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Archive for the ‘statins’ Category

How statins work 2: atherosclerosis and LDL cholesterol

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Recent studies have revealed that children 8-10 years old are being diagnosed with Type II diabetes, high cholesterol, and high blood pressure at an alarming rate.

Lee Haney

Picture taken from ‘LDL in atherosclerosis and heart disease’ by Axel Sigurdsson, MD, PHD

As I said in my previous post, biochemistry is almost infinitely complex, so bear with me as I crawl towards an understanding of the role of statins in reducing LDL cholesterol in the blood stream, thus reducing atherosclerosis, a major feature of heart disease.

Remembering, first, that cholesterol is a sterol, which is a modified steroid with a hydroxyl (alcohol) group coming off carbon 3. It’s a mostly hydrophobic lipid with this tiny polar hydroxyl group added. It’s carried around in the bloodstream by lipoproteins.

I’ll turn now to atherosclerosis – though I don’t currently know whether statins can perform roles other than reducing the build-up of plaque in the arteries.

So, generally, our arteries carry oxygenated blood from the heart to other organs and regions of the body. Atherosclerosis is sometimes called ‘hardening of the arteries’, as sklerosis is from Greek, meaning ‘hardening’, but it’s really a narrowing rather than a hardening, or perhaps it’s better described as both, as we’ll see. Arteriosclerosis is a more general name, while atherosclerosis means blockage or narrowing (stenosis) due to an atheroma, an abnormal accumulation of ‘debris’ or plaque consisting of fat (mostly), calcium and sometimes fibrous tissue in the inner arterial wall (endothelium). These atheroma are difficult to detect before they cause heart attacks or disease, because heart arteries are very small and hidden deep within the chest. They’re also quite mobile and elastic with blood flow. Heart attack and stroke sometimes happen when the atheroma ‘bursts’ – the fibrous cap (of smooth muscles cells, cholesterol-rich foam cells, collagen and elastin) which surrounds the atheroma is ruptured, or breaks free from the arterial wall, causing a blood clot (thrombus). These are sudden events, not easily detected beforehand. Alternatively, major problems arise when the atheroma becomes large enough to defeat arterial flexibility.

There can be symptoms, apart from such major dramas as heart attacks and stroke, which may act as warning signs for atherosclerosis. The narrowing of the arteries means that less blood and oxygen is reaching the cardiovascular system (ischemia), and this may result in vomiting, angina (chest pain), and general feelings of faintness and anxiety. Atherosclerosis of the carotid artery, which feeds the brain, may have different symptoms, including headaches, dyspnea and facial numbness. Atherosclerosis can also affect the function of the liver, kidneys and other organs, and the vascular system.

So what causes atheromas? It seems that these accumulations of plaque are the result of monocyte-macrophage activity. Macrophages are types of white blood cells (leucocytes) that perform immune and cleansing functions. However, we don’t really know why the plaque build-up occurs – though it might be initiated by damage to the endothelium. We do know that atherosclerosis can begin early, and that blood LDL cholesterol is a major factor in the activity that leads to this build-up. That’s why researchers have been rather single-minded about ways of reducing LDL cholesterol, and even on increasing HDL cholesterol levels, though there’s little evidence, apparently, that higher HDL levels are beneficial. Nor, interestingly, is there much evidence that lowering triglycerides has a positive effect on heart disease, while study after study has shown that low LDL cholesterol levels are key to avoiding cardiovascular problems.

Okay, now I’m going to take a few steps back to look more deeply at the role of LDL cholesterol in building atheromas and so causing atherosclerosis. Returning to my vague mention of macrophages and monocytes, here’s a clearer picture, drawn mainly from this excellent video.

