Caffeine consumption was inconsistently associated with clinical dementia, according to the results of a study published in Annals of Neurology.
The relationship between habitual caffeine consumption and age-related cognitive impairment is unclear. Previous studies of cognitive decline or dementia associated with caffeine consumption tend to show beverage-specific findings, not caffeine-specific associations. Meta-analyses of studies on coffee consumption show a non-linear association while a few studies have indicated that tea consumption has a positive linear association with onset dementia.
The objective of the present study was to investigate associations between habitual caffeine consumption, incident cognitive impairment, and neuropathology.
The researchers assessed participants at the Rush Memory and Aging Project (MAP) and the UK Biobank. The average caffeine consumption was 74 ± 57 mg/d in the MAP group (888 individuals aged at least 59) and 259 ± 153 mg/d in the UKB group