The results of this study, along with the associated podcast and commentary have been presented in a way that is extremely favourable to statins. However, there is an obvious fundamental flaw with this study that, in my opinion, has not been adequately discussed.

The new study relates to a follow-up of the Heart Protection Study (HPS), which was a statin clinical trial that ran for just over 5 years. At the end of this study the researchers continued to monitor the participants for a further 5 years. 

During the follow-up period, increasing numbers of people who were in the original placebo group started to take a statin. By the end of the study, the number of people taking a statin in each group was the same. 

The table below shows how many people (as a percentage) were taking a statin in each group.

Obviously, the study was no longer comparing a statin against a placebo – it was comparing statins against statins. Just to make it even more confusing; we do not even know which statin people took during the follow-up period and at what dosage.

This did not stop the researchers describing the results of this study as definitive evidence in favour of statins. 

Most doctors who prescribe statins will not have the time to read the full study and will have to rely on the summary and the podcast. This will leave them with an interpretation of these results that is heavily skewed in favour of statins.  

As far as I am concerned, the fact that just as many people in the placebo group took a statin is enough to nullify this study. However, there are several additional issues. 

All of the people included in this study are categorised as having very high risk. Almost half had already had a heart attack, and everyone else had either other forms of cardiovascular disease or conditions that would place them at high risk.  All of the evidence from statin clinical trials has consistently shown that any 'benefit' varies greatly according to the level of risk the trial participants have. Therefore, if any statin benefits were found during this study, it is simply unthinkable to try and extrapolate this to the general population or the majority of people who take statins.

In addition, the study report and commentary describe the results in terms of relative percentages. This is a very common problem with statin clinical trials. The relative percentage is meaningless to patients and it grossly exaggerates any suggested 'benefit'. For example, in terms of vascular related deaths a risk reduction of 18% is quoted for the initial trial period. However, the real risk reduction in absolute terms was 1.7%. 

Incidently, this 1.7% risk reduction in vascular related deaths reduced to 0.1% during the follow-up period. Therefore, there is not any real evidence to support the claim that the 'benefits' of statins increase if a person starts taking the statin earlier in life. 

It is also worth mentioning that statins have a wide range of adverse effects (some very serious) that were not included in this study. 

References:

Reuters: Cholesterol drugs safe, even after a decade of use. 23 November 2011

MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20 536 high-risk individuals: a randomised placebocontrolled trial. Lancet 2002; 360:7-22

Heart Protection Study Collaborative Group. Effects on 11-year mortality and morbidity of lowering LDL cholesterol with simvastatin for about 5 years in 20 536 high-risk individuals: a randomised controlled trial. ; published online Nov 23.

Kohli, P and Cannon, CP Statins and safety: can we finally be reassured?Lancet 2011;  published online Nov 23

However, a recent study published in the Journal of the American Medical Association, found that people who have the above risk factors are LESS likely to die after a heart attack than people who do not have the above risk factors. 

The study included more than 500,000 people who had a heart attack without any previously known  about cardiovascular disease. The researchers also accounted for other influences such as age and weight. 

In this study, the people who had NONE of the above risk factors were 50 percent MORE likely to die after a heart attack, than people with all of those risk factors. 

Some of the people who had these risk factors would have been on medications, so there is a suggestion that these medications may have prevented some of them from dying after the heart attack. In some cases this may be true, however, we know the 'benefits' of medications are all too often exaggerated, so it is impossible to say how much the medications would have influenced the results.

Of course, some of the above risk factors are valid, but overall, this study is telling us that the conventional model of how heart disease develops is fundamentally flawed. 

The conventional view of  cardiovascular disease is very narrow-minded and puts far too much emphasis on risk facts, in particular, risk factors that pharmaceutical companies have medications to treat. 

Cardiovascular disease is caused by a wide range of nutritional, lifestyle and environmental factors. The basic mechanism involves a build-up of inflammation that becomes in effect, out of control. Several nutritional factors are associated with this. Toxins can also damage our arteries. So can infections. In addition, excessive stress and a lack of social support are far more damaging to the heart than an arbitrary cholesterol reading.  This broader understanding of how cardiovascular disease develops is much more scientifically coherent than a short list of profit-driven risk factors. 

