Caffeine intake was inconsistently associated with clinical dementia, according to study findings published in Annals of Neurology.
The relationship between habitual caffeine consumption and age-related cognitive impairment is unclear. Prior studies of cognitive decline or dementia associated with caffeine intake tend to present beverage-specific results, not caffeine-specific associations. Meta-analyses of studies of coffee consumption show a non-linear association while a few studies have indicated tea consumption has a linear positive association with incident dementia.
The objective of the current study was to investigate the associations between habitual caffeine intake, incident cognitive impairment, and neuropathology.
Researchers evaluated participants in the Rush Memory and Aging Project (MAP) and the UK Biobank. Mean caffeine intake was 74±57 mg/d in the MAP group (888 individuals aged at least 59 years) and 259±153 mg/d in the UKB group (303,887 individuals aged at least 55 years).
Researchers tested MAP participants’ cognition annually and collected UKB participants’ hospital and death records. Researchers found that 266 MAP participants developed dementia at a mean age of 89.8±5.9 years, including 252 who developed Alzheimer disease (AD) at a mean age of 90.0±5.9 years.
MAP participants reported regular coffee, non-herbal tea, soda, and chocolate intake at each annual clinical evaluation while UKB participants reported regular coffee and black/green tea intake at their baseline visit.
Compared with MAP participants who consumed no more than 100 mg/d of caffeine, those who consumed more than that amount were more likely (HR 1.35 95% CI 1.03-1.76) to develop all-cause dementia and AD (HR 1.41 95% CI 1.07-1.85).
Caffeine intake was inversely associated with postmortem Lewy bodies. Those who consumed more than 100 mg/d were more likely to have lower neocortical type Lewy bodies (OR 0.40 95% CI 0.21-0.75).
Caffeine intake was not linked with cognitive decline.
Among UKB participants, those who consumed more caffeine daily were less likely to develop all-cause dementia compared with those who consumed no more than 100 mg/d (HR 0.83 100≤200, HR 0.72 200≤300, HR 0.74 300≤400, HR 0.92 >400mg/d), with similar results for AD.
Study limitations included possible misdiagnosis of dementia, long pre-symptomatic phases of dementia, possible reverse causation, and lack of information on other caffeine sources in UKB.
Caffeine intake was found to be inconsistently associated with clinical dementia, possibly due to cohort differences in underlying dementia etiology, the researchers explained.
“Caffeine consumption was inversely associated with postmortem [Lewy bodies] LB but not associated with other neuropathologies. Inconsistencies in the broader epidemiological literature of caffeine and dementia may partly be due to cross-study differences in underlying dementia etiology,” the researchers concluded.
Cornelis MC, Bennett DA, Weintraub S, et al. Caffeine consumption and dementia: are Lewy bodies the link? Annals of Neurol. Published online March 15, 2022. doi: 10.1002/ana.26349
This article originally appeared on Neurology Advisor