Under-reporting or over-reporting?
I am going to start part two by looking at the evidence for statins causing ‘non-imagined’ adverse effects. Or, to put it another way, real effects. My own view on this is that the adverse effects of statins are significantly under-reported. Mainly because patients often don’t associate the drug with the problem. Such as muscle pain or weakness. This is especially true if it takes weeks or months for problems to develop. In some cases, even years.
Even if patients do report symptoms, doctors do not record many, if any, of the adverse effects. Which is true of all drugs, not just statins. The US does have an adverse drug reaction reporting system. But less than 1% of adverse reactions are captured by it 1:
As the article confirms: ‘Underreporting significantly delays the dissemination of critical information about such reactions.’ You don’t say.
In the UK, we have a yellow card system, specifically designed to make it a complete pain to report any problems. If you do fill in a yellow card, you find yourself bombarded with requests for masses of additional information. Past medical history, drug history, days and dates of starting the medication, exact adverse effect, lab tests etc. etc. This can all take many, many, unpaid, hours to gather. Which means that doctors rarely bother to use the system, and patients have never even heard of it.
The issues of adverse effect reporting has many other complexities. A few years ago, an interesting study caught my eye. It was not large, but telling. I have not seen the same research done, before or since. I may have missed it. It can be tricky to keep up with all the research done. Seventy-five patients were taking blood pressure lowering tablets – anti-hypertensives. They were asked the following questions:
- Did their quality of life improve on medication?
- Did it stay the same?
- Did it get worse?
Two other groups, the patient’s doctor, and the patient’s closest relative/partner were asked the same questions … about the person taking the tablets.
A little background. High blood pressure causes no symptoms. Because of this, hypertension is often referred to as the ‘silent killer’. Anti-hypertensives, on the other hand, are well known for causing a number of unpleasant effects. Therefore, you would probably expect that taking anti-hypertensives would have a negative effect on quality of life. Or, at best, it would remain about the same. Here is how the three groups answered.
Doctors: Quality of life improved: 100% agreed
Patients: Quality of life improved: 50% agreed
Patient’s relatives: Quality of life improved: 0% agreed
Possibly most telling is that seventy-four out of seventy-five of the patient’s relatives reported that the quality of life worsened 2. What can we learn from this? Well, I might start by giving the doctors involved a good slap. I wouldn’t learn anything, but it might be a good lesson in humility for them. ‘Stop seeing what you want to see, and start seeing what is.’
The point here is that if there is a significant bias in the reporting of adverse effects, the bias is heavily weighted towards not reporting them. Not by patients, and certainly not by the doctors – remember that 1% figure. Which means that nothing is recorded for posterity. See no evil, hear no evil, speak no evil.
Another issue in play here, specifically, is that the authors of the Lancet paper do not appear to have heard of the placebo effect:
The placebo effect is a phenomenon where a person’s physical or mental health improves after receiving an inert, “dummy” treatment (like a sugar pill or saline injection). Triggered by the belief in, and expectation of, improvement, the brain induces real, measurable physiological changes—such as releasing endorphins or dopamine—that reduce symptoms like pain, fatigue, and anxiety.
One of the main reasons why we have such massive, complex, double-blind placebo-controlled trials is precisely because of the placebo effect. The drug could initially appear brilliant, but it may be achieving nothing; it may be that the ‘placebo effect’ is doing the heavy lifting.
Because of this significant ‘confounding factor’ clinical trials need to be ‘controlled’ by giving everyone a pill, or an injection. A percentage get the active drug, the rest get the dummy placebo. It is a major reason why clinical trials are so huge, complex, and costly.
However, the impact of taking an unknown ‘placebo’ is far less than being handed a real tablet by a doctor. Who will likely inform you, with great enthusiasm, that it is going to do you good 3. Especially if they add, as they do with statins. ‘And it will stop you dying from heart disease.’ Or words to that effect. [And if you dare stop taking it, you will die].
Strangely, it appears to have escaped the attention of the CTT in Oxford that there is such a thing as the placebo effect. For them, the only bias that exists with statins is that you read about nasty effects, then suffer from them. The Nocebo effect. Why did they not mention the placebo effect? Which does the exact opposite – far more powerfully. I leave it to you, dear reader, to decide on that matter.
