

factors to get better and better prediction of coronary heart

disease. But all this does is give you a better prediction. You still

can't predict CHD 100% of the time, which means you still haven't

found the causal factor.

*Low cholesterol levels are associated with increased rates of

cancer, stroke, and overall mortality. In 's

comprehensive survey of the literature(92), he found that low

cholesterol was a risk factor for increased overall mortality in 26

epidemiological studies including the three most famous: Framingham,

Mr.Fit and Ancel Key's 7 countries study. No association was found in

11 studies and a reduced overall mortality rate was found in two, one

of which was a study only of young adults and in the other the lowest

measured cholesterol levelwas 226 mg/dl, which is too high to be at

increased risk for other disease. 's review has been

corroborated by more recent studies as well(93,94,95,96). This gives

rise to the U shaped cholesterol curve in which the bottom of the U,

the lowest overall mortality rates, is found among people with

average cholesterol values. Indeed there is little change in overall

mortality rate between cholesterol levels of about 140 to 240(97).

But all of the above is irrelevant because cholesterol has been

tested clinically. Even if it were powerfully and consistently

correlated to CHD, the epidemiology must take a back seat to the

clinical trials.

The Japanese Paradox

Comparisons between nations instead of individual people are called

ecological studies. These studies have fallen out of favor because

they are less able to separate correlation from causation than

epidemiology, but are important for historical reasons. An example of

an ecological study is Ancel Keys' six countries study(103), which

found a striking correlation between a nations rate of heart disease

and fat consumption. You might be thinking that it seems odd that he

would study so few countries - only six. It turns out he had data on

22 countries and threw out those that didn't fit his theory. When you

consider all this data the correlation is much weaker. In

's review(92) of the literature of ecological studies, other

studies have found correlations between a nation's rate of CHD and

consumption of sugar, carbohydrates, fish, tea, and protein as well

as obviously non-causal factors like GNP and per-capita use of paper.

So while much is made of the French Paradox, you could just as easily

speak of the Japanese Paradox - a nation that eats a diet high in

carbohydrates but has a surprisingly low rate of heart disease. This

doesn't mean that carbohydrates cause heart disease, but shows how

limited ecological studies are.

Another type of ecological study compares one nation at two different

times. In an attempt to understand the rise in CHD in the United

States, many such studies have compared our fat intake over time. It

turns out that over the course of the 1900s, ourconsumption of animal

fat declined slightly while our consumption of vegetable oils doubled

(105-115). Whatever is causing the rise in CHD in the US, consumption

of animal fat is not a likely suspect!

Is the Diet-Heart Theory Non-Falsifiable?

The first time a cholesterol lowering drug reduced coronary and total

mortality was in 1994 when the first trial of the new statin drugs

published the data on mortality(127). Prior to that, cholesterol

reduction had produced a succession of failures. The first large

scale cholesterol reducing trial was actually four separate trials in

one study. Two of those trials, estrogen and thyroid hormone,

actually increased coronary and total mortality (11,12,13), the other

two, niacin and clofibrate (14), had noeffect. The next two large

scale trials were the Mr.Fit trial(7) and the Lipid Research Clinic's

trial(15). They both failed to lower coronary or total morality. Six

large scale clinical trials of cholesterol reduction, six failures.

You might think that at this point diet-heart supporters would go

back to the epidemiology and develop a new hypothesis. Instead they

turned the Lipid Research Clinics trial, a prospective clinical study

(121), into a retrospective study. In particular they lowered the

preset level of statistical significance from 99% to 95%, and

switched from a two-tailed t-test to a one-tailed t-test. For those

of you that slept through stats class, a one-tailed t-test is only

use to analyze data that can only change in one direction. When you

use it to analyze something that can either increase or decrease, in

this case mortality rates, it has the effect of further lowering the

degree of statistical significance. Taken together, this

retrospective analysis resulted in a " statistically significant "

reduction in " coronary events. " Retrospective analysis can be useful

in science as a form a brainstorming to think about why the results

of your expirement were not what you expected. But this was something

completely differant. The researchers violated the protocol that they

decided on before they got the results. This would be like a sports

team cheating on the agreed upon rules in order to win. In science

the word for this is post-hoc analysis and by post-hoc analysis you

can prove that black is white, up is down and cholesterol causes

coronary heart disease.

