Lancet: Statins (Lipitor, Zocor, Cr... 
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If 49 of 50 is considered most! According to an article being published in the medical journal The Lancet this week - the statins (worth billions to the pharma industry) are worthless to patients.
I feel that they are not worthless. I feel that they are harmful. Overweight, those not exercising, those eating poorly, all take what they feel is a magic pill AND THEY DON'T CHANGE A THING. They see their overall cholesterol numbers go down and think they are protected. Cheeseburger and Zocor = not perfect together.
A preview of the Lancet article:
http://www.dailymail.co.uk/pages/live/articles/health/healthmain.html?in_arti...
Have we been conned about cholesterol?
by MALCOLM KENDRICK
Conventional medical wisdom about cholesterol and the role of statins is now being challenged by a small, but growing number of health professionals. Among them is Dr Malcolm Kendrick. A GP for 25 years, he has also worked with the European Society of Cardiology, and writes for leading medical magazines:
When it comes to heart disease, we have been sold a pup. A rather large pup.
Actually, it's more of a full-grown blue whale. We've all been conned.
If you've got a raised risk of heart disease, the standard medical advice is to take a cholesterol-lowering statin drug to cut your chances of having a heart attack because, as we all know, cholesterol is a killer.
Indeed, many of you already believe that you should take statins for the rest of your natural lifespan.
Nearly everybody is in agreement about the need to lower your cholesterol level. The NHS spends nearly £1 billion a year on prescriptions for statins and possibly the same amount administering the cholesterol tests, surgery visits and the rest.
But is it all worth it? According to an article being published in the medical journal The Lancet this week, the answer is probably no.
A leading researcher at Harvard Medical School has found that women don't benefit from taking statins at all, nor do men over 69 who haven't already had a heart attack.
There is a very faint benefit if you are a younger man who also hasn't had a heart attack - out of 50 men who take the drug for five years, one will benefit.
Nor is this the first study to suggest that fighting cholesterol with statins is bunk. Indeed, there are hundreds of doctors and researchers who agree that the cholesterol hypothesis itself is nonsense.
What their work shows, and what your doctor should be saying, is the following:
• A high diet, saturated or otherwise, does not affect blood cholesterol levels.
• High cholesterol levels don't cause heart disease.
• Statins do not protect against heart disease by lowering cholesterol - when they do work, they do so in another way.
• The protection provided by statins is so small as to be not worth bothering about for most people (and all women). The reality is that the benefits have been hyped beyond belief.
• Statins have many more unpleasant side effects than has been admitted, while experts in this area should be treated with healthy scepticism because they are almost universally paid large sums by statin manufacturers to sing loudly from their hymn sheet.
So how can I say saturated fat doesn't matter when everyone knows it is a killer? Could all those millions who have been putting skinless chicken and one per cent fat yoghurts into their trolleys really have been wasting their time?
The experts are so busy urging you to consume less fat and more statins that you are never warned about the contradictions and lack of evidence behind the cholesterol con.
In fact, what many major studies show is that as far as protecting your heart goes, cutting back on saturated fats makes no difference and, in fact, is more likely to do harm.
So how did fat and cholesterol get such a bad name? It all began about 100 years ago, when a researcher found feeding rabbits (vegetarians) a high cholesterol carnivore diet blocked their arteries with plaque.
But it took off in the Fifties with the Seven Countries study by Ancel Keys, which showed that the higher the saturated fat intake in a country, the higher the cholesterol levels and the higher the rate of heart disease.
The countries he chose included Italy, Greece, the USA and the Netherlands. But why these particular ones?
Recently I did my own 14 countries study using figures from the World Health Organisation, and found the opposite.
Countries with the highest saturated fat consumption ? Austria, France, Finland and Belgium ? had the lowest rate of deaths from heart disease, while those with the lowest consumption ? Georgia, Ukraine and Croatia ? had the highest mortality rate from heart disease.
