Trolls and censorship

Two cholesterol skeptics have recently been subjected to a Wikipedia trolling attack, with their entries being dissed and removed. The authors of the attacks are cowardly enough to hide behind pseudonyms and have tried to discredit their victims by suggesting that  their opinions are those of fringe lunatics.

That Wikipedia appears to have caved in to their demands for censorship is scandalous. One does not need to be a multipublished researcher to have sound opinions based on evidence. The trolling appears to be part of a sustained assault by vested interests against skeptics without any attempt to analyse or even read the scientific rationale they are setting out. The number of edits suggests a concerted trolling effort and its apparent success undermines the credibility of Wikipedia itself.

Wikipedia can restore its credibility by naming the anonymous trolls so that reasoned debate may continue.  Without that it will always be subject to the charge that it promulgates fake news. Which would be a pity as there is much to admire.

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Now I know how Galileo felt

An astonishing article appeared in “The Guardian” on 30th October.  You can find it at https://www.theguardian.com/lifeandstyle/2018/oct/30/butter-nonsense-the-rise-of-the-cholesterol-deniers.  Basically it states that accepted wisdom over the dangers of cholesterol is correct, and those that seek to deny this are dangerous lunatics.  The article is shot through with snide digs at the deniers, implying they are not proper researchers because they don’t hold tenured posts, that their opinions are published in obscure or second-rate journals and that their views are as damaging as Andrew Wakefield’s views on MMR vaccine causing autism.

When Galileo (and Copernicus for that matter) first suggested, with good scientific evidence, that the earth went round the sun he was subjected to abuse, vilification and was ostracised.  Every attempt was made by the scientists of the day to rubbish his theory. Oh well, it was suggested, he isn’t a proper astronomer, so what does he know to produce a theory that all we experts refute categorically?

Sounds familiar, perhaps.

Let’s get a few things straight. I was a rheumatologist in my working life, so deferred to my cardiology colleagues on matters cardiac.  When I found my serum cholesterol was very high I consulted my GP and readily accepted the prescription of a statin.  I developed an odd inflammation in my shin shortly after the first statin.  The technical term was tenosynovitis of the tibialis anterior muscle; in lay terms this was pain on walking, with a peculiar grating feeling if I put my hand over my shin and worked the muscle.  I had never encountered this among the myriad soft tissue lesions I saw in my clinics so consulted the Internet, where I found a case report of the condition related to statin intake.  So I stopped my statin .  The problem went away.  I sought further advice.  My GP gave me another one.  This time within 24 hours I had developed severe shoulder and hip girdle muscle pains, so bad during the night that I was unable to sleep.  I attributed this to the new statin, and stopped that.  After an interval I was prescribed yet another.  I had no adverse effects for a couple of months, and then found I was struggling to climb hills and could not lift heavy garden items.  On a long slope I simply ran out of steam, and had to stop and wait a few minutes.  Normally I could lift two 50 litre bags of compost together; now i could not lift even one.

By this time I had discovered the existence of statin myalgia, so took myself to the hospital lab to get my blood checked.  My creatine kinase level (that’s an enzyme which goes up with muscle damage, or rhabdomyolysis) was significantly elevated.  I consulted a lipid specialist and we agreed I should not take them any more.  My cholesterol remains high.

I write this preamble because the anti-Galileans of the cholesterol world talk blithely of a nocebo effect – one where you get a side-effect because you are expecting to get one. – which explains, in their eyes, the reports of side-effects that they claim are grossly exaggerated in numbers.  But you can’t suffer from a nocebo effect if you don’t expect it.  Neither can such an effect cause significant enzyme changes on blood tests.  Never mind; whatever the real incidence that’s not entirely relevant to this piece, but my experience led me to a new world of the cholesterol-heart hypothesis, and to the statin skeptic network called THINCS.  And we are, I believe, modern Galileos, whose questioning of received wisdom (if you can call it that) is beginning to lead to denigration and persecution.  Will we be proved right?  Let’s look at some facts.

