Last month I noticed several reports in the news about a study concerning the relationship between statins and dementia (see here for an example). The study in question was presented at a cardiology conference in Amsterdam, the Netherlands. This research found that, over a 4 and a half-year period, statin use was associated with a significantly reduced risk of developing Alzheimer’s disease. I saw a cardiologist comment on this study on the TV. He talked about previous concerns that statins might adversely affect brain function, and how this new study can give us confidence that statins are safe after all in this respect.
This study, from Taiwan, is epidemiological in nature, which means all it’s really good for is establishing the relationship between statins and Alzheimer’s disease. It does not, actually, tell us much about what the effects statins have on the brain. This is partly because the supposed benefits of taking statins may not be due to the statins at all, but due to other factors associated with the taking of statins.
One potential so-called ‘confounding factor’ here is the fact that, by and large, those who see doctors and take medications as prescribed are generally more health-conscious than those who don’t. For example, these people may be less likely to and be more likely to take exercise. It may be these or other factors, and not the statins per se, that are responsible for the lower risk of Alzheimer’s disease seen in those who take statins.
This sort of bias is further compounded by the fact that one of the reasons people may not take statins is because they tried them in the past, but had side-effects such as fatigue and muscle pain. It is possible, then, that those who tolerate statins are generally healthier than those who do not – another factor that can bias results in favour of statin-takers.
Anyone who has suffered mental symptoms such as memory lapses and confusion as a result of taking statins is quite likely to stop taking them and may appear in the ‘no-statin’ group. In this way, genuine problems with statins may effectively disappear from the statistics, making statins appear better and safer than they are in reality.
To properly assess the effect of statins on the brain we need to look at data from ‘clinical’ studies, such as those where individuals are treated with a statin or placebo and the effects compared. Unfortunately, even here there can be biases that can skew results. For example, as I mentioned in a blog post last week, many studies include a ‘run-in’ period where all potential study subjects are given the active drug. Those who react adversely to the statin are then removed from the study before it starts in earnest. Again, this can make statins look safer than they are in reality.
Despite this sort of bias, clinical studies are still generally more illuminating than epidemiological ones. Unfortunately, there is not a lot of clinical evidence relating to statins and dementia. That’s partly because many studies have simply failed to record dementia as a potential side effect.
However, in 2010 researchers from the respected ‘Cochrane Collaboration’ conducted a review of the clinical evidence regarding the impact of statin therapy on mental symptoms in individuals with a diagnosis of dementia [1]. The review isolated three relevant studies (lasting 26, 52 and 72 weeks respectively). When the results of these studies were put together, there was no evidence of improvement in the symptoms of dementia, though there was no evidence of harm either.
My clinical experience tells me that statins can indeed have adverse effects on brain function, and this is a recognised issue. The Food and Drugs Administration in the US, for instance, has alerted us to the potential for problems here by warning us that: “There have been rare post-marketing reports of cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) associated with statin use.”
Also, last year saw the publication of some interesting clinical research in which elderly individuals with Alzheimer’s disease had their statin medication stopped for six weeks, and then restarted [2]. The results showed that during the six weeks when their statins were stopped, the basic brain function of the individuals improved. When the drugs were restarted, brain function got worse again. One possibility here is that the changes were as a result of the placebo effect. However, it may also be true that the statins can genuinely worsen the symptoms of some people with Alzheimer’s disease or other forms of dementia.
References:
1. McGunness B, et al. Statins for the treatment of dementia. The Cochrane Library 2010
2. Padala KP. Et al. The effect of HMG-CoA reductase inhibitors on cognition in patients with Alzheimer’s dementia: a prospective withdrawal and rechallenge pilot study. Am J Geriatr Pharmacother. 2012;10(5):296-302
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When I heard about the Taiwan study I was stunned. I hope this isn’t a big setback for the anti-statin movement. It’s well documented that statins can cause memory loss even being required to state this as a side effect on the label (at least here in the US). I’d love to know who funded this study – was it Pfizer?
As a carrier of the Alzheimer’s gene (ApoE4) and the son of a father crippled by the disease, I have a great interest in this topic. I will never take statins and deprive my brain of precious cholesterol and cholesterol sulphate. Recommend people read Grain Brain by neurologist/nutritionist (what a combination!) David Perlmutter which was just published and makes it clear that carbs/sugar drive free radical production, inflammation and glycation and Alzheimer’s not to mention most heart disease.
