Category Archives: Dr Malcolm Kendrick

I am a GP living in Macclesfield, having graduated from Aberdeen medical school many moons ago. This blog is my best effort at providing some balance to the increasingly strident healthcare lobby that seems intent on scaring everyone about almost everything. Is there a foodstuff that is safe to eat anymore? Is there any activity that does not cause cancer or heart disease? Sausages…..get thee behind me Satan.

Replies to the vitamin D article by the guest contributor

11th July 2020

Having published the guest article by ‘Bob’ there have been a lot of comments. I have not replied, as it was not my article. However, Bob has put together a kind of generic reply to people’s posts which I think may be useful and informative.

Hello Everybody – I wrote the article and have read your comments.  First, I want to thank Dr. Kendrick for publishing my thoughts in his esteemed blog.  I started following Dr. Kendrick’s blog around 2015 and am a devoted reader.   My favorite single post is the one titled “Salt Is Good for You.”

I was introduced to the wonderful world of Vitamin D in 2010 when a physician directed me to the Vitamin D Council website, now defunct.  John Cannell’s articles on influenza, and on autism, were compelling for me.  I started taking 5000 IU per day in December 2010 (at age 60) and I noticed that I no longer got colds or influenza in the winter.  Before 2010 I would get one or two colds every winter, with the usual sore-throat – head cold – chest congestion sequence.  Since then I have had exactly 5 colds, all very mild.  I now take a higher dose but I think people should look at the advice provided in the Grassrootshealth article and make up their own minds as to appropriate dose.

My article sketches out a theory that yields a series of hypotheses which can be tested.  Thus, one notes a general pattern, and scratches one’s head over exceptions.  Hence my discussion of Ecuador and South America.

I propose that an underlying difference in susceptibility to coronavirus arises from the fact that the New World was epidemiologically isolated from the rest of the world until about 500 years ago.  Before then the indigenous populations of the New World and the Old World were exposed to and therefore developed adaptive mechanisms to ward off different groups of pathogens.

This is illustrated by the well-known susceptibility of New World populations to Old World pathogens like measles and smallpox.   The higher death rates in many South American countries suggests that the indigenous New World genome has not yet fully adapted to Old World coronaviruses.  Thanks, Terry Wright, for the Guayaquil reference.

Thank you, John Stone, for the reference to the Stadler article observing that there is a significant level of immunity to Covid19 already present in the population.   We had another clue to this fact early in the pandemic with outbreaks on two ships, the cruise ship Diamond Princess, and the US aircraft carrier Theodore Roosevelt.  Both occurred before people took protective measures, and it can be argued that the close quarters of shipboard life are ideal for the transmission of the disease.  On both ships, everybody was tested for Covid19.   Results were remarkably similar.  On both ships, 17 percent of the people tested positive for the virus, and of those, 50 percent were asymptomatic.  It looks like 83 percent of the shipboard populations were immune to the virus.  Why?

Several of you have pointed out that death rates from various countries are inconsistent with the sunshine theory.  First, do not confuse cases with deaths.  Case totals are the creatures of testing programs, which vary from place to place.  Deaths are a much harder statistic.

That said, country-specific factors come into play.  In comments, Andrew Larwood and Simon C pointed out Finland’s vitamin D supplementation program would reduce deaths.  Their death rate per million is 59, which seems very low for a country in the winter at such a high latitude.  Now I know why. Another factor may be fatty fish, a dietary source of Vitamin D, which is consumed in quantity in ScandinaviaHåkan, your comment about Sweden is relevant.

Many people attribute the higher rate of Covid19 deaths to the lack of a lockdown.  However, an equally good case can be made that the dark-skinned immigrant population in Sweden is more deficient in vitamin D and thus more susceptible to the illness.  See this article by Dr. David Grimes where he notes that 1 percent of the Swedish population may be responsible for 40 percent of deaths: http://www.drdavidgrimes.com/2020/04/vitamin-d-and-immunity-important.html and this one: https://www.bmj.com/content/368/bmj.m1101/rr-10  If you have read Dr. Kendrick’s last blog post, “Distorting science in the COVID pandemic,” you would know that the very low death rate (7 per million) in Morocco may be due to their use of hydroxychloroquine to treat sick patients.

Does implementation of hydroxychloroquine treatment explain the abrupt decline of coronavirus deaths in the UAE on May 12? https://www.palmerfoundation.com.au/preliminary-injunction-sought-to-release-hydroxychloroquine-to-the-us-public-studies-show-benefits/  If you look at the death rate graphs for a number of Muslim countries, there is a distinct uptick in cases at the end of May.  Does this have something to do with Ramadan, which was April 23 to May 23 this year?

David Bailey, your comment is spot-on.  Look at the seasonality of acute myocardial infarction.   In the higher latitudes one gets daily doses of sunshine in the summer, but not in the winter, and it is the dailiness of the dose that is key to protection of the endothelium.  This is also why randomized clinical trials of vitamin D tend not to show a strong protective effect against CVD, because most do not use a daily dose, rather, dose intervals are weekly or longer (and the dose is usually too small and the duration of the trial too short).

Thank you all for your comments.

 

A Good Cause

15th April 2020

I have known Steve Bennett for a few years now. He became a convert to the high fat low carb world (primal living and eating) and has set up Primal Living to promote this dietary message to the world, using his considerable financial muscle to do so.

In the midst of lockdown, he is running a series of youTUBE programmes, and interviews, discussing a number of topics, and from the resultant publicity he is hoping to gain donations to food banks – which are really struggling at the moment. He will match donations up to £100,000 to do this.

I hope you can watch some of the programmes. I hope you can donate, if you feel able. I am appearing on a couple of the shows. I think this is a very good cause. I support Steve Bennett and his team in the endeavour. Below is a slightly amended press release…

THE FOOD BANK SHOW – YouTube channel: The Primal Living.

Guests on the shows include politician Tom Watson and Dr Aseem Malhotra and Dr Malcolm Kendrick – amongst others (we are also waiting for conformation of singer Liam Payne – Liam is a huge supporter of food banks). The show will also be connecting live to the Trussell Trust, who with their army of amazing volunteers keep many of our food banks operational.

Every morning thereafter, we will be broadcasting live on youTUBE providing food and health advice. Steve Bennett The Food Bank Show host will be joined by doctors, medical experts and chefs, many of whom contributed to his latest health book FAT and Furious. Together – they will be taking your questions from around the country and additionally during the shows we will video link to food banks across the UK and discover new ways we can all help offer support.

With fast food chains closed, we want to seize this opportunity to reshape the eating habits of our nation and improve everyone’s health and whilst we are doing this together –  help feed those most in need during this crisis.

Join Steve and his family, as they put on a truly interactive show and please encourage everyone you care and love to join them too.

Further Info

  • We aim to generate as many donations to the Food Banks as possible. Steve Bennett is going to match donations up to the first £100,000.
  • People can donate via a text or a justgiving page.
  • The show has 3 aims;
    • Help viewers learn about how to eat healthily
    • Raise money for foodbanks, with our partnership with the Trussell Trust
    • Entertain people
  • 2% of UK families currently rely on food banks, but the virus has resulted in fewer donations and fewer volunteers being able to help.
  • After keeping social distance and washing hands, the next best thing we can do to help our immune and defences is to be metabolically healthy, this will be discussed at detail in the shows.
  • Most vulnerable are those with metabolic syndrome. In Italy while the average age of death was 81, the average person who died suffered from 2.7 underlying chronic medical conditions. Including High blood pressure, cancer, diabetes. Lowering blood pressure, reversing diabetes, high sugar levels, can happen quickly with the right advice and that is the message the doctors will be promoting.
  • In Wuhan, more than 60% of people who died, or had serious complications had high blood pressure or type 2 diabetes.
  • UK over 60% adults are overweight or obese. Only 17.4% of American adults are metabolically healthy.

For more information contact:

Contact the Show Writers Nick.Davies@primalliving.com  or Poppy Hadkinson poppy@primalliving.com
Jack Bennett Show Producer JB3015@bath.ac.uk
The Show Host Steve Bennett Steve@tggc.com

CORONAVIRUS [COVID-19]

18th March 2020

I thought I should say something about the coronavirus for readers of this blog. I need to state that the situation is fast moving, facts are changing, and I am not asking anyone to go against any current medical advice.

Here, I am simply providing advice that I believe, currently, may be of benefit to people out there. I am acutely aware that there is controversy swirling about, but I will not promote anything that can cause any significant harm – but may cause significant good.

I have tended to look back a few years in time for some evidence, because current, emerging evidence is subject to massive bias and controversy, with various vested interests getting involved. The ‘older’ evidence has not been done in a rush and is therefore more measured.

1: Anti-inflammatories (NSAIDs)

COVID-19 appears to impact the lungs more than any other organ and COVID-19 can be thought of as a ‘viral’ community acquired pneumonia. There has been evidence for several years that anti-inflammatory agents e.g. ibuprofen, naproxen (NSAIDs) may worsen community acquired pneumonia. As highlighted in this 2017 paper:

‘Non-steroidal Anti-inflammatory Drugs may Worsen the Course of Community-Acquired Pneumonia: A Cohort Study:

CONCLUSIONS:

Our findings suggest that NSAIDs, often taken by young and healthy patients, may worsen the course of CAP with delayed therapy and a higher rate of pleuropulmonary complications.’ 1

There is now anecdotal evidence, particularly from France, that patients who take NSAIDs do considerably worse. It has been suggested they may lead to an increased death rate.

ADVICE: Avoid NSAIDs if possible

2: Vitamin C

Vitamins always cause massive controversy, and the mainstream medical community tends to be highly critical of the use of vitamins. However, vitamin C has been found to have many, many, positive impacts on the immune system. It also protects the endothelium lining blood vessels – thus preventing/delaying passage of pathogens from the bloodstream.

I include the full abstract from the 2017 paper ‘Vitamin C and Immune Function.’ It contains a great deal of medical jargon, but I have highlighted the most important parts.

Vitamin C contributes to immune defense by supporting various cellular functions of both the innate and adaptive immune system. Vitamin C supports epithelial barrier function against pathogens and promotes the oxidant scavenging activity of the skin, thereby potentially protecting against environmental oxidative stress.

Vitamin C accumulates in phagocytic cells, such as neutrophils, and can enhance chemotaxis, phagocytosis, generation of reactive oxygen species, and ultimately microbial killing. It is also needed for apoptosis and clearance of the spent neutrophils from sites of infection by macrophages, thereby decreasing necrosis/NETosis and potential tissue damage.

The role of vitamin C in lymphocytes is less clear, but it has been shown to enhance differentiation and proliferation of B- and T-cells, likely due to its gene regulating effects. Vitamin C deficiency results in impaired immunity and higher susceptibility to infections. In turn, infections significantly impact on vitamin C levels due to enhanced inflammation and metabolic requirements.

Furthermore, supplementation with vitamin C appears to be able to both prevent and treat respiratory and systemic infections. Prophylactic prevention of infection requires dietary vitamin C intakes that provide at least adequate, if not saturating plasma levels (i.e., 100–200 mg/day), which optimize cell and tissue levels. In contrast, treatment of established infections requires significantly higher (gram) doses of the vitamin to compensate for the increased inflammatory response and metabolic demand.’ 2

In short, Vitamin C can help prevent respiratory infections. It can also help to treat established infections, although much higher doses are required. This seems to fit with emerging Chinese data which appears to be showing considerable success with high dose intravenous Vitamin C in treating coronavirus.

It is unlikely that anyone working in the medical system in the West will agree to using high dose Vitamin C as part of any management plan. However, if your loved one is extremely ill in hospital I would recommend speaking to the doctors and asking if this can be added.

Whilst it is possible that vitamin C may prove ineffective, it also does no harm. Those who are currently attacking the use of Vitamin C and attacking those who believe vitamin C may be beneficial are, I believe, mainly concerned with their personal reputations.

ADVICE: Take at least 2g of Vitamin daily C to ‘prevent’ infection, probably more like 5g. Increase the dose to at least 10g if you are suffering symptoms.

3: ACE-inhibitors/ARBs

COVID-19 appears to enter the body using the ACE2 receptor (found on the surface of many cells, particularly in the lungs. Also found in high concentrations in the heart and kidneys.

Because of its affinity to ACE2 receptors (and the more widespread Renin Aldosterone Angiotensin System or “RAAS”) COVID-19 is causing upset with the whole system – in complex ways. The system itself is complex.

To remind those of a more technical bent, here is the system:

 

I wished to make it clear that if COVID-19 impact on the RAAS system, trying to work out the resultant abnormalities, is not easy.

There are two main drugs that are designed to lower blood pressure by ‘interfering’ with the RAAS system. ACE-inhibitors (angiotensin converting enzyme inhibitors), and ARBs (angiotensin II receptor blockers). They are very widely prescribed.

Some people have suggested that these drugs should be stopped. Others have suggested that they should be continued. You may be able to see why the advice is contradictory, given all the possible interactions.