It is undeniable that statins do reduce the risk of a major cardiac event.  But the first question is – by how much?  If you read the statin-favourable reports and research studies you will think that the risk reduction is around 50%, which is pretty impressive.  However you must ask first what the risk was in the first place.  If the risk is 4%, then a reduction of 50% means it becomes 2%.  So it’s not really very impressive at all.  Statistics are not easy; I have seen many examples of trials conducted by perfectly respectable researchers who have used the wrong statistical analysis method by accident (or ignorance) and not-so-respectable ones who find a method, or select data, so they produce an apparently significant result.  But quoting a risk reduction of 50% – the relative reduction – is deception when the absolute reduction is only 2%.  Why do people do this?  It makes the results look better, but in the end they start believing their own myths.  And if you look at the prolongation of life it amounts to a few days, let alone years.  Not a lot, as Paul Daniels would have said.

So the effects of statins are overstated and misrepresented.

The next question is why do statins reduce risk (although perhaps, as the reduction is so piddling, we shouldn’t bother).  But I did bother, because I found something that blew the whole cholesterol thing out of the water.

There is unimpeachable evidence that if you suffer from severe rheumatoid arthritis (RA) then your risk a a major cardiovascular event is very high – possibly even higher than if you are diabetic.  If you successfully treat the arthritis with so-called disease-modifying drugs, this risk reduces substantially.  But the cholesterol level in the blood goes up.

Here we have an oxymoron. Give statins, cholesterol falls and cardiac risk falls (a bit).  Give drugs that make RA patients better, cholesterol rises, but cardiac risk falls (quite a lot).  Explain.

For about seven years I put this paradox to rheumatologists, physicians and others. No-one could explain it.  They huffed and puffed and mumbled and came up with all manner of crazy theories.  So we have a Black Swan.  Received wisdom in the eighteenth century was that all swans were white. Then Australia was discovered and lo! there were black ones. So the received wisdom was wrong. It only takes a single contrary observation to destroy a theory.  In medicine one tests a theory exactly thus; you make a hypothesis, and set out to disprove it (it’s called a null hypothesis).  The null hypothesis is that statins  reduce cardiac risk because they reduce cholesterol.  Yet if we reduce cardiac risk by treating a disease characterised by inflammation, cholesterol goes up.  So the null hypothesis is by definition proved to be false.  You can have any number of things supporting a null hypothesis, but it takes just one that doesn’t to turn things over.

Enter Malcolm Kendrick, another cholesterol skeptic, a deep thinker, careful research analyst, and GP without some giant research department (therefore suspect in the eyes of the anti-Galileans). What if the mechanism of action of statins has nothing to do with cholesterol?  Suppose that cardiovascular risk is increased because of blood vessel inflammation and that statins reduce this?  Well.  It all fits, doesn’t it? And by golly there’s plenty of evidence for coronary artery inflammation.  You get it in RA and other connective tissue diseases.  You find it on pathological examination under a microscope.  And it explains otherwise inexplicable things.  Like – how does a large cholesterol molecule get through the blood vessel wall?  It can’t, if the wall is intact, because it’s too big.  But suppose the wall is damaged, and tries to repair itself, but the process doesn’t quite work.  Why, then you can find cholesterol the wrong side of the wall lining.  It’s there as part of an incomplete healing process.  It has nothing whatever to do with its concentration in the blood but will happen more often where there is blood vessel damage.  Oh, and by the way, that occurs in diabetics and smokers too.  There are an awful lot of scientists and cardiologists who find this hypothesis attractive, and despite asking the anti-Galileans to pick it to pieces for some reason they haven’t.  Perhaps they can’t but I would like to see them try.

I would prefer to explain this as follows: Statin use (A) causes a small reduction in cardiac risk (B).  A also causes a fall in cholesterol (C).  A leads to B, and A leads to C.  But that does not mean that C leads to B.  A fall in cholesterol is more likely to be a side-effect, or epiphenomenon – something clearly observable but irrelevant.

Another question of mine has been why you find cholesterol deposits in arteries, but not in veins, where the pressure is less and the flow can be sluggish.  If cholesterol was to be deposited anywhere it ought to be here, like silt in a river. Explain. (Actually don’t bother, because there’s more coming that makes that unnecessary).

So statins work by reducing inflammation; that they reduce cholesterol is by the by.  Now I don’t really care whether severe statin side-effects occur in 20 % or 2% but others do, on the basis that if patients cannot take a statin they MUST HAVE SOMETHING!!!  You would be amazed at the number of people I saw with clear-cut statin side-effects (effect occurs, stop, effect disappears, restart, effect reappears – that’s called re-challenge, and QED for cause and effect) who were otld, 0redered even, to carry on because otherwise they would DIE!

