Re: Statins & heart disease (was fats & cholesterol)

[Guest guest]

I'm not sure that discrepancy actually exists. I have read both ways

> on whether they are protective in these populations, and also read

> that it is very understudied. Do you have a reference for this? I

> realize I am saying things without providing all the references but

> since there is conflicting information on this point I can't really

> address it without seeing the data.

>

Here are some studies on statins you should look at if you haven't already seen

them:

- No statin primary prevention study has ever shown reduced mortality in healthy

men and

women with only an elevated serum cholesterol and no known CHD (CMAJ. 2005 Nov

8;173(10):1207; author reply 1210.)

- An analysis of large, controlled trials prior to 2000 found that long-term use

of statins

for primary prevention of CHD produced a 1% greater risk of death over 10 years

compared to placebo ( PR. Br J Clin Pharmacol 2001;52:439-46.)

- Honolulu Heart Program 2001: " Our data accords with previous findings of

increased

mortality in elderly people with low serum cholesterol, and show that long-term

persistence of low cholesterol concentration actually increases risk of

death...the earlier

patients start to lower cholesterol concentrations, the greater the risk of

death. " (Lancet.

2001 Aug 4;358(9279):351-5.)

- ALLHAT 2002: in the largest North American cholesterol-lowering trial ever and

the

largest trial in the world using Lipitor, mortality of the treatment group and

controls after

3 or 6 years was identical. (The ALLHAT Officers and Coordinators for the ALLHAT

Collaborative Research Group. JAMA 2002;288:2998-3007.)

- Heart Protection Study 2002: received widespread press coverage indicating

" massive

benefits " from cholesterol-lowering; those who took simvastatin (Zocor) had an

87.1%

survival rate after five years, compared to an 85.4% survival rate for the

controls, and these

results were independent of the amount of cholesterol lowering. (Heart

Protection Study

Collaborative Group. Lancet 2002;360:7-22.)

- J-LIT 2002: a 6-year study of 47,294 patients treated with simvastatin;

results showed

higher mortality at the lowest serum cholesterol (both total and LDL), and the

lowest

mortality at the highest serum cholesterol (both total and LDL). The higher

mortality at

low cholesterol levels was due to increased cancer. (Matsuzaki M and others.

Circ J. 2002

Dec;66(12):1087-95.)

- CARE 1996: risk of death from CHD for those with pre-existing CHD went from

5.7% to

4.6% (Sacks FM, et al. New England Journal of Medicine 1996;335:1001-1009.)

- WOSCOPS 1995: risk of death from CHD for those with pre-existing CHD went from

2.6%

to 2.2% (Shepherd J, et al. New England Journal of Medicine 1995;333:1301-1307.)

- " The statins correct plasma lipid levels optimally, yet the real magnitude of

their benefits

is marginal and certainly not better than attained with agents that do not

affect plasma

lipid levels. It is suggested that some of our recommendations and actions

relating to

plasma cholesterol levels and to atherosclerosis are based on concepts that are

fundamentally flawed and need to be revised. " (Krut LH Am J Cardiol 1998.)

- " The beneficial effects of statins on clinical events may involve nonlipid

mechanisms that

modify endothelial function, inflammatory responses, plaque stability and

thrombulus

formation...These nonlipid properties of statins may help to explain the early

and

significant cardiovascular event reduction reported in several clinical trials

of statin

therapy. " (Rosenson RS JAMA 1998)

- In people older than 85 years, high total cholesterol concentrations are

associated with

longevity owing to lower mortality from cancer and infection. The effects of

cholesterol-

lowering therapy have yet to be assessed. (Lancet. 1997 Oct

18;350(9085):1119-23.)

- Our findings do not support the hypothesis that hypercholesterolemia or low

HDL-C are

important risk factors for all-cause mortality, coronary heart disease

mortality, or

hospitalization for myocardial infarction or unstable angina in this cohort of

persons older

than 70 years. (JAMA. 1994 Nov 2;272(17):1335-40.)

** ACCORDING TO THE FIGURES FROM THE WOSCOPS TRIAL, If you treated someone for

30 years you can expect to provide them with 30/700 added years of life. This is

15.64

days... In short, if a fifty year old man asked you how much longer he could

expect to live

if he took a statin for thiry years you can inform him " just over two weeks —

max. " (Dr.

Malcom Kendrick, " The Great Cholesterol Con " )

There is more but perhaps I should stop here. The conclusions are as follows:

1) Statins MAY reduce CHD mortality in primary prevention populations (people

who've

never had heart disease), but they do not reduce total mortality in this

population

2) Statins do not reduce CHD rates or total mortality in women

3) Statins do reduce CHD mortality in secondary prevention populations (people

who have

or had heart disease), but do not reduce total mortality in this population

4) Statins do not reduce CHD or total mortality. In fact, elderly people with

low cholesterol

die twice as often as elderly people with high cholesterol.