However, it does seem the COVID-19 creates hypokalaemia (a low blood potassium level). A rising potassium level indicates recovery from the virus. This is probably due to interference with the hormone Aldosterone due to degradation of many ACE-receptors in the body.

ADVICE – currently not enough information to provide any advice on ACE-inhibitors and ARBs. However, increased consumption of potassium, if symptomatic, can be advised. Dose?

People who eat large amounts of fruits and vegetables tend to have a high potassium intake of approximately 8000 to 11,000 mg/d,’ 3

So, up to Ig a day appears perfectly safe, and if more is being lost through the kidneys with COVD-19, there appears to be little danger of overdosage.

4: Chloroquine and Hydroxychloroquine

These drugs normally used to treat/prevent malaria (and are also used to treat various ‘immune’ disease). However, they have been found to be effective in treating other viruses and seem to have been highly effective against COVID-19 4. These drugs will only be available as part of medical management. They cannot be bought over the counter (in any country, as far as I know).

If you, or a loved one, is seriously ill, I would urge you to ask for – one or the other – to be used. Hydroxychloroquine has fewer side effects (drug related adverse effects)

ADVICE – Ask for one of these drugs if you, or a loved one, is seriously ill with COVID-19.

5: Vitamin D

This one is simple. Vitamin D has important effects on the immune system 5. A low vitamin D level in the winter is almost certainly why flu epidemics occur in the winter months. [Vitamin D is synthesized in the sun by the action of sunlight].

ADVICE – take at least 2000iu vitamin (preferably D3) daily.

I hope some people have found this useful. If anything I have written here proves to be wrong, or dangerous, I will change it. However, I am working on the basis here of ‘first, do no harm.’ The worse thing that any of this advice can do, I believe, is to NOT work.

1: https://www.ncbi.nlm.nih.gov/pubmed/28005149

2: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5707683/

3: https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/485434

4: https://www.connexionfrance.com/French-news/French-researcher-in-Marseille-posts-successful-Covid-19-coronavirus-drug-trial-results

5: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3756814/

The Great Placebo scandal

25th February 2020

In this blog I am going to have a closer look at an issue that has niggled away at me for a long time. Placebos. In part I was stimulated to write on this following an article that Maryanne Demasi published on the CrossFit site ‘Sometimes a placebo is not a placebo.’ 1

There are many, many different issues about placebos. Most of which people don’t even consider. Such as, is there really such a thing as the placebo effect? And if there is, how come we haven’t managed to sort out what it actually might be? I know most people reading this will retort. ‘Of course, there’s a placebo effect. It’s a known thing.’ Personally, I am not so sure. Like many known things it begins to fall apart under a bit of critical examination.

For example:

‘Whether you know you’re taking a placebo pill or not, it will still have a beneficial effect, new research has revealed. Scientists from Harvard University and the University of Basel prescribed a group of minor burn victims with a “treatment” cream, telling only some of them that it was a placebo. After the cream was applied, both groups reported benefits, despite the placebo cream containing no medicine.

The study goes against traditional medical thinking surrounding the placebo effect, which has always revolved around the idea that it was necessary to deceive patients in order for “sugar pills” to be clinically effective.’ 2

In short, you get the placebo effect whether you know, or don’t know, that you are receiving a placebo. Which kind of blows a major hole in rationale underpinning double-blind, placebo controlled clinical trials.

However, I am not exploring that particular rabbit hole today.

Today I am going to look at the question. What is in a placebo? You may well believe you know the answer to this. A placebo is an inert formulation containing no active ingredients.

This is a reasonable assumption to make as the medical definition of a placebo, as taken from the Merriam-Webster medical dictionary, is:

‘1a: a usually pharmacologically inert preparation prescribed more for the mental relief of the patient than for its actual effect on a disorder

b: an inert or innocuous substance used especially in controlled experiments testing the efficacy of another substance (such as a drug)’

A few years ago, I was speaking to an investigative journalist from the Netherlands who was trying to get hold of the placebo tablets used in a particular clinical trial. He wanted to establish exactly what was in them, and if they were truly inert. No such luck, these placebos were very carefully guarded, as was any information about what they contained.

He gave up, but I did file his tale in my mind, recognising this was something that needed to be looked in greater detail at some point in the future. Can it be true that placebos are not actually inert?

Surely, it’s possible to ask the pharmaceutical company running the trial what’s in the placebo. Well, you can try. To quote a section of Maryanne’s article

‘The process of obtaining regulatory documents, however, is by no means straightforward. In fact, it is often complicated and time consuming. I have made multiple appeals to a European drug regulator (Medicines Evaluation Board) to obtain information (Certificate of Analysis) regarding the ingredients of a placebo used in a controversial statin study (JUPITER trial), but so far, they have fallen on deaf ears. So, too, have my requests to the trial’s lead investigator, Dr. Paul Ridker.

Medical journals will need to take responsibility and insist that published papers report on the methodological details of “inactive” placebos. Recently, Shader of Clinical Therapeutics stated, “It will no longer be sufficient to simply indicate that a placebo was used.”

“We will require that a full description of any placebo or matched control used in a clinical trial be given in the Methods section. This means that color; type (capsule or pill or liquid); contents (e.g, lactose), including dyes; taste (if there is any); and packaging (e.g, double-dummy) must be noted,” he stated. “We are instituting this change as part of our ongoing effort to facilitate replication of findings from trials. All too often this valuable information is omitted from published trial results.”

In short, you can’t find out what is contained within the placebos. Or at least, it is exceedingly difficult – to impossible.

This is very disturbing indeed, because it has become increasingly clear that placebos are often far from inactive or inert. In fact, they often contain some quite unpleasant substances. For example, here from an article in Medical News Today

‘The authors outline an example where a particular placebo skewed the results of several studies. In studies that investigated oseltamivir, which people may know by its brand name Tamiflu, scientists often added dehydrocholic acid to the placebo.

Dehydrocholic acid has a bitter taste, as does oseltamivir. The researchers chose to add this chemical to the placebo so that the participants would not know whether they had received the active drug or the placebo.

However, both dehydrocholic acid and oseltamivir cause gastrointestinal side effects. When scientists attempted to calculate the rate of gastrointestinal side effects due to oseltamivir, they compared them with side effects from the placebo.

As the placebo also caused these types of symptoms, scientists underestimated the overall gastrointestinal side effect rate for oseltamivir.3

Essentially, and you may find this rather shocking, a company doing a clinical trial can stick almost any nasty substance they like into a placebo and tell no-one. There are no regulations to prevent this happening, or at least none that I can find.

From time to time, however, the secret ingredients are revealed, or discovered, such as dehydrocholic acid. Here is Maryanne on the Gardasil (HPV) vaccine. In this case the ‘secret ingredient’ in the placebo was also identified.

‘In trials of the human papilloma virus (HPV) vaccine, participants were told they were either receiving a “vaccine or placebo.” The vaccine manufacturer defines a placebo as an “inactive pill, liquid, or powder that has no treatment value.”

However, participants in the placebo group did not receive an inactive substance of no treatment value. “Instead,” RIAT researchers state in the BMJ, “they received an injection containing amorphous aluminium hydroxyphosphate (AAHS), a proprietary adjuvant system used in the Gardasil vaccine to boost immune response.” 4

[RIAT = Restoring invisible and abandoned trials. Good people]

This is worrying. Many of those who are concerned about the potential for vaccine damage, believe it may well be the amorphous aluminium hydroxyphosphate (AAHS) itself which is the substance that can cause the adverse effects seen with many vaccines.

If both placebo, and vaccine, contain this adjuvant, then… it’s a free pass for the vaccine. In order to hide adverse effects with the vaccine, the placebo contained the substance suspected to cause adverse effects. Anyone who thinks that is remotely acceptable needs a long hard look in the mirror…

However, important thought it may be, it is time to move onto my favourite subject, statins – and placebos. For years I been highly suspicious of the adverse effect rates seen in the statin clinical trials. My concerns, and the concerns of others, formed part of a letter written to the then Health Secretary (Jeremy Hunt), and also to the National Institute for Health and Care Excellence 5

Here was the section on adverse events:

  1. Conflicting levels of adverse events

In emphasising the cost per Quality Adjusted Life Year (QALY), NICE is clearly making a major assumption that the key issue is mortality reduction, and that statins lead to very few adverse effects. We would question this very strongly.

The levels of adverse events reported in the statin trials contain worrying anomalies. For example, in the West of Scotland Coronary Prevention Study (WOSCOPS, the first primary prevention study done), the cumulative incidence of myalgia was 0.6% in the statin arm, and 0.6% in the placebo arm*

However, the METEOR study found an incidence of myalgia of 12.7% in the Rosuvastatin arm, and 12.1% in the placebo arm

Whilst it can be understood that a different formulation of statin could cause a different rate of myalgia, it is difficult to see how the placebo could, in one study, cause a rate of myalgia of 0.6%, and 12.1% in another. This is a twenty-fold difference in a trial lasting less than half as long*.

Furthermore, the rate of adverse effects in the statin and placebo arms of all the trials has been almost identical. Exact comparison between trials is not possible, due to lack of complete data, and various measures of adverse effects are used, in different ways.

However, here is a short selection of major statins studies.

AFCAPS/TEXCAPS: Total adverse effects lovastatin 13.6%: Placebo 13.8%

4S: Total adverse effects simvastatin 6%: Placebo 6%

CARDS: Total adverse effects atorvastatin 25%: Placebo 24%

HPS: Discontinuation rates simvastatin 4.5%: Placebo 5.1%

METEOR: Total adverse effects rosuvastatin 83.3%: Placebo 80.4%

LIPID: Total adverse effects 3.2% Pravastatin: Placebo 2.7%

JUPITER: Discontinuation rate of drug 25% Rosuvastatin 25% placebo. Serious Adverse events 15 % Rosuvastatin 15.5% placebo

WOSCOPS: Total adverse effects. Pravastatin 7.8%: Placebo 7.0%

Curiously, the adverse effect rate of the statin is always very similar to that of placebo. However, placebo adverse effect rates range from 2.7% to 80.4%, a thirty-fold difference.

How can the adverse effects of placebo range from 2.7% to 80.4%? Yes, there can be differences in the way that adverse effects are recorded, and that could explain, perhaps a five-fold difference – being extremely generous. But a thirty-fold difference?

Also, how can it be possible that the adverse effects of the placebo, and the statin, are always, almost exactly the same, in all trails – no matter the absolute figure. I believe that this could not possibly occur unless:

  • The placebos in each trial were carefully formulated to cause adverse effects at the same rate as the statin
  • The statistics on adverse effects were manipulated

Neither possibility should fill anyone with joy, nor confidence in the regulatory systems.

I have raised this issue with a number of different people, but they all seem determinedly disinterested. I suppose that if either of my two statements are true, it means that the entire database of randomised double-blind placebo-controlled trials can no longer be trusted. This is not a nettle to be grasped. It is a fifty-thousand-volt power line with a sign reading ‘Danger of Death!’ attached.

I can well understand the reluctance to investigate. However, I do not believe that we can possibly allow the formulation of placebos to remain a well-kept secret in future, current, or past trials.

If my suspicions about placebos are wrong, then can someone please prove me wrong.

*in the letter I had calculated this figure wrongly. It was not 0.06%, it was 0.6%. So, I have changed the text in the blog to reflect that.

1: https://www.crossfit.com/health/sometimes-a-placebo-is-not-a-placebo

2: https://www.independent.co.uk/life-style/health-and-families/placebo-pills-work-no-medication-know-even-treatment-study-harvard-basel-a7969716.html

3: https://www.medicalnewstoday.com/articles/326505#Problems-with-placebos

4: https://www.bmj.com/content/346/bmj.f2865/rr-7

5: https://www.nice.org.uk/Media/Default/News/NICE-statin-letter.pdf

Writer’s block

June 4th 2019

Several people have asked after my welfare as I have not updated this blog for some time. The answer is that I am okay. Thanks for your concern. There have been a few things going on, one of which I will be able to speak about – at some point in the future – that have been taking up inordinate amounts of my time.

I am also writing, but for some reason, every time I sit down to write a new blog my mind goes completely blank. A very difficult thing to explain. It is as if a million thoughts all gather and just mangle each other up. Things seem very clear when I am walking about, but the moment I try to get started – glomp.

I am not sure if this is what is called writer’s block. It cannot really be, because I am writing other things – such as another book. However, it is very frustrating. I did fear maybe that I have run out of things to say – but in truth each day sees a newspaper headline, or a medical research paper, that has me itching for the keyboard. How can there be so much nonsense written in the world?

So, instead I am writing this rambling nonsense, that is of very little interest to anyone I suspect, but it may get me started again. Re-set my brain into super-blog mode – if there is such a thing.

Because I still believe there is a need for voices to question the misleading rubbish   being churned out by people who claim to be scientists. Especially medical scientists, such as my great friends in Oxford who can write the most outrageous gibberish and get it published.

