Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label rhabdomyolysis. Show all posts
Showing posts with label rhabdomyolysis. Show all posts

Monday, August 31, 2026

I’m a cardiologist. This is what you need to know about the side effects of statins

Sorry, but cholesterol is not the problem; INFLAMMATION IS! Without inflammation the arteries wouldn't be grabbing cholesterol to pack into plaque. Medical personnel took the shortcut and left the real cause still out there. And solving the correct problem would negate use of statins, Big Pharma will never allow such research to be completed.

Why doesn't your doctor know about this? Your doctor, like mine, will use the excuse that statins reduce inflammation.

Inflammation video explaining it here:

The accent is a bit hard to understand and needs to be rerecorded to a laypersons understanding.

Inflammation In Atherosclerotic Plaque Formation YouTube 

The latest here:

I’m a cardiologist. This is what you need to know about the side effects of statins

Our new series The Expert View brings you specialist health advice from professionals. In this article, we hear from Dr Ricardo Petraco, an internationally recognised consultant cardiologist and researcher based at Imperial College London and the Mayo Clinic in London. He specialises in cardiovascular screening, coronary artery disease and intervention.

Around seven to eight million people in the UK are on statins, and every week I see patients who are either on or considering taking them. More than with any of their other pills, many are worried about side effects. So what are their real risks?

First, an important disclosure: I have no conflict of interest in recommending or prescribing statins. I don’t make money from doing so, and I have no relationship with the pharmaceutical companies that make and sell them to the NHS.

It’s mystifying to me that statins are so vilified, because if you had to pick the one medication in the history of cardiology with the clearest benefit, it would be them.

Statins work by lowering low-density lipoprotein (LDL), the so-called “bad” cholesterol in the blood that leads to heart attacks, strokes and early death. Across the board, people taking a statin are roughly 25-40 per cent less likely to have a heart attack or stroke, regardless of their cholesterol level at the start of treatment. And the myths about the alleged risks – cancer, dementia, cognitive impairment, sexual dysfunction – have all been robustly debunked.

 Related video: New cholesterol guidelines: What you need to know (WCNC-TV Charlotte)

A study led by Oxford Population Health and published in The Lancet in February 2026 pooled 23 blinded trials involving more than 154,000 people. It found no excess risk from statins for 62 of the 66 conditions listed in their package leaflets, including memory loss, depression and sleep disturbances.

However, side effects can happen and some patients have genuine concerns. Dismissing them is wrong. What we should say is: “Yes, there is a small risk of side effects with statins, but let’s talk about it. Let’s weigh that risk against the risk of having a heart attack, and then you can make a rational decision about your treatment.”

Whatever you do, don’t give up on statins because you’re worried about side effects. That daily pill could save your life.

The side effects – should you be concerned?

Muscle aches

It is estimated that around one fifth of patients refuse or stop taking statins because of muscle aches, fatigue or joint pain. Yet true statin-caused muscle ache is uncommon. A 2022 study led by researchers from Oxford Population Health found that “for every 1,000 people taking a moderate intensity statin, the treatment would cause 11 generally mild episodes of muscle pain or weakness in the first year, with no significant excess in subsequent years”. The occurrence is just over 1 per cent, and only at the start.

A lot of complaints around muscle ache are largely down to the “nocebo effect”. That means the symptom is real but the drug is not causing it – the expectation of feeling unwell is. In studies where people don’t know whether they’re taking a statin or a dummy pill, aches are reported at nearly the same rate in both groups.

At Imperial, where I’m based, my colleagues carried out a study in 2020 that recruited 60 people aged between 37-79 who had stopped taking statins because of side effects, and restarted them, but with a twist. Over a year, each patient received bottles containing a statin, bottles containing a dummy pill, and bottles containing nothing at all, rating their symptoms each day via an app. The results were illuminating. Symptoms were nearly identical whether people took the statin or the placebo.