  1. Structure of arterial wall

First, we need to know that the arterial walls are layered. The first layer surrounding the lumen (the tunnel space where the blood flows and where you find red blood cells or RBCs, leukocytes and lipoproteins, etc) is the epithelium, a thin layer of squamous cells. This layer is surrounded by the tunica intima (sometimes the epithelium is described as part of the T intima), an elastic layer quite rich in collagen. It also contains structural cells called fibroblasts, and smooth muscle cells (SMCs). Surrounding the T intima is the tunica media (particularly rich in SMCs), which in turn is surrounded by the thicker, tougher tunica adventitia. In general, the arterial wall becomes stiffer and more fibrous as you move from inner to outer. Atherosclerosis is apparently more of a problem in large and middle-sized arteries which contain more of the protein elastin.

2. Plaque formation

Plaque formation begins, it’s believed, when there’s damage to the thin endothelial layer (only one cell thick) as well as an abundance of circulating low density lipoproteins (LDLs). LDLs (mostly lipid with a small amount of protein) can then move through the damaged layer into the T intima where they become oxidised by ‘reactive oxygen species’ (free radicals) and other enzymes such as metallo-proteases, released by the endothelial cells. These oxidised LDLs, which are now ‘trapped’ in the T intima, will activate endothelial cells to express receptors for white blood cells (leukocytes), particularly the largest types of leucocyte, known as monocytes. So we have this accumulation of oxidised LDLs activating endothelial cells to express adhesion molecules for leucocytes, which brings monocytes and T helper cells into the T intima layer. This movement into tissue transforms monocytes into macrophages (not sure how that happens), and these macrophages then ‘take up’ or engulf the oxidised LDLs and form foam cells. By this time the lipid material dumped into the T intima has created something like a lake of fat, known as a ‘fatty streak’. Foam cells are central to the process of plaque formation and atherosclerosis, as they induce more SMCs into the T intima from the T media by means of a released growth factor, IGF-1 (insulin-like growth factor), and this leads to increased synthesis of collagen in the region, which hardens the plaque build-up, a build-up further fostered by foam cell death which releases more lipid material. Foam cells also release pro-inflammatory cytokines and reactive oxygen species as well as chemokines which attract more macrophages to the site. Upon death they also release DNA material that attracts neutrophils, a very common type of white blood cell. All of this will increase inflammation or plaque build-up in the region.

3. Effects

As mentioned, SMCs contribute to the containment of this inflamed lipid area by releasing proteins such as collagen and elastin, which is used to build a fibrous cap around it. They also stiffen the formation, the atheroma as it’s called, by adding calcium. All of this has the effect of enlarging the atheroma and so reducing the diameter of the arterial lumen in the area, which raises blood pressure as the blood tries to maintain an adequate flow. The calcification of the area also considerably reduces the flexibility of the arterial wall, again resulting in increased blood pressure. Rupture of the fibrous cap may result, which may lead to thrombosis.

So where do statins come in here? Let me quote from an abstract of one academic paper: Statins in atherosclerosis: lipid-lowering agents with antioxidant capabilities, published in 2004:

Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are the first-line choice for lowering total and LDL cholesterol levels and they have been proven to reduce the risk of CHD [chronic heart disease]. Recent data suggest that these compounds, in addition to their lipid-lowering ability, can also reduce the production of reactive oxygen species and increase the resistance of LDL to oxidation. It may be that the ability of statins to limit the oxidation of LDL contributes to their effectiveness at preventing atherosclerotic disease.

Note that oxidation of LDL has the effect of fixing it in the T intima, as mentioned above, so if it’s true, as I presume it is, that statins inhibit LDL oxidation, as well as having other benefits, then they can’t be a bad thing, as long as there aren’t serious side-effects. I’ll continue to explore this topic, as it’s teaching me a lot about the blood, the liver and the circulatory system, inter alia – and it’s great fun. Dr Ben Goldacre has written a book Do statins work? the battle for perfect evidence-based medicine, which hasn’t been released yet, but I intend to get my hands on it and devour it, along with more videos and articles. In the meantime I hope it’s not too controversial to go on saying that the best way to reduce that nasty (but not too nasty) LDL cholesterol is to eat a healthy diet and engage in effective exercise.

PS: haha I know this’ll be unreadable to most, but if anybody finds any egregious error in this, let me know.


