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Do Statins Really Prevent Alzheimer’s? An Exercise in Data Mining
If you have been paying attention to any of the non-Trump-related news this week, you may have noticed headlines about how statin drugs prevent Alzheimer’s disease. Some of the headlines are pretty breathless. The Daily Mail touts “The Pill That Could Stop Millions Getting Dementia;” and Science Daily leads with an even more definitive conclusion: “Cholesterol-Fighting Drugs Lower Risk of Alzheimer’s Disease.” CNN (perhaps chastened by recent events?) is somewhat more circumspect: “Are Statins a Key to Preventing Alzheimer’s disease?”
As a recovering cardiologist, and as an Old Fart who (reluctantly) has been taking a statin drug for several years, I am always on the lookout for new evidence that might convince me that it would be reasonable to stop the drug, or alternately, that it’s really a good thing that I’m taking it. But anyone who wants to learn the objective truth about statins must soon confront the fact that statins are sort of the cardiology world’s equivalent of climate change. That is, a consensus of experts agree that statins substantially reduce the risk of nasty cardiovascular events in people at elevated risk, and that a large majority of people older than 60 should be taking them; but a vocal minority holds statins to be mainly toxins foisted upon an unsuspecting public by people with a special agenda. The debate has become very nasty and vociferous, and we have come to a place where each group tends to simply anathemize the other.
That’s science for you. This is not a new phenomenon; it’s been like this ever since science became a thing. I expect it will remain this way until science is no longer conducted by people.
Anyway, as someone personally affected by the statin debate, I have made a consistent effort for many years to seek objective truth about these drugs. So far, as evidenced by the fact that I continue to swallow one each day, I think that (for people like me at least), the potential benefits probably outweigh the potential risks.
Still, in this long-term effort I have learned never to accept what people say about statins at face value. So when all the news media began barking at me this week that my statin was going to keep me in fine cognitive fettle, I immediately began looking for reasons to disbelieve it. (This is what scientists are supposed to do — to be skeptical of everything.)
In this case it wasn’t hard to find the bulls—t. I simply read the study.
The study was published this week in JAMA Neurology by researchers from the University of Southern California’s Sol Price School of Public Policy.
Note: School of Public Policy. We need to be aware of a couple of things when we consider health-related research produced by public policy experts. First, these are people who don’t take care of patients; they take care of data. Second, they mine the data to come up with stuff they can do to the herd that they believe will improve the average outcome for the herd. Third, they must necessarily assert that mining data is the ultimate pathway to Truth.
Here is what these researchers did: From the vast databases kept by Medicare they took a 20% sample of Medicare beneficiaries, and linked data about enrollment, demographics, vital statistics, and Medicare Parts A, B, and D claims. They identified a group of beneficiaries who had no diagnosis of Alzheimer’s disease, and who had filled at least two statin prescriptions between 2006 and 2012. This produced a sample of 399,979 statin users. They then divided this group into two cohorts according to how many times they filled prescriptions for statins between 2006-2008. The top 50% were said to have high exposure to statins, and the bottom 50% were said to have low exposure to statins. They then assessed which patients were formally diagnosed with Alzheimer’s disease between 2009 and 2013.
They concluded that the “high exposure” statin patients were 10% less likely to develop Alzheimer’s disease than “low exposure” statin patients. Like most public health experts, they chose to report their results as a relative risk reduction (10%) rather than as an absolute risk reduction (which was from about 1.62% to about 1.44%, or a difference of only about 0.18%). This is because when you’re treating the herd, you don’t care that an individual’s odds of a benefit are minuscule, as long as the people managing the herd can measure an appreciable benefit to themselves.
The study went on to further demonstrate the great benefit of data mining as a method of truth-seeking by dividing the 400,000 patients into various subgroups, and attempting to show the differential abilities of particular statin drugs to prevent Alzheimer’s in various genders and races. The more subgroups you look for in these data mining expeditions, the more remarkable things you find. Accordingly they conclude, “The right statin type for the right person at the right time may provide a relatively inexpensive means to lessen the burden of (Alzheimer’s disease).”
Wow.
Does this study really indicate that statins might reduce the risk of Alzheimer’s? It is possible, I suppose, but if so it’s a fluke. Data mining expeditions in general can be useful in drawing interesting associations, but are useless in determining cause-and-effect. But even to accomplish this much the data mining exercise must be carefully designed so as not to build in predictable bias. This study did not do that.
What do we already know about patients who go to their doctors, accept a prescription for statins (or anything else), and then regularly take the prescribed drug for a period of at least a couple of years? We know that they tend to go to their doctors regularly, and faithfully follow their prescribed medical regimen. If they agree to take statins chronically, we also suspect that they may have at least a modicum of interest in taking personal preventive measures against cardiovascular disease.
What do we know about patients who accept prescriptions for statins and then fill them only very irregularly if at all? Some of them, of course, may have carefully reconsidered the risks and benefits of statins, and reasonably concluded that statins weren’t for them after all. And no doubt that among the 200,000 “low statin exposure” patients there were some like this. But much more likely, many tended to be those people who simply neglect to take their prescribed medication. And if so, it seems reasonable to suppose that they may also have been less likely to follow other important preventive measures, such as not smoking, taking care of their diabetes and hypertension, getting plenty of exercise, and eating a Mediterranean-type diet. All of these lifestyle measures, when not followed, are associated with a higher risk of Alzheimer’s disease. In addition, the “low exposure” group likely included an excess of individuals who, while not yet diagnosed with Alzheimer’s, already had some pre-clinical cognitive decline. Such people often forget to take their medication as prescribed, or to refill their prescriptions.