Nonetheless, it does occasionally happen, and it is a genuine concern. If a patient feels that statins are causing aches and pains, we monitor the situation, temporarily stop the statin and restart it to see how they feel. For many, symptoms lessen with time, particularly if you start on a lower dose and increase gradually. And if muscle problems persist, we can find another way to lower their LDL cholesterol. There are always alternatives.

Severe muscle damage

Rhabdomyolysis (severe muscle breakdown) is a genuine but extremely rare side effect of statins. It happens in about one to three people out of every 100,000 taking statins each year, and less commonly still at lower doses. It is more likely if you’re on a higher dose, if you’re taking certain other medications at the same time, or if you have kidney or liver problems or an underactive thyroid.

The problem is that because people occasionally experience muscle aches on statins, they immediately associate this with rhabdomyolysis and become very concerned. Yet the chances of it occurring are negligible, and that small risk needs to be weighed against the benefit.

A 2016 report published in The Lancet remains the clearest quantification: treating 10,000 people for five years with a type of statin called atorvastatin at 40mg would cause about five cases of muscle injury. One of those five might progress to rhabdomyolysis, and 50 to 100 people would report muscle symptoms.

Over the same five years, it would prevent 500-1,000 major vascular events, including deaths and disability from strokes and heart attacks. The benefits outweigh the harms many times over.

Slightly higher risk of diabetes

Taking a statin does slightly increase your average blood-sugar level, and over five years it raises the chance of being diagnosed with diabetes by about 0.5 to 1 per cent – somewhere between one in 200 and one in 100 people.

If you are fit and well, with a normal blood sugar, you will not suddenly become diabetic by going on a statin. It’s the patients who are already borderline – with insulin resistance or obesity – who may be taken over the line from pre-diabetes to diabetes. But those are precisely the patients at highest risk of a future cardiac event, so they are the ones the statin protects most. In these cases, lifestyle interventions such as diet changes, exercise and quitting smoking are recommended alongside taking statins.

Raised liver enzyme levels

With many medications, such as paracetamol, ibuprofen and antibiotics, there is a very small risk of liver failure. With statins, this is not a clinical concern: they do not measurably increase your risk of dying from liver failure.

It’s true that about four in 1,000 people have raised liver enzyme levels on blood tests when they start taking statins, but this usually causes no symptoms and is rarely a reason to stop.

Dementia (and the brain cholesterol myth)

There is a widespread myth that taking statins causes dementia. It is based on the fallacious claim that “20 per cent of your brain is cholesterol and yet your doctor is giving you medication to lower your cholesterol”. Biologically this makes no sense. Your brain cholesterol is produced locally, by specialised cells, and has nothing to do with the cholesterol circulating in your bloodstream in LDL particles.

Cognitive impairment is not a side effect of taking statins – The Lancet’s 2026 review confirmed as much. If anything, there is a theoretical gain, because you are decreasing the chance of vascular damage in the brain. Observational studies suggest that long-term statin use may even reduce your risk of developing dementia, although that is not yet proven.

Recommended

The truth about statins, memory and dementia

Read more

Sleep problems

Clinical trials have shown no consistent association between statins and sleep problems, but this is something patients do worry about. Again, the picture is confounded: people on cardiac medication tend to be older, and to have other conditions that disturb sleep. The statin itself has never been shown to cause them.

A few people taking statins that cross the blood-brain barrier – such as simvastatin or atorvastatin – report vivid dreams or disturbed sleep. This is rare, and although it’s hard to conclude whether the drug is the cause, we pragmatically recommend moving the dose to the morning; and if symptoms persist, an alternative such as rosuvastatin can be tried, as it is known not to cross into the brain so easily.

Erectile dysfunction

Statins causing erectile dysfunction is another common chapter in the book of online misinformation, but the link is unfounded. Sexual dysfunction is common among patients with cardiovascular disease, and some heart drugs, such as beta-blockers, can indeed cause it.