Atherosclerosis video – Nucleus Medical Media (2009)

Atherosclerosis – pathophysiology, video by Armando Hasudungen (2014)

Atherosclerosis – part 1, Khan Academy video

Cholesterol metabolism part 1, video by Ben1994 (2015)

Cholesterol metabolism part 2, video by Ben1994 (2015)

Cholesterol metabolism part 3, video by Ben1994 (2015)

Written by stewart henderson

September 21, 2019 at 5:20 pm

How statins work 1 – stuff about cholesterol, saturated fats and lipoproteins…

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filched from Wikipedia – don’y worry, I don’t understand it either – at least not yet

Statins are HMG-CoA reductase inhibitors, according to Wikipedia’s first sentence on the topic. HMG-CoA reductase is an enzyme – a macromolecule that accelerates or catalyses chemical reactions in cells. The enzyme works in the mevalonate pathway, which produces cholesterol and other terpenoids (terpenoids are very common, varied and useful forms of hydrocarbon).

So what does HMG-CoA stand for, and what’s a reductase?

3 hydroxy -3 methyl-glutaryl coenzyme A, which may be explained later. A reductase is an enzyme which catalyses a reduction reaction, and I’m not sure if that refers to redox reactions, in which case reduction involves the gaining of electrons…

But let’s look at cholesterol, which statins are used against. Sterols are lipid molecules with a polar OH component, and ‘chole’, meaning bile, comes from the liver. So cholesterol is a type of lipid molecule produced largely by the liver or hepatic cells of vertebrate animals. Cholesterol is essential for life, and it’s synthesised in the cell via a complex 37-step process (the mevalonate pathway makes up the first 18 of these). It makes up about 30% of our cell membranes, and its continual production is necessary to maintain cell membrane structure and fluidity. In high food-intake countries such as Australia and the US, we ingest about 300mg of cholesterol a day on average. We also have an intake of phytosterols, produced by plants, which might vary from 200-300mgs. Of course, this is massively dependent on individual diets (increased phytosterol intake may reduce LDL cholesterol, but it comes with its own quite serious problems).

The (very basic) structure of cholesterol is shown below.

The body of the molecule (centre) contains 4 rings of carbon and hydrogen – A, B and C are 6-carbon rings, while D has 5. The bonds between rings A and B, and C and D, represent methyl groups. On the left is a hydroxyl group, which is hydrophilic and polar, though the massive body of the molecule is extremely hydrophobic, which is reinforced by the cholesterol tail connected to the D ring. The hydroxyl polarity creates a binding site, which builds structure as the molecule binds to others.

Interestingly, the need for cholesterol synthesis varies with temperature, or climate. This has to do with fluidity and melting points. People who live in colder climates require less cholesterol production because, in cold weather, solid structure remains intact. Hotter climates cause greater fluidity and increased entropy, so more cholesterol needs to be synthesised to create and maintain structure.

So now to the 18-step mevalonate pathway, by which the liver produces lanosterol, the precursor to cholesterol. Well, on second thoughts, maybe not… It’s fiendishly complex and Nobel Prizes have been deservedly won for working it all out and I’m currently thinking that physics is easy-peasy compared to biochemistry (or maybe not). What I’m coming up against is the interconnectivity of everything and the need to be thorough. For example, in order to understand statins we need to understand cholesterol, and in order to understand cholesterol we need to understand lipids, lipoproteins, the liver, the bloodstream, the digestive system… So I sometimes feel overwhelmed but also annoyed at the misinformation everywhere, with chiropractors or ‘MDs’ announcing the ‘truth’ about statins, cholesterol or whatever in 500-word screeds or 5-minute videos.