One of the things that made me give up statins was severe memory loss. I thought I was getting dementia and started writing even simple things down because I was forgetting them from one minute to the next. Needless to say my docotr probably didn’t report this as an adverse event.
We still don’t know what drives Alzheimer’s disease but in most cases it starts late in life and may have been gathering steam in the brain for decades before it manifests. How then could a 4 year study demonstrate that any one factor was responsible for a decrease in Alzheimer’s among an already elderly population? Or am I missing something?
The following information was told me by my pal about her friend who is a doctor, and his son is also a GP.
“My friend actually came off them a second time as the side effects reappeared and he then learned through his GP son from a leading neurologist that the tingling in his fingers and toes is likely to be permanent although might improve with time. This neurologist said that side effects which appear a second time can be permanent even when the statins are stopped for a second time. We seem to be being used as profit making guinea pigs by the big pharma companies – no surprise there!”
With reference to Tony’s comment regarding statins appearing to cause memory loss and Dr Briffa’s last 2 paragraphs where the FDA say there are ‘rare’ post-marketing symptoms of cognitive impairment – I really believe that these side effects are not nearly as ‘rare’ as they would have us believe. Speaking to several people over the past year, both friends and work colleagues, they told me that they themselves or relatives they knew were having memory problems. When I mentioned statins they all said that, yes, they were on statins and realised that the symptoms had arisen after they had been taking them. However, doctors seem reluctant to attribute these memory issues to the statin drugs partly because they don’t appear to have heard about the FDA’s new warning and partly because they still believe that statins are ‘essential’ to ‘control’ (apparently) high cholesterol, being told what to do by the NICE guidelines. Therefore these adverse effects are not actually finding their way back to the MHRA…….
My mother-in-law developed dementia after being put on statins four years ago after a mild heart attack. No one thinks the statins caused her memory problems, but I’ve kind of wondered.
How often does dementia follow statins? it is never going to be reported, just blamed on age. And maybe it is just age, or other problem completely unrelated to the statins (and low fat-high sugar diet). How in the world can you prove it one way or another.
Stephanie Seneff addresses this issue in part 8 of her article, How Statins Really Work. http://people.csail.mit.edu/seneff/why_statins_dont_really_work.html
That’s a great link Gregory, and I like this particular quote from Stephanie’s concluding remarks to her essay and analysis:
“Mobility is a great miracle that cholesterol has enabled in all animals.”
I have been thinking much the same for some time but have never been able to say it so summarily, and I think it worth adding a line or two to Stephanie’s wsidom.
There is a great divison with biology. Species either have to rely on either of two quantum prospects. Species must either photosynthesise or metabolise. Many of those who photosythensise get by with phyto-sterols and have very limited use of cholesterol. In contrast the species that metabolise and move, that have an accompanying sense of thier surroundings and purpose of movements, that have more interesting sex lives, invest greater significance to the propspects afforded by cholesterol, and much less on the run-of-the-mill phyto-sterols.
Indeed the business of digestion shows a marked preference if the claims of the makers of sterol enriched functional foods and margarines are true in this; that the phyto sterols are passed out with stools and take some of the dietary cholesterol with them. Cholesterol is a key constitutent in the business of digestion itself, and a key constituent in the provisions made for conveying important and health promting fats and proteins accross the gastro-intestinal divide and into our body proper. Cholesterol is a key component vital for the constituency of chylomicrons which transport these things accross the GI divide.
So if we free our minds of the dogma and doggydodos we see yet another aspect directing that our assocation with cholesterol and lipoproteins is one which is essentially ‘adaptive’ (purposeful and natural), while it seems our association with phyto-sterols is not especially.
I read a fascinating book about Alzheimer research. In essence, Alzheimers is caused by an inflammatory reaction to beta amyloid proteins. Lepers who take a strong anti-inflammatory for the condition do not get Alzheimers, and those with arthritis similarly have a very reduced prevalence. As well as an anti-cholinergic effect statins are also anti-inflammatory. Heart disease patients are also often put on aspirin along with the statins, another anti-inflammatory and make lifestyle changes that lead to lower inflammation eg eat more fruit and veges. This study does not look at whether taking statins is better than taking a much less damaging anti-inflammatory, even natural ones such as turmeric, ginger, and fish oils