5) CONCLUSION: statins do not, therefore, reduce overall mortality in >95% of

the human

population

If you have data that indicate otherwise, I'd love to see it.

The problem this raises for me is that if oxidized LDL was a primary cause of

CHD and

CHD mortality, and statins reduce levels of ox-LDL across the board (which is

not in

dispute by anyone, it seems), then why aren't statins reducing CHD rates in

women and

the eldery?

K.

[Guest guest]

> It seems from scanning to me that you provided too much information.

> I can't possibly look at all of it for participation in a discussion

> like this, and it seems that only a few of them concern whether women

> or elderly benefit from statins, which I believe was your original

> question. Perhaps you could provide one or two studies and/or

> meta-analyses showing that statins have failed to reduce CHD in women

> and elderly.

>

Sorry about that! I have looked into this in great detail and have a lot of

studies handy

since I'm preparing for a presentation.

Here is a good summary of the studies on elderly & statins:

http://junkfoodscience.blogspot.com/2008/01/reading-evidence-closely-statins-

for.html

See here for info on women and elderly:

- Abramson and contend that statins did not reduce coronary heart disease

events

in the almost 11 000 women in pooled trials, nor in men and women older than 69

(n=3239). (http://www.medscape.com/viewarticle/551324)

K.

[Guest guest]

> Ultimately, however, your question of how statins cannot provide

> benefits in certain population if they lower ox-LDL and ox-LDL

> contributes to heart disease is similar to asking how they can boost

> nitric oxide functioning and provide no benefit in these populations

> if nitric oxide is protective, or how they can inhibit platelet

> aggregation and smooth muscle cell migration and not provide benefit

> in these populations if these factors are known to be part of the

> disease process.

>

> We would want to know how effective they were at lowering ox-LDL in

> the individual trial, and want to know if it correlated with risk

> reduction -- information we don't have. We would want to know, if

> there was not reduction in CHD deaths, was there a reduction in or

> reversal of the disease process. For example, was there a reduction

> in stenosis and intima-media thickness, a reduction in calcification,

> etc.

>

Exactly. The deeper I get into the data and analysis of the data, the more

clear it becomes

that we just can't be sure of the exact mechanisms of CHD. Nor can we be sure

exactly

how statins work.

However, most people simply aren't interested in the finer points of this

debate. What

most people want to know is " what can I do to promote health and well-being and

improve

my quality of life as I age " ? " What should I eat? " " Should I take statins? "

And ultimately,

as a future health-care professional, those are the questions I'm most

interested in as

well.

From my reading of the data, we can answer those questions with some certainty.

That's

why in my mind the total mortality data is so much more important than the rates

of CHD,

and even CHD-related deaths. Who cares if a statin reduces CHD events when it

raises

mortality from cancer and other diseases at the same time? Personally, I'd much

rather die

from a massive MI than a long, painful cancer.

What I feel very good about telling the people I work with is this:

1) There is absolutely no evidence that eating cholesterol and saturated fat in

the diet

raises cholesterol levels in the blood.

2) A diet high in saturated fats and cholesterol is far more healthy for your

heart (and the

rest of your body) than a diet high in PUFAs and refined carbohydrates (the

so-called

" heart healthy " approach).

3) The only aspect of your cholesterol levels you should (probably) be aware of

is the L(p)a

(as an indicator of the level of oxidization of LDL) and the ratio of ApoB100 to

LDL (as an

indicator of the density/size of LDL particles). The way to reduce ox-LDL and

minimize

the small, dense LDL particles is to avoid PUFAs and trans fats in the diet and

eat plenty of

egg yolks (see #3 above).

4) Statins do not reduce total mortality in >95% of the population. They have

serious and

significant side effects and risks, many of which are underreported. They have

been shown

to cause cancer in every animal study done to date. In the highest risk

population

(middle-aged men who already have CHD), a 50-year old man would have to take a

statin

for 30 years to extend his lifespan for 2-weeks. Statins do not reduce total

mortality in

primary prevention populations or women, and they actually increase total

mortality in the

elderly (high cholesterol is protective in this population).

On a practical level, for most people, I think the four points above are what it

really boils

down to. The details we are hashing through are only relevant (in my mind) to

the extent

that they change the recommendations above in some way. Otherwise, they are

mostly

academic. (No judgment there! I enjoy learning about this stuff and talking

about it. But

I'm speaking of what I think is relevant to our daily lives.)

K.

[Guest guest]

> This is false. It has long been established that substituting SFA for

> PUFA raises levels of cholesterol in the blood in very tightly

> controlled metabolic ward studies. Your point about cholesterol is

> more true. However, to be more precise, at least with egg

> cholesterol, about 70% of people have no response or a very slight but

> relatively insignificant increase, and about 30% have substantial

> increases in cholesterol levels, but no change in the LDL:HDL ratio

> and a general shift from pattern B (bad) LDL to pattern A (good) LDL.

> This is dependent on certain genes.