Added to this, the biggest ever trial on dietary modification put 50 million people on a low saturated fat diet for 14 years.
Sausages, eggs, cheese, bacon and milk were restricted. Fruit and fish, however, were freely available. I?m talking about rationing in Britain during and after World War Two. In that time, deaths from heart disease more than doubled.
Even more damning is what happened in 1988. The Surgeon General's office in the US decided to gather all evidence linking saturated fat to heart disease, silencing any nay-sayers for ever.
Eleven years later, however, the project was killed. The letter announcing this stated that the office "did not anticipate fully the magnitude of the additional expertise and staff resources that would be needed".
After eleven years, they needed additional expertise and staff resources? What had they been doing? If they'd found a scrap of evidence, you would never have heard the last of it.
Major trials since have been no more successful. One involved nearly 30,000 middle-aged men and women in Sweden, followed for six years.
The conclusion? "Saturated fat showed no relationship with cardiovascular disease in men. Among the women, cardiovascular mortality showed a downward trend with increasing saturated fat intake." (In other words, the more saturated fat, the less chance of dying from heart disease).
Even stronger evidence of the benefits of increased fat and cholesterol in the diet comes from Japan. Between 1958 and 1999, the Japanese doubled their protein intake, ate 400 per cent more fat and their cholesterol levels went up by 20 per cent.
Did they drop like flies? No. Their stroke rate, which had been the highest in the world, was seven times lower, while deaths from heart attacks, already low, fell by 50 per cent.
It's a bit of a paradox, isn?t it? That's one of the features of the dietary hypothesis - it involves a lot of paradoxes.
The most famous is the French Paradox. They eat more saturated fat than we do in Britain; they smoke more, take less exercise, have the same cholesterol/LDL levels, they also have the same average blood pressure and the same rate of obesity.
And you know what? They have one quarter the rate of heart disease we do.
The official explanation is that the French are protected from heart disease by drinking red wine, eating lightly cooked vegetables and eating garlic.
But there is no evidence that any of these three factors are actually protective. None. By evidence, I mean a randomised, controlled clinical study.
Every time a population is found that doesn't fit the saturated fat/cholestrol hypothesis - the Masai living on blood and milk with no heart disease, the Inuit living on blubber with low heart disease - something is always found to explain it.
One research paper published more than 20 years ago found 246 factors that could protect against heart disease or promote it. By now there must be more than a thousand.
The closer you look the more you find that the cholestrol hypothesis is an amazing beast. It is in a process of constant adaptation in order to encompass all contradictory data without keeling over and expiring.
But you don't need to look at foreign countries to find paradoxes - the biggest one is right here at home. Women are about 300 per cent less likely to suffer heart disease than men, even though on average they have higher cholesterol levels.
For years there was an ad hoc hypothesis to explain this apparent contradiction - women were protected by female sex hormones.
In fact, there has never been a study showing that these hormones protect against heart disease in humans.
But by the Nineties, millions of women were being prescribed HRT to stave off heart disease.
Then came the HERS trial to test the notion. It found HRT increased the risk of heart disease.
So what to do? Put them on statins; bring their cholesterol level down ? below 5.0 mmol is the official advice.
But, as The Lancet article emphasises, women do not benefit from statins. The phrase "Statins do not save lives in women" should be hung in every doctor's surgery.
But it's not just hugely wasteful handing out statins to women and men who are never going to benefit; it also exposes them to the risk of totally unnecessary side effects.
These include muscle weakness (myopathy) and mental and neurological problems such as severe irritability and memory loss.
How common are they? Very rare, say experts, but one trial found that 90 per cent of those on statins complained of side effects, half of them serious.
Only last week, a study reported a link between low LDL cholesterol and developing Parkinson's disease.
Statins are designed to lower LDL. In the face of anticholesterol propaganda, it is easy to forget cholesterol is vital for our bodies to function.