I have always liked to believe that science is a self-correcting system. Researchers can head of in the wrong direction for many years, decades even, but in the end the scientific truth will always catch up with them, tap them on the shoulder and make it very clear they are just being silly.

The days when there were special devices for blowing smoke up the rectum have faded from memory:

When an “apparently dead from drowning” person was pulled from the Thames [river running through London], it was thought that two things needed to happen to successfully resuscitate them: warming of the body and stimulation. Tobacco was becoming popular in Europe thanks to its exportation from the Americas, and a well known stimulant thanks to the alkaloid nicotine. The nearly dead drowning victim can’t smoke themselves, and certainly can’t swallow anything. And since hypodermic needles weren’t to be fully-invented for another hundred years, the only logical way to administer tobacco was rectally. Plus, the warm smoke would warm the individual from the inside. Win-Win. Thus, the tobacco smoke enema was born, and devices placed all along the Thames river.’ 1

From here came the mocking expression ‘Blowing smoke up your arse.’ Yes, doctors have always been keen on such activities. The first Chinese Emperor was advised by his doctors to inhale vaporised mercury – which was a magical substance so incredibly healthy that everyone should be ingesting it.

Inevitably he went mad through mercury poisoning, and started running around the forests naked before being overthrown and murdered. Still he did leave a nice tomb with terracotta soldiers and even, so it is said, an underground lake of mercury – to keep him healthy in the afterlife.

My how we laugh now at such silly ideas. But medicine has continuously felt the need to do something, anything, for the patient – even if they have not the faintest idea what will happen. Good, or bad. Bernard Shaw wrote about this over a hundred years ago in Doctors Dilemmas.

‘When your child is ill or your wife dying,” when you are confronted by “the spectacle of a fellow creature in pain or peril, what you want is comfort, reassurance, something to clutch at, were it but a straw. This the doctor brings you. You have a wildly urgent feeling that something must be done; and the doctor does something. Sometimes what he does kills the patient.”

Leeches, other forms of bloodletting, trepanning, full frontal lobotomies, removal of the toxic colon, the radical mastectomy, strict bed rest following a heart attack – all these things and many more. The ‘sometimes’ that kill the patient.

These things have all gone – mostly. Evidence, science, got rid of them. Stupidity cannot run forever. At least this was once true. Today, I am not so sure. The need to do something, anything, still runs deep in the psyche of all doctors. The concept of ‘sorry, I can’t really do anything about that’ has never been front of mind.

My personal motto is ‘Don’t just do something, stand there.’ I call it masterful inactivity; others may call it laziness.

Anyway, to return to the main issue here, which is that medical science may now be incapable of self-correction. Erroneous ideas will be compounded, built on, and can never be overturned. Because of a thing called non-reproducibility.

In most areas of science, there is nothing to stop a researcher going back over old research and trying to replicate it. The correct term is reproducibility. In every branch of science there is currently an acknowledged crisis with reproducibility.

‘Reproducibility is a hot topic in science at the moment, but is there a crisis? Nature asked 1,576 scientists this question as part of an online survey. Most agree that there is a crisis and over 70% said they’d tried and failed to reproduce another group’s experiments.’ 2

This is not good, but in medical research this issue is magnified many times. Because there is another in-built problem. You cannot reproduce research that has been positive. Take clinical trials into statins. You start with middle aged men, split them into two groups, give one a statin and one a placebo. At the end of your five-year trial, you claim that statins had a benefit – stopped heart attacks and strokes and suchlike.

Once this claim has been made, in this group, it becomes unethical/impossible to replicate this study, in this group – ever again. The ethics committee would tell you that statins have been proven to have a benefit, you cannot withhold a drug with a ‘proven’ benefit from patients. Therefore, you cannot have a placebo arm in your trial. Therefore, you cannot attempt to replicate the findings. Ever.

Thus, if a trial was flawed/biased/corrupt or simply done badly. That’s it. You are going to have to believe the results, and you can never, ever, have another go. Ergo, medicine cannot self-correct through non-reproducibility. Stupidity can now last for ever. In fact, it is built in.

We face a rather dismal eternity of blowing smoke up our arses.

1: https://naturespoisons.com/2014/07/29/the-exciting-history-of-blowing-smoke-up-ones-arse-tobacco-smoke-enema/

2: https://www.nature.com/articles/d41586-019-00067-3

Dr Malcolm Kendrick – deletion from Wikipedia

I thought I should tell you that I am about to be deleted from Wikipedia. Someone sent me a message to this effect. It seems that someone from Manchester entitled User:Skeptic from Britain has decided that I am a quack and my presence should be removed from the historical record.

I have no idea who this person is, perhaps it is possible to find out? It seems a bit harsh as I recently contributed money to Wikipedia to keep it going. Was this a terrible mistake?

To be frank, I am not entirely bothered if I no longer appear on Wikipedia, but I am increasingly pissed off that self-styled anonymous ‘experts’ can do this sort of thing without making it explicit why they are doing it, what their motives are, and if they have any disclosure of interest.

Perhaps user Skeptic from Britain would like to reveal himself and provide some information as to why he is so interested in trying to wipe me out? Perhaps one or two of you here could join in the discussion and see what emerges.

His reasons for trying to get rid of me are the following

Malcolm Kendrick is a fringe figure who agues(sic) against the lipid hypothesis. He denies that blood cholesterol levels are responsible for heart disease and in opposition to the medical community advocates a high-fat high-cholesterol diet as healthy. Problem is there is a lack of reliable sources that discuss his ideas. His book The Great Cholesterol Con was not reviewed in any science journals. Kendrick is involved with the International Network of Cholesterol Skeptics, I suggest deleting his article and redirecting his name to that. Skeptic from Britain (talk) 20:29, 2 December 2018 (UTC)

Come out, come out, whoever you are.

Meeting in London

4th March 2018

A bit on the late side, but I want to make readers of the blog aware of a meeting to be held in in London 17th/18th March.

It is part of the Health Icons Lecture Series. The main guest will be Gary Taubes. It will be in London at 1 America Square. Details are here: https://re-findhealth.com/event/health-icons-lecture-series-gary-taubes/

Other guests/speakers will be

  • Ivor Cummins
  • Campbell Murdoch
  • David Unwin
  • Aseem Malhotra
  • Andreas Eenfeldt
  • Me

Here is some of the blurb

For the past half a century, the concept of a healthy diet has been synonymous with a diet low in fat, and particularly low in what is all-too-often referred to as “artery-clogging” saturated fat, the fat found in quantity in eggs, butter, meat and dairy products. The result has been a national dietary prescription to eat ever more plant-based diets: copious fruits, green vegetables and whole grains, while we minimize our consumption of animal products.

For those of us who are overweight or obese, this advice has been accompanied by the insistence that we got that way merely by eating “too much” and that the only way to solve our problems is to eat less and exercise more. And yet this now ubiquitous dietary advice has coincided with unprecedented increases in the prevalence of obesity and diabetes, raising the obvious question of whether this advice and the belief system associated with it may somehow be to blame.

Are they based on sound science? And if they’re not, which the evidence strongly suggests, then how did we come to believe them and why? And, perhaps most important, what’s the alternative? Why do we get fat and diabetic, and what can we do about it?

By asking these questions for the past 20 years, Gary Taubes has become perhaps the single most influential journalist covering nutrition and health today. He’s certainly the most controversial. His investigative reporting on the science of nutrition and the dietary triggers of obesity and diabetes are fundamentally changing the way we eat and live. Michael Pollan has described him as the closest thing we have to a “scientific Alexksandr Solzhenitsyn,” exposing the intellectual bankruptcy of current nutrition science. The Atlantic recently described his investigative journalism as so tenacious and obsessive that he had “fallen through a wormhole from reporting into expertise.”

Taubes’s skeptical, rigorously scientific approach to nutrition science is unparalleled and now he wants to share both the approach and the implications to our health and how to eat to remain healthy.

I hope some people can get along.

What causes heart disease part XXXIX (thirty nine)

9th October 2017

In this blog I would like to highlight some of the evidence that is not there. The missing link, the lost chord. The thief that steals in, in the night. The thing that is not there when you look for it.

“As I was going up the stair

I met a man who wasn’t there!

He wasn’t there again today,

Oh how I wish he’d go away!”

 

When I came home last night at three,

The man was waiting there for me

But when I looked around the hall,

I couldn’t see him there at all!

Go away, go away, don’t you come back any more!

Go away, go away, and please don’t slam the door…”

 

There was a theory, indeed there still is, that a myocardial infarction starts with damage to the heart muscle (myocardium), and the blood clot forms afterwards. Carlos Monteiro, a Brazilian researcher with whom I often communicate, promotes and supports this, the ‘myogenic theory of heart disease’. He is not alone.

Now, superficially this idea may sound completely daft. However, there is a great deal of evidence that can be gathered to support it. First, in a significant number of myocardial infarctions, no blood clot can be found. Here, from a paper entitled ‘Myocardial infarction without obstructive coronary artery disease.’

‘A substantial minority of myocardial infarction (MI) patients have no obstructive coronary artery disease (CAD) at angiography. Women more commonly have this type of MI, but both sexes are affected.1

So, how can you have an MI, if there is no blood clot, and no blockage of a coronary artery? A very good question M’lud.

There is also an increasingly recognised form of ‘heart attack’ called Takotsubo cardiomyopathy, named after the Japanese octopus pot. This is where you have all the signs and symptoms of a myocardial infarction, but it is not a myocardial infarction. It is due to extreme levels of stress – both positive or negative. Here I quote from the British Heart Foundation:

Takotsubo cardiomyopathy

This condition is also called acute stress-induced cardiomyopathy, broken heart syndrome and apical ballooning syndrome.

Takotsubo cardiomyopathy was first reported in Japan in 1990. The word ’Takotsubo’ means ‘octopus pot’ in Japanese, as the left ventricle of the heart changes into a similar shape as the pot – developing a narrow neck and a round bottom.

The condition can develop at any age, but typically affects more women than men. The good news is that often the condition is temporary and reversible.

What are the symptoms of Takotsubo cardiomyopathy? The main symptoms of Takotsubo cardiomyopathy are chest pain, breathlessness or collapsing, similar to a heart attack. In some cases, people may also suffer palpitations, nausea and vomiting.’2

You can, in fact, die from Takotsubo cardiomyopathy. Another myocardial infarction that is not a myocardial infarction.

Equally, you can find that people can suffer from a myocardial infarction days, or even weeks, after a blood clot blocked the artery. Here is a paper entitled ‘Plaque Instability Frequently Occurs Days or Weeks Before Occlusive Coronary Thrombosis.’

‘In at least 50% of patients with acute STEMI, coronary thrombi were days or weeks old. This indicates that sudden coronary occlusion is often preceded by a variable period of plaque instability and thrombus formation, initiate days or weeks before onset of symptoms.’3

So, there you go. You can have four types of myocardial infarction:

  • A myocardial infarction with no obstructive arterial disease
  • A myocardial infarction cause by stress, with no obstructive arterial disease
  • A myocardial infarction that happens weeks after the thrombus forms
  • The ‘classic’ myocardial infarction with thrombus formation followed rapidly by infarction.

What are we to make of this gentle reader? Three forms of ‘myocardial infarction’ that cannot be linked in time, or in any other way, to thrombus formation. Or, to put it another way the infarction a.k.a. the bit where the heart muscle becomes seriously damaged, is not related to a blockage in the artery either immediately, or at all.

In addition to this, there is the observation of ‘the completely blocked coronary artery, without myocardial infarction’. Here is a case history from the British Medical Journal:

A 75 year old man was admitted because of stable angina pectoris without any history of myocardial infarction. His risk profile consisted of arterial hypertension and hypercholesterolaemia. At the time he was being treated with 100 mg aspirin, 100 mg metoprolol, 20 mg pravastatin, and 40 mg isosorbide mononitrate daily. ECG showed sinus rhythm, no Q waves, and slight T wave inversions at lead aVL and I. A bicycle stress test resulted in horizontal ST segment depression of 2 mm at 75 W. Coronary angiography was performed and revealed coronary artery disease with complete occlusion of the proximal part of the left coronary artery.4

At this point you could very reasonably argue that there truly is no consistent association between blood clots, arterial obstruction, and myocardial infarction. Or, to put it another way, the widely held view that the blood clot, and subsequent arterial occlusion, immediately precedes the infarction, is contradicted by evidence.

Which leads to the inevitable conclusion that something else must be going on. Perhaps it is true that the infarction, due to extreme stress and build of lactic acid does come first. Then, as a consequence, the clot forms in the artery.

Hmmmm. I don’t think so. However, in order to understand what is actually going on it is necessary, unfortunately, to dig even deeper, to find the man that isn’t there. Banksy, a man who paints on walls, is never seen, but we know he was there because, otherwise, you can’t explain the painting.