Anyway, back to work. Cholesterol is a lipid molecule, and lipids are generally hydrophobic (they don’t mix with water, or to be more exact they’re not very soluble in water), but cholesterol has a hydrophilic hydroxyl side to it. Lipids that have this hydrophilic/hydrophobic mix are called amphipathic. Phospholipids in cell membranes are an example. and they interact with cholesterol in the ‘phospholipid bilayer’. As an indication of the complexity involved, here’s a quote from an abstract of a biochemical paper on this very topic:

Mammalian cell membranes are composed of a complex array of glycerophospholipids and sphingolipids that vary in head-group and acyl-chain composition. In a given cell type, membrane phospholipids may amount to more than a thousand molecular species. The complexity of phospholipid and sphingolipid structures is most likely a consequence of their diverse roles in membrane dynamics, protein regulation, signal transduction and secretion. This review is mainly focused on two of the major classes of membrane phospholipids in eukaryotic organisms, sphingomyelins and phosphatidylcholines. These phospholipid classes constitute more than 50% of membrane phospholipids. Cholesterol is most likely to associate with these lipids in the membranes of the cells.

Anyway, perhaps for now at least I won’t explore the essential role of cholesterol in cell structure and function, but the role of ingested cholesterol, the difference between LDL and HDL cholesterol, and how it relates to saturated fats and heart disease, particularly atherosclerosis. As Gregory Roberts explains it in a Cosmos article, saturated fats (found in butter, meat and palm oil) definitely raise total cholesterol…

But what is saturated fat, as opposed to polyunsaturated or mono-unsaturated fat? Most of us have heard of these terms but do we really know what they mean? Here comes Wikipedia to the rescue (because there’s a lot of bullshit out there):.

saturated fat is a type of fat in which the fatty acid chains have all or predominantly single bonds. A fat is made of two kinds of smaller molecules: glycerol and fatty acids. Fats are made of long chains of carbon (C) atoms. Some carbon atoms are linked by single bonds (-C-C-) and others are linked by double bonds (-C=C-). Double bonds can react with hydrogen to form single bonds. They are called saturated, because the second bond is broken and each half of the bond is attached to (saturated with) a hydrogen atom. Most animal fats are saturated. The fats of plants and fish are generally unsaturated. Saturated fats tend to have higher melting points than their corresponding unsaturated fats, leading to the popular understanding that saturated fats tend to be solids at room temperatures, while unsaturated fats tend to be liquid at room temperature with varying degrees of viscosity (meaning both saturated and unsaturated fats are found to be liquid at body temperature).
Various fats contain different proportions of saturated and unsaturated fat. Examples of foods containing a high proportion of saturated fat include animal fat products such as cream, cheese, butter, other whole milk dairy products and fatty meats which also contain dietary cholesterol. Certain vegetable products have high saturated fat content, such as coconut oil and palm kernel oil. Many prepared foods are high in saturated fat content, such as pizza, dairy desserts, and sausage.
Guidelines released by many medical organizations, including the World Health Organization, have advocated for reduction in the intake of saturated fat to promote health and reduce the risk from cardiovascular diseases. Many review articles also recommend a diet low in saturated fat and argue it will lower risks of cardiovascular diseases, diabetes, or death. A small number of contemporary reviews have challenged these conclusions, though predominant medical opinion is that saturated fat and cardiovascular disease are closely related.

Saturated Fat, Wikipedia. I’ve removed links and notes – they’re just too much of a good thing! Apologies for the lengthy quote but I think this is essential reading in this context.

High density lipoprotein (HDL) cholesterol can be a problem if your levels are low. HDL absorbs cholesterol and carries it back to the liver, from where it’s removed from the body. So generally high levels of HDL will reduce your chances of heart attack and stroke.

As Roberts notes, from the 1950s, heart disease has risen to be a major problem. Heart attack victims have been regularly found to have arteries clogged with ‘waxy plaques filled with cholesterol’. Further proof that cholesterol was to blame came with studies of people with a genetic disease – familial hypercholesterolemia (FH) – which meant that they had some five times the normal levels of blood cholesterol, and suffered heart attacks even as children or teenagers. Also, the rise in blood cholesterol levels and the rise in heart attacks, and heart disease generally, were correlated. This was unlikely to be coincidental.