So a new injectable drug was produced called evolucumab.  Its cholesterol-lowering effects are remarkable.  It’s far, far better than a statin.  It’s also very, very expensive.  Does it reduce cardiac events far, far better than a statin?  No!  Why not? Perhaps it doesn’t have any anti-inflammatory properties, but we won’t know in all probability as the major trial looking at outcomes was terminated early.  The death rate in those on the active drug was higher.  There is a suspicion that it would have been higher still if the trial had continued.  Even Sir Richard Thompson, past president of the Royal College of Physicians, said any benefit was “amazingly small”.  So here is another oxymoron.  Statins reduce cholesterol a bit and reduce cardiac events a bit.  Evolucumab reduces cholesterol a lot but doesn’t reduce cardiac events.  Explain.

Well, the obvious explanation is that any cardiac benefits of statins have nothing to do with cholesterol.

Next question.  Where does cholesterol come from?

You thought you ate it, didn’t you?  It’s in all that butter and other saturated fat that forms such a large part of your diet.  Actually it’s not that large a part, but anyway most of the cholesterol you find in the bloodstream (80% or so) is made in the liver.  From what, you ask? How about carbohydrate?  Whatever, an increase in dietary cholesterol slows the liver’s own production (this is called homeostasis).  So fiddling with your cholesterol intake is not much use, as your liver will defy your good intentions and simply make more.  If your level is high, probably your genes made you that way.

I wonder whether you are beginning to doubt received wisdom.  It is interesting, if sad, that the whole concept of cholesterol irrelevance was effectively proposed several decades ago by Dr John Yudkin, who saw sugar as the villain, but who was himself vilified and ostracised.  And the work of Ancel Keys who was key (sorry) to the adoption of the cholesterol-heart hypothesis, was fatally flawed.  Out of the countries from which demographic data was analysed he picked those that best fitted his hypothesis.  Had he used it all he would not have found any significant correlation.  Indeed most of the trials looking at serum cholesterol and heart disease conducted before 2000 have methodological flaws.  Confine reviews to trials after that date and even the relative risk improvement begins to look unexciting.

So there it is.  The hypothesis is based on shaky data analysis, falls over under intense scrutiny because of inherent contradictions and is also suspect because some of the later trials cannot be independently assessed.  Sceptics have persuaded erudite journals that trial data should be made available for independent analysis.  Yet one of the most strident anti-Galileans, Sir Rory Collins, refuses to do this for his own work.  If it’s so cast iron right, what is there to hide, one might ask.  And what need is there for the anti-Galileans to make snide remarks questioning the credibility and integrity of their critics? Likening us to the disgraced Andrew Wakefield, who has fooled people with fraudulent data, is frankly offensive.  We have faked no data, falsified no trials, merely picked major holes in those of others.  We have raised no scares, unlike those who have accused us of killing people by telling them to stop their statins.

What did Socrates say?  “When the debate is lost, slander becomes the tool of the loser.”

Remember: all of us sceptics were reared on the heart-cholesterol hypothesis but it is us who have been open-minded enough to question its validity.  If we are wrong, give us the evidence.  Prove that our hypothesis has fatal flaws.  In other words, put up or shut up.

 

Rain, rain, don’t go away

I know Spain needs rain as much as we do here in England (and New South Wales needs even more) but watering the allotment twice a day plays havoc with my elbows (no hoses, only watering cans filled from a tank).  So we are hoping for a thunderstorm or two.  The weather forecast has predicted several.  None has yet materialised.

But of course the forecast is only that, and the chance of rain is given as a probability.  So if there’s an 80% chance of rain, there is a 20% chance of no rain.

James Stagg changed the date of the D-Day landings in 1944 because his forecast was believed over that of the American advisers.  Michael Fish said there wouldn’t be a hurricane in 1987.  OK, it wasn’t a hurricane by the strict definition of the term, but it was a pretty powerful storm.  We slept through it, actually, but the damage around us the following morning was horrendous.

It all puts me in mind of the old Lake District forecast: if you can see Ireland from the top of Scafell Pike it’s going to rain.  If you can’t, it’s raining already.

But the finest “forecast” was promoted by “Private Eye”, which produced a floppy EP record distributed inside one issue, with a series of John Bird’s Idi Amin confections.  I suppose nowadays it is politically incorrect, or culturally appropriative, but it doesn’t stop it being funny.  Go to https://www.youtube.com/watch?v=4zlMO4z2T74 for the full effect…

The skies are grey.  It’s humid as anything.  But still no bloody rain.

