For all the scares about cancer, heart disease is still the number-one killer disease in the West. The immediate causes of death are often heart attack and stroke, but a more insidious cause is congestive heart failure (CHF).
This chronic disease tends to develop slowly, with symptoms of fatigue, shortness of breath and swelling in the legs. The underlying cause is a loss of pumping capacity by the heart, which may be due to persistent high blood pressure, irregular heartbeats, hardened arteries, a previous heart attack, lung disease or thyroid gland problems.
Early on, the body compensates by increasing the heart rate and even the size of the heart. However, as the heart weakens, fluid collects in the lungs (hence the word ‘congestive’) or is trapped in the circulatory system, causing swelling of the blood vessels and organs such as the liver.
Heart failure is now the leading cause of hospitalisation in those over 65 – and the problem is getting worse by the year. Experts tell of a ‘growing epidemic of CHF’ (Cardiol Clin, 2001; 19: 547-55), particularly over the last 20 years. In the US, nearly five million people suffer from heart failure; in the UK, it is believed to affect 1 per cent of the population – or around 500,000 people – at any given time. Some experts find this CHF epidemic puzzling, given the fall-off in other heart diseases (MMWR, 1994; 43: 77-81). Others warn that CHF is ‘highly lethal’, killing over 80 per cent of men within six years of diagnosis (Am Heart J, 1991; 121: 951-7).
Mortality rates like these have been one of the reasons why health authorities are prepared to spend huge amounts of money on statins, the so-called miracle drugs that are meant to prevent heart disease.
The miracle of statins
With most of the world’s major pharmaceutical companies offering a statin, this is now the biggest drug sector – worth a staggering $20 billion each year. Introduced less than 20 years ago, they have become the most profitable drugs in the history of medicine.
Statins don’t cure; they reduce cholesterol levels in blood to below the figure thought to cause heart disease. As such, statins are primarily prescribed as preventative medications and often given in perpetuity. But these ‘patients’ don’t have a true illness; they are simply those who have a particular lab-test reading – and may have no symptoms whatsoever.
Moreover, the cholesterol-heart disease connection is still largely only theoretical, and not always borne out in practice: for example, 50 per cent of people who die from heart attacks don’t have high cholesterol.
So, according to the best analysis, statins may only prevent some heart conditions – and that’s assuming they work. Nevertheless, cardiologists – especially those in the US – recommend that at least half of the adult population should be permanently taking statins. Even in the cash-strapped NHS, British GPs are urged by drug companies to give statins to anyone whose cholesterol levels fall outside of the recommended ‘target’ values.
But statins are now increasingly coming under fire. First, although marketed as safe, bitter experience has revealed serious side-effects (see box, p 2). But the major concern is that, although statins may lower cholesterol by as much as 30 per cent, this does not translate into any significant prolongation of life – which is why they are given in the first place.
The evidence that statins don’t deliver the goods has been steadily accumulating over the past decade. Keen-eyed medical statisticians have pored over the data from drug company-sponsored clinical trials, and found some interesting facts hidden behind the headlines.
Last year, for example, researchers at the University of British Columbia concluded that statins may harm as many people as they help. Pooling the data from five separate large-scale trials, the UBC team found that statins indeed reduced heart attacks and strokes – but only by a meagre 1.4 per cent. This means that 71 people with high cholesterol would have to be treated with statins for up to five years to prevent just one heart attack or stroke.
Furthermore, setting this modest gain against a 1.8 per cent increase in the serious side-effects caused by the drugs effectively cancels the benefit, concluded the UBC team leader Dr James Wright, (Therapeutics Initiative, April-June 2003, University of British Columbia).
British researchers arrived at an even starker conclusion – that statins can kill. The University of Sheffield’s Department of Clinical Pharmacology looked at the risk-to-reward ratio of statins, comparing the mortality rates of people taking statins with their underlying risk of death. The figures suggest that statin use ‘could be associated with an increase in mortality of 1 per cent in 10 years’ (Br J Clin Pharmacol, 2001; 52: 439-46).
A small band of doctors are now beginning to ask: could there be a connection between the huge rise in statin use and the current epidemic of CHF?
One of the doctors leading this heresy is Texas cardiologist Dr Peter Langsjoen. ‘In my practice of 17 years, I have seen a frightening increase in heart failure secondary to statin usage – I call it ‘statin cardiomyopathy’,’ he says. ‘Are we causing this epidemic through our zealous use of statins? In large part, yes.’
But how can a drug meant to prevent heart failure possibly cause it? The answer has been unfolding since 1985, when a team led by University of Texas biochemist Dr Karl Folkers found that those suffering from heart failure had a deficiency of the enzyme ubiquinone in their heart tissue – the less ubiquinone, the worse the heart failure (Proc Natl Acad Sci USA, 1985; 82: 901-4).
Ubiquinone got its name because it is found everywhere in the body – it’s ubiquitous. Later recognised as necessary for glucose production, its name was changed to ‘coenzyme Q10’ (CoQ10). It was soon found to be at its greatest concentrations in the heart, where it is now known also to act as a powerful antioxidant.
