Recently a major new review on the safety of statins was undertaken by an international team led by Professor Rory Collins. Published in the prestigious journal the Lancet, and touted by the BBC and other media with little scrutiny, is this just another attempt at a propaganda coup in the wake of increasing concerns about one of the world's biggest selling drugs?
The Review by Collins, et al, creates the impression that statins are safe and appropriate medicines for the prevention of myocardial infarction (heart-attack), based on the assumption that lowering cholesterol prevents the build up of atherosclerosis and therefore the potential occlusion of arteries which could give rise to a cardio-vascular event.
The statin drug Crestor made by AstraZeneca had sales over of over $5 billion as of 2013, according to the Guardian, however AstraZeneca's patent expired as of July 2016. When a patent expires more generic forms of a drug can appear on the market, affecting profits and market shares.
More importantly statin drugs have been coming under increasing criticism for a raft of side-effects, which have been largely played down in the review by Collins, et al. For example Green Med Info provides reports on over 300 different adverse reactions from statins recorded in the medical literature.
So how can we know if this new review is to be trusted? The international team involved in the review come from some of the top echelons of medical science and yet, 23 of the 28 authors of the review have conflicts of interest, according to a report by the Alliance for Natural Health. Collins himself is active in the CTT collaboration. This means that there could be considerable bias at the centre of the report, which in turn undermines the trustworthiness of the data.
The presentation of an international collaboration like this is in some ways seems like a last ditch attempt at stabilizing the shaky paradigm that is the cholesterol myth. There are many critics of this myth which, according to Dr Steven Sinatra, has never been clinically proven. Cholesterol is actually a very important substance in the body, involved in everything from the construction of cell walls to your sex hormones to your memories. Does it make scientific sense to reduce it?
Importantly cholesterol is also involved in the repair of damaged tissue. For example when there is damage in the arterial wall, the liver releases cholesterol to repair the damaged tissue. A problem arises when the resulting repairs, which forms like pollyfilla in a gap, may generate a plaque which does not dissolve once repairs are complete. This can give rise to a thickening of the plaque over time, and potentially occlusion of the artery and a potential cardiovascular incident. However this raises several questions.
1. How does the arterial wall become damaged in the first instance?
2. In normal function what causes plaques to be broken down dissolved into the blood stream?
There are a number of possibilities in regards to the original insult to the intima, but essentially inflammation is the precursor to the release of cholesterol. Therefore it seems appropriate to reduce inflammation first, which would itself lead to lower levels of cholesterol? The generation of free radicals (reactive oxygen species) is damaging to tissue. This then begs the question about the role of antioxidants which can check free radical generation (usually by pairing off electrons and restablising molecules). Antioxidants include Vitamins A, C, E, Selenium and zinc among others. What this suggests is that plaque formation and development in the arterial wall may be largely dependent on nutritional status. If appropriate levels of antioxidants are present then plaques may be dissolved and broken down once they have carried out their repairs.
The idea of reducing cholesterol with statin drugs becomes questionable when we appreciate the vital roles that cholesterol carries out in the body. Reducing a vital substance with so many important roles could account for the many side effects reported from taking statins. But statins also negatively influence the important Co-enzyme Q10 potentially leading to, among other issues, musculo-skeletal problems; while statins, being amphiphilic, may cause cellular damage which would normally be repaired by cholesterol itself (in this case LDL is the transport mechanism) but which is reduced by statins.
A more rigorous approach, focused on patient-centred care and prevention, might involve dietary changes with an emphasis on high vegetable and fruit intake, providing key antioxidants, a strategy not mentioned in the Collins Review. There are other natural agents which could prove useful. The enzyme serapeptase may also dissolve arterial plaque for example. There are also several herbal medicines which may help to dissolve plaque. Herbs rich in phytoestrogens can dissolve plaque in post-menopausal women for example. The herb Salvia miltihoriza may be useful, and there are many others which, it is worth noting, may also be more cost-effective than the drug approach.
An independent study, tasked with evaluating both quantitative and qualitative data, could produce important data to allow patients to make informed decisions about their health. For example, the use of individualised polyherbal formulae or nutritional protocols could be put through randomized controlled trials, but who will pay for this?
Readers may check for patient-reported side-effects from individual statin drugs here.
To conclude, the new review by Collins, et al, raises more questions than it answers. Research culture itself is in need of independent and judicious review - it is easy to see how selective criteria can focus the outcome of a systematic review for example; and it is obvious that the epistemological bias which favours positivism over holism may actually negate patient-centred care. And conflicts of interest may generate bias and questionable data. Finally we must ask if statins actually cure anything, or do they simply suppress certain symptoms, and in the long term, generate a greater risk of serious side effects as a consequence?