Some evidence of causality
It is very difficult to know what the true rate of adverse effects with statins may be. So much heat, so very little light. I cannot possibly cover all adverse effects in this blog. Instead, I will focus primarily on muscle pain and damage. This is probably the most common problem, and the most easily explained and understood.
I want to make it exceedingly clear that, far from being an imagined problem, we have a well-established biochemical pathway that directly links from statins to muscle damage, pain and weakness. With all steps proven, multiple times, in multiple studies.
In its simplest form, the pathway goes like this. Statins block an enzyme known as HMG-CoA reductase. This inhibits an early step in the long and complex – thirty-six step process – that ends up with the synthesis of cholesterol. This mainly takes place in the liver, which synthesizes around five grams of cholesterol, per day. About twenty eggs worth.
However, if you block HMG-CoA reductase this is not the only pathway you inhibit. You are also blocking the production of many other highly important compounds at the same time. You can perhaps think of cholesterol synthesis as a tree that grows from the ‘root’ of a chemical compound called Acetyl CoA.
As the chemical reaction ‘tree trunk’ grows upwards it starts to branch out, leading to the creation of many other, vital, substances. Such as dolichols, Heme A, prenylated proteins, co-enzyme Q10 etc, etc. Don’t worry there won’t be a test at the end.
Forgetting the others, important though they are, I will focus on Co-enzyme Q10 here. Which is also known as ubiquinone. This co-enzyme is critical in the synthesis of Adenosine Triphosphate (ATP). This molecule is, in turn, the power source that drives everything in our bodies. When ATP is broken down to ADP, energy is created, and used. This is how we work. From ‘professor’ Wikipedia:
‘ATP (adenosine triphosphate) is the primary energy carrier and “molecular currency” of the cell, storing and transferring energy to power essential processes like muscle contraction, nerve impulses, chemical synthesis, and active transport.’
You could think of ATP as the fuel in our car, or the battery in an EV. ATP doesn’t’ last long, and is being constantly replenished within the mitochondria – the little energy factories that live inside our cells. But without ATP, everything stops, and you die.
So, you could say it is kind of important. And, yes, statins have a significant and detrimental effect on the production of coenzyme Q10 (CoQ10), and then on ATP production. If you want some ‘real’ boring science about what this does. Read this paper:
‘Simvastatin impairs ADP-stimulated respiration and increases mitochondrial oxidative stress in primary human skeletal myotubes 4.’
‘These data demonstrate that simvastatin induces myotube atrophy and cell loss associated with impaired ADP-stimulated maximal mitochondrial respiratory capacity, mitochondrial oxidative stress, and apoptosis (death) in primary human skeletal myotubes, suggesting that mitochondrial dysfunction may underlie human statin-induced myopathy (muscle damage and pain).’
Paper highlights – taken from the paper itself:
- Statins can induce muscle weakness/myopathy.
- In culture, simvastatin induced dose dependent atrophy of human myotubes.
- Statin exposure decreased mitochondrial respiratory function and increased ROS (reactive oxygen species…ROS = ’bad’) production.
- Activation of apoptosis (muscle cell death) also evident.
- Findings suggest mitochondrial dysfunction underlies statin-induced myopathy.
It all sounds pretty damned unpleasant, does it not. The primary problem is that, without sufficient CoQ10 mitochondria cannot make enough ATP. This, in turn, ‘impairs ADP-stimulated respiration’ which leads to mitochondrial dysfunction then activation of apoptosis. Apoptosis means cell death.
In short. If the mitochondria can’t make enough ATP, the cell does not have enough ATP/energy to survive, and may commit suicide. Which is what ‘activation of apoptosis’ means.
You think the pharmaceutical companies didn’t notice this… this (imaginary) muscle cell destruction and death? Of course they did. They may be many things, most of which are far too rude to print here, but they are very good at science, and they certainly do notice stuff.
They knew very early on that statins block CoQ10 synthesis, and then ATP synthesis. Not entirely, but up to a fifty per-cent reduction. At one point it looked as if this could be such a significant problem that Merck took out two patents outlining how to neutralise it. The first was US4933165A:
Key Aspects of US4933165A
- Assignee: Merck & Co., Inc.