In my view it seems as likely as not that this study simply divided Medicare patients up into two groups that, from the outset, had slightly different probabilities of developing overt Alzheimer’s disease. The statin prescriptions were merely the mechanism by which these two inherently different groups happened to be identified. It is easy to think of other ways of differentiating these groups that might have been used instead.
Even if this study is accepted at face value as a reasonable hypothesis-generating exercise, it ought to be noted that the hypothesis has already been tested in at least two, published, randomized clinical trials, in which statins were assessed as an Alzheimer’s disease preventive measure. In both trials, statins failed to offer any benefit.
The authors of the JAMA Neurology study were aware of this fact, and argued in their paper that these RTCs were flawed (which is always the case), and that their new analysis offers information that is potentially more compelling than the RTCs. The bottom line is that I find their concluding statement astounding, and so I repeat it: “The right statin type for the right person at the right time may provide a relatively inexpensive means to lessen the burden of (Alzheimer’s disease).”
I will continue to take my statin for now, but this study offers me no comfort. In fact, it gives me some pause that public health experts now seem to be growing in favor of statins for the herd. This is the one thing about this study that seems new to me, and perhaps it is significant.
I’ve posed this riddle before on Ricochet, but I will repeat it here because it makes an important point:
Q: What is the main difference between public health experts and serial killers?
A: Serial killers usually kill only one person at a time.
Published in General
Elderly people often have strange and unpredictable reactions of many commonly used drugs. Several times in my practice I became a hero after being asked to see some 85 year old person with some sort of cardiac arrhythmia who seemed to have terminal lethargy and inanition, and who was on the way to the nursing home or hospice. Everyone expected me to pile on with some new medication. Instead, I would beg the family and the attending doctor to stop ALL medications for 72 hours. (“What the heck to we have to lose?”) The recovery was occasionally miraculous. After that the issue became: are any of the diagnoses being treated with any of these drugs worse than the reaction to the drugs we have all just witnessed?
What I have just relayed, of course, cannot be construed in any sense as a medical recommendation. It is not. It is simply an anecdote you might want to think about and discuss with the doctor.
Fellow readers of Ricochet: If your doctor has a treatment philosophy substantially different from that of @DocJay, you need to shop around.
Have you tried pravastatin? It’s the least likely to cause muscle pain. I’ve heard another good option is long acting fluvastatin.
Gotta love the “elderly hispanic woman effect.”
The Alzheimer’s Drug Discovery Foundation (ADDF) is very explicit in stating that there is no evidence that statin use in late life will prevent or slow the progression of Alzheimer’s disease or dementia. They only believe that statins help in cholesterol management, which in turn may reduce the risk.
My doctor has prescribed statins for me, not because I have high cholesterol, but because I am a male over 60 with a family history of heart disease, and he believes the data that show that statins reduce the risk of heart disease for such a population. Alzheimer’s was never mentioned.
According to an Officially Apocryphal Study recently completed at a leading Midwestern University at Taxpayer Cost of $3.4 Billion the Leading Cause of Mayhem and Death related to Dietary Intake in Modern Americans is…..Worrying about what we Eat!!
Not really, I got this information 2nd third hand after they changed the meds. I think it was lipitor that did the deed.
G-I-G-O
How? I have recently developed a GERD problem at the age of 36. My doc thinks it is stress. How do you manage stress, when you know you are stressed, but you don’t feel stressed?
Don’t stress about it. Try avoiding coffee, chocolate , late night meals, alcohol, anti-inflammatories, and drop some weight. Or take a drug. Or both. But don’t stress. My work here is done.
Activity crowds out stress. Go fishing (per your avatar). Go to the gym, or for a run or hike. Volunteer. Tidy your garage or attic. Works for me.
Great article! Looking forward to more…
The sarcasm makes it more entertaining to read!
Great article! I agree with most of the comments, and I’ll add that the term “data mining” is new enough and vague enough that it means whatever the user wants it to mean. Good breakdown of the actual study.
As long as we’re on the subject of preventing Alzheimer’s, has anyone heard about Longvida, a specialized form of Curcumin that’s been shown to reduced brain plaques associated with the disease?
Something smells of quackery. The DiSilvestro et al. paper deals with plasma beta amyloid protein concentrations. It is another step to conclude this means the brain plaques were reduced. It is yet another step to conclude that reducing the plaques per se slows the disease.
There’s evidence that brain plaques are reduced, at least in mouse brains, in vivo. Also true in vitro in human brains. Longvida has been shown to result in free curcumin passing the blood brain barrier. Maybe not absolute proof of anything, but it is promising.
I’m late to this party and have not read all previous posts but think it worthwhile to point out that not all cognitive disorders are Alzheimer’s and so-called vascular dementia is common. In that at risk group, statins and antihypertensives would be beneficial to prevent but not treat cognitive impairment.
Thanks. One of the best written, most insightful and informative articles I’ve read on Ricochet all year.