Why do you think an egg yolk is full of cholesterol? Because it takes a lot of cholesterol to build a healthy chicken.
It also takes a hell of a lot to build and maintain a healthy human being.
In fact, cholesterol is so vital that almost all cells can manufacture cholesterol; one of the key functions of the liver is to synthesise cholesterol.
It's vital for the proper functioning of the brain and it's the building bock for most sex hormones.
So it should not be such a surprise to learn that lowering cholesterol can increase death rates.
Woman with a cholesterol level of five or even six have a lower risk of dying than those with a level below four.
The Lancet reported that statins didn't benefit anyone over 69, not even men; in fact, there's good evidence that they may hasten your death.
The Framingham study in the US found that people whose cholesterol levels fell were at a 14 per cent increased risk of death from heart disease for every 1mg/dl.
Set up in 1948, the study screened the whole population of Framingham near Boston for factors that might be involved in heart disease and then followed them to see what happened to them.
It is still going today, making it the longest running and most often quoted study in heart-disease research.
A massive long-term study that looked specifically at cholesterol levels and mortality in older people in Honolulu, published in The Lancet, found that having low cholesterol concentration for a long time increases the risk of death.
This may be because cholesterol is needed to fight off infections or there may be other reasons ? but many other studies have found exactly the same thing.
Low cholesterol levels greatly increase your risk of dying younger. So the cholesterol hypothesis looks something like this:
There is no evidence that saturated fat is bad - and there are lots of 'paradoxes' where countries with a high cholesterol intake don't have a higher death rate from heart disease.
But there is an even more fundamental problem. The theory claims fat and cholesterol do things in the body that just don't make sense.
To begin with, saturated fat and cholesterol are talked of as if they are strongly connected. A low-fat diet lowers cholesterol; a high-fat diet raises it.
What is never explained is how this works. This isn't surprising because saturated fat doesn't raise cholesterol. There is no biochemical connection between the two substances, which may explain all those negative findings.
It's true that foods containing cholesterol also tend to contain saturated fats because both usually come from animals.
It's also true that neither dissolve in water, so in order to travel along the bloodstream they have to be transported in a type of molecule known as a lipoprotein - such as LDLs (low-density lipoproteins) and HDLs (high-density lipoproteins).
But being travelling companions is as close as fats and cholesterol get. Once in the body, most fat from our diet is transported to the fat cells in a lipoprotein called a chylomicron.
Meanwhile, cholesterol is produced in the liver by way of an incredibly complicated 13-step process; the one that statins interfere with.
No biochemist has been able to explain to me why eating saturated fat should have any impact on this cholesterol production line in the liver.
On the other hand, the liver does make fat - lots of it. All the excess carbohydrate that we eat is turned first into glucose and then into fat in the liver.
And what sort of fat does the liver make? Saturated fat; obviously the body doesn't regard it as harmful at all.
Recently, attention has been shifting from the dangers of saturated fat and LDL "bad" cholesterol to the benefits of HDL "good" cholesterol, and new drugs that are going to boost it.
But the idea that more HDLs are going to fight off heart disease is built on equally shaky foundations.
These lipoproteins seem to be cholesterol "scavengers", sucking up the cholesterol that is released when a cell dies and then passing it on to other lipoproteins, which return it to the liver.
Interestingly, the "bad" LDL lipoproteins are involved in the relay. The idea seems to be that HDLs can also get the cholesterol out of the plaques that are blocking arteries.
However, there is a huge difference between absorbing free-floating cholesterol and sucking it out of an atherosclerotic plaque which is covered by an impermeable cap.
• Extracted from The Great Cholesterol Con by Malcolm Kendrick, published by John Blake on January 29 at £9.99.
http://www.bobmantz.com
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This is a reply to # 822,300Cholesterol :: Cholesterol drugs, statins, Lipitor over-prescribed - The Lancet
Award-winning physician John Abramson argues that clinical trials provide no evidence of lowering cholesterol in women and elderly.
more..