- Inventor: Michael S. Brown (Note: The patent is often associated with the work of Dr. Karl Folkers regarding CoQ10, though the listed assignee in the 1990 publication is Merck).
- Purpose: The invention describes a method for reducing the side effects of HMG-CoA reductase inhibitors (statins) by combining them with Coenzyme Q10.
- Mechanism: Statins work by blocking the HMG-CoA reductase pathway. This same pathway is used by the body to produce CoQ10. The patent addresses the depletion of CoQ10 caused by statins, which can lead to muscle pain (myopathy) and potential heart damage.
- Scope: The patent covers the combination of CoQ10 with various statins, including lovastatin, simvastatin, and pravastatin.
They didn’t act on this patent. Perhaps it wasn’t seen as a great sales idea to stuff the antidote into the same packet as the statin. ‘These are perfectly safe, you say. So, what it this other tablet here for – precisely?’
One man who did take out a patent with regard to the muscle damage caused by statins was none other then Professor Sir Rory Collins himself, in 2009.
A leading Oxford medical researcher who says statins are safe is at loggerheads with a company that makes “misleading” claims about the drugs’ side effects to sell a diagnostic test he invented.
More than 6m people take statins — drugs which reduce cholesterol and save an estimated 7,000 lives a year — but there is a fierce debate about the benefits and side effects.
Sir Rory Collins, a professor of medicine and epidemiology at Oxford University, led a review into statins, published in The Lancet earlier this month, which found that not more than one in 50 people will suffer side effects.
Collins, who believes millions more Britons could benefit by taking statins, is also co-inventor of a test that indicates susceptibility to muscle pain from them.
In 2009, he and three co- inventors filed the patent for a genetic marker that identifies patients at increased risk of myopathy (muscular pain). The patent says the incidence of myopathy is around one in 10,000 patients per year on a standard statin dose*.
The test, branded as Statin–Smart, is sold online for $99 (£76) on a website that claims 29% of statin users will suffer muscle pain, weakness or cramps. The marketing material also claims that 58% of patients on statins stop taking them within a year, mostly because of muscle pain.
Oxford University said Collins had raised his concerns “several times” about “misleading” marketing claims made by Boston Heart Diagnostics, the American company granted the exclusive licence for Collins’s patent by the university5. [Lois Rogers was health editor for the Sunday Times].
*Muscle pain and myopathy are not quite the same thing. Myopathy is a serious adverse effect – assocatied with a significant rise in an enzyme called creatine kinase (CK). When muscles are damaged and/or, die they – usually – release enzymes, with CK being the main one. Myopathy can be the precursor to rhabdomyolysis (very widespread muscle death) which has an extremely high fatality rate. And yes, all statins can cause rhabdomyolysis – albeit rarely.
I think of it this way, as a spectrum.
Muscle pain = Moderate muscle damage/death ± moderate rise in CK
Myopathy = Severe muscle damage (often, not always, a rise in CK)
Rhabdomyolysis = Catastrophic muscle damage, CK through the roof
Myopathy may be considered relatively rare 1:10,000 per year (according to Collins). But the diagnosis is not straightforward, and it is heavily reliant on the finding of raised CK levels. But…here is a small study looking at patients with severe myopathy, and no rise in CK. ‘Statin-associated myopathy with normal creatine kinase levels.’
‘Four patients with muscle symptoms that developed during statin therapy and reversed during placebo use… Muscle biopsies showed evidence of mitochondrial dysfunction…These findings reversed in the three patients who had repeated biopsy when they were not receiving statins. Creatine kinase levels were normal in all four patients despite the presence of significant myopathy 6.’
So, we have a condition that is considered rare … but which may not be as rare as you think it is. Because you are relying on a blood test that may, or may not, actually diagnose it. You may get a lot of false negative tests. [A test which says you do not have a condition, when you do]. And when does muscle pain transform into myopathy? It is arbitrary.
Enough of this, I think.
What do we now know? We know that statins block CoQ10 production, and this reduces the amount of ATP being manufactured by the mitochondria – by up to fifty per cent. This is a well-researched, and inarguable, scientific fact. It will be a particularly significant problem in cells that have a high energy requirement e.g. skeletal muscle, or heart muscle, or neurones.