But what’s a lipoprotein and why the different densities? Here we get into another area of extraordinary complexity. Lipoproteins are vehicles for transporting hydrophobic lipid molecules such as cholesterol, triglycerides and phospholipids through the watery bloodstream or the watery extracellular fluid (blood plasma – the yellowish liquid through which haemoglobin and lipoproteins etc are transported – is a proportion of that fluid). They act as emulsifiers, ‘encapsulating’ the lipids so that they can mix with and move through the fluid. Lipoproteins don’t just come in HD and LD forms – we classify them in terms of their density much as we classify colours in the light (electromagnetic) spectrum. According to that density classification we recognise five major types of lipoprotein in the bloodstream.

Cholesterol arrives in the blood via endogenous (internal) and exogenous (external) pathways. Some 70% of our cholesterol is produced by the liver, so, though diet is an important facet of changing cholesterol levels, finding ways of modifying or blocking liver production was clearly another option. Through studying the way fungi produced chemicals such as penicillin that break down cell walls (a large part of which are cholesterol), Akira Endo was the first to produce a statin from a mould in oranges – mevastatin. That was the beginning of the statin story.


Cholesterol metabolism, part one – video by Ben1994 (excellent)

Cholesterol structure, part 1/2, by Catalyst University

Written by stewart henderson

September 15, 2019 at 10:24 am

The statin controversy

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Never edit your own writing! Brian J Ford.

one thing thing you can be sure of – this claim (posted by a British chiropractor) is meaningless bullshit

I read Ben Goldacre’s quite demanding book Bad pharma some years ago, and that’s where I learned about statins, but I don’t recall much. I do recall that, not long after I read the book, I was at a skeptics meet-up when Dr Goldacre’s name came up. The man next to me started literally spitting chips at the mention – he was eating a massive bowl of chips and was grossly overweight (not that I’m assuming anything from this – just saying, haha). He roolly didn’t like Dr Goldacre. What went through my head was – some people may be really invested in having a magic pill that allows them to live forever and a day no matter what their diet or lifestyle.

I’ve just discovered that Goldacre has a new book out, entirely on this topic, which I intend to read, but my current decision to explore the issue is based on listening to Dr Maryanne Demasi’s talk, ‘statin wars – have we been misled by the evidence?’, available on YouTube. I very much recall the massive Catalyst controversy a few years ago, when a two-part special they did on statins led finally to the demise of the program. Without knowing any details, I thought this was a bit OTT, but when I heard Dr Norman Swann, a valued health professional and presenter of the ABC’s Health report, railing about the irresponsibility of the statin special, I frankly didn’t know what to think.

So statins are lipid-lowering medications that come in various flavours, including atorvastatin, fluvastatin, lovastatin and rosuvastatin. Lipitor, a brand name for atorvastatin manufactured by Pfizer, is the most profitable drug in the history of medicine. I’ve never taken statins myself, and I’m starting this piece as a more or less total beginner on the topic. I’ve read the Wikipedia entry on statins, which is quite comprehensive, with a very long reference list. Of course it’s not entirely comprehensible to a lay person, but that’s not a criticism – immunobiology and related research fields are complex. It’s also clearly pro-statin. It includes this interesting sentence:

 A systematic review co-authored by Ben Goldacre concluded that only a small fraction of side effects reported by people on statins are actually attributable to the statin.[63]

It’s interesting that Goldacre, and nobody else, is mentioned here as a co-author. It makes me wonder…

My only quibble, as a lay person, is that the positive effects of these statins, and their relatively few side-effects, seems almost too good to be true. I speak, admittedly, as a person who’s always been ultra-skeptical of ‘magic bullets’.

Which brings me to issues raised in Dr Demasi’s talk, and not addressed in the Wikipedia article. They include the idea, promoted by an ‘influential group’, that statin use should be prescribed for everyone over 50, regardless of cholesterol levels. Children with high cholesterol levels are being screened for statin use and Pfizer has apparently designed fruit-flavoured statis for use by children and adolescents. Others have suggested using statins as condiments in fast-food burgers, and even adding statins to the public water supply. It’s easy to see how such ‘innovations’ involve making scads of money, but this isn’t to deny that statins are effective in many if not most instances, and we should undoubtedly celebrate the work of the Japanese biochemist Akiro Endo, who pioneered the work on enzyme inhibitors that led to the discovery of mevastatin, produced by the fungus Penicillium citrinum.