PS.  Half an hour after I posted this the rain began!  Magic in the Internet?

HS2: the gravy train

The fron page of today’s “The Times” carries the news that large numbers of employees of the HS2 rail project are on large salaries of over £100,000 per annum.  The thing hasn’t even started building yet and the release of these figures undoubtedly plays into the hands of the naysayers who wish the whole thing would go away, and be replaced by the currently mothballed plans to upgrade the east-west routes in the north of England.  It would be cheaper and of more benefit to the economy, they say, citing “evidence” that the speed of HS2 will not result in any change in passenger numbers or convenience, It would also relieve the pressure on those whose estates are in the way of HS2 who, it must be admitted, have been treated pretty shabbily by the compensation-wallahs.

It all sounds very reasonable.  But haven’t we been here before?  The furore over HS1 is all but forgotten; all the same arguments were raised – poor homeowners forced from their land, those left bordering the line subjected to unbearable noise, shortage of passengers making the whole thing unnecessary, high fares to cover costs will be scorned by travellers.  Well.  All I can say is that it has been an unmitigated success.  I declare an interest, as I use HS1 to get to London from Ashford, but the trains are full, the speed is amazing with a halving of the old journey time, and the only complaints I ever hear are when a train is cancelled or late.

But we have been here even before that.  If we return to 1865 we find that the tunnel on the railway from London Bridge to Chislehurst at Elmstead Woods is only there because the landowner refused permission for access, and refused to allow a cutting, forcing the railway to drive a tunnel which in places is only a metre or so below the surface.  There are numerous examples of major landowners seeking special treatment during railway mania; insisting on diversions or their own stations (or both) and making just as much of a NIMBY noise as today’s complainers.  And a hundred years or so before that exactly the same happened with the canals, and in both cases people were bought off, intimidated or otherwise persuaded to give ground (pun not intended).

That isn’t to say that I lack sympathy for those in the way of HS2.  There is a clear need, though for a reassessment of the comparative costs and benefits of HS2 and HS3.  Whether, given the government’s entrenched position, this will happen is doubtful, but there must come a time when a bold decision to cancel might be wise.  Think planes, and TSR2 (look it up).

 

Why back pain treatments don’t work

A recent study suggested that many treatments for back pain do not appear to be effective.  I am unsurprised.  The first reason is that the wrong diagnosis has been made.  The second is that the treatment is, actually, ineffective.

Back pain has several causes; pain can come from a number of different structures.  It’s no good treating a disc prolapse with a muscle injection.  If the pain does not arise from a facet joint then injecting that joint will do nothing.  If the issue is a pulled back muscle then manipulation may actually make things worse.  And surgery to remove a bulging disc won’t help if the disc is not the problem.  MRI scans may help, but you can be sure if a disc bulge is on the left, and all the symptoms are on the right, then that disc bulge is irrelevant.  It is difficult, though, to persuade patients that an “abnormality” does not signify.

Thus the first key is – be sure which structure is the source of the pain.  I have an algorithm that helps, but is not infallible.  I failed to diagnose my own disc prolapse for a couple of weeks because the algorithm pointed me the wrong way.  But it’s a start.

The second key is patience.  How do you treat a bruise?  You treat the affected area with a bit of respect (not a lot) and wait for it to get better on its own.  So should you with back pain.  95% get better in four to six weeks – even disc prolapses resolve themselves quite often.  Mine did.  However there are some symptoms that should prompt the seeking of help; severe pain at night, nerve symptoms (loss of sensation or power in the leg); and especially any disturbance of bladder and bowel control.  The worrying causes of back pain are cancer or osteoporosis.  The former produces unremitting pain, the latter may have a sudden onset as a bone collapses.  The history is vital.

Treating cancer in bones is possible.  Treating pain from an osteoporotic fracture is possible, but trying to treat the osteoporosis itself will make no difference.  Time will heal the fracture and the pain will go off; anti-inflammatory drugs will help with the pain meanwhile.