In truth, the adverse effect issue mainly boils down to this. Do you have the reserves to overcome the mitochondrial damage that statin cause … or not. If you do have the reserves, you may not notice much, if anything. If you don’t, you could end up stuck in a chair, hardly, able to rise. Which I have seen happen to several patients. And my father-in-law. An early statin user.
One lady I was looking after in an elderly care unit was judged to be so physically and mentally incapacitated that she was going to be admitted to a nursing home with frailty and dementia. I stopped the statins, and she walked out of the unit two weeks later, bright as a button. The nurses were stunned. I got a letter from her GP a week later, condemning me for stopping her life saving medication. That was just one of many patients where I had very similar results. She was just the most dramatic.
Do I have other terrible tales about statins? Of course. I recall another lady with such severe abdominal pain that she ended up having a laparoscopy (sticking a camera into the abdominal cavity to have a look around). Nothing was found, a mystery. She stopped the statin, on my recommendation, and the pain went away. Completely and forever.
Yes, I am biased, yes these are ‘anecdotes’, easily dismissed – and, boy, they will be. But I have seen so very many. Far more cases of rhabdomyolysis, for example, than I should ever have seen in my career …statistically. And so many more have written to me, telling me how they have suffered, and then been dismissed by their own doctors.
Here is one such. I could dredge up a thousand more, given a couple of days.
‘Thank you, Dr. Kendrick. I am one of the many unfortunates who suffered permanent muscle damage from a needless prescription of simvastatin from 2008 to 2012. No monitoring, but my CK reading of 20 x normal was discovered by chance and the alarm was raised. When referred to NHS specialists their attitude was very strange, complete denial and hostility. Now permanently disabled on the right side of my body.’ Georgina H (Reproduced with consent).
Before I finish this blog. I would like to return to my court case, and all the interesting documents that emerged, blinking into the light. Barney Calman was the Health Editor of the Mail on Sunday which ran the defamatory article against me. He put out a call for case histories from people who had stopped taking statins, then suffered a major event e.g. heart attack, or stroke, or suchlike. What he got was the following:
From: Barney Calman Sent: Tue, 26 Feb 2019 08:44:40 +0000From: “Barney Calman” To: “Fiona Fox” , “Rory Collins” , “Colin Baigent” , “samanin@bhf.org.uk” , “Sever, Peter S” , “Liam Smeeth” CC: “Greg Jones” Thread To: Fiona Fox Rory Collins Cc: Greg Jones Sensitivity: Normal Colin Baigent samanin@bhf.org.uk Sever, Peter S Liam Smeeth
‘Dear all, thank you again for all your input into this article so far. I wanted to readdress the issue of finding a case study. One of the key factors in your collective argument is that criticism of statins discourages use amongst high-risk patients, and this is a public health threat. Since putting calls out we have been inundated by stories of people who have stopped taking statins and felt far healthier.
We’ve had two quite dramatic stories of patients who have been taken off statins by their doctors because of developing serious liver problems, and then died. The families themselves both naturally question whether statins caused the problems. What we haven’t had is a single story which backs your thesis, and obviously I’m concerned.’
Yes, he was ‘inundated’ with stories of people who felt far better having stopped their statins. The only two case histories he had managed to get hold of, at this point, were two people who took statins which then (almost certainly) caused liver failure, then death. [Statins are known to cause liver failure leading to, in extreme cases, death].
One would hope, in an ideal world, that if an investigative journalist was running a story on the unrivalled benefits of taking statins, and the harm that would befall those who stopped taking them … then. Then, when he found himself literally, his word, ‘inundated’ with stories of people who felt far better after stopping statins, and two cases of people who were almost certainly killed by statins then … Then you may pause to wonder if you are grabbing the right end of the stick.
But no, he did not let this put him off in the slightest. He had his eyes on the prize.
Next, a few surprising facts about statins and the unpleasant effects they can cause. Before finally, my direct criticism of the Lancet paper. And the nonsense that it is.