References:

Reuters News Story: More "healthy" patients die after heart attacks. November 15 2011

Canto, JG et al. Number of Coronary Heart Disease Risk Factors and Mortality in Patients With First Myocardial Infarction JAMA 2011;306(19):2120-2127

I am pleased to say that we have made significant progress with the documentary. We have now interviewed several of the leading experts in this field including: 

• Dr Malcolm Kendrick

(Author of The Great Cholesterol Con)

• Dr Natasha Cambell-McBride

(Author of Gut and Psychology Syndrome, and Put Your Heart in Your Mouth)

• Barry Groves, PhD

(Author of Trick and Treat)

• Professor Kausik Ray

(Professor of Cardiology, lead author on several key studies related to statins)

We have also interviewed people who have been affected by the adverse effects associated with statins.

During the next few weeks we will be releasing clips from these and other interviews as we progress with our investigation. If you would like to be kept informed of our progress, please sign-up for updates using the form to the right.

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This will be of no surprise to anyone who has looked into this subject, and the media reports do not go far enough, but at least some of the issues regarding statins are now starting to reach the general public.

The news reports do not go far enough because they still suggest that cholesterol is a risk factor for heart disease. After all this time it still absolutely amazes me that so many doctors have not bothered to take even the most casual look at the evidence.

“Research by BHF-funded scientists has shown that when it comes to cholesterol, ‘lower seems to be better’ for protecting us against heart attacks... The researchers looked at the effects of increasing the dosage of statins, a medicine that reduces cholesterol. They showed that a bigger drop in cholesterol – from more intensive treatment with statins – cut risks even more.”

This refers to a study just released in the Lancet. This study, and the media hype that the BHF have created about it, is nothing more than an attempt to confuse and mislead people.

If you read the headlines and the summary report you could certainly be forgiven for thinking that statins are wonder drugs and cholesterol really is humanity’s nemesis. This study did indeed find a reduction in heart attacks associated with more intensive use of statin drugs. However, there are at least four major reasons why the results are misleading.

The first reason is that the reduction in risk quoted in the interpretation of the study refers to a reduction in LDL cholesterol that is not normally seen in real life. This exaggerates the perceived benefits.

The interpretation refers to reductions in LDL levels of 2-3 mmol/l. The authors state that this reduction in LDL cholesterol would reduce the risk of a vascular event (such as a heart attack) by 40-50 percent.

Well, LDL cholesterol is typically around 2-3 mmol/l anyway, so the suggestion that it could be reduced by 2-3 mmol/l is nonsense – most people would have to be clinically dead to achieve this drastic reduction. So, the suggested risk reduction is completely academic and for most people could never happen.

The second reason is that, as usual, relative percentages are used instead of absolute percentages. This problem is ubiquitous in statin clinical trials and I have commented on it many times before. The risk reductions of 40-50 percent are relative percentages, which can only mislead people. In real terms, the percentages come down to single digits or less.

The third reason is that, as usual, the issue of deaths from all causes is not addressed. Statins can reduce the risk of suffering a heart attack or other cardiovascular event, but at the same time, these drugs can also increase the risk of dying from other causes, and overall, there is usually no net benefit.

There is not much point in taking an expensive medication if the risk for one disease is reduced at the cost of increasing the risk for another disease within the same time period.

I called the BHF today and asked them for the data concerning deaths from all causes. The press office said they didn't know, but they did kindly send me the full report for the study.

In this trial, the risk of dying from any cause was reduced from 2.3 percent to 2.1 percent. So, in real terms, the benefit of more intensive statin use equates to a risk reduction of just 0.2 percent.

But even this meagre 0.2 percent risk reduction may not be experienced by real people who take statins. This issue relates to the fourth problem with this study.

The forth reason why the results are misleading is that the analysis did not distinguish between people at a lower risk for a heart attack and people at a higher risk.

Around 7 million people are taking statins in England alone, and in America it is estimated that more than 20 million people may be taking them. The vast majority of these people are taking statins for primary prevention. This means that they do not have cardiovascular disease but are given the medications in the hope of preventing future disease.

To date, there is no convincing evidence that statins provide any net benefit to people when they are taken for primary prevention - they do not reduce the overall death rate. This was the conclusion of the latest analysis in the Archives of Internal Medicine.