1: https://www.ncbi.nlm.nih.gov/pubmed/22941122

2: https://www.bhf.org.uk/heart-health/conditions/cardiomyopathy/takotsubo-cardiomyopathy

3: http://circ.ahajournals.org/content/circulationaha/early/2005/02/21/01.CIR.0000157141.00778.AC.full.pdf

4: http://heart.bmj.com/content/83/6/672

British Society of Lifestyle Medicine Conference

On the weekend of the 1st July I am giving a talk at the British Lifestyle Conference in Bristol UK.

This is a great grassroots movement of people, and many doctors, who are trying to achieve a more holistic approach to health. I hope some of you can come along. Here is what the organiser, Dr Rob Lawson, has put together for a mention on my blog.

Vital optimism at work – and play.

Lifestyle Medicine has been shaped by the natural evolution of Medicine. It is an established approach that focuses on improving the health and wellbeing of individuals and populations. It combines the broad facets of modern healthcare practices with the deeper understanding of being human. In the 21st century it has never been more important as a concept. And that is to create a society and an environment, from cell to community, which nurtures healthy longevity.

It requires an understanding and an acknowledgement of the physical, emotional, environmental and social determinants of disease and wellbeing. Hence the LM practitioner will engage with us as patients and operate within a boundary of evidence-informed medicine. A boundary in which our ideas, values, mind-set and social context blend not only with the clinicians’ expertise but also with clinical research outcomes.

Importantly, Lifestyle Medicine has a wider responsibility to recognise upstream determinants of disease and to promote population health, to protect ecological health and to reduce health inequity. This requires a realistic team approach and recognition that not one discipline or profession alone can meet our health needs.

On 1st July 2017 in Bristol Dr Malcolm Kendrick will be joining other world renowned speakers in Bristol at the inaugural Conference of the British Society of Lifestyle Medicine, the Science and Art of healthy longevity, https://bslm.org.uk/event/vital-optimism/, to which you are warmly invited. If you have never heard him speak – this is your chance! No better way to spend a Saturday in July

Mike Cawdery – a tribute

It is not often you are passed such terrible news. But sadly, Mike Cawdery, a regular and highly impressive contributor to this blog, was murdered along with his wife, on the 26th of May.

‘The devastated family of an elderly couple murdered in their home on Friday say they are struggling to understand what has happened. Michael and Marjorie Cawdery, both aged 83, were the victims of a brutal knife attack leaving them both with fatal injuries.

A family spokesperson said: “The awful and incomprehensible events of Friday 26 May have deprived our family of two wonderful people Michael and Marjorie who were our father, mother, brother, sister and grandparents. “We thank the police for their prompt response and professional actions. We also thank everyone who has expressed sympathy in whatever way and offered help.”

Mr Cawdery, a retired veterinary surgeon who trained at Trinity College Dublin, and his wife Marjorie, were attacked in their home and died at the scene.’ http://www.belfastlive.co.uk/news/belfast-news/marjorie-michael-cawdreys-family-say-13101196

I found out about this from his GP, who was kind enough to e-mail this news. He knew that Mike posted comments to this blog on a very regular basis, and he thought that I should know what had happened. Thank goodness, he did, otherwise I would have had no idea. I would have simply wondered why Mike Cawdery, our statistician par excellence, had fallen silent. [In truth, other people have since, e-mailed me with the news].

I never met him, I never spoke to him, but I believe that I – and other readers of this blog- knew him well. He seemed ferociously intelligent, and still driven to do what he thought was right. I felt he was an admirable man. Funny how the Internet brings people together into a ‘family’ that converses and argues and supports and occasionally falls out.

In the last month, Mike Cawdery posted 117 comments on the blog, all of them were worth reading. Here was one of his last ever posts.

‘May I plead with you all to keep a watch on the BMJ and to use their RAPID RESPONSE system just as one uses Dr Kendrick’s comment section. Many of the comments and references cited here are equally valid on some relevant editorials, news items and even reports. All one has to do is give name and rough address and answer a question or two. Open to all including doctors.

May I take this opportunity to suggest that any one, a patient, carer and particularly doctors as the ultimate carers sign up as “patient reviewers”. Interesting and gets patients and carers involved. Too long have patients been treated little better than pets (may be with less respect??). It is people like Dr Kendrick that have given patients an outlet to express their views and knowledge.’

At 83, he was still active, still getting involved, and still trying to make the world a better place. Mike, you will be missed, by us all.

What causes heart disease part XXVII

Lumen: The lumen of the artery is the hole in the middle that the blood flows through.

The artery wall: The artery wall is made up of three layers: Endothelium/intima, media and adventitia

The endothelium: Usually thought of as a single layer of endothelial cells than line the lumen of the artery. [The layer may be more than one cell thick]. This layer of endothelium acts as a barrier to blood, or anything in the blood, leaking from the lumen into the artery wall. There is a bit of space, sometime called the intima just under the endothelial cells.

The media: This layer is mostly made up smooth muscle cells and elastic tissue. The muscle can contract or relax, depending on circumstances

The adventitia: This outermost layer is mainly made up of collagen. It is very strong and keeps the artery in shape.

The atherosclerotic plaque: The areas of thickening and narrowing of arteries (in heart disease). These are usually found between the endothelium and the media – smooth muscle layer. They lie beneath the endothelium – within the artery wall itself. The area often referred to as the intimal layer of the artery.

The elevator pitch

Various people who work in business tell me of something called the ‘elevator sales pitch’. So-called, because of a (highly unlikely) situation whereby you find yourself in an elevator (which we in the UK call a lift) with a rich, famous, person. You have a short space of time to outline your idea to them, what it is, what it means, and why it is of value. They then hand over a hundred million dollars to invest in you, and your idea. Or something like that anyway.

Whilst the elevator pitch is clearly a mythical beast, the general point is reasonable. You should be able – or you should at least attempt – to condense your ideas into a very short space of time, before people get bored and walk away. Well, clearly I have miserably failed on this, as I am now writing part twenty-seven of my idea(s) on heart disease. In truth, I am planning on the elevator breaking down for about ten hours between floors to give me the time needed.

Recently, though, I have been speaking to a number of people who have successful careers in business, music, the arts and suchlike. I have been trying out my elevator pitch on them. Admittedly the elevator I am thinking of is in the Burj Khalifa in Dubai, but I am trying. So, here goes. Doors close on the elevator. Me and Bill Gates…

Me. ‘Forget diet, forget cholesterol, the real cause of heart disease is blood clotting.’

Bill Gates looks at his watch. ‘You have one minute.’

Me. ‘Blood clots can form and stick to the inside of artery walls. They then get absorbed into the artery wall itself where, normally, they are cleared away by specialised white blood cells. But if blood clots keep forming rapidly, at the same point, or the blood clots are bigger and more difficult to shift when they form, they cannot be cleared away quickly enough and so end up stuck inside the artery wall. This leads to a build-up of blood clot residue, and remnants, in the artery wall itself. Which means that repeated episodes of clotting, over time, build into thickenings, and narrow the larger arteries, mainly in the heart and the neck, growing somewhat like tree rings. These areas of damage are usually called atherosclerotic plaques.

In time, the process of blood clotting, over a vulnerable area, leads to heart attacks and strokes as the final, fatal blood clot forms over an area of the artery that is already thickened and narrowed. In short, atherosclerotic plaques are the remnants of blood clots. Heart attacks and strokes are the end result of the same processes that caused plaques to form in the first place. Heart disease is a disease of abnormal blood clotting. It is as simple as that. The end.’

Ping. Elevator door opens and Bill Gates walks out.

Do you think he believed me? Of course not. Heart disease is caused by cholesterol, end of.

Bill Gates: ‘Who was that complete idiot in the lift, make sure he never gets the chance to speak to me again.

Man in black suit: ‘OK boss.’

I should point out that I have never spoken to Bill Gates, and almost certainly never will. I merely used his name as an example of someone that you might try to convince using an elevator sales pitch.

I also know that my sales pitch will just seem like the most complete nonsense to most people. How can I possibly claim that atherosclerotic plaques are blood clots, when no-one else in the entire world is saying it? Am I not simply a flat-Earther? Indeed, am I not a lonely flat-Earther baying at the moon. At least the moon currently passing overheard, to join all the other moons that clearly fall into a big basket on the other side of the Earth – to be returned from time to time by an enormous dung beetle.

I like to think not, because the ‘blood clotting’ hypothesis fits all known facts about cardiovascular disease. In fact, many people have proposed the ‘blood clotting theory’ of CVD over, what is now, hundreds of years. From Rokitansky to Duguid to Smith – and many more. Here, from a paper written in 1993 called ‘Fibrin as a factor in Atherosclerosis’, co-authored by Elspeth Smith.

[Just to first remind everyone that Fibrin is a critical element of blood clots (along with platelets). Fibrin is made up of short strings of a protein called fibrinogen. When the clotting system (clotting cascade) is activated, the end result is that fibrinogen is stuck together end to end, in order to create long sticky strands of fibrin that entangle themselves around the clot and bind it all together.]

After many years of neglect, the role of thrombosis in myocardial infarction is being reassessed. It is increasingly clear that all aspects of the haemostatic system are involved: not only in the acute occlusive event, but also in all stages of atherosclerotic plaque development from the initiation of atherogenesis to the expansion and growth of large plaques.

Infusion of recombinant tissue plasminogen activator (rt-PA) into healthy men with no evidence of thrombotic events or predisposing conditions elicited significant production of crosslinked fibrin fragment D-dimer. Thus, in apparently healthy human subjects there appears to be a significant amount of fibrin deposited within arteries, and this should give pause for thought about the possible relationship between clotting and atherosclerosis.

It also provides in vivo biochemical support for the numerous morphological studies in which mural fibrin and microthrombi have been observed adherent to both apparently normal intima and atherosclerotic lesions. It should be noted that these observations are based on the human and not just the animal model.

In 1852 Rokitansky discussed the “atheromatous process” (sic) and asked “In what consists the nature of the disease?” He suggests “The deposit is an endogenous product derived from the blood, and for the most part from the fibrin of the arterial blood”.

One hundred years later Duguid demonstrated fibrin within, and fibrin encrustation on fibrous plaques, and small fibrin deposits on the intima of apparently normal arteries. These observations have been amply confirmed but, regrettably, the emphasis on cholesterol and lipoproteins was so overwhelming that it was another 40 years before Duguid’s observations had a significant influence on epidemiological or intervention studies of haemostatic factors in coronary heart disease.

Unfortunately, since that paper was written the emphasis on cholesterol and lipoproteins has become even more overwhelming, and research into blood clotting and atherosclerosis has faded to almost nothing. It appears that the vast sums of money to be made from cholesterol lowering has completely distorted research into this area. All the funding, and all the international experts, have charged into the blind-alleyway that is the cholesterol hypothesis.

In a kind of supreme irony, in 1992 Pfizer were also travelling down the blood clotting route. I have (mentioned before) possibly the only remaining copy of a small booklet entitled ‘Pathologic Triggers New Insights into cardiovascular risk.’ And I quote:

‘Several features of mature plaques, such as their multi-layered patterns, suggests that platelet aggregation and thrombus formation are key elements in the progression of atherosclerosis. Platelets are also known to provide a rich source of growth factors, which can stimulate plaque development.

Given the insidious nature of atherosclerosis, it is vital to consider the role of platelets and thrombosis in the process, and the serious events that may be triggered once plaque are already present.’

Of course, this leaflet was promotional, for their product doxazosin. Doxazosin lowers blood pressure and also has effects on urinary retention. However, in this leaflet, they were trying to promote its effects on blood clotting factors. Basically, doxazosin reduces fibrinogen levels and plasminogen activator inhibitor – 1 (PAI-1). Plasminogen is activated by tissue plasminogen activator (tPA) which then becomes plasmin, an enzyme that slices fibrin apart, and breaks down blood clots. PAI-1 stops this happening, so makes clots more difficult to break down.

To quote, again.

‘These recent studies suggest that doxazosin may have a range of significant antithrombotic effects in many patients, in addition to its proven beneficial effects on hypertension and hyperlipidaemia. Following doxazosin treatment, a reduction of platelet aggregation and a tendency towards dissociation, together with a reduction in fibrinogen levels, might prevent excessive degrees of thrombosis at the site of vascular injury. In addition, reduced levels of PAI-1, and increased tPA capacity with doxazosin might stimulate fibrinolysis and early clot dissolution at these sites, and prevent the evolution of an acute coronary event.’

So there, couldn’t have put it better myself.

Then Pfizer bought Warner-Lambert, who made atorvastatin/Lipitor. The focus became Lipitor and lipids, lipids, lipids. Lo it came to pass that Pfizer never mentioned blood clotting ever again, lest it interfere with the LDL story. Pity really, because mighty Pfizer got it right in 1992. Smith got it right in 1993, Duguid got it right in the 1940s, and Rokitansky was right in 1852. Of course, there have been many others who got it right too. Many, sadly, lost to history.