1: https://www.ncbi.nlm.nih.gov/books/NBK599521/
3: Unraveling the mystery of placebo effect in research and practice: An update – PMC
4: https://www.sciencedirect.com/science/article/abs/pii/S0891584911011130
5:Statins expert in row over level of risk to patients – Lois Rogers
6: Statin-associated myopathy with normal creatine kinase levels – PubMed
Dr. Malcolm Kendrick 
Amazing work! I hope you still have free time for other things…
I trust you and your witted sense of humour.
Which make me wonder, are there any other doctors in other fields that we should follow to have a good understanding of what they try to prescribe to us?
Sent from my iPhone
I had muscle weakness severe enough to affect my job. I was so tired I was wearing me out walking from my car to my work station. After work I had more energy. It took a while for me to notice that after I took my statin, that I would be tired and would get worn out just by walking from car to job. Then I noticed how much better I felt after work when the statins had mostly left my system. Against my doctor’s advice I quit the statins. Everything improved greatly. I was put on statins because my LDL was 101, and my doctor said it shouldn’t be above 100.
I ran an acupuncture practice from 2020 to 2024 in a major American city. Whenever I would refer a statin-taking patient to Dr. Kendrick’s work and some other articles off the web, and the patient listened to what was written and took action, half of their symptoms would go away. Including a lady who dropped her cane after two weeks of discontinuing statins. It was crazy how easy it was to “treat” their symptoms in this way. Most of the patients never connected the myriad of their symptoms to statins. And neither did their physicians.
Muscle destruction caused by statins leads to a long-term explosion of kidney failure cases. A Swiss pathologist stated that 100% of the people he autopsied who were taking statins had liver damage; he declared that statins should never have been authorized.
CoQ10 – Ubiquinol. I was taking this daily, on recommendation of my younger sister (who was also the person responsible for my finding you !) until informed that I must stop taking it because I also take rivaroxaban.
This blood-thinner is the bane of my existence. I would give ANYTHING to stop taking it.
The Ubiquinol restored some some lost energy; but I’m not allowed it. Is this a correct prohibition ?
Dear MR,
You can dump the blood thinners and replace with raw garlic. This should be eaten (crushed) after 5 to 10 minutes exposure to air in order to release the allicin etc properly. Sprinkle on hot/cold food, salads, toast, whatever you like.
Garlic IS a natural blood thinner and in my experience much more powerful than those horrible drugs which cause bruising, tummy upsets, etc – you don’t need them. If you can’t stomach raw garlic straight away try in small amounts daily with meals and note, maximum per day should never exceed 2 cloves.
Alternatively there is always low dose coated aspirin, but only if you can’t take raw garlic. Please look up various research papers both at UK universities and elsewhere, on eating garlic, and please read the summary conclusions.
Kind regards & good luck
Mike
I say !! – how helpful are you ??!! You might be my favourite Pom of all times, if this works … sending a grateful hug from a very old Aussie ! 🙂
As always, an interesting & powerful read. Thanks for these articles. (should the title read Lancet paper & not peper?)
You are right, have changed, thanks. Silly error.
Missing is any mention of the effect on GLP-1 – considering the much stronger correlation of CVD with metabolic disease who wants to cut their GLP-1 levels in half?
Or the idea that Tadalafil might have the same benefits without the side effects?
This link is dead – refers to Bullet point 2
https://www.ncbi.nlm.nih.gov/pmc.articles/PMC1971011/pdf/jroyalcgprac00086-0041.pdf
I will try to track it down.
Dr Kendrick has fought the corner for unwitting statin users, (pressed by remunerated medical professionals), and fought his own corner against Barney Calman’s derogatory and reputationally damaging Article in the Mail on Sunday. Kudos to Dr Kendrick’s tenacity and the important research comprised within.
I’d be interested in an article on the adverse side effects of anti hypertensives. I currently take 5, and am eager to cut down, but none of the doctors will give me any advice on how to, esp the beta blockers
Easy, throw them in the bin and stop measuring, no numbers no problem. Has worked for me.
As we age so do our arteries along with everything else. The body may well need to keep the blood pressure high for one reason or another. The systolic used to be 100 plus your age but of course that doesn’t sell the drugs.
It’s probably a similar situation for the cholesterol numbers. What’s normal is not permitted.
All a bit of a farce really. We should trust our bodies a bit more, eh?