But Demasi made some other interesting points, firstly about how drug companies like Pfizer might seek to maximise their profits. One obvious way is to widen the market – for example by lobbying for a lowering of the standard level of cholesterol in the blood considered dangerous. From the early 2000s in the US, ‘high cholesterol’ was officially shifted down from as high as 6.5 down to below 5, moving vast numbers of people onto having a ‘need’ for these cholesterol-lowering drugs. Demasi points out that this lowering wasn’t based on any new science, and that the body responsible for these decisions, the National Cholesterol Education Program (NCEP), was loaded with people with financial ties to the statin industry. To be fair, though, one might expect that doctors and specialists concerned with cholesterol to be invested, financially or otherwise, in ways of lowering it. They might also have felt, for purely scientific reasons, that the level of cholesterol considered dangerous was long overdue for adjustment.

Another change occurred in 2013 when two major heart health associations in the US decided to abandon a single number in terms of risk factors for heart disease/failure. Instead they looked at cholesterol, blood pressure, weight, diabetes and other factors to calculate ‘percentage risk’ of cardiovascular problems. They evaluated this risk so that if it was over 7.5% in the next 10 years, you should be prescribed a statin. A similar percentage risk system was used in the UK, but the statin prescription started at 20%. Why the huge discrepancy? Six months later, the Brits brought their threshold down to 10%. The US change brought almost 13 million people, mostly elderly, onto the radar for immediate statin prescription. The method of calculation in the US was independently analysed, and it was found that they over-estimated the risk, sometimes by over 100%. Erring on the side of caution? Or was there a lot of self-interest involved? It could fairly be a combination. The term for all this is ‘statinisation’, apparently. It’s attributed to John Ioannidis, a Stanford professor of medicine and a noted ‘scourge of sloppy science’. If you look up statinisation, you’ll find a storm of online articles of varying quality and temper on the issue – though most, I notice, are five years old or more. I’m not sure what that signifies, but I will say that, while we’ll always get the anti-science crowd baying against big pharma, vaccinations and GM poison, there’s a clear issue here about vested interests, and the need to, as Demasi says, ‘follow the money’.

This brings up the issue of how trials of these drugs are conducted, who pays for them, and who reviews them. According to Demasi, the vast majority of statin trials are funded by manufacturers. Clearly this is a vested interest, so trial results would need to be independently verified. But, again according to Demasi (and others such as Ioannidis and Peter Gotzsche, founder of the nordic Cochrane Collaboration) this is not happening, and ‘the raw data on statin side-effects has never been released to the public’ (Demasi, 2018). This data is held by the Cholesterol Treatment Triallists’ (CTT) collaboration, under the Clinical Trial Service Unit (CTSU) at Oxford Uni. According to Demasi, who takes a dim view of the CTT collaboration, they regularly release meta-analyses of data on statins which advocate for a widening of their use, and they’ve signed agreements with drug companies to prevent independent examination of research findings. All of this is described as egregious, which might seem fair enough, but Elizabeth Finkel, in a long-form article for Cosmos magazine in December 2014, takes a different view:

.. [the CTT] are a collaboration of academics and they do have access to the raw data. It is true that they do not share that data outside their collaboration and are criticised by other researchers who would like to be able to check their calculations. But the trialists fear mischief, especially from drug companies seeking to discredit the data of their rivals or from other people with vested interests. Explains [Professor Anthony] Keech, “the problem with ad hoc analyses are that they can use methods to produce a particular result. The most reliable analyses are the ones done using the methods we published in 1995. The rules were set out before we started.” And he points out these analyses are cross-checked by the academic collaborators: “Everything is replicated.”

As a regular reader of Cosmos I’m familiar with Finkel’s writings and find her eminently reliable, which of course leaves me more nonplussed than ever. I’m particularly disturbed that anyone would seriously claim that everyone over fifty (and will it be over forty in the future?) should be on these medications. I’m 63 and I take no medications at all, which I find a great relief, especially when I look at others my age who have mini-pharmacies in their homes. But then I’m one of those males who doesn’t visit doctors much and I have little idea about my cholesterol levels (well yes, they’ve been checked and doctors haven’t raised them to me as an issue). When you get examined, they usually find something wrong….