At some point this, the blood clotting hypothesis, the correct hypothesis will win. Maybe that time will be now.

Postscript

I realise some people may still wonder (if they have not read what I have written before) how the blood clot ends up within the artery wall/beneath the endothelium.

The reason is as follows. If the endothelium is damaged, a clot will form, sitting on the inside of the arterial wall. Once the clot has stabilised, and been reduced in size by fibrinolysis, the remainder of the clot will be covered over by Endothelial Progenitor Cells (EPCs) that float around in the bloodstream and are attracted to areas of endothelial damage.

After a layer of EPCs has grown over the clot, and converted themselves into mature endothelial cells the blood clot will now, effectively, be sitting inside the artery wall. Underneath a new layer of endothelium. Thus, clot becomes plaque.

http://circ.ahajournals.org/content /92/5/1355.full

What causes heart disease part IV

I have entitled this little series ‘What causes heart disease?’ But I have been at pains to point out that you cannot possibly establish potential causes heart disease, until you are clear about the underlying process.

By this I mean you can say that smoking causes heart disease – and you would be right. You can also say that Systemic Lupus Erythematosus (SLE) causes heart disease – and you would also be right. You can say that type II diabetes causes heart disease – and you would be, guess what, right. You could say that obstructive sleep apnoea causes heart disease and you would be… right again. Steroids…right again. High levels of fibrinogen…right once more. Cushing’s disease…right. Depression… bang on the button.

But you have to be able to answer the question, how can these very different things lead to the same disease? Or, perhaps you are going to argue they all cause different diseases, that look exactly the same? If so we are doomed, as this would mean that there are a hundred different types of heart disease each with their own individual cause. (I believe this to be unlikely, and am not further discussing it as a possibility).

In short, you cannot simply go around stating that you have identified cause after cause, after cause after cause. Or you can, but it does not help in the slightest with understanding what is going on. It just becomes increasingly confusing. You must establish the process, or processes, that can link all of these potential causes together. Until you can answer this, you are basically just floundering about.

I spent thirty years floundering about in this unending kaleidoscope of risk factors before I decided that it was mission critical to work out what was the actual disease process underpinning CVD. In the end, it came down to this.

The four stage process

Heart disease – or the development of atherosclerotic plaques, followed by the final, fatal, blood clot – consists of four stages. These stages obviously overlap, and interact, and separating them out is a somewhat artificial process. However, I think a degree of separation is necessary for understanding. You can jumble them all around again afterwards.

I should also say that; in this particular blog, I am only going to look at the first stage of the four stage process. And the first stage is endothelial damage.

The endothelium

The endothelium is a single layer of cells that lines all arteries, and veins. At one time endothelial cells were believed to be essentially inert. They just sat there, lining the blood vessels, and not doing much. But, of course, these cells are gigantically, mind-bogglingly, complex.

However, for the sake of this discussion, I am only going to look at three aspects of endothelial cells.

  • Nitric oxide synthesis
  • What happens when endothelial cells are damaged
  • Tissue factor

Nitric oxide synthesis

A critical role of endothelial cells is to manufacture nitric oxide (NO). When it comes to CVD, this little molecule is absolutely key. First, it relaxes the smooth muscle in artery walls, causing them to relax, which opens up the surrounding artery. This then lowers blood pressure.

Within conventional medicine various ‘nitrates’ are given to people with angina, which opens up the coronary arteries, improves blood flow and the oxygen supply improves. The first of these to be discovered was nitro-glycerine. Renamed glyceryl tri-nitrate, and put into tablets to dissolve under the tongue.

NO is also a very powerful anticoagulant – it stops the blood clotting. This is clearly essential as you do not want clots forming on normal blood vessel walls, and when NO levels fall, accidental blood clotting becomes a real possibility.

Healthy endothelial cells produce lots of NO. Stressed and damaged endothelial cells do not. Which means if you have stressed or ‘dysfunctional’ endothelial cells, your arteries are narrower ‘constricted’ and the blood within them more likely to clot.

In recent years it has been recognised that damage to endothelial cells is an early marker of atherosclerosis, as made clear in this paper, entitled: ‘Endothelial dysfunction: the early predictor of atherosclerosis.’

‘Endothelial dysfunction, characterised by reduced NO bioavailability, is now recognised by many as an early, reversible precursor of atherosclerosis.’ 1

Which means that damaged, or dysfunctional, endothelial cells can be recognised by their failure to produce NO. On the flip side, if there is abundant NO in the body this seems, in reverse, to keep endothelial cells healthy.

There are some drugs, supplements, and activities, that can actually increase NO synthesis in endothelial cells, and also the rest of the body. Possibly the most powerful single factor that can do this is sunlight. As highlighted in this paper, where the rather snappy title actually says all that needs to be said: ‘Whole body UVA irradiation lowers systemic blood pressure by release of nitric oxide from intracutaneous photolabile nitric oxide derivates.2

Essentially, if you sunbathe, NO is released throughout the body, and your blood pressure drops (as your arteries open wider). Other studies have found many other major benefits of sun exposure on lung, breast, prostate and colo-rectal cancer, but that is a story for another day.

For now, the focus here is simple. Endothelial cells produce NO, this chemical is vital for CVD health. Any factor that reduces NO synthesis is unhealthy, any factor that increases NO synthesis will protect against CVD.

What happens when endothelial cells are damaged

I am not looking in any great detail here at how endothelial cells are damaged, although there are many, many, things that have a negative impact on the health and wellbeing of endothelial cells. High blood sugar, low blood sugar, steroids, smoking, cocaine, SLE, Obstructive Sleep Apnoea (OSA), and suchlike.

Perhaps the single most important factor that can damage endothelial cells is this – biomechanical stress. By biochemical stress I mean turbulent blood flow, stretching and bending of the blood vessel, high shear stress, high blood pressure, rapid blood flow, points where the blood has to change direction violently.

Violent direction occurs where smaller arteries branch off from larger one e.g. where carotid arteries (that supply blood to be brain) branch from the aorta at the base of the neck. Such points are called bifurcations, and bifurcations are where the biggest and most ‘vulnerable’ atherosclerotic plaques are almost always to be found.

In reality, extreme biomechanical stress only takes place in the larger arteries in the body, where the pressure is high and there are great forces for the endothelium to deal with. A raging white water river. Place a pebble on the side of this maelstrom and it will soon be ripped off and dragged downstream. Veins and the arteries in your lungs, on the other hand, are more like the lazy rivers of East Anglia, slowly meandering along through flat fields.

It is almost certain that the massive difference in the biomechanical stress that endothelial cells have to deal with, in arteries, in comparison to veins and pulmonary blood vessels (the blood vessels in the lungs) fully explains why atherosclerotic plaques never develop in veins and never develop in the pulmonary blood vessels (blood vessels in the lungs). Despite that fact that these blood vessels are exposed to exactly the same ‘risk factors’ as the arteries.

Moving on. It is possible to do more than simply stress endothelial. They can simply be stripped off. If and when this does happen, not only is there no NO at that location, something else far more important comes into play….

Tissue factor

Sitting within all artery walls (and all vein walls too) is a substance called Tissue Factor (TF). It is by far the most powerful clotting agent known to nature. If you expose blood to it, a clot will immediately form, right on top.

This makes sense. If a large blood vessel is damaged, you will bleed to death very rapidly, unless a very strongly constructed blood clot forms right on top of the damaged area, to block the hole. Another point to mention is that TF triggers the ‘extrinsic’ clotting system which simply bypasses a large part of the blood clotting system. Clot right here, right now!

In truth, the system of blood clotting is incredibly complex, and I have not the slightest intention of covering it all here. Probably because I don’t fully understand it myself. However, at its simplest, blood clots consist of two key components. Platelets and fibrin.

Platelets are small ‘sticky’ cells. They are activated by exposure to Tissue Factor (TF), at which point they start clumping together to get the clot started. Whilst doing this they release about five hundred other substances that further activate the entire ‘clotting cascade.’ Then all hell breaks loose.

The end result of all of these clotting factors activating is that small strands of protein called fibrinogen are stuck together for form a long, very strong, string of protein called fibrin. This wraps round platelets, and anything else floating past, and binds everything together in a tight and very strong blood clot.

This clot then sticks very firmly to the site of damage, and grows, until all the damage is covered up. At which point the other five hundred factors that are designed to stop blood clots forming and/or getting too big, stop the clotting process in its tracks.

After the clotting process has been whipped into action, then brought to a halt, we have a blood clot stuck to the inside of the artery wall. Obviously if it grew too big it will have completely blocked the artery – resulting in a heart attack, or suchlike. Assuming, however, that it stopped growing, before completely blocking the artery. What then happens to it?

To be continued.

References:
1: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3721957/
2: http://www.ncbi.nlm.nih.gov/pubmed/19797169

Study 329 – where the hell is the outrage?

To quote from the BMJ ‘No correction, no retraction, no apology, no comment…’

Study 329 was started in 1994 by Smith Kline Beecham, which shortly become part of the larger conglomerate Glaxo Smith Kline (GSK). Study 329 looked at the use of paroxetine, an anti-depressant, in adolescents with depression.

Following this study paroxetine was promoted and marketed heavily by GSK as demonstrating, in the words of GKS marketing materials: ‘REMARKABLE Efficacy and safety’. Over two million prescriptions were then written for children and adolescents in the US.

However, in 2002 the FDA considered study 329 to be a ‘failed trial.’ In 2003 the UK recommended that paroxetine should not be used in children and adolescents with depression because it increased the risk of self-harm and potentially suicidal behaviour.

In 2004 the FDA placed a black box warning on all antidepressants in adolescents and children stating that they increased the risk of suicidal thinking and suicidal behaviour in these groups. In 2012 GSK finally agreed to pay £2Bn for fraudulently promoting paroxetine.

But the story does not end here. A group of researchers, who had been heavily critical of this trial, finally managed to get hold of the raw data and carried out a re-analysis under the restoring invisible and abandoned trials (RIAT) initiative. Yes, this saga has been a long one.

The reanalysis was recently published in the BMJ with sadly predictable results. The primary conclusion was that ‘Neither paroxetine nor high dose imipramine showed efficacy for major depression in adolescents, and there was increase in harms in both groups.’

This is in stark contrast to the original trial results. When it was first published it appeared to demonstrate very clearly that paroxetine was both safe and effective in adolescents with depression. According to GSK it demonstrated ‘.remarkable efficacy and safety’ However, using exactly the same trial data, reanalysed by independent researchers, we now find that paroxetine was both useless and damaging.

So, what has been the consequences for those involved in the initial trial and the writing up thereof? For those who read the BMJ, you will know that I am now quoting verbatim here:

  • Despite subsequent FDA and MHRA warning about increased risks of suicidal thinking and behaviour and GSK receiving a record fine, partly for illegal off-label promotion of the drug, the original report has not been retracted or even had a correction
  • Academic and professional institutions have failed to publically address the many allegations of wrongdoing
  • None of the named authors had intervened to correct the record. An internal enquiry by the Journal of the American Academy of Child and Adolescent Psychiatry (JAACAP) concluded that no further action was necessary
  • Brown University remains silent over its involvement in the study. It refuses even to confirm or deny whether any investigation took place1

I will add to this that a co-author of study 329, Karen Wagner, named eight times in the 2011 US Department of Justice complaint against GSK, is currently the president elect of the American Academy of Child and Adolescent Psychiatry – whose journal, the JAACAP, is where the original study was published.

Taking stock. What do we have? A study was done, and published, demonstrating that paroxetine was safe and effective. The trial data were heavily promoted, resulting in millions of children and adolescents being prescribed paroxetine.

The reality is that this drug was completely ineffective and increased the risk of suicide (amongst other things). This has all been known for many years. The latest re-analysis simply confirms everyone’s worst fears.

So surely someone, somewhere, got punished? No they did not. Not only that, but the original published study has not even been retracted. It still sits in the medical database. A young and innocent researcher could come across it, and reference it, and use data from it to support a grant application for a study to use antidepressants in children.

If this were not all completely and absolutely one hundred per-cent fact, you might think we have a possible plot line for a dystopian novel here. A story of terrible corruption where large corporations can distort data through one hundred and eighty degrees, and get away with a fine. A world where bent researchers promote research that results in more children committing suicide, and then move on positions of greater power and authority – with no censure from anyone. To become presidents of major medical societies, for example.

Frankly I don’t think I would dare to write a novel with a plot so completely outrageous. Surely someone, somewhere, would be punished for this behaviour. Surely the paper would be retracted. Surely a co-author of such a study would not be in line for a prestigious position. Surely the public would rise up in outrage.

In truth, it seems, nothing is going to happen at all. I must dig out 1984 and read it again, just to depress myself even further.

1: BMJ 2015;351:h4629

Medicine – science or religion?