Exactly! Prescribed Coversyl (blood pressure medication) 9 years ago. Fit, active and now 70 (high cholesterol, quelle horreur!). Side effects after 8 months of taking this medication. Loss of hair, anxiety, bleeding gums and nose (at 4am!), 4 BCC (basal cell carcinoma) out of my head and neck in 18 months period to the surprise of the dermatologist as I have olive skin and tan easily without burning. Glaucoma in right eye with perfect vision test, treated with laser and now all fine. I dropped this medication and all symptoms are gone….that was 6 years ago, love to find out more about it!
The sheer evil evidenced here is mind-blowing. I certainly feel vindicated in my own refusal to accept statins. Several of my friends who started them report fatigue and muscle pain.
falls risks in elderly certainly linked to statins and the meds – no one connecting the dots. Drs not even following protocol as prescribe hypertensives on one visit rather than tracking bp over some weeks before prescribing.
great article as usual. Thanks very much for sharing your insights. I will never take statins.
Norma Bailie
That new cardiologist who, upon learning I don’t “do” statins, advised me to consider some newer LDL lowering potions*, also deserves some credit: I recall he mentioned CoQ10, too.
*ezetimibe, inclisiran
Did you ask him why he thinks a low LDL is better?
When I asked my GP that his reply was that you can never get it too low.
The Science, eh?
Keep up the good work, doc; maybe you’ll grind the buggers down.
My husband was on 80 mg of rosuvastatin for at least 15 years and was having stomach issues and leg cramps. Strangely he was started on 80 mg a day and not 5 or 10 mg, why not start with the lowest dose and work your way up? Anyway, they put him on another one, same thing. Then his cardiologist put him on Ezetimibe. Months later, I was on the verge of leaving him, because I just couldn’t live with him anymore – couldn`t say anything to him without him becoming angry and aggressive. Eventually I realised it was the Ezetimibe. Did some research, found Dr Kendrick (thank the lord!), and after ceasing Ezetimibe he went back to normal and has never taken a cholesterol lowering drug since. Everyone I know that has taken a statin has had issues. Don`t bother with them!
My mother was on statins for some years. In the end she had so much pain in her legs she could barely walk. Her doctor said it was because she didn’t take enough exercise … She died of kidney failure.
The kidney failure could, of course, have been due to the statins. Severe muscle breakdown floods the kidneys with damaged muscle debris, leading to failure. This is why people who suffer rhabdomyolysis (rhabdo – muscle: myolysis-destruction and breakdown) die.
Thanks for the reply. I wondered about this.
Is Atorvastatin (Lipitor), which has been prescribed for me, bad? I tend not to trust the pharmaceutical companies, who are just in it for the money. Rapacious is a good word for them. I tend to trust you. Thank you for your articles Dr. Kendrick.
Kenneth Straus, Petaluma, California
All statins have the same spectrum of adverse effects, it is simply a matter of ‘does’
The phrase “the poison is in the dose” (or “the dose makes the poison”) is most commonly translated into Latin as “Sola dosis facit venenum”
Your URL in footnote 2 is broken, but this one works:
https://pmc.ncbi.nlm.nih.gov/articles/PMC1971011/pdf/jroyalcgprac00086-0041.pdf
Thanks very much. Will change over.
Wow! What an incredibly informative read that was. Thank you. Very unhappy about my 5mg daily Rosuvastatin. I was on Atorovastatin (much higher dose when I stopped years ago now) I don’t understand why I have to take it. My ratios are ‘perfect’ according to the cardiac nurse. After two or more years of hell with a dementia affected husband and an awful lot of high stress I developed two bad blockages in my arteries for which I was stented in January. Very successful, I have to say. Now I am on a blood thinner (Ticagrelor) plus Lansoprolole to protect my stomach from Ticagrelor, plus 5mg Rosuvastatin for goodness knows what. I now take 8 medications related to my heart failure (which came on very suddenly one week after a Pfizer booster for you know what) before which I was fighting fit. Now suddenly, I’m an old woman (okay, I am 83) but never felt in any way old before. Don’t mind me. I’m just venting but if there is a clever person out there who can advise me??? Not you, of course, Dr. K as I know you can’t. keep up all your good work, Dr. K. You are a lifeline.
