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Statins don’t stop heart disease

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Heart disease stubbornly persists as the world’s major killer despite the billions spent on low-fat foods and cholesterol-lowering statin drugs. Two years on since the introduction of tougher thresholds, with almost everyone over the age of 50 invited to start statin therapy, mortality rates have barely shifted.

It’s not because the drugs don’t work: they are indeed lowering levels of the “bad” LDL (low-density lipoprotein) cholesterol, the fats targeted by statins that, as the theory has it, deposit themselves around artery walls until blood flow to the heart is blocked, causing a heart attack.

But nonetheless, statins aren’t achieving the ultimate aim of a reduction in cardiovascular disease (CVD) and fatal heart attacks. That could be because the whole cholesterol and fats theory is wrong, as a new research paper suggests.

Researchers led by Robert DuBroff at the University of New Mexico analyzed the results from 35 clinical trials that had assessed three types of cholesterol-lowering drugs, including statins and the new kid on the block, PCSK9 inhibitors, prescribed to people at the highest risk of heart disease based on their LDL levels. Others with a similar risk profile were instead given a placebo, or dummy pill.1

But in more than 75 percent of the trials, those given a cholesterol-lowering drug didn’t live any longer than those on a placebo, and in half of the studies those taking the drugs still developed CVD.

In almost all the trials, the drugs were doing their job: cholesterol levels fell. In one of the reviewed studies, the drugs reduced LDL by 13 percent, and yet the number of deaths and rates of cardiovascular disease were higher than in the placebo group, whose cholesterol levels didn’t drop.

The PCSK drugs are even more effective at lowering cholesterol levels. One of the first on the market, Repatha (evolocumab), achieved a 60 percent reduction – and yet that didn’t protect people from a fatal heart attack.

The results of the FOURIER trial, which tested the new drug on 27,564 patients with heart disease, were extolled by the world’s media. Finally, here was a medication that could dramatically lower cholesterol levels and, as a result, was going to make heart disease history.

Sensing the moment of triumph, one of the researchers, Professor Peter Sever at Imperial College London, enthused: “The end result was cholesterol levels came down and down and down, and we’ve seen cholesterol levels lower than we have ever seen before in the practice of medicine.”

But that isn’t the end result – that should be the number of people who die from heart disease. Hidden in the data, and away from the media glare, the real picture emerged. A total of 251 patients taking Repatha died from heart disease, as did 240 who were instead given a placebo, but whose cholesterol levels had not fallen. Total deaths from any cause were 444 in the Repatha group and 426 among those taking a placebo.2

Mysteriously, the study was stopped two years prematurely, and Dr Michel de Lorgeril, a cardiologist with the French government’s National Centre for Scientific Research, suspects foul play. He has described the study as “junk science.”

The missing link

Looking beyond the studies they reviewed, the New Mexico researchers found further evidence to support their findings suggesting there is little, if any, connection between LDL cholesterol and heart disease.

Belgian health authorities reported a small decline in heart disease between 1999 and 2005, but only among the elderly who weren’t even taking a statin, while Sweden hasn’t seen any decline in heart attack deaths despite a ramping-up of statin prescriptions.

In the US, statin prescriptions doubled between 2002 and 2013, and, not surprisingly, average cholesterol levels fell – yet cardiovascular deaths rose.

Since 2018, the American Heart Association (AHA) has lowered the threshold for prescribing cholesterol-lowering drugs even further, suggesting many more will join the millions already taking them.

This has boosted the revenues of manufacturers, who have already racked up more than $1 trillion in sales since the first statin was licensed 40 years ago, and the new PSCKs look to inflate those figures even higher. Dr Malcolm Kendrick, a cholesterol skeptic, estimates that converting all statin patients to a PSCK would cost the UK £28 billion a year, equivalent to the country’s entire defense budget.

Hide the evidence

Why does statin therapy persist when there is so much contradictory evidence? There is “substantial evidence” for statins, the New Mexico researchers admit, but it could be because of the drugs’ “off-target” benefits. They also act as an anticoagulant, which can stop blood from clotting and, in extreme cases, prevent a heart attack.