Folkers immediately set about testing oral supplements of CoQ10 on patients with CHF. His reported results were spectacular. ‘These patients, steadily worsening and expected to die within two years under conventional therapy, generally showed an extraordinary clinical improvement,’ he wrote (Proc Natl Acad Sci USA, 1985; 82: 4240-4).
These results, together with his earlier discovery, strongly suggested that CoQ10 is an important contributory factor in CHF.
The CoQ10-statins connection
During the next five years, Folker teamed up with fellow Texan Langsjoen, the cardiologist who had expressed such concerns about statins causing heart failure. Combining Folker’s biochemical evidence with Langsjoen’s clinical experience, they asked: could statins be depleting CoQ10?
This possibility had never been investigated in any of the official trials of statins, so it was virgin scientific territory.
Folker’s biochemists set about testing their hunch in the laboratory by feeding rats lovastatin, the most widely prescribed statin drug.
What they found was a bombshell: lovastatin depleted as much as 20 per cent of the CoQ10 in the rats’ blood, and about 10 per cent from their heart tissue (Proc Natl Acad Sci USA, 1990; 87: 8928-30). Folker and Langsjoen then went on to test their findings on human volunteers and confirmed the animal findings – lovastatin destroys CoQ10 (Proc Natl Acad Sci USA, 1990; 87: 8931-4).
Since then, confirmation of their results has come in thick and fast, strongly implicating most of the statins in CoQ10 depletion. Italian physicians found that simvastatin caused a 20 per cent reduction in blood CoQ10 levels (Int J Clin Lab Res, 1994; 24: 171-6), and similar results were obtained by Russian doctors using cerivastatin (Bull Exp Biol Med, 2002; 134: 39-42). French physicians achieved the same results with all the statins they prescribed (Br J Clin Pharmacol, 1996; 42: 333-7).
So, all of this suggests that Langsjoen’s once heretical idea that statins cause heart failure may well be on its way towards becoming established fact. The logic seems clear: if statins deplete CoQ10, and low levels of CoQ10 are associated with CHF, then statins may be a causal factor in CHF.
In a crowning irony, Merck (which manufactures simvastatin, marketed as Zocor) has filed a patent proposing to add CoQ10 to its formulation – a tacit acknowledgement of the core problem with these drugs.
Nevertheless, the widespread use of statins increases unabatedly, with over a million prescriptions a month in the UK alone – a 10-fold increase in less than a decade.
Nearly three years ago, 14 experts from across the globe, most of them professors of medicine, signed an open letter (dated 5 September, 2001) to the US Food and Drug Administration, the supreme American health authority. In this communication, they pointed out the dangers of statins and pleaded: ‘It is urgently incumbent upon the scientific community . . . and the regulatory bodies to be certain that we are not inadvertently creating a life-threatening deficiency . . . in many millions of patients.’
Since then, however, regulatory bodies have done nothing. The silence has been deafening.
The mercury connection
Besides statins, what other factors might lie behind the CHF epidemic? Groundbreaking research from Italy says one major environmental cause could be dental amalgam fillings. Researchers at the Catholic University in Rome have tested patients with advanced CHF and found a ‘marked elevation’ of mercury in the heart tissue – in the order of a massive 22,000 times higher than normal. None of these patients worked or lived in areas that would have exposed them to mercury, so the source of this toxin in their bodies must have been the silver-mercury amalgam fillings in their mouths.
Interestingly, most of the mercury was concentrated in the heart, with very little found elsewhere in the body. Quite why this happens is not known, but the researchers speculate that the mercury can ‘adversely affect . . . heart metabolism and worsen cellular function’ (J Am Coll Cardiol, 1999; 33: 1578-83).
That mercury is a major poison has been known for more than a century, but dentists have always claimed that, when chemically amalgamated with silver, it becomes harmless. But, in the last 20 years, this view has been seriously called into question as study after study has shown that amalgam fillings leach mercury into the body, mainly through mercury vaporisation while chewing.
Dentists have been forced to retreat to a fall-back position in which they now admit that fillings do give off mercury, but at such low levels that they’re non-toxic. However, this convenient side-step appears to have been scuppered by the new Italian research demonstrating that mercury is not harmlessly distributed throughout the body, but accumulates into potential killer loads in the heart.
The Italian findings tie in with older US research that found that people with amalgam fillings had significantly more heart-related problems than those with healthy teeth. Amalgam-filled patients also had more irregular heartbeats and fatigue – typical of CHF (Sci Total Environ, 1990; 99: 23-35).
Similarly, when Soviet doctors studied workers exposed to mercury, they found that the heavy metal had a profound effect on the heart, interfering with its normal contractions, electrical conductivity and overall regulation. Like the Italians, they too found that mercury accumulated in the heart tissue and valves (Cardiotoxic Effects of Mercury, DHEW (NIH) Publication No 74-473, 1974: 109-34, 199-210).
So, with mercury accumulating in the heart, could it be affecting levels of CoQ10, which is also primarily found in the heart? Nobody knows for sure because the research hasn’t been done, but such a mechanism seems plausible.