An article published today in one of the leading medical journals claims that anti-cholesterol drugs are over-prescribed and could spell big trouble for pharmaceutical companies such as Pfizer, maker of industry-leading medication Lipitor.
The article, co-authored by Harvard Medical School clinical instructor John Abramson, appeared in the January_20th edition of The Lancet medical journal, and shows that clinical trials for coronary heart disease prevention fail to prove that anti-cholesterol drugs, such as Lipitor, provide benefit for many in the U.S. who are taking them.
If the medical community accepts Abramson's conclusions, it could negatively impact sales for drugs such as Lipitor.
Dr. Abramson and co-author Dr. Jim Wright of the Therapeutics Initiative in British Columbia say that statins, a class of cholesterol-lowering drugs, should not be prescribed for the primary prevention of heart disease to women of all ages or to men older than 69 years of age.
According to Abramson, the article titled "Are Lipid-Lowering Guidelines Evidence-Based?" shows that no studies have shown statin drugs to be effective for women and men 69 years of age or older who do not already have heart disease or diabetes. It also suggests that U.S. cholesterol treatment guidelines should be revised, taking in to consideration the lack of evidence that such drugs are beneficial to many Americans.
"The displacement of effective approaches to preserving our overall health is an enormous national scandal," said Abramson. "Americans are being misled about what the scientific evidence really shows."
Lipitor is the best-selling drug in the world, with sales in 2004 of more than $10 billion.
http://www.spiritindia.com/health-care-news-articles-5889.html
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This is a reply to # 823,159Statins can do harm
Created: Wednesday, January 24, 2007
Healthy women and healthy older men should not take cholesterol-lowering statin drugs in an attempt to prevent heart disease, suggests a US-Canadian study in the current issue of the The Lancet medical journal.
The researchers analysed data from eight previous studies that compared statins with placebo in people at increased risk for cardiovascular disease. They found that statins did reduce overall risk of heart attack or stroke but did not reduce total deaths, reported the National Post newspaper in Canada.
When the researchers analysed data from specific groups, they found that statins did not reduce the risk of heart attacks in healthy women or in healthy men older than 69 years.
Not for primary prevention
"Our analysis suggests that lipid-lowering statins should not be prescribed for true primary prevention in women of any age or for men older than 69 years," the researchers wrote.
"Most people have the impression that statins are going to make them live longer. For primary prevention, there hasn't been demonstrated to be any survival advantage," study co-author Dr Jim Wright, a professor at the University of British Columbia, told the Post.
He noted that, in rare cases, statins can cause muscle damage that results in muscle pain and weakness. The drugs can also cause nerve damage that leads to numbness and pain in the feet. – (HealthDayNews)
http://www.health24.com/news/Heart_Cardiovascular/1-958,39001.asp
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This is a reply to # 823,161Sharon Kirkey, CanWest News Service
Published: Tuesday, January 23, 2007 Article tools
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Font: * * * * No otherwise healthy woman of any age should be on a cholesterol-lowering drug to prevent heart disease, suggests a new analysis of the fastest-growing drug class in Canada.
Millions of Canadians take cholesterol reducers, called statins, to lower their risk of heart attacks and cardiovascular disease. For people who already have artery disease, statins saves lives.
More controversial is whether people who don't have evidence of occlusive vascular disease, which leads to clogged arteries, should be taking the drugs.
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About three-quarters of people on statins fall into that category. ``It's not a trivial, minor thing. It's the bulk of the prescribing,'' said Dr. Jim Wright, medical director of the B.C.-based Therapeutics Initiative and a professor at the University of B.C.
In a brief article published in the most recent issue of the journal, The Lancet, Wright and co-author Dr. John Abramson of Harvard Medical School pooled data from eight randomized trials comparing statins with a placebo in people at increased risk of cardiovascular disease. The statins did not reduce total deaths. And, when they looked at women alone, they found no benefit.
