Sherlock Holmes "A Study in Scarlet"
However, that is exactly how science works. Usually there is a hypothesis that the researcher tries to prove (strangely by trying in fact to fail at disproving it), which informs the collection of experimental data. In the eyes of science, exploratory projects, which in Sherlock Holmes's view would be ideally non-biased, are actually seen as less worthy than traditional hypothesis driven - and as such inherently biased - science.
An interesting case of this scientific conundrum is illustrated by the strange case of how physical exercise (PE) goes after Alzheimer's dementia (AD). In a prior post I discussed some of the ways in which physical exercise might be good for the brain (which you can find HERE).
To summarize, we know that that the brain likes physical exercise. Yet if I may paraphrase Mr. Holmes "What we don't know dear Watson is how it does it."
While it is generally agreed that people who exercise have a lower risk for AD, a cause and effect it is yet to be demonstrated. In other words we don't know if exercise directly decreases the risk of AD, if there is something different about people who are at lower risk for AD that somehow increases their propensity to exercise, or if this is just an indirect effect of decreasing other risk factors for AD (such as diabetes, metabolic disorders, or cardiovascular disorders) or maybe a diffuse effect of an overall improved state of physical health on the brain.
How could we not know?
The problem is that most of the exercise-AD data comes from correlational retrospective studies. For example, at a level of a population, if one compares AD-individuals with non-AD individuals (healthy controls), the healthy people usually have higher levels of physical exercise.
However, when two things happen at the same time it does not mean that one is the cause of the other. No matter how solid, correlation does not necessarily imply causation, and that is one of the major hurdles in interpreting the findings of the PE-AD research.
So I get excited when there is new data that can help us better understand what's at stake here. This is the case with a study that just came out of Washington University looking at how physical exercise affects the amyloid levels (one of the main culprits in the Alzheimer's drama) in seniors.
But before looking at the study let's talk about a couple of relevant characters in the "Alzheimer and Who Is at Risk for Memory Loss" saga.
First, meet the ApoE-ε4, a genetic factor that's been shown to have the strongest associations with late-onset Alzheimer's. When ApoE-ε4 is present, conferring the status of (ApoE-ε4) carrier, this distinction comes at the price of a much higher risk for AD.
Second, meet another somber character, a villain with poor boundaries who, like those guests who overstay their welcome, tends to stick around (the ageing brain) for way too long: the amyloid. Clumping up in places where it does not belong, and wreaking havoc wherever it chooses to camp in the brain, the amyloid is the number one on the wanted list for anti-AD interventions at this time. So, when it comes to cognition in the older brain it makes sense to measure the amyloid in whatever way we can (e.g. brain imaging or CSF quotes) and see if we can understand what makes it stay or go.The Wash U researchers tried to do exactly this. They first determined the ApoE-ε4 status for about 200 cognitively intact subjects, then measured the brain amyloid. They also asked the subjects to complete a questionnaire about the physical exercise history over the last 10 years. Their research question: Can exercise changes one's propensity to store brain amyloid?
What did they find?
ApoE-ε4 brains like exercise or amyloid but not both. If you are a carrier and you don't exercise your amyloid level is up; exercise and you will bring your level down to that of a non-carrier.
However, if you are a non-carrier, your amyloid levels would not change much with exercise. They tend to be low to start with, and they stay about the same regardless of how much time you log in at the gym.
In other words, exercising seems to have sort of a leveling effect on amyloid. Without knowing what your amyloid levels are, and without knowing your ApoE-ε4 status (which might be possible in the future, however is not a routine test your doctor can order for you at this time) the take home point is fairly obvious.
When it comes to amyloid and exercise, there is little to lose and there is a lot to gain. Or, you can think about it this way: exercise and you might just "melt" some of that excessive amyloid that you carry around your brain. Not bad for a cheap and safe treat.
And remember: surfing the net doesn't quite count as as a real sport.ApoE-ε4 brains like exercise or amyloid but not both. If you are a carrier and you don't exercise your amyloid level is up; exercise and you will bring your level down to that of a non-carrier.
However, if you are a non-carrier, your amyloid levels would not change much with exercise. They tend to be low to start with, and they stay about the same regardless of how much time you log in at the gym.
In other words, exercising seems to have sort of a leveling effect on amyloid. Without knowing what your amyloid levels are, and without knowing your ApoE-ε4 status (which might be possible in the future, however is not a routine test your doctor can order for you at this time) the take home point is fairly obvious.
When it comes to amyloid and exercise, there is little to lose and there is a lot to gain. Or, you can think about it this way: exercise and you might just "melt" some of that excessive amyloid that you carry around your brain. Not bad for a cheap and safe treat.
Enough for today: time for you to hit the gym. But before you do, remember to bookmark this page and come back for the next installment of my discussion of this study. Without giving too much away I'll just say that: don't let the fact that this is yet another correlational study stand between you and your exercise routine.
For a summary of this check my Psychology Today blog HERE.
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