Thank you.
JB
“I don’t understand why I have to take it”
Respectfully, I would not take anything without thoroughly understanding why. Make them explain it.
Thank you for your articles Dr. Kendrick.
My mother was on statins for some years. In the end she had so much pain in her legs she could barely walk.
great article as usual. Thanks very much for sharing your insights. I will never take statins.
A ‘related’ article on BP, Statins, Salt, etc. with a shoutout to Dr K.
https://articles.mercola.com/sites/articles/archive/2026/02/27/understanding-blood-pressure.aspx
Will Q10 supplementation do any good to mitigate statin adverse effects?
I took two different statins 30-35 years ago. I was in my mid 30s. My doctor was concerned about my high LDL level (which I later found out was normal for someone of my age).
The first was an older statin. I stopped taking it when I started seeing double one day. I was advised by my doctor to stop taking it. My vision returned right away. I was switched to another statin and in a short while developed two problems: a stiffness in my joints and memory problems – I had trouble coming up with common words, similar to what an older person experiences (like I do now). These both disappeared almost immediately.
As I thought about my family health history I realized neither of my parents nor their siblings had heart problems. I decided the risk of my developing heart problems was unlikely. At 74 I continue to not have heart problems.
i am surprised that the lancet published the paper at given that the authors would not provide references and source research data.
the lancet has further undermined its credibility.
have you come across a book called ‘turtles all the way down’? Fascinating reading about clinical trials all using previous erroneous trial data to ‘prove’ efficacy of new interventions. The resources for the book are also all in the public domain – about 1200 of them!
worth a read
marcia
I’ve read it, thanks
Dr. Kendrick wrote a great book about hanky-panky in pharmaceutical trials called Doctoring Data.
Despite all the drugs of which 99% are useless, the medical mafia will never be concerned with discovering the conditions that lead to heart problems. The idea that you need “something” like a drug or supplement to fix some problem never considers the reason why the problem exists to begin with.
There is always a direct reason. It may be called the root problem. Stop taking the “cure” and the trouble is likely to still exist.
Of course there is never going to be a robust method of collecting drug blow backs and adverse events. That might negate the billions of dollar spent on endless marketing. If drugs actually worked to provide better health, no marketing would be needed. The news would spread like wild fire on its own.
Marketing, unfortunately, is very effective. That’s why the pharma industry spends more on marketing than it does on research.
To illustrate, Lipitor was the first statin to appear on our market, back in the ’90s. At the time I was a programmer working for a small health fund. The way it worked in those more primitive times is people would buy their prescriptions at the pharmacy then mail the invoice to us. We would manually capture the data then send them a cheque based on the standard rate for the medication, not what the pharmacy charged. (Most pharmacies charged the standard rate so there were few complaints.)
We had a qualified doctor as a medical advisor. He told me to be sure the computer would not pay out anything for Lipitor because in his opinion it was a worthless drug and people only wanted it because of all the hype around it.
The reaction from our members was violent. They accused us of trying to kill them because they believed they would die of a heart attack if they didn’t take Lipitor. We had no option but to reverse our policy or we would be burned at the stake. Qualified medical opinion be damned. That pill was their savior and they were determined to have it.
As I say, marketing works.
Excellent, can’t wait to read the rest. I have been told to take statins twice and have simply not told the physicians that I did not follow their instructions. There are other ways to control/decrease the problem.
“I have been told to take statins twice and have simply not told the physicians that I did not follow their instructions.”
I always make sure to tell a doctor when I’m not going to follow their instructions. They need to know there’s pushback.
Not to mention, I don’t want an erroneous note in my records that I took something they wanted to give me (and I refused to take).
More Paradoxes,
Or
The systemic corruption of the “expert boards” that define cardiovascular “guidelines”?
“Residual coronary atherosclerotic risk and low LDL-cholesterol in chronic coronary syndromes “ European Heart Journal – Imaging Methods and Practice, Volume 4, Issue 1, January 2026,
It is impressive how many studies are published annually that directly contradict official cardiovascular guidelines. This one, recently published in the journal of the European Society of Cardiology, is yet another addition to the already extensive medical literature that refutes the demonization of cholesterol as a cause of cardiovascular disease.