[Never admit that you are wrong]

Medicine has always occupied an often uncomfortable space between science and belief. I remember when I started medical school the Dean of the medical school welcomed us to the main lecture hall. He told us how wonderful it was that we had chosen to become doctors, and waffled on for a bit about how we were the chosen few. He finished his speech with these words, which etched themselves into my brain… ‘Welcome to the brotherhood.’

Of course the parallels between medicine and religion have always been obvious to anyone who has eyes to see. The patient consultation as confessional. The use of long latin words that the patient cannot understand. The rituals and incantations of medicine have clear parallels with religion. Or would that be the other way round. You could go on and on.

It is easy to understand why many aspects of medicine and religion mirror each other. Particularly if we look at one very important aspect of religion. Namely, protection against terrible things happening to you. Humans, once they became aware of their mortality, very rapidly felt the need for protection against an unpredictable and dangerous world. Earthquakes, storms, crop failures, plagues, early death… that type of thing.

Very early on, religious leaders realised the power and status you could command if you claimed to be able to understand why such terrible things happened. And, more importantly, how to stop them. Build a big temple, pray to a god, don’t shave your hair, sacrifice a pig, don’t eat pigs…. give the priests lots of money, and suchlike. The people, in turn, were extremely eager to do these ‘right’ things in order to feel a sense of protection, a removal of fear.

Of course, none of this actually stopped anything. But when terrible things still occurred it was because you (you sinner) didn’t pray in the right way, or someone else (a heretic) was deliberately praying the wrong way and causing bad things to happen. ‘Find the heretic in our midst and burn them.’ Or whatever. A good idea not to have ginger hair or a club foot at such times.

Over time, a million and one reasons were developed by clever priests to explain why, despite all the incantations, gifts, temples built, and sacrifices, bad things were not prevented. However, there was one reason that could never be countenanced. Namely that the priests were completely wrong, and had no idea what they were talking about. For, if the priests were wrong then…well then, terrible things just happened and there was nothing you could do to stop them.

How frightening is that. Thus, it was not just were the priests desperate to keep their power that kept their religion going, the people were equally desperate to believe that the priests knew what they were doing. It could be described as a conspiracy of the willing. ‘I will protect you. Yes, you will protect me.

It was usually only when plagues and earthquakes and lack of rain and suchlike went on for a prolonged period of time that the people rose up against the priesthood and bashed their skulls in. Usually to be replaced by the ‘new model priesthood’, with another bunch of newly discovered incantations. ‘The absolutely new true truth is revealed,’ rpt.

Then, luckily, along came science and we started to learn what caused bad things to happen in the first place. Earthquakes weren’t due to the displeasure of Gods. Infections were caused by viruses and bacteria and suchlike. More and more that used to be unknown, and terrifying, became explained and, at least in some cases, controlled.

As science advanced, and became the best way to explain the physical world medicine, which used to be a branch of the priesthood, moved towards becoming more scientific. However, one of the primary social drivers behind medicine remained ‘this is how the world works, and we can protect you from it’.

Thus, although in many ways, medicine became more scientific, it maintained of the key social functions previously carried out by religion. ‘We can stop bad things happening to you. You do not need to be frightened. If you do as we say’

This form of mutual dependency works extremely well when the medical profession really does know how to stop things happening, and the medical leaders know exactly what they are doing. However, there is a heavy price to be paid for establishing yourself in the position of ‘certainty’. A position of belief requirement.

Primarily, it becomes extremely difficult for you, or the rest of the brotherhood, to admit that you don’t know something? Or that things you have been telling people, or doing, are in fact useless or wrong. Because if you start doing that, you fear you may lose your hard won authority, control and respect. Equally, if patients no longer believe, or trust in you, or your advice, what then? Fear stalks the land. Metaphorical skull crushing looms.

This is why, if you are a patient who feels that your treatment has not worked as you were told it would, or should, you will not find an eager audience for your complaints within the medical profession. Equally if you question or refuse the sacrament, sorry treatment, your doctor is likely to become very angry with you.

Additionally, if a doctor cannot discover what is causing your symptoms, or they have no tests to diagnose you, you are likely to be told that there is nothing actually wrong with you. The medical profession cannot easily admit to ignorance. In such situations, the only explanation that can be countenanced is that ‘you are making it up.’ Unexplained symptoms become ‘somatisation’. Side effects from drugs, such as statins, are due to ‘nocebo’ effects.

A million reasons will be found as to why the treatment has not worked in your case. Or why you got worse. The only explanation that cannot be allowed is that the doctors are completely wrong, and do not know what they are talking about.

If you find a whole group of patients who feel that their condition is not being treated well, and you band together to get the medical profession to think again, you will run up against a brick wall. You will simply be written off as cranks, and dismissed. The priesthood does not take kindly to being exposed as wrong.

See under, treating thyroid patients like children.

Treating Thyroid patients like children

Here is an imagined, but not far off the truth, conversation between a doctor and a patient.

‘Why can’t I have T3 doctor? I feel so much better when I do?’

‘Because I say so, now go away.’

Nowadays doctors, at least when they are in training, are repeatedly told that they must NEVER be paternalistic. To do so will result in immediate censure. In the UK it is also a very rapid way of failing the GP entrance exams. We are told that we must explore the patients’ expectations, listen to their worries and fears, and work with them in partnership to lead to a therapeutic partnership…. or some such left wing bollocks. [Joke]

How exactly that fits within the National Institute of Health and Care Excellence (NICE) guidelines is up for grabs. For those who don’t know, NICE decide on which drugs and interventions can be prescribed, or paid for, within the NHS. So you can explore expectations with your patient till the cows come home, only to find that you cannot prescribe what the patient wants, even requires. Even if it makes them feel much better and costs very little. Would you call this paternalism? Oxford entrance exam, discuss.

Don’t get me wrong, I think rationing is increasingly vital for healthcare provision, and at one point I supported NICE. I now realise how naïve and misguided I was…but that is a discussion for another day.

Where was I? Oh yes, T3. Most people have never heard of it. But I am willing to bet that if you have heard of it, and you are a patient, you will certainly know all about this particular hormone. You will definitely know about a thousand times as much as your GP, who may nod sagely when you mention T3. But frankly they are unlikely to have any idea what it is, or does.

To be honest, until about a year ago I had no real idea what T3 was either, but I have learned quite a lot since. Wikipedia states that: ‘The thyroid hormones, triiodothyronine (T3) and its prohormone, thyroxine (T4), are tyrosine-based hormones produced by the thyroid gland that are primarily responsible for regulation of metabolism.’ I would like to draw your attention to the fact that, in Wikipedia, at least, T3 is mentioned before T4 – which makes it more important?

In reality, in a physiological sense at least, T4 comes before T3, in that T4 is produced almost exclusively by the thyroid gland in a ratio of about 17:1 T4 to T3. Once inside various tissues and organs T4 is then converted to T3, where it becomes the biologically active hormone.

Whichever does come first, it can be argued that T3 that is the key thyroid hormone, because T4 is basically a ‘prohormone.’ From Wikipedia again: ‘A prohormone refers to a committed precursor of a hormone, usually having minimal hormonal effect by itself. The term has been used in medical science since the middle of the 20th century. Though not hormones themselves, prohormones amplify the effects of existing hormones.’ Although the figures are not absolutely clear cut, it is usually stated that T3 is five times more biologically active than T4.

Therefore, if someone is hypothyroid, which is normally taken to mean that the thyroid gland is not producing a sufficient quantity of thyroid hormone, you would want to prescribe the active hormone T3, would you not?

This is a rather rhetorical question because what doctors do, at least since the 1960s, is to prescribe synthetic T4 (levothyroxine). Once T4 is in the body it is converted to T3 (through the kidneys, liver, spleen and brain – and numerous other thyroid hormone receptors throughout the body) and does its thing. In most cases this is a perfectly good treatment. However, there is a kicker, which I will get to.

At this point I feel I need to add that hypothyroidism is a very, very common condition. By the age of 60, 10% of people have ‘lab’ test abnormalities that would define them as having subclinical hypothyroidism. At least 2% of the population has overt, clinical, symptoms. Which means that we are talking about millions of people in the UK, possibly tens of millions in the EU and US.[It affects women ten times as much as men].

TSH

I now need to bring in another player called Thyroid Stimulating Hormone (TSH). As with all systems in the human body, a negative feedback loop controls the function of the thyroid gland, and it works something like this:

If you have a high T4 level, this is detected by the pituitary gland, which sits deep within your brain. At which point the pituitary gland reduces the production of Thyroid Stimulating Hormone. As TSH is the hormone that instructs the thyroid gland to produce T4/T3, production of T4/T3 falls. [There are actually a couple of other steps, but this is essentially what happens].

If T4 falls too far, the pituitary gland swings into action to produce more TSH. In turn stimulating the thyroid gland to manufacture more T4…and so it goes. Up and down, up and down, up and down. Endlessly until, of course, you get too old and drop dead. And there ain’t no feedback loop for that.

TSH is also important in that it is usually the substance you measure to decide whether or not someone is hypothyroid. If TSH is very high this means it is trying to ‘drive’ the thyroid gland into action – and failing. You also use the TSH level to determine the dose of T4 that is required as replacement therapy. If the level of TSH is low, this suggests you may be giving too much T4. If the level of TSH is high, this suggests you may be giving too little.

As you may have noticed, at this point I have slipped into talking about TSH and T4, with T3 getting very little mention. That is because this is where the medical profession now stands. Hypothyroidism means high TSH and low T4. You are getting adequate thyroid replacement hormone if TSH in the ‘normal’ range. End of.

Here is what the Royal College of Physicians (RCP) and the British Thyroid Association (BTA) have to say on the matter. Key points only

  • The only validated method of testing thyroid function is on blood, which must include serum TSH and a measure of free thyroxine (T4).
  • Overwhelming evidence supports the use of Thyroxine (T4) alone in the treatment of hypothyroidism. Thyroxine is usually prescribed as levothyroxine. We do not recommend the prescribing of additional Tri-iodothyronine (T3) in any presently available formulation, including Armour thyroid, as it is inconsistent with normal physiology, has not been scientifically proven to be of any benefit to patients, and may be harmful. [Then again, it may not be – harmful, that is]

An aside – (Additional information, as provided to me)

I should mention here that I have been told that the RCP has been asked on numerous occasions to cite references to research/studies showing “overwhelming evidence supports the use of thyroxine (T4 alone)”, but to date, they have provided none. A Freedom of Information (FOI) request that the RCP provide such evidence – again met with no response. A request was made via the ‘Ask for Evidence’ website, run in association with ‘Sense About Science’ asking for evidence on the safety and efficacy of L-T4 as a treatment for hypothyroidism. This request was directed to the RCP who eventually responded stating “The RCP’s guidance is based on the opinion of an expert panel which was temporarily formed for this purpose. The evidence they used to form their individual opinions has not been collated and therefore the RCP cannot provide any evidence list”1 (Jolly, as they say, good)

Restricting the diagnosis and treatment of hypothyroidism to measuring T4 and TSH, and nothing else, is the approach that seems to be used by conventional medicine in the rest of the World. I recently received an e-mail from someone in Singapore telling me that their doctor was about to be struck off for prescribing T3 to patients- against Singaporean medical rules. In the UK, T3 testing is virtually banned, and the medical authorities are making it virtually impossible to prescribe T3 in any form.

In the UK, a doctor called Gordon Skinner was repeatedly dragged in front of the General Medical Council (GMC) for prescribing thyroxine to patients whose T4 and TSH levels were in the ‘normal range’. He was also attacked for prescribing natural thyroid extract (NDT) (a combination of T4 and T3) to his patients – who he felt would benefit. He is now dead. It has been suggested that constant and repeated efforts to strike him off the medical register may have had an impact on his health. I couldn’t possibly say.

Now, there is no doubt that this area is highly complex and for those who know this area, you will be aware that I am keeping things as simple as possible. But I think it is important to make a few points:

The lab tests, especially for TSH, are far from 100% reliable, to say the very least. In fact the man who developed the test in the UK, at Amersham International in Wales, has told me that the test is virtually worthless in many cases (especially continuous testing when patients are taking thyroid hormone replacement).

The conversion of T4 into T3 can be significantly reduced in some people. So these individuals can have normal T4 and TSH, but they are still effectively hypothyroid. For those who are interested in a bit more detail, there is a population with a defective DIO2 gene. This blocks T4 to T3 conversion, and results (amongst other things) in reduced T3 levels in the brain, which can lead to mood disorders2. I mention this single example to make it clear that there is solid scientific evidence to back up the conjecture that it is possible to be functionally ‘hypothyroid’ with normal blood tests.

A lot of people have reported significant improvements in their health through taking thyroxine, with normal blood tests, and also natural thyroid extract when their laboratory tests were ‘normal’. Please look at this article in the Daily Telegraph3…then look at the comments section – which is very, very telling. A cry of despair!