That confuses the picture, as those are the same patients who take statins. But there is no scientific evidence that statins cause sexual dysfunction. In fact, some studies suggest they can help, possibly by improving vascular health which then improves blood flow to the genitals.

Oedema (swollen ankles)

Three weeks after stopping my amlodipine  for high blood pressure the swollen left ankle is still there. Right ankle(good leg) never swelled up. I wasn't warned about edema when I started taking the drug. Now on nifedipine.

Oedema – essentially swollen ankles – does happen, but the numbers are very small and it’s not something we worry about. The 2026 analysis previously found roughly seven extra cases per 10,000 people per year, or 0.07 per cent. For comparison, amlodipine, a blood pressure tablet frequently prescribed alongside statins, causes dose-dependent ankle oedema in 5-10 per cent of users.

As told to Damon Syson

Recommended

Why I'm taking statins after avoiding them for nearly a decade

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Thursday, May 26, 2016

Molecular mechanisms of statin intolerance

Your doctor should be able to give you the exact percentage risks of developing these side effects. How many of their patients have discontinued statins because of side effects?
http://www.termedia.pl/Molecular-mechanisms-of-statin-intolerance,19,27579,0,1.html

Anna Gluba-Brzozka, Beata Franczyk, Peter P. Toth, Jacek Rysz, Maciej Banach

Arch Med Sci 2016; 12, 3: 645–658
DOI (digital object identifier): 10.5114/aoms.2016.59938
Statins reduce cardiovascular morbidity and mortality in primary and secondary prevention. Despite their efficacy, many persons are unable to tolerate statins due to adverse events such as hepatotoxicity and myalgia/myopathy. In the case of most patients, it seems that mild-to-moderate abnormalities in liver and muscle enzymes are not serious adverse effects and do not outweigh the benefits of coronary heart disease risk reduction. The risk for mortality or permanent organ damage ascribed to statin use is very small and limited to cases of myopathy and rhabdomyolysis. Statin-induced muscle-related adverse events comprise a highly heterogeneous clinical disorder with numerous, complex etiologies and a variety of genetic backgrounds. Every patient who presents with statin-related side effects cannot undergo the type of exhaustive molecular characterization that would include all of these mechanisms. Frequently the only solution is to either discontinue statin therapy/reduce the dose or attempt intermittent dosing strategies at a low dose.

Wednesday, April 18, 2012

Report validates risk of high-dose simvastatin

More stuff on rhabdomyolysis.  Make sure you ask your doctor to explain in detail your risks and symptoms on this.
 http://www.theheart.org/article/1386379.do?utm_campaign=newsletter&utm_medium=email&utm_source=20120418_EN_Heartwire
Statins were responsible for rhabdomyolysis in 7.5% of patients diagnosed with the skeletal muscle condition, according to a review of International Classification of Disease, Ninth Edition (ICD-9) codes from a large nonprofit healthcare system in Seattle, WA.
Publishing their findings as a letter to the editor in the Journal of the American Medical Association, Dr James Floyd (University of Washington, Seattle) and colleagues also confirmed a significantly higher risk of rhabdomyolysis in patients treated with high doses of simvastatin.
Incidence rates of statin-related rhabdomyolysis

Statin Person-years of use Validated rhabdomyolysis cases, n Incidence rates per 100 000 person-years
Simvastatin <20 mg/d 21 832 0 0
Simvastatin 20-39 mg/d 75 082 4 5.3
Simvastatin 40-79 mg/d 56 703 8 14.1
Simvastatin >80 mg/d 16 876 1 64.8
All doses 170 605 23 13.5
Other statins 116 54 6 5.2
All statins 286 756 29 10.1

In total, 22 cases of statin-related rhabdomyolysis were validated among 292 statin users with an ICD-9 code for rhabdomyolysis (positive predictive value 7.5%). Seven other patients were confirmed as having statin-related rhabdomyolysis using other criteria. Overall, the risk of rhabdomyolysis was significantly elevated among patients treated with simvastatin. The incidence rate ratio (IRR) for simvastatin compared with other statins was 2.61 (95% 1.03-7.84) using all validated cases of rhabdomyolysis.
"These results confirm in a community setting findings from a recent clinical trial that prompted the US Food and Drug Administration to issue a warning about the use of high-dose simvastatin," write the researchers.