But, more significantly, the statin drug trials have not been independently validated. In other words, the drug manufacturers have sponsored the trials that returned positive results, but the underlying data has not been published for review. Drug companies have also been reticent to reveal the results of other studies that were never published, despite the efforts of the European Medicines Agency to have the raw data released.3

It’s also a statistical sleight of hand, the researchers say. To make a drug appear more effective, investigators often use a measure known as relative risk. The relative risk calculation includes everything a person is doing: he is taking the drug, but he may also have improved his diet or started exercising. Yet the combined benefit of all those changes is attributed only to the drug.

While drug companies maintain that around half of people taking a statin see a benefit, it is actually just one percent, and this is probably among the highest risk groups, researchers from the University of South Florida estimate.4

They looked at some of the major statin trials – including Jupiter, Crestor and the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) – to discover the original researchers had “used statistical deception to create the illusion that statins are wonder drugs when the reality is that their modest benefits are more than offset by their adverse effects.” Major reactions included cancer, cataracts, diabetes, cognitive impairment and musculoskeletal disorders.

Hero, not villain

These reactions may be happening not as a response to the statin but to the lowering of LDL cholesterol. Far from being a biological accident, the fat is important to our mental and physical wellbeing, especially as we get older.

One study discovered that LDL was actually preventing a build-up of cholesterol in the arteries, and so protected against heart disease and atherosclerosis, or hardening of the arteries.5

In another study, an international research group found that among 68,096 people aged 60 and older, 80 percent of those who lived the longest also had the highest levels of LDL cholesterol. This was because the cholesterol was counteracting micro-organisms that cause fatal diseases such as cancer, respiratory problems and, paradoxically, heart disease, the researchers concluded.6

LDL even plays a part in keeping people alive when they’re in end-of-life care. A group of 381 terminally ill patients fared better when they stopped taking statins. Those who came off the drugs reported a higher quality of life, and they also lived a little longer – an average of 39 days – than those who continued taking statins.7

In most sciences, when enough evidence contradicts the prevailing view or paradigm, a new theory is established. That isn’t happening in medicine with the cholesterol theory, but then, with £1 trillion of revenues banked,
why change?

So what is heart disease?

If “bad” LDL cholesterol and trans fats aren’t causing heart disease, what is? Here are a few of the theories that have been put forward in recent years:

It’s inflammation: Adding natural anti-inflammatories to the diet – such as tomatoes, spinach and kale, fatty fish and berries – could reduce your risk of heart disease. Researchers monitored more than 10,000 heart patients, and those whose inflammation levels were lowered pharmaceutically were also less likely to suffer a second heart attack. Their risk dropped by up to 17 percent, researchers at Brigham and Women’s Hospital in Boston found.1

It’s refined sugar: People who get a quarter or more of their daily calories from refined sugar triple their risk of dying from cardiovascular disease (CVD). The US Centers for Disease Control and Prevention (CDC) discovered the risk when they analyzed the diets of thousands of Americans. Consuming processed food and drinks also makes you overweight and raises the risk of diabetes, which further increase the likelihood of CVD.2

It’s stress: People who feel they aren’t in control of a situation, such as at work or home, are twice as likely to die from heart disease. A study in Finland tracked the lives of 800 people working for an engineering company. While high workloads and tight deadlines didn’t increase CVD risk, it was the stress – including negative psychological factors such as feeling trapped or powerless – that did the damage.3

It’s air pollution: Cigarettes, car exhaust and industrial pollution are the real cause of CVD, several studies claim. CVD risk has nearly doubled in Chinese cities that have recently industrialized, a CDC report found, while people living near busy roads are also more likely to suffer from heart disease.



BMJ Evid Based Med, 2020; bmjebm-2020-111413


N Engl J Med, 2017; 376: 1713-22


BMJ, 2015; 350: g7811


Exp Rev Clin Pharmacol, 2015; 8: 201-10


J Lipid Res, 2014; 55: 1648-56


BMJ Open, 2016; 6: e010401


JAMA Intern Med, 2015; 175: 691-700

So what is heart disease?



New Engl J Med, 2017; 377: 1119-31


JAMA Intern Med, 2014; 174; 516-24


BMJ, 2002; 325: 857-60

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