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The actual study (1) is observational and makes no causal claim, only that there exists a statistical association between caffeine consumption and dementia. Nevertheless, people are apt to misinterpret the finding as “caffeine consumption prevents dementia”:
Caffeine -> Dementia
However, the two variables would be correlated if the causal arrow were reversed and dementia influenced the propensity to consume caffeine:
Caffeine <- Dementia
And we would also observe the correlation if a person's general health influenced both the propensity to consume caffeine and dementia risk:
Caffeine <- General Health -> Dementia
Since caffeine is a stressor, we would expect to see reduced consumption among people with reduced general health. But we would also expect increased dementia among that same group. So the relationships in the diagram immediately above are plausible and would give rise to a spurious correlation between caffeine consumption and dementia risk.
While studies can try to “control for confounding factors,” it’s easy to overlook or misunderstand the true causal relationships in play, causing spurious correlations. In other words, you can create false “causal” relationships through imperfect identification and control of confounding variables.
In short, take this article’s claims with a suitable dose of suspicion.
”After adjusting for potential confounders and pooling results across cohorts, higher caffeinated coffee intake was significantly associated with lower dementia risk (141 vs 330 cases per 100 000 person-years comparing the fourth [highest] quartile of consumption with the first [lowest] quartile; hazard ratio, 0.82 [95% CI, 0.76 to 0.89]) and lower prevalence of subjective cognitive decline (7.8% vs 9.5%, respectively; prevalence ratio, 0.85 [95% CI, 0.78 to 0.93]).”
So about 18% relative reduction. But if your risks are already low (e.g. active and healthy diet) the relative reduction is less impactful (e.g. 4% to 3.28%).
Makes you wonder. Coffee is tasty, so we drink it, and find out much later it also has these awesome side effects. What if there are plants out there that have even better health effects, but we'll never get decades worth of data on their consumption because they taste bad?
Is that right? Isn't it more related to the fact that people in education/etc. actually drink more coffee for culture reasons but also use their brain more? could that be the actual reason? Because I don't see how all the coffee zombies in my workplace would last longer long term when they're already useless and aggressive today (until they had their coffee)
Confounding variables are the first thing that breaks in prod. You can't control for "brain usage" in a retrospective study, and nobody's funding the 20-year RCT to prove it either way.
Has anyone looked at whether they controlled for socioeconomic status? Coffee consumption patterns correlate heavily with income and education, which themselves correlate with brain health outcomes. Without that adjustment, the correlation probably just reflects a lifestyle cluster, not coffee specifically.
Coffee, like other beans, is loaded to the hilt with antioxidants, particularly once it’s hyper-concentrated, and the roasting and brewing process eliminates all the mechanisms beans normally use to avoid animals wanting to eat them.
The caffeine-as-deterrent point is right and it's wild how well it works -- I've seen coffee plants absolutely hammered by aphids when caffeine production was experimentally reduced. On the antioxidant thing though, the ORAC story is genuinely complicated; some specific polyphenols do show measurable effects in cell culture even if the broad "antioxidants good" framing is overblown.
"Excessive coffee consumption was significantly associated with an increased risk of all-cause neurodegenerative diseases and vascular neurodegenerative diseases. The results also showed that tea intake was associated with a reduced risk of all-cause neurodegenerative disease, vascular neurodegenerative disease, other neurodegenerative diseases, and VD. Moreover, coffee and tea had an interactive relationship with all-cause neurodegenerative diseases and AD, with specific combinations significantly associated with reduced risk of disease" onset.
The dose-response relationship in coffee studies is genuinely tricky. That conclusion about "excessive" consumption aligns with most of the literature — protective effects tend to peak around 3-4 cups and invert at higher doses. So both studies are probably right, just describing different parts of the curve.
Isn't this all about brain hypoperfusion coming from some sort of dysautonomia and/or mitochondrial dysfunction and worse blood vessels as we age? We know that medication that helps blood flow and endothelium improves brain long-term, like sildenafil.
Only a few years ago, there was a study showing that regular caffeine use reduces blood flow to the brain by up to 30%, leading to lower brain volume and increased risk of dementia.
We've had a rule at every company I've worked at: no important decisions before the first cup. Half joke, but the sharpness difference is real. Nice to have data backing what everyone already knew operationally.
Caffeine -> Dementia
However, the two variables would be correlated if the causal arrow were reversed and dementia influenced the propensity to consume caffeine:
Caffeine <- Dementia
And we would also observe the correlation if a person's general health influenced both the propensity to consume caffeine and dementia risk:
Caffeine <- General Health -> Dementia
Since caffeine is a stressor, we would expect to see reduced consumption among people with reduced general health. But we would also expect increased dementia among that same group. So the relationships in the diagram immediately above are plausible and would give rise to a spurious correlation between caffeine consumption and dementia risk.
While studies can try to “control for confounding factors,” it’s easy to overlook or misunderstand the true causal relationships in play, causing spurious correlations. In other words, you can create false “causal” relationships through imperfect identification and control of confounding variables.
In short, take this article’s claims with a suitable dose of suspicion.
(1) https://jamanetwork.com/journals/jama/article-abstract/28447...