Tuesday, April 17, 2012

Coding Muddies Stats on Statin Side Effect - Rhabdomyolysis

This was a poor article, I had to look up the definition of  Rhabdomyolysis myself. Be careful out there.
http://www.medpagetoday.com/Cardiology/Dyslipidemia/32210
 definition first, from NIH,
Rhabdomyolysis is the breakdown of muscle fibers that leads to the release of muscle fiber contents (myoglobin) into the bloodstream. Myoglobin is harmful to the kidney and often causes kidney damage.

Symptoms

  • Abnormal urine color (dark, red, or cola colored)
  • Decreased urine production
  • General weakness
  • Muscle stiffness or aching (myalgia)
  • Muscle tenderness
  • Weakness of the affected muscles
Other symptoms that may occur with this disease:
 The article:
Relying on use of the standard diagnostic code for rhabdomyolysis, a serious but rare side effect of statin therapy, to gauge incidence of the condition may lead to both under- and overestimates, researchers said.
Analysis of patient records maintained by the Group Health Cooperative over a 5-year period indicated that 292 charts of statin-treated patients had the ICD-9 code for rhabdomyolysis, but only 22 were validated by elevated creatine kinase levels and muscle symptoms, according to James S. Floyd, MD, of the University of Washington in Seattle.
Another seven cases of probable rhabdomyolysis were identified for which the ICD-9 code was not used, the researchers reported in a research letter appearing in the April 18 issue of the Journal of the American Medical Association.
In short, an ICD-9 code for the condition had a positive predictive value of just 7.5% (95% CI 5.0% to 11.1%), Floyd and colleagues wrote, while its sensitivity was 76% (95% CI 58% to 88%).
The researchers also found that the inaccuracy was not spread evenly across different types of statin therapy. In particular, it led to an underestimate of the actual rhabdomyolysis risk associated with high-dose simvastatin (Zocor), which was the subject of an FDA warning last year.
A higher proportion of the validated rhabdomyolysis cases were in patients taking simvastatin at 80 mg/day or more than among those with the ICD-9 code, Floyd and colleagues found.
As a result, the incidence rate ratio for validated cases in patients on high-dose simvastatin, relative to those taking doses of 20 to 39 mg/day, was 12.2 (95% CI 3.6 to 52.3), whereas use of ICD-9 codes produced an incidence rate ratio of only 1.77 (95% CI 1.05 to 2.88).
The researchers' analysis also showed a trend toward an increase in risk associated with more moderate simvastatin doses -- an incidence rate of 14.1 per 100,000 person-years (95% CI 6.1 to 27.8) at doses of 40 to 79 mg/day, whereas for all other statin drugs combined -- mostly lovastatin (Mevacor) or atorvastatin (Lipitor) -- the rate was 5.2 per 100,000 person-years (95% CI 1.9 to 11.2).
"The use of administrative data alone in studies of adverse drug reactions with multiple causes may fail to detect actionable and clinically important harms," Floyd and colleagues concluded.
To validate a case of rhabdomyolysis, the researchers looked for chart records indicating muscle symptoms with a peak creatine kinase level of 10 times the upper limit of normal or higher.
When peak creatine kinase fell between 5 and 10 times the upper limit of normal, they classed the event as myopathy. The rate of myopathy also appeared to be elevated in patients on high-dose simvastatin versus those taking other statins or lower simvastatin doses.
Floyd and colleagues noted that they did not adjust for potential confounding factors and also may have missed some cases of statin-associated rhabdomyolysis.
In searching for rhabdomyolysis cases that lacked the ICD-9 code, the researchers looked for clear records of the defining symptoms and also for the words "rhabdo" and "statin" appearing near each other anywhere in the record.