Let’s start by looking at the most commonly prescribed drugs, aspirin and statins, so we know what nutrients are up against. It is extraordinary that, for decades, doctors have been dishing out aspirin as a convention for reducing heart disease risk fully knowing that over 2,000 people die each year from drug-induced internal bleeding, the net effect being no lives saved. Finally, authorities such as the British Heart Foundation, are coming clean and pointing out that the risks outweigh the benefits. To give you an example, in one meta-analysis of several studies
(1) the risk of a non-fatal heart attack was reduced by 0.7% per year, while the risk of a gastrointestinal bleed, which can be fatal, was 0.3% a year. There was no difference in mortality between those on placebo or aspirin. In another meta-analysis of large trials
(2), reviewers concluded that treatment with aspirin for an average of 6.4 years resulted in around 3 cardiovascular events prevented per 1,000 women and 4 cardiovascular events prevented per 1,000 men. However, this was offset by an additional 2.5 major bleeding events per 1,000 women and 3 for men. Out of the frying pan into the fire. But what if you are in a high risk group, perhaps with diabetes or high blood pressure? In one large trial involving almost 20,000 people the tiny risk reduction (0.5%) was smaller than the increased risk (0.65%) of a major bleed
(3). So no benefit there either. For diabetics the story is just the same. You’d be much better off ditching the aspirin, eating some oily fish and/or taking an omega 3 fish oil and eating a low GL diet. But what about statins, the golden drug dished out to millions of people who haven’t had a heart attack, including those with low cholesterol levels ‘just in case’. One meta-analysis
(4) involving 42,800 people reported no difference in mortality or coronary heart disease deaths between those on placebo and statins, although there was a small (1.7% ) reduced risk of a non-fatal heart attack after about four years of use. Once again the side-effects are significant, estimated to affect possibly one in ten. Last year the UK’s drug agency, the MHRA, told drug companies that "Patients should be made aware that treatment with any statin may sometimes be associated with depression, sleep disturbances, memory loss, and sexual dysfunction”. That’s on top of the risk of heart rhythm abnormalities, muscle aches and fatigue. One year on most drug product information has yet to be updated. Against these rather pathetic results how do nutrients compare? For over a decade I’ve been recommending niacin, that’s vitamin B3, both for lowering high cholesterol and reducing risk. It stops platelets clumping together, making the need for aspirin largely redundant and not only lowers high cholesterol, but raises the so-called ‘good’ cholesterol fraction, HDL. More than a decade ago research published in the American Journal of Cardiology
(5) showed that two grams of niacin a day drops high cholesterol by 28% in twelve weeks, raising HDL fraction by 23%, without side-effects. But it’s not just cholesterol that comes down. This simple vitamin also unblocks your arteries. Recent research shows that 2 grams of niacin reduced the thickness of carotid arteries. This study compared the results of combining statins with the drug ezetimibe, which further lowers LDL cholesterol by stopping its absorption, or niacin (B3) which increases HDL cholesterol, as well as lowering LDL. Doctors often give both statins and ezetimibe, and get rewarded for producing a lower cholesterol score as a result. But does it help the patient? No, according to an editorial in the New England Journal of Medicine "The findings, obtained in a modest sample of 208 patients, followed for only 14 months, show a clear superiority of niacin over ezetimibe. In fact, the addition of extended-release niacin to statin therapy led to a decrease in the common carotid intima–media thickness, whereas the addition of ezetimibe merely prevented an increase in this thickness.
The authors emphasize the additional post hoc finding that large reductions in the LDL cholesterol level, induced by ezetimibe, were associated with an increase in the carotid intima–media thickness." You can expect more good news on the niacin front because two drug companies have found a way to patent a combination of niacin with a drug to make it ‘slow-release’ and hence non-blushing, which is the only side-effect of niacin – that is apart from its ability to improve your memory and make you feel good. I just took 500mg, the blushing kind, and stopped a potential migraine dead in its tracks. It also helps schizophrenia, a condition characterised by losing touch with reality.
With some government advisors recommending that ALL men over 50 and women over 60 should be on statins, one wonders whether they too may benefit from taking niacin. The NHS already waste enough tax payers money on next to useless drugs. Of course, there’s loads more that you can do to reduce your risk with nothing but benefit from increasing your intake of magnesium, vitamin C, E and folic acid, in the case of stroke risk, and, most of all, eating a low GL diet. Jerome Burne and I have written about this extensively in our book Food is Better Medicine Than Drugs. If you’d like to know more about niacin and cholesterol read my Special Report High Cholesterol and if you are concerned about high blood pressure read the Special Report Lowering High Blood Pressure Naturally.
References 1. Antithrombotic Trialists’ Collaboration. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials. Lancet 2009; 373: 1849–60. 2. Berger JS et al. Aspirin for the primary prevention of cardiovascular events in women and men: a sex-specific meta-analysis of randomized controlled trials. JAMA 2006; 295: 306–13 3. Hansson L et al. Effects of intensive blood-pressure lowering and low-dose aspirin in patients with hypertension: principal results of the Hypertension Optimal Treatment (HOT) randomised trial. Lancet 1998; 351: 1755–2 4.P.Thavendriranathan et al, Archives of Internal Medicine, November 2006 5. Morgan JM et al. Am J Cardiol 1998;82(12A):29U–34U