I would like to see the data from which you draw this conclusion. Where can I

find those

metabolic ward studies?

Because I have seen a lot of studies that indicate the opposite (regarding the

effect of

saturated fat consumption on serum cholesterol).

- " In Framingham, Massachusetts, the more saturated fat one ate, the more

cholesterol

one ate, the more calories one ate, the lower people's 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. " (1992)

- In a study of 10,000 Israeli civil servants, intake of animal fat ranged from

ten grams up

to two hundred grams daily. Yet there was absolutely no relationship between

intake of

dietary fat and cholesterol levels. (Kahn HA, and others. Israel Journal of the

Medical

Sciences. 1969;5:1117 1127.)

- A survey of South Carolina adults found no correlation of blood cholesterol

levels with

" bad " dietary habits, such as use of red meat, animal fats, fried foods, butter,

eggs, whole

milk, bacon, sausage and cheese (Lackland DT, et al. J Nutr, Nov 1990.

120:11S:1433-

1436)

- The Masai tribe in Africa subsist largely on whole milk, blood and beef. Yet

their

cholesterol is among the lowest ever measured in the world, and about 50% of the

average

Americans' (Lapiccirella V., and others. Bulletin of the World Health

Organization 1962;27:

681-697.)

- There is not a single long-term study showing that a high-cholesterol, or high

saturated fat diet, has any impact on blood cholesterol levels in a normal,

healthy

population (Farr, M.D., " Why the Cholesterol-Heart Disease is Wrong " ,

http://www.thincs.org/)

If the above statement by Dr. Farr is incorrect, I would like to see that study

if you have

the reference.

K.

[Guest guest]

> This is false. It has long been established that substituting SFA for

> PUFA raises levels of cholesterol in the blood in very tightly

> controlled metabolic ward studies. Your point about cholesterol is

> more true. However, to be more precise, at least with egg

> cholesterol, about 70% of people have no response or a very slight but

> relatively insignificant increase, and about 30% have substantial

> increases in cholesterol levels, but no change in the LDL:HDL ratio

> and a general shift from pattern B (bad) LDL to pattern A (good) LDL.

> This is dependent on certain genes.

>

One more question. Since you advocate eating saturated fat, and since you

believe ox-

LDL is a contributor to CHD whereas " normal " (light, fluffy) LDL is not, I'm

assuming that

you believe saturated fat increases the " normal " LDL and not ox-LDL. (That's a

lot of

assumptions about what you think, so please correct me if I'm wrong!)

In the study you reference, did total, HDL, LDL or all three go up after eating

SFA? How

much?

Of what relevance do you believe this finding is, in light of the fact that you

support eating

SFAs over PUFAs?

K.

[Guest guest]

I'm just one person BUT last June, I began eating a whole foods, no

sugar no grain diet. The only fats I use are butter, coconut oil and

once in a while, a small amount of olive oil. I eat plenty of meat,

mostly chicken. My total Cholesterol went from around 300 to 150 in

that amount of time. HDL increased from 30 to 50 and LDL came down a

little, but still high. So, for me personally, I certainly don't fit

what was written and from my research, something sounds very wrong with

that conclusion.

" It has long been established that substituting SFA for PUFA raises

levels of cholesterol in the blood in very tightly

controlled metabolic ward studies " .

[Guest guest]

>

> I'm just one person BUT last June, I began eating a whole foods, no

> sugar no grain diet. The only fats I use are butter, coconut oil and

> once in a while, a small amount of olive oil. I eat plenty of meat,

> mostly chicken. My total Cholesterol went from around 300 to 150 in

> that amount of time. HDL increased from 30 to 50 and LDL came down a

> little, but still high. So, for me personally, I certainly don't fit

> what was written and from my research, something sounds very wrong with

> that conclusion.

>

> " It has long been established that substituting SFA for PUFA raises

> levels of cholesterol in the blood in very tightly

> controlled metabolic ward studies " .

>

M. will likely weigh in, but what makes this more complicated is that you

were not

simply substituting SFA for PUFA in your diet and keeping carbohydrate intake

constant. It

sounds like you dramatically reduced your carbohydrate intake, which would lower

your

cholesterol. You were substituting SFA for both PUFAs and carbs, so although

the SFAs

may have had a very slight cholesterol raising effect vs. the PUFAs, the huge

reduction in

carbs had a much more significant effect in lowering your cholesterol.

And of course, many like Dr. Ravnskov and Colpo would simply say that

SFA

consumption and serum cholesterol aren't correlated.

K.

[Guest guest]

I just want to say thanks for the explanations to both Chris's. That

makes sense. I'm fairly new to this way of life and although I knew

the correlation between HFCS and triglycerides, I didn't realize all

carbs affected it to. Learn something every day. Actually, I learn

more somethings every day here and other places than I can keep up

with:) I just want to say how much I appreciate ya'll (and everyone

else) being so willing to share their knowledge and answer questions.

God Bless,

Patty