Overall, statins reduced the risk of heart attack or stroke. But the absolute risk reduction of 1.5 per cent ``is small (and) means that 67 people have to be treated for five years to prevent one such event," according to the researchers.
When they looked closer, the benefit appeared to be limited to high-risk men aged 30 to 69.
The drugs did not reduce heart attacks in 10,990 women in the primary prevention trials. Statins also did not reduce heart attacks or strokes in men older than 69.
``Our analysis suggests that lipid-lowering statins should not be prescribed for true primary prevention in women of any age or for men older than 69 years,'' the researcher write in the Lancet.
``If someone says that they should, then give us the evidence,'' Wright said in an interview.
``It doesn't make sense to me. Each doctor prescribing these drugs and each patient taking them wants to know, what is the magnitude of the potential benefit and harm in people like me?''
But Dr. George Fodor, one of the authors of the Canadian cholesterol-lowering guidelines said a study published last year involving 8,000 people found giving statins to low-risk men significantly reduced their risk of cardiovascular disease, and that there was a ``trend'' toward improvement for women.
``The efficacy and safety of the drugs is outstanding,'' said Fodor, a spokesman for the Heart and Stroke Foundation and head of research in preventive cardiology at the University of Ottawa Heart Institute.
In the United Kingdom, statins are available over the counter, without a doctor's prescription.
Fodor said the drugs ``are much safer than Aspirin.
``Somebody who has no detectable risk and is apparently healthy should not take (statins). But how many middle-aged people in Canada do not have some atherosclerosis? We cannot detect them easily at the moment.''
More than 23.6 million prescriptions for cholesterol reducers were dispensed from Canadian retail drug stores for the 12-month period ending Sept. 30, according to the drug-tracking firm IMS Health. In Canada alone, statins are a $2-billion market.
There were more than 12.3 million prescriptions over the same period for Pfizer's Lipitor, the No. 1-selling drug in the country.
``Most people have the impression that statins are going to make them live longer,'' Wright said. ``For primary prevention, there hasn't been demonstrated to be any survival advantage.''
In rare cases, statins can cause muscle damage that can lead to muscle pain and weakness. ``In the worst form, patients can die due to muscle breakdown leading to kidney damage,'' Wright said. ``It's not a trivial thing.''
As well, doctors are seeing more cases of statin-induced peripheral neuropathy, where the long nerves in the body die off, causing numbness and pain in the feet.
Abramson is an expert consultant to plaintiffs' attorneys on lawsuits involving the drug industry, including Pfizer for its marketing of Lipitor.
http://www.canada.com/topics/bodyandhealth/story.html?id=ddc034f2-7c00-46d1-9...
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This is a reply to # 823,163January 25, 2007 Shelley Wood
London, UK - Authors of a Comment in the January 20, 2007 issue of the Lancet are calling for a revision of the 2001 US National Cholesterol Education Program guidelines, saying that statin therapy for primary prevention in women or in people over age 65 is not supported by the bulk of the evidence [1]. But others counter that while the magnitude of the benefit may not be as large in primary-prevention patients as in secondary prevention, there is clear benefit, particularly in higher-risk groups.
"In support of statin therapy for the primary prevention of this disease in women and people aged over 65 years, the guidelines cite seven and nine randomized trials, respectively. Yet not one of the studies provides such evidence," Dr John Abramson (Harvard Medical School, Boston, MA) and Dr Jim Wright (University of British Columbia, Vancouver) write in the Lancet.
The authors of the Comment drew their conclusions after looking at eight randomized clinical trials that compared statins with placebo and included primary-prevention populations at increased risk of developing CAD. Overall benefit was estimated on the basis of total mortality and total serious adverse events. They report that total mortality was not reduced by statins. In the two trials that reported total serious adverse events, these events were not reduced or increased by statins.