I am not going into further detail of how T4 binding and conversion in various organs can be affected by stress hormones, inflammation, trauma, adrenal insufficiency, lack of converting enzymes in tissues, and infection of various sorts. I shall just keep this simple by stating that it is possible to have enough T4, even T3 in your bloodstream, but these hormones have reduced ‘bioavailability’. This is not crank ‘woowoo’ stuff. This is real and measurable and you can find studies on this in peer-reviewed medical journals.

Far more telling, from my point of view, is the fact that hundreds, indeed thousands of patients report that, although their blood tests were normal, they felt terrible, and that they have felt so much better when they have been given ‘excess’ T4 and/T3, or NDT (natural desiccated thyroid). Whilst there is no doubt that some of them are, to quote a medical colleague, ‘not tightly wrapped.’ I have spoken to many, many, people who are calm, rational and reasonable, and their stories are compelling. A hellish existence that was ‘cured’ by Dr Skinner and his like. I refuse to believe that all of these patients are ‘somatising’ fruitcakes.

Comparing the use of SSRIs and ‘Unconventional’ Treatments for Hypothyroidism

At this point I will change tack slightly. For I think it is fascinating to compare and contrast the treatment of depression using SSRIs, with hypothyroid patients who complain that they are unwell, despite ‘normal’ T4 and TSH tests.

Today, almost all doctors you speak to believe that depression is due to a low level of serotonin in the brain. This is why they prescribe SSRIs (Selective Serotonin Reuptake Inhibitors) by the lorry-load. Drugs such as Prozac, Zoloft, Paxil etc.To quote from a recent article in the BMJ ‘Serotonin and depression, the marketing of a myth’4.

‘…the number of antidepressant prescriptions a year is slightly more than the number of people in the Western World.’

This all happens despite the fact that:
‘There was no correlation between serotonin reuptake inhibiting potency and antidepressant efficacy. No one knew if SSRIs raised or lowered; they still don’t know. There was no evidence that treatment corrected anything.’

In short, with depression, there is no lab test, no way of measuring the impact of anti-depressants. They are prescribed purely and simply on the basis of the patient history. Equally, there is no doubt at all that SSRIs have significant side-effects, some of which are very, very serious e.g. increased suicidal tendency. They are also addictive and patients can end up stuck on them for years. So, they do cause harm.

Equally, as you may be aware, clinical trial data in this area have been horribly distorted….

“…That said, the fact that the class of antidepressants known as the selective serotonin reuptake inhibitors (SSRIs), are basically useless in treating depression in children and adults is not news to the FDA. Back on September 23, 2004, during testimony at a hearing before the House Oversight and Investigations Committee on Energy and Commerce, Dr Robert Temple, the FDA’s Director of the Office of Medical Policy, discussed the agency’s review on the efficacy of SSRIs with the children.”

He noted that it was important in a risk-benefit equation to understand the benefit side. “Of the seven products studied in pediatric MDD (Prozac, Zoloft, Paxil, Celexa, Effexor, Serzone and Remeron),” he testified, “FDA’s reviews of the effectiveness data resulted in only one approval (Prozac) for pediatric MDD.”

“Overall,” Dr Temple said, “the efficacy results from 15 studies in pediatric MDD do not support the effectiveness of these drugs in pediatric populations.”

Also in 2004, a study of previously hidden unpublished data as well as published studies on five SSRIs, was conducted by Tim Kendall, deputy director of the Royal College of Psychiatrists’ Research Unit in London, to help analyze research to draw up the clinical guidelines for British regulators, and published in the Lancet.

Following his evaluation, Mr Kendall stated: “This data confirms what we found in adults with mild to moderate depression: SSRIs are no better than placebo, and there is no point in using something that increases the risk of suicide.”

In 2005, the British Medical Journal published another study that concluded that SSRIs are no more effective than a placebo and do not reduce depression.

In December 2006, at the most recent FDA advisory committee meeting held to review studies on SSRI use with adults, SSRI expert, Dr David Healy, author of, “The Antidepressant Era,” told the panel that the efficacy of SSRIs has been greatly exaggerated, while the actual studies reveal that only one in ten patients responds specifically to an SSRI rather than a nonspecific factor or placebo.

In February 2008, Irving Kirsch’s study at the Department of Psychology at the University of Hull is the first to examine both published and unpublished evidence of the effectiveness of selective serotonin reuptake inhibitors (SSRIs), which account for 16 million NHS prescriptions a year. The largest study of its kind concluded that antidepressant drugs do not work. More than £291 million was spent on antidepressants in 2006, including nearly £120 million on SSRIs. 4

Critics complain that industry funded studies are presented in ways to exaggerate benefits and obscure side effects. “These include failure to publish negative results, the use of multiple outcome measures, and selective presentation of ones that are positive, multiple publication of positive study results, and the exclusion of subjects from the analysis,” according to the paper, “Is Psychiatry For Sale,” by Joanna Moncrieff, in People’s Voice.”5

So we have an interesting medical conundrum, do we not? On one hand, doctors are more than eager to prescribe antidepressants at the drop of a hat, based entirely on the patients reported symptoms. No need for any blood tests, and no evidence that they work for the vast majority of people.

On the other hand, if a patient dares to say that they feel better taking T4 when their blood tests are normal, or if they say they feel better taking a combination of T3 and T4/NDT, they are dismissed as ‘somatising.’ Which is a posh medical way of saying, you are making your symptoms up and we don’t believe you. Equally, if a patient complains of continuing symptoms and that they don’t feel better when they are taking T4 (or T3 and T4) and their blood test results show ‘normal’ they are again accused of ‘somatising’6

The world, my friends, has gone nuts and, in a bitter irony, the medical profession – at least in this area – has become institutionally paternalistic. ‘You cannot be feeling better, because your blood tests say you were never unwell. So you cannot have treatment. And you, Dr Skinner and your like. If you dare treat patient’ symptoms you will be attacked and struck off from medical practice.’ Now I have looked long and hard, and I have found no evidence, from anywhere, that giving T3, in the dose that’s needed, causes any significant medical problems, and I have listened to repeated testimony from people who feel they have greatly improved.

As for antidepressants, these mostly useless addictive drugs that can increase suicide risk. ‘Have as many as you like for as long as you like. Because we fully believe everything you say about your symptoms….’ No need for any silly tests, or anything like that.

Compare and contrast, then try to make some sense of the medical world that we now live in.

Sigh.

P.S. Because I am considered to have alternative views about medical matters, many people contact me to help promote their ‘alternative’ ideas. Some I believe to be completely whacko, I smile sweetly and move on. Some I cannot decide. Other issues, once I start looking into the evidence, I find the evidence compelling.

I certainly find the evidence that a large number of people are effectively hypothyroid, with ‘normal’ thyroid blood tests, to be virtually overwhelming. Both from a scientific/physiology basis, and also from a patient testimonial basis.

I now firmly believe that the medical profession is currently doing these people a great disservice, and that the guidelines on the treatment of ‘hypothyroidism’ are rigid, autocratic, and just plain wrong (for a significant minority).

As with all medical matters that I write about, I have no axe to grind, no horse in the race, no financial links to anyone or anything with regard to treating thyroid patients. I simply hope this article can have some positive impact. For it seems very clear to me that many thousands, hundreds of thousands, of people are suffering unnecessarily. And I would like it to stop.

References:

  1. http://www.scottish.parliament.uk/S4_PublicPetitionsCommittee/General%20Documents/PE1463_AAA_Petitioner_19.11.14.pdf
  2. “Common Variation in the DIO2 Gene Predicts Baseline Psychological Well-Being and Response to Combination Thyroxine Plus Triiodothyronine Therapy in Hypothyroid Patients”http://press.endocrine.org/doi/pdf/10.1210/jc.2008-1301
  3. http://www.telegraph.co.uk/news/health/alternative-medicine/10985192/Could-a-renegade-doctor-save-your-life.html
  4. Serotonin and Depression, the marketing of a myth.’ BMJ2015;350:h1771
  5. Kirsch I, Deacon BJ, Huedo-Medina TB, Scoboria A, Moore TJ, et al. “Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration.” 2008, PLoS Med 5(2): e45 doi:10.1371/journal.pmed.0050045: Access full article at http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0050045
  6. http://www.lawyersandsettlements.com/articles/ssri_birth_defects/ssri-secret-00642.html#.VT-ycCG6eUk
  7. Professor A Weetman – http://www.medscape.com/viewarticle/524955

 

Further postscript

Malcolm – we need to clear up the fact regarding the definition of ‘hypothyroidism’ which is “underactivity of the thyroid gland” according to the RCP Policy Statement on the diagnosis and management of hypothyroidism. Hypothyroidism is easily diagnosed and more often than not, easily treated with L-thyroxine only. However, what is being missed by everybody is that over 300,000 UK citizens (15% of the thyroid community – millions worldwide) have a normally functioning thyroid GLAND, but the hormone it is secreting is not getting into the cells where it does its work. These are the folk who need T3, in combo. with T4, T3 alone or in NDT. The RCP teaching curriculum makes no mention of the possibility of a non-thyroidal condition where patients suffer the same symptoms and signs of hypothyroidism that may need to be treated with a different medication or hormone. When these patients complain of continuing symptoms when treated with L-T4 monotherapy, many are given an incorrect diagnosis of ME, CFS, FM, depression, functional somatoform disorder – or even old age blah, blah, blah – and sent on their way without further investigation or treatment. This is a serious business, which the RCP and BTA choose to ignore.

Doctoring Data

I am pleased to announce that my book is finally written and edited and available to buy, on-line at http://doctoringdata.co.uk

The full, formal launch will not be until next year. But for those who cannot wait (hopefully several hundred million people), you can pre-order it now on a restricted print run. First come, first served as they say.

It has been a mighty effort to write, and I hope that people can both enjoy reading it, and feel that they have learned something by so doing. I am but your humble servant.

My father

My father died recently, so I have been rather busy with other things. I wrote a short eulogy to him and I thought I would share it, and my memories of him, on my blog. I am not certain that this is the ‘done’ thing, but I am doing it anyway. I sort of feel the need to share it with those who are kind enough to read my blog.

My father was not a man who suffered fools gladly. In fact his favourite expression was BF, as in, bloody fool. We were all, at times, BFs. I am sure I was referred to as a BF on more occasions than I ever knew. Politicians were most certainly all BFs.

But beneath the façade of referring to everyone and most of their actions as those of a BF was a man who would, after he had finished his obligatory two minute rant, then do all that he possibly could to help someone out.

Crashed your car….you BF….then he would fix it. Needing help… he would invite foreign students into his house for the night. At heart he was, basically, a big softie. A velvet fist in a steel glove. He would forgive anyone anything – in the end.

I remember he used to sing a little song at times. At the time I never knew where it came from. Some of you may recognise it. It is incredibly rude, and incredibly sad. This is the chorus – which is the only bit I heard him sing.

It’s the same the whole world over,

It’s the poor that get the blame,

It’s the rich that get the pleasure,

Ain’t it all a bloody shame

This never seemed, to me, to be a favourite song of a man who did not care deeply about the world, and who would like to see it become a better place.

Yes he could be irascible – we all know that. Yes, he could be difficult and argumentative… and we all most certainly all know that. Yes, he too, he was a fully functioning BF at times, with bells and whistles, and there were most certainly moments when he drove me – and everyone else – completely mad. But my thoughts and memories now are almost entirely positive. As I think are those of everyone else gathered here.

As we know he did many, many things. A man of great energy and boundless enthusiasm for life. Whilst I was thinking about writing this short eulogy I remember a quote about Winston Churchill that I think best sums up my father.

When you first meet him, you see all his faults. It takes a lifetime to appreciate his virtues.

Silence was the stern reply

I thought I should share with you, a letter written to Professor Sir Rory Collins by a reader of my blog. Mr David Bailey. Of course I have ensured that I have his permission to re-print this here.

He sent the letter to me some time after he wrote to Professor Sir Rory Collins. I told I thought it was very well written and interesting. But then, as a confirmed statin/cholesterol geek, I think everything about statins is interesting [More meds please nurse].

Anyway, David Bailey wrote the letter, with the following cover note to me:

Malcolm,

I followed your GOOGLE link in your latest blog, and of course I found Sir Rory’s email address! I sent him the following letter, but I didn’t explicitly CC you, because I thought he might be less likely to take me seriously!

I hope perhaps a few of your other readers will do the same, but I don’t intend to suggest this on your blog – I don’t want this to seem organised.

All the best,

———————————————————

I replied

David

Excellent letter.

The reply will be, as follows

Dear Mr Bailey,

Thank you for you letter. Professor Sir Rory Collins is unable to respond to personal issues of this type. Message ends….

Still a good letter though. Could I put it on my blog in a couple of weeks, once you fail to gain any response at all?

Malcolm

———————————————————

That is the background, here is the letter. It is typical of many hundreds that I receive from people suffering severe and significant statin related adverse effects. In virtually every case their doctor has dismissed the adverse effects as even existing.