In her talk, Demasi made a comparison with the research on Tamiflu a few years ago, when Cochrane Collaboration researchers lobbied hard to be allowed to review trial data, and it was finally revealed, apparently, that it was certainly not as effective and side-effect free as its makers, Roche, claimed it to be. The jury is still out on Tamiflu, apparently. Whether it’s fair to compare the Tamiflu issue with the statin issue is a matter I can’t really adjudicate on, but if Finkel is to be believed, the CTT data is more solid.

There’s also an issue about more side effects being complained of by general users of statins – complaints made to their doctors – than side effects found in trials. This has already been referred to above, and is also described in Finkel’s article. Many of these complaints of side-effects haven’t been able to be sheeted home to statins, which suggests there’s possibly/probably a nocebo effect at play here. But Demasi suggests something more disturbing – that many subjects are eliminated from trials during a run-in period precisely because the drug disagrees with them, and so the trial proper begins only when many people suffering from side-effects are excluded. She also notes, I think effectively, that there is a lot of play with statistics in the advertising of statins (and other drugs of course) – for example a study which found that the risk of having a heart attack on statins was about 2% compared to 3% on placebos was being advertised as proving that your heart-attack risk on statins is reduced by a third. This appears to be dodgy – the absolute percentage difference is very small, and how is risk actually assessed? By the number of actual heart attacks over period x? I don’t know. And how many subjects were in the study? Were there other side-effects? But of course we shouldn’t judge the value of statins by advertising guff.

Another interesting attack on those expressing doubts about the mass prescription of statins has been to call them grossly irresponsible and even murderers. This seems strange to me. Of course doctors should be all about saving lives, but they should first of all be looking at prevention before cure as the best way of saving lives. Exercise (mental and physical) really is a great form of medicine, though of course not a cure-all, and diet comes second after exercise. Why the rush to medicalise? And none of the writers and clinicians supporting statins are willing to mention the financial bonanza accruing to their manufacturers and those who invest in them. Skepticism is the lifeblood of science, and the cheerleaders for statins should be willing to accept that.

Having said that, consider all the life-saving medications and procedures that have preceded statins, from antibiotics to vaccines to all the procedures that have made childbirth vastly safer for women – who cares now about the pharmaceutical and other companies and patentees who’ve made their fortunes from them? They’re surely more deserving of their wealth than the Donnie Trumps of the world.

So, that’s my initial foray into statins, and I’m sure the story has a way to go. In my next post I want to look at how statins work. I’ve read a couple of pieces on the subject, and they’ve made my head hurt, so in order to prevent Alzheimer’s I’m going to try an explanation in my own words – to teach myself. George Bernard Shaw wrote ‘those who can, do, those who can’t teach (it’s in Man and Superman). It’s one of those irritating memes, but I prefer the idea that people teach to learn, and learn to teach. That’s why I love teaching, and learning…

By the way, the quote at the top of this post seems irrelevant, but I keep meaning to begin my posts with quotes (it looks cool), so I’m starting now. To explain the quote – it was from a semi-rant by Ford in his introduction to the controversial dinosaur book Too big to walk (I’ve just started reading it), about writers not getting their work edited, peer reviewed and the like, and being proud or happy about this situation. This, he argues, helps account for all the rubbish on the net. It tickled me. I, of course, have no editor. It’s hard enough getting readers, let alone anyone willing to trawl through my dribblings for faults of fact or expression. Of course, I’m acutely aware of this, being at least as aware of my ignorance as Socrates, so I’ve tried to highlight my dilettantism and my indebtedness to others. I’m only here to learn. So Mr Ford, guilty as charged.


Dr Maryanne Demasi – Statin wars: Have we been misled by the evidence?

Written by stewart henderson

September 9, 2019 at 9:44 pm