RESULTS:
“Patients with low-moderate LDL-C levels had a lower prevalence of absent, non-obstructive and less extensive CAD and a higher prevalence of more severe (CAD-RADS2 = 3-4-5 or SG) and/or extensive CAD (P 3-4) (Secondary OUTCOME).
Patients with low-moderate LDL-C levels had higher values of the Leiden CAD Risk score, and a higher prevalence of either high CAD risk category (Leiden score > 20) and moderate-to-high CAD risk category (Leiden score ≥ 5, Primary OUTCOME).
Patients with low-moderate LDL-C levels had a higher plaque burden as expressed by the total number of segments with any plaque, non-calcified/mixed or calcified plaques. Non-calcified/mixed plaques were particularly overrepresented in the lowest LDL-C group (LDL-C < 70 mg/dL).
In this subpopulation, patients in the lower LDL-C groups still demonstrated a significantly higher prevalence of more severe/extensive CAD, a higher Leiden CAD Risk score and greater overall plaque burden, confirming the consistency of the main findings.”
Facts, don’t bother me with facts. My mind is already made up.
In 2014 (aged 61), visiting a new GP I was advised to take statins. I declined, pointing out the evidence for cholesterol in reasonable amounts being rather beneficial. On another occasion, I mentioned nattokinase. The GP was at least willing to admit he’d never heard of it.
So, I’ve never been near them. But an older friend (now 78) stopped taking them last year after having unpleasant side-effects.
Off-topic slightly, I’ve been (re-)reading ‘The Clot Thickens’. It’s notable how a few major factors determine health and longevity and all the rest are pretty minor. From reading Arthur Firstenberg’s ‘The Invisible Rainbow’ (2017) could non ionising radiation be one of the fairly major factors?
Sources of exposure in 2026 are considerably more abundant than in 2006, let alone 1996 by when Firstenberg noticed that the entire planet was now affected. He claimed that people vary widely in sensitivity to NIR, also that it disrupts carbohydrate metabolism.
Not that the relevant industries are keen on discussing the subject. Indeed, it seems to have gone very quiet. Firstenberg sadly died in 2025 at only 74.
“Next, a few surprising facts about statins…”
Well, please make it snappy. You’ve lain low too long. Much too long!
Here’s a eulogy from The Times of a chap who, purportedly, proved conclusively that high cholesterol causes heart disease.
https://archive.ph/zxMWC
I can’t reasonably suggest that you pull it to bits so soon after his death but perhaps you’d care to do it “in due course”?
De mortuis nil nisi bonum dicendum est
In her seventies my mum had a stent put in, as she had angina. She was already on one tablet for high blood pressure. But her health was much worse! I went to her six month check with her, and discovered she’d been put on NINE drugs. She was too ill to even bother reading – she was very well read. The doctor took her off five of the drugs.Dr James Lefanu had a column at the time in the Telegraph. It always finished with a comment from one of his readers. One day it was from a man who had got on holiday to Hawiii, forgotten his statins, and come back a new man. Dr Lefanu then had the largest post bag he had ever had from people who had been made ill by statins, and devoted the whole column to the letters. We persuaded my mum to have a statin ‘holiday’, and within a week she was much, much better – from being exhausted by a conversation when we visited, to coming to visit us on the train, chatting animatedly, coming to a concert, climbing stairs. Another friend was falling and we were all worried she was getting dementia. Same story, she gave up all her pills, and is still alive and with it in her nineties.
We met a lady on holiday who had been ill, looked at the inserts in the tablets she was on, realised she had all the side effects, threw them away, and was restored to health.It makes my blood boil. Of course it’s all in our heads.
I am 77 years of age, Taking 10mg atorvastatin for the last 15 years, Total cholesterol reduced by 50 % without obvious side effects. lately having muscle aches every where. Tried eliminating atorvastatin last year to no effect Now deciding to try again. I have no opinion on the cholesterol debate other than my own experience. Having never experienced a heart attack I don’t consider myself at risk but it is worrying that the debate seems to be going nowhere. Nevertheless I will continue with my own experiment and give it a few months to see whether it makes any difference.