When only cardiovascular events were considered, Abramson and Wright report that statins reduced this outcome to a statistically significant degree; however, the absolute risk reduction of 1.5% was small. Moreover, this would mean that 67 people would have to be treated for five years to prevent one event. Furthermore, they argue, this benefit might be confined to high-risk men between the ages of 30 and 69. Abramson and Wright 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).
Relative risk by event and group
Outcome
RR
95% CI
Mortality, all
0.95
0.89-1.01
Serious adverse events, all*
1.01
0.97-1.05
CVD events, all
0.82
0.77-0.87
CVD events, women
0.98
0.85-1.12
CVD events, men and women over age 69
0.94
0.77-1.15
*Reported in two trials only
To download table as a slide, click on slide logo below
In an interview with heartwire, Wright explained that their analysis was conducted in response to the 2005 meta-analysis reported by the Cholesterol Treatment Trialists (CTT) collaborators, which found a benefit of statins in a combined cohort of primary- and secondary-prevention populations and in a cohort of patients with no coronary heart disease at baseline, many of whom had preexisting cerebrovascular or peripheral vascular disease [2].
"Because they have individual participants' data, the CTT collaborators have the unique opportunity to analyze the data for the 41 354 people in the true primary-prevention group," Abramson and Wright contend.
To heartwire, Wright elaborated: "Our information, which is the best that's available in the published literature, is not as good as what the CTT collaborators have. They basically are in a better position to publish this information specifically in the primary-prevention group and have the world be able to look at it and have doctors be able to see that the evidence isn't there, for some groups of people.
"It appears to me that they are deliberately not providing that information. . . . If you look at their paper, they're academics, but they do have relationships with a number of the companies that market these drugs. Maybe they honestly believe that [public access to data] could mislead, or that they don't have all the answers yet, or all those things, but personally I find it shocking that they wouldn't just provide access. And if they don't want to analyze it and publish it themselves, then make it available for other people to do so. We'd be more than happy to do that."
In the meantime, Wright thinks physicians should be honest with their patients about the lack of evidence in low-risk patients and the low absolute difference in relative risk, even in higher-risk patients requiring primary prevention.
'If you take a male who is 50 years old, a smoker, with high blood pressure, who eats the worst diet in the world . . . then if I were an honest physician, I would tell him that maybe he should be taking a statin. And if he asked how much would that reduce his risk, I would have to tell him that it would reduce his risk by 2% over the next five years. If he understood that information, he would say, You're expecting me to take a pill everyday for five years? And it's going to cost me two dollars a day? You're crazy! I'm not going to do it."
If physicians were truly honest with their patients, Wright concludes, "I think there probably would be very few people being treated for primary prevention with a statin."
The CTT responds
In response, Dr Colin Baigent (Clinical Trial Service Unit [CTSU], University of Oxford, UK) co-primary investigator for the CTT, told heartwire he considers the CTT database a resource and said he was unaware that Wright and Abramson wanted access. "If people are interested in the data, they can write to us and we'll do our best."
He also stated that he has every intention of doing the analysis proposed by the Comment authors. "They've suggested we should also look at effects in people with no known coronary disease at baseline. We haven't had the opportunity to do that, but I do plan to do those analyses, and I will discuss them with my coprincipal investigators and we'll decide whether we want to formally respond in print [to the Lancet Comment]."
But Baigent also underscores the pitfalls of proving benefit—or lack of benefit—in a very low-risk population. "My suggestion would be that if we are looking at a group of patients with no history of vascular disease, what we should be doing is looking at that group of people and also looking at the effects in people with vascular disease and testing to see whether there are any differences between these groups; rather than just looking at primary prevention in isolation, we should use all the data and ask the question: is it clear that the effects of statins differ substantially in those without disease? Because inevitably what will happen is that we'll have many fewer events in people with no history of disease, so the risk is that we'll inappropriately conclude that statins don't work."