A consensus conference was convened and the Lipid Research Clinic's

trial became the conclusive proof the high cholesterol causes CHD. It

was the study responsible for Time Magazine's cover that read " Sorry,

its true, cholesterol really is a killer, " with the subsequent

article that begins, " No whole milk, no butter, no fatty meats... "

The fact that cholesterol was found not to be a killer was dismissed

as a trifling detail. This study was also responsible for the

creation of the National Cholesterol Education Program ( " Ask your

doctor about cholesterol " ), the program to screen every single

American for high cholesterol and put up to a quarter of them on

cholesterol lowering drugs for the rest of their lives. This is in

violation of another basic statistical practice against generalizing

from one population, middle-aged men screened to have the highest 1%

of the populations cholesterol levels, to another, up to a quarter of

all Americans.

The Lipid Research Clinic's trial is the most notorious example of

post-hoc analysis, but it is not the only one, there's also the Oslo

Anti-Smoking Trial (123). Other times, the major results of the study

simply aren't published, as in the Excel trial(123), a practice that

has lead the leading research journals to demand that scientists have

greater control over privately funded research(125). The evidence in

favor of cholesterol reduction has been further distorted by

selective citation; studies felt to be supportive of the diet-heart

theory are cited six times as often as studies that aren't supported

(126). I bring this up not to point fingers but because at this time

a large body of research on cholesterol has been created. Drawing

conclusions from the body of research is now the crux of the debate.

The CHD research community has already held a consensus conference

that concluded that the Lipid Research Clinic's trial proved the link

between cholesterol and CHD. Are they capable of doing a thorough and

objective review of the literature?

Some facts about omega-3's

*The plant based versions of omega-3 fatty acids are not biologically

active. Only 0.2% of the plant form (LNA) in blood plasma ends up

being converted to the " fish oil " forms found in animal products

(130). This trait is shared with other omnivorous and carnivorous

species and is a result of animal products being a staple in the

diet. Vegetarian species make the conversion readily.

* The absorption of omega-3's is increased substantially when

consumed with ample saturated fat(131)

* Fish are not the only source of " fish oils " . Grass-fed animals have

up to 10 times more omega-3 fatty acids, in the more beneficial " fish

oil " form, than grain fed animals(132). The same thing applies to

eggs from pastured chickens(133).

Assuming that larger studies corroborate the benefits of omega-3's,

this means that animal fat is your best source of the only nutrient

that will lower the rate of coronary heart disease. And when you get

your omega-3's from fish, be sure to have them with a nice cream

sauce to ensure efficient absorption!

Conclusions

The scientific method that we follow today was created by Francis

Bacon in 1594. One of the most basic tenets is to revise your

hypothesis if it fails experimental testing. Cholesterol has

consistantly failed experimental testing, but rather than develop a

new hypothesis, it is recreated in disguised forms in which the

bottom line remains to lower your cholesterol and avoid fatty foods.

This is why nutrition has become a joke among the general public and

given rise to cartoons with punch lines like " Good news, Mr. Dewlap.

While your cholesterol has remained the same, the research findings

have changed. " In the void of responsible leadership from the

scientific community, our bookstores are filled with crank theories

that are doing untold harm to the public's health. Meanwhile the real

cause of heart disease remains unknown and unstudied; a tragedy that

could have been prevented if early researches heeded the advise of

Francis Bacon back in 1970 when the first large scale test of a

cholesterol lowering drug was aborted because it was causing heart

attacks.

Further Reading

Articles

The Soft Science of Dietary Fat by Taubes. Science, vol 291, pp.

2536-2545

The Cholesterol Myth by . The-Atlantic, VOL:v264, ISS:n3,

DATE: Sept 1989, PAGE:37(25),

Books

The Cholesterol Myths by Uffe Ravnskov. New Trends Publishing

Coronary Heart Disease, the Dietary Sense and Nonsense by

Mann. Janus Publishing

The Cholesterol Conspiricy by . Janus Publishing.

Know Your Fats by Enig. Bethesda Press.

Websites

http://www.ravnskov.nu/cholesterol.htm

http://www.second-opinions.co.uk/cholesterol_myth_1.html

http://www.westonaprice.org/know_your_fats/oiling.html

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[Guest guest]

Hi ,

I would like to give this to some friends/family to read; do you

mind? If you don't mind, how would you like to be attributed?

Thanks!

[Guest guest]

> Hi ,

>

> I would like to give this to some friends/family to read; do you

> mind? If you don't mind, how would you like to be attributed?

>

Nope, I don't mind. Anything to put an end to the low-fat nonsense!

As far as the attribution, I guess as long as my name's on it, it

should be fine.