I have had dramatic results from injecting anaesthetic and steroids around facet joints.  Such success may be gratifying not because it works but because it confirms the diagnosis of facet origin pain.  Spinal manipulation is positively dangerous in some circumstances.  I saw a patient who had had his neck manipulated when the cause of the pain was a large cancer deposit in one of the vertebrae which had made it vanish on X-ray; he was lucky that the manipulation did not dislocate the spine and transect the spinal cord.  I have also seen patients whose disc prolapse has been worsened by a quick tweak.  I have also seen a patient who had been diagnosed with polymyalgia (multiple central muscle pains now thought to be due to blood vessel inflammation) whose exacerbations of pain were treated with large increases in their steroid dose.  But the cause of the pain was not polymyalgia, but recurrent osteoporotic crush fractures – which the bursts of steroids were helping to create.  Folk are ever so keen to have an osteopath or chiropractor manipulate them, but there’s an awful lot of them who go back time after time for repeat treatments because they don’t last (or work).

So the first step is to make sure you have the right diagnosis, and the second is to administer the right treatment for it – or none at all.  Nothing can be a treatment.  But it’s not easy to persuade someone that nothing is better than something.  My rule was – if it’s that painful, rest it, but when it starts to improve get moving ASAP.  Bedrest can not only prolong recovery but also lead to chronic problems.  Keeping up muscle strength is vital.

There is a story of an old villager in France who had an astounding reputation for correctly identifying wines.  He could pick types, origins, even years.  Eventually during a tasting competition one of the judges slipped in a glass of water.  The old boy nosed the glass, took a sip, swilled it round and spat.  He looked puzzled.  He had a piece of bread and repeated the process, and then a third time.  Eventually he turned to the judges.  “I have never been wrong, or beaten by something” he said “but I confess that this has defeated me.  I don’t know what it is.  But I do know one thing.  It won’t sell.”

 

Sugar and spice and all things horrible

I may be boring but I have never smoked, eaten or taken cannabis in any form.  It has been around should I have wanted it but I was thoroughly put off by my father, who told terrible tales of street scenes in Bombay (now Mumbai) in his youth in the 1920s.  Men (and it was usually men) were addicted, and sat around in a zombie-like state, and he was convinced that chronic use led to serious mental illness.

Back in the 1960s, when I was a medical student, my friends pooh-poohed his lurid accounts.  “Go on! Try it!” they said.  We were in time of free love, Woodstock, California dreaming and all that.  Everybody did it.  But I never did.

Well.  Hasn’t the worm turned. The appearance of new, highly potent preparations has led to – zombie-like states, chronic addiction and the unmasking, or generation, of serious mental illness such as schizophrenia.  We have been treated to graphic scenes of drug abuse in prisons (BBC – Prison from the inside) showing not only the distressing state of users but the violence surrounding the supply of drugs.  And Spice is the big problem.  For years people have denied that cannabis and its derivatives are harmful.  I cannot believe that any denier could watch these prison scenes and persist in their denial.  Some of the users are clearly vulnerable adults and no-one is looking after them.  Perhaps no-one can.  There’s a lot of money involved so there is no incentive for suppliers to desist.

My father died forty years ago next week, but I bet he is sitting on his cloud wagging his finger and saying “I told you so”  At least it makes a change from me saying it!

 

What’s in a title?

The Times Literary Supplement this week contains a letter from Lydia Davis detailing the struggle she had in translating the title of Proust’s “Du Côté de Chez Swann”.  I had enough trouble with the English title of my book about the origins of modern facial surgery.  No-one has yet suggested it should be translated into French, and I did not, to be truthful, have that as a consideration.

For nearly 15 years its working title was “The Queen’s Hospital and all the King’s Men”, referring of course to the nursery rhyme, which seemed apposite:

Humpty Dumpty sat on a wall,

Humpty Dumpty had a great fall;

All the King’s horses and all the King’s men

Couldn’t put Humpty together again.

Except, of course, that the surgeons did manage to put their 5000 Humpties together pretty well.

But it seemed a bit long.  So I switched to “Faces of War”.  A quick Google revealed several such titles, as did “The Face of War”, which anyway left out 4999 from the equation.  Oh dear.  Then I came up with “Faces from the Front”.  This had no overlaps; if you look now you will find a few sites indicating how to draw faces from the front.  It was short and alliterative.  It resonated both with my diligent editor and daughter, and my publisher.

So “Faces from the Front” it became, although for clarity it had appended a rather long subtitle.  But the book cover makes this suitably sub.  So you can see for yourself and purchase from any number of bookselling sites worldwide.

“Faces from the Front: Harold Gillies, the Queen’s Hospital, Sidcup and the origins of modern plastic surgery” is published by Helion Press (2017).