The analysis that the BHF are supporting includes data from higher risk groups - the results do not represent the majority of people who currently take a statin.

The film, The Living Matrix, provides a good introduction to some of the modalities that will be used in the future.

Back in 2005, there was a similar study published in the Journal of the American Medical Association (JAMA). But this study went back and traced cholesterol levels from 1960. When you look at the JAMA study and the more recent one, it is clear that cholesterol levels have been steadily declining regardless of any intervention or public 'health' messages. 

This trend is also seen in countries like the UK, where cholesterol levels were also going down before billions of pounds was spent on cholesterol-lowering.

Governments in developed countries spend billions of dollars each year trying to tackle a fictitious cholesterol problem. All the attention directed towards cholesterol leads us to assume that our cholesterol levels have risen. But it is crystal clear that cholesterol levels have been reducing on their own for the last five decades.

Cholesterol levels are now lower than back in the days when so few people had blocked arteries that doctors didn't even bother to study heart disease. 

The cholesterol hypothesis is nonsense, and a complete waste of more than 100 billion dollars: the more we reduce our cholesterol, the more heart disease we get.

The recent study also showed, unsurprisingly, that obesity has increased. But this has happened while cholesterol levels have gone down. Have you ever felt uncomfortable about the way that cholesterol and obesity are thrown together and described as somehow related? I certainly have. For example, the justification for giving kids cholesterol-lowering drugs is that we have a childhood obesity problem - we have fat kids, so we must feed them toxic cholesterol medications for the whole of their life. Cholesterol is linked with obesity in order to reinforce this illusionary cholesterol problem.

Triglyceride levels are also still increasing according to the study. This is a direct result of the advice people are given to follow a low-fat/high-carbohydrate diet – which has been shown in at least twelve published dietary trials to increase triglycerides.  

This may seem slightly trivial, but it really isn't. How long a drug is consumed can have a significant effect on the risk/benefit balance. Especially where statins are concerned – since any benefit of statins already hangs by a thread. 

Some adverse effects of statins can occur quickly (like muscle aches and pains) and others (like diabetes) may take longer to develop. The full extent of the adverse effects associated with statins is not seen in just 5 years – it would take much longer to see the full effects.

So, drug companies can effectively choose the duration of the trial that will show their drugs in the best possible light. Drug companies also have a history of not publishing studies that show their drugs to be ineffective or harmfull – well lets face it, they are a business at the end of the day, with immense pressures to increase profits for shareholders.

The fact that no longer-term studies have been published on statins should make us very concerned. At the very least, our health authorities (who are supposed to protect us) should be asking for at least one long-term trial. We know that money is not an issue, because the drug companies keep doing more and more relatively short trials. Instead of this repetition we could have a longer trial that might tell us something new. 

In 2008, the results of the JUPITER trial were published. This trial attracted a lot of media attention around the world and I have commented on it several times before. In summary, the statin used only managed to reduce deaths from all causes by a mere 0.55 percent (despite the nonsensical relative percentages that the drug company put out to the media to exaggerate the results).

One of the many interesting aspects of the JUPITER trial is that it was stopped early. It was stopped after just 1.9 years. 

I have always suspected that this trial was stopped early because if it was allowed to continue even the miniscule 0.55 percent benefit would disappear.

A few days ago, a study was published in the Journal of the American Medical Association (JAMA), that looked at the effects of stopping trials early. This study found that trials stopped early almost always show much better results for the drug being tested than if the trial was allowed to run its full duration. 

In fact, the JAMA study showed that any drug benefits may be doubled by stopping the trial early. This means that the 0.55 percent reduction in deaths found in the JUPITER trial would have almost completely disappeared if the trial was allowed to run its full course.

The statin used in the JUPITER trial caused more people to develop diabetes, and all statins cause a long list of other adverse effects (some of which result in permanent damage). Knowing this, was it wise for the FDA to approve the wider use of statins based on the results of the JUPITER trial?

References:   

Bassler, D et al. randomized trials early for benefit and estimation of treatment effects: systematic review and meta-regression analysis. JAMA 2010; 303(12):1180-7

Ridker PM et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. New England Journal of Medicine 2008; 359:2195–2207