Baigent also dismissed the idea that ties to industry had any effect on the CTT collaborators' conclusions. The CTT, he reminded heartwire, is a joint collaboration of the CTSU at Oxford and the University of Sydney, Australia, made up of clinical trialists who have participated in major statin trials, many of which were publicly funded, without industry involvement. The CTSU itself has a policy of not accepting honoraria from industry, as do several of the collaborators individually, and travel funding for the CTT to meet during the annual AHA meeting is provided by government funding, he explained. Any industry representatives who attend the CTT meetings, like all other collaborators who are not on the writing group, have no influence or veto powers in the writing of the CTT's conclusions.
"I'm very disappointed to hear that they think there's in some way some conflict of interest, " Baigent summed up. "I don't think there's any justification in the implication that we have been in any way influenced by industry. We are independent research scientists."
A question of interpretation?
Also commenting on the Comment for heartwire, Dr Niteesh Choudhry (Harvard Medical School) took issue with the emphasis by Abramson and Wright on mortality outcomes. Choudhry and colleagues published their own meta-analysis of statins in primary prevention, as reported by heartwire, in November 2006. At that time, Choudhry told heartwire that the guidelines are supported by the data, particularly for higher-risk patients requiring primary prevention.
"[Abramson and Wright] are saying that statins reduce the risk of nonfatal events in a significant way but don't reduce the rate of fatal events, and that's basically what we found as well," Choudhry stated. "But the difference is in the interpretation of whether nonfatal events are important or not. These authors make the argument that because statins don't reduce mortality in a primary-prevention population maybe it's not worth the cost of providing them to patients who don't have proven vascular disease. The argument I would make in contrast to that is that statins do reduce nonfatal events—MIs and other vascular events—and those are important. Even if they don't reduce deaths [in primary prevention], which is debatable, preventing heart attacks is still an important outcome."
Magnitude of benefit vs money matters
Where both Baigent and Choudhry appear to agree with Abramson and Wright is that the magnitude of benefit in a low-risk primary-prevention population is unclear.
"Risk stratification is of course the key point, because we've got so much information now on statins and their effects: it's very clear that they are effective."
Some sort of risk score for primary-prevention patients to determine the absolute benefit of statins based on level of risk would be useful, he notes. Indeed, CTT collaborators have a paper "in gestation" examining the use of a risk score for diabetics, and such an index could also be devised for other, lower-risk patients, Baigent agreed.
"We're conscious of the fact that there is interest in looking to see how low the benefits go. But really, the evidence of benefit of statins is so immense that I would be very surprised if we find a group that clearly doesn't benefit, when appropriate allowance is made for the multiple comparisons that we would have to do. . . . If you were treating middle-aged women with no history of disease and their risk is very low, the number of women you'd have to treat to avoid one event would be enormous, and that would be very expensive," Baigent continued. "So society would tend to agree that that wasn't an appropriate use of money, but that wouldn't be the same as saying that statins don't work in those people. Very likely they do, but their benefits are so small that they're not worth it."
But Baigent is adamant: "I don't recall writing—or even thinking—that statins should be used in everyone. That's simply not something we advocate."
What price point would be deemed worthwhile is fodder for further study, says Choudhry. Until then, he believes clinicians should feel comfortable using statins in primary prevention. "For patients who are at high risk by virtue of their risk factors but don't have proven vascular disease, who have average or above-average cholesterol levels, they should receive statin therapy," Choudhry proposed. "I think the data on that are relatively clear. What I believe the data also support is that there is benefit for intermediate-risk patients, although maybe not in terms of mortality. The unresolved question that the data do not answer, and even data from the CTT won't answer, is whether the magnitude of benefit in those intermediate-risk folks is worth the cost of paying for these drugs for tens of millions of people."
http://www.theheart.org/article/767615.do
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This is a reply to # 823,163"As well, doctors are seeing more cases of statin-induced peripheral neuropathy, where the long nerves in the body die off, causing numbness and pain in the feet."
That's safer than aspirin?
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