When, rarely, their doctor has accepted they are having adverse effects they have NEVER, according to those who write to me, made any attempt to inform the authorities that their patient has suffered a statin related adverse effect. Medwatch in the US, the Yellow Card system in the UK…

Dear Sir Rory,

I am not a medical doctor, though I have a PhD in chemistry, but I am writing to tell you of my experiences taking Simvastatin.

As I understand it, you are of the opinion that statin side effects are rare, and not important when weighed against the chance to avoid cardiovascular events.

I took Simvastatin for 3 years, and for most of that time I suffered no obvious side effects. I felt extremely positive towards this drug, because although I have not had a stroke or heart attack, anything that reduced the risk seemed like a good idea.

The side effects started rather suddenly – with extreme cramps in my right leg, which was weakened by polio when I was a child. I naturally thought I was getting Post Polio Syndrome (PPS) – a problem that I understand has no specific test. Because there was some delay before I could see a specialist, and I was struggling as my symptoms got worse, I decided to stop my Simvastatin as a precaution because I remembered that it could cause ‘muscle pains’. By that time my leg was extremely painful in the muscles and the knee joint, and it had weakened further so that my right foot would drop as I walked – potentially causing me to trip on it.

By the time I saw a polio specialist, I was not diagnosed with PPS because the symptoms were receding – I got no specific diagnosis. As I continued to improve, I decided to restart my Simvastatin, assuming that it had had nothing to do with my problems, and within a week I could feel the symptoms returning.

All in all, I stopped Simvastatin 3 times, and each time the symptoms started to reduce after a delay of about a week, and returned after I restarted the drug!

Had I not realised that Simvastatin might be causing my problems; I think I might have ended up confined to a wheelchair in considerable pain, still taking the drug! As it was, once I gave up on Simvastatin, I recovered completely over a period of about 9 months.

Of course, my situation was a bit special, but I discovered from informal discussions with others in their late 50’s and 60’s that maybe half had had problems with statins, or knew someone else who had! Some had simply discarded their tablets without discussing it with their GP, others had been given prescriptions for a succession of different statins, and had trouble with all!  One man had suffered muscle cramps and severe memory problems – both reversed after he stopped taking statins.  These were personal contacts, but of course, the internet is overflowing with stories of statin side-effects. I realise that the internet may encourage such stories, but when I combine them with my own experience and those of others I know, I am very concerned that you are so ready to endorse an even wider use of statins in people who are currently well.

I would particularly like to draw your attention to the following aspects of my case:

1)           My side effects took 3 years to manifest themselves – making it less obvious what was happening.

2)          Only my polio leg was affected, which suggests that statin side effects may start in a part of the body already damaged in some other way. This must give particular concern because it suggests that there are people out these suffering statin side effects and still taking the drug!

3)          Because I was very positive about the value of Simvastatin, it is hard to attribute what happened to me as a nocebo effect. Furthermore, the fact that I tried stopping the drug several times and observed the symptoms recede each time, means that I can be essentially certain that my troubles were indeed caused by Simvastatin!

After this experience, I have read around the entire subject of statins, cholesterol levels, and saturated fats. What I read disturbs me greatly.

1)            The evidence against saturated fats is weak except for one graph by Ancel Keys, who cherry picked his data to ‘prove’ the result he wanted!

2)           Cholesterol in the blood (or LDL/HDL) seems far less well correlated with heart attacks than I would have expected.

3)           Even though statins also block the synthesis of Co-Enzyme Q10, doctors do not seem to be warned to combine statin treatment with this supplement.

4)           Many medical researchers are concerned by the consequences of taking statins – some even suggest that statin induced muscle damage may be responsible for a rise in the incidence of heart failure in recent years!

We live in an age of openness, and I really think it would help if you debated your views with medical critics – verbally or in written form. Simply repeating that statins are safe and good for you (I paraphrase slightly) doesn’t seem to be sufficient.

Sincerely yours,

David Bailey

‘You are killing my patients’ – again

[Bring it on]

A few months ago I was part of a group that wrote a letter to the National Institute of Health and Care Excellence (NICE) criticising their proposed guidance on the use of statins in primary prevention. I drafted the letter and it was signed by such people as the President of the Royal College of Physicians, past president of the Royal College of Physicians etc. This was not, in short, a group of fringe lunatics.

It caused a bit of a stir, and generated a considerable amount of air time. After receiving the letter, NICE reviewed their guidance and decided that they had been perfectly correct to promote the use of statins in primary prevention in the UK after all. NICE, in effect, judged NICE, and found itself not guilty of anything. Well, that’s one of the benefits of being judge, jury and executioner all wrapped up together in one body.

This letter, and the dismissal of all its points, followed a nasty outbreak of hostilities in which Professor Abramson and Dr Malhotra had been attacked by Rory Collins for publishing separate, but related, papers in the BMJ. These papers suggested that adverse effects from statins were quite common. Professor Rory Collins demanded retraction of the articles and also attacked the editor of the BMJ very publically. Generating articles such as this one:

‘Professor Sir Rory Collins, from Oxford University, said he believes GPs and the public are being made unjustifiably suspicious of the drug, creating a situation that has echoes of the MMR vaccine controversy.

The academic, one of the country’s leading experts on the drug, is particularly unhappy with the British Medical Journal (BMJ), which has run well-publicised articles by two critics of statins that he argues are flawed and misleading.

“It is a serious disservice to British and international medicine,” he said, claiming that it was probably killing more people than had been harmed as a result of the paper on the MMR vaccine by Andrew Wakefield. “I would think the papers on statins are far worse in terms of the harm they have done.”’ 1

Stung by this attack, the BMJ brought together an independent panel in response to Rory Collins criticism. The result, as reported by Forbes, was as follows:

“As previously reported, Rory Collins, a prominent researcher and head of the Cholesterol Treatment Trialists’ (CTT) Collaboration, had demanded that The BMJ retract two articles that were highly critical of statins. Although The BMJ issued a correction for both papers for inaccurately citing an earlier publication and therefore overstating the incidence of adverse effects of statins, this response did not satisfy Collins. He repeatedly demanded that the journal issue a full retraction of the articles, prompting The BMJ’s editor-in-chief, Fiona Godlee, to convene an outside panel of experts to review the problem.

The report of the independent statins review panel exonerates The BMJ from wrong doing and said the controversial articles should not be retracted:

“The panel were unanimous in their decision that the two papers do not meet any of the criteria for retraction. The error did not compromise the principal arguments being made in either of the papers. These arguments involve interpretations of available evidence and were deemed to be within the range of reasonable opinion among those who are debating the appropriate use of statins.”

In fact, the panel was critical of Collins for refusing to submit a published response to the articles:

“The panel noted with concern that despite the Editor’s repeated requests that Rory Collins should put his criticisms in writing as a rapid response, a letter to the editor or as a stand-alone article, all his submissions were clearly marked ‘Not for Publication’. The panel considered this unlikely to promote open scientific dialogue in the tradition of the BMJ.””2

In short, Professor Sir Rory Collins was told that he was utterly wrong to demand retraction of the papers, and that by refusing to take part in an open discussion was trying to strangle scientific debate.

That, if you like sets the scene. A scene whereby anyone who dares to criticise statins, even a prestigious journal such as the BMJ itself, is subjected to vitriolic attacks and a demand for silence. Rory Collins tried to keep all correspondence with Fiona Godlee secret, which kind of backfired on him. Hoorah. Type ‘Rory Collins and Fiona Godlee e-mails’ into Google, and you can see for yourself.

Of course, things have not stopped here. The ‘statinators’ although briefly thwarted in their initial attack on Abramson, Malhotra and the BMJ – and less directly me – have switched track. The British Cardiovascular Society (which you will not have heard of), have decided to run a survey of their members. They are trying to gather information about the damaging impact of the articles, and the letter to NICE:

Here is an e-mail which was sent to all members:

The British Cardiovascular Society is keen to know of any potential adverse effect on cardiovascular disease prevention which may have resulted from recent media stories and articles such as those published in the BMJ (1,2) and in an open letter to NICE (3). 
We would be grateful if members would complete this short survey. Your response will be anonymous and the link below is unique to you allowing you to complete the survey once only. 
The survey closes on 30th September and results will be made available subsequently on the BCS Website and in the BCS newswire.

References

(1) Abramson JD, Rosenberg HG, Jewell N, Wright JM. Should people at low risk of cardiovascular disease take a statin? BMJ 2013; DOI:10.1136/bmj.f6123.
(2) Malhotra A. Saturated fat is not the major issue. BMJ 2013; DOI:10.1136/bmj.f6340
(3) http://www.nice.org.uk/News/Press-and-Media/nice-responds-to-criticisms-of-its-draft-guidance-on-statins
PLEASE CLICK HERE TO COMPLETE THE SURVEY 

Now, why would they be doing this? I do not think it is that difficult to work it out. The BCS is trying to gather evidence that the articles by Abramson, Malhotra and the open letter to NICE have caused harm to patients. They will be asking their members if they know of people who have stopped taking statins, or who will not go on statins, because of what they have read in the BMJ and suchlike.

Once they have done this, they will then extrapolate the raw figures to the entire population of the UK, in order to claim that ‘Thousands have died.’ Abramson will be attacked, along with Malhotra and the BMJ. I will get a few attacks as well for drafting the letter to NICE. This is a very unsubtle variation of the ‘You’re killing my patients’ tactic which is regularly used to silence any who dares criticise currently medical opinion.

At this point you may be wondering what the British Cardiovascular Society (BCS) may be, and could it possibly have any conflicts of interest with the pharmaceutical industry? Well, of course it does. The BCS is heavily reliant on the industry for its very existence. I would say totally reliant, but such bodies do not reveal detailed financial information.

However, you can start looking at what they charge for sponsorship at their conference, and begin to multiply. For example, if you want an exhibition stand at said conference, here is what you pay for an Option 1 stand3.

Option 1 – £33,500 + VAT
To include:

  • Stand – 8mx8m (64msq) island site
  • Full Page Colour advert in Heart Journal
  • Table (10 guests) at BCS Annual Dinner (Tuesday 3 June)
  • 4 x Conference Badges (company name only so transferable)
  • 20 x Stand/Exhibition Badges
  • 50 word entry in the Conference Programme and on the website
  • Opportunity to purchase additional adverts in Heart Journal

with up to a 50% discount of card rate

The BCS helpfully explains the benefits of exhibiting:

Why Exhibit?

The BCS Annual Conference is the most highly attended and respected cardiovascular event in the UK. The Exhibition is a crucial component to the success of BCS event, enabling cardiologists, physicians, scientists, physiologists and nurses to keep up to date with innovative and developing technologies, pharmacology, diagnostic equipment, educational materials and more.

Access over 2,300 cardiovascular healthcare professionals face to face – including top cardiologists, physicians, scientists, physiologists and nurses

Promote and demonstrate products and services directly to key cardiovascular healthcare professionals and gain first-hand feedback

Associate your brand/company with the Society for Cardiovascular Care – the British Cardiovascular Society

Introduce new products/services and test the market

Opportunity to network with industry peers

Of course there are other sponsorship opportunities, such as Advertising in the BCS Conference Programme, which will set you back another £10K:

Advertising in BCS Conference Programme

A copy of the Conference Programme is given to each delegate upon arrival to the event. This is the perfect opportunity to reinforce your presence and support of the BCS Annual Conference 2014.

Inside Front Cover: £2,000 + vat (exclusive)

Inside Back Cover: £2,000 + vat (exclusive)

Outside Back Cover: £2,000 + vat (exclusive)

Double Page: £2,000 + vat

Single Page: £1,200 + vat

There are limited opportunities available

I could go on, but I think you get the general drift. The BCS are funded and supported by the pharmaceutical industry. An industry that is not, currently, that bothered about statins – as the patents have run out. But it is an industry that remains extremely interested in the whole idea of lowering cholesterol. Which remains THE multi-multi-billion dollar market.

Any attack on statins threatens the foundations of this market, one that has been painstakingly constructed over the last thirty years. Keeping the cholesterol lowering idea alive, vibrant, and expanding, will make it far simpler to sell the next generation of cholesterol lowering agents that are currently lurking in the wings, engines purring.

To cut a long story short, the forthcoming attack by the BCS can be considered, to all intents and purposes, an attack by the pharmaceutical industry on anyone who dares to suggest that drugs lowering cholesterol may not be such a brilliant idea. So when you see the headlines in the newspapers damning and rubbishing Aseem Malhotra, John Abramson, and me (and a few others), you now know exactly where this attack originated, and why. Knowledge is, as they say, power.

References:

1: http://www.theguardian.com/society/2014/mar/21/-sp-doctors-fears-over-statins-may-cost-lives-says-top-medical-researcher

2: http://www.forbes.com/sites/larryhusten/2014/08/02/no-retraction-for-you-review-panel-exonerates-medical-journal-in-statin-kerfuffle/

3: http://www.bcs.com/pages/exhibition_09.asp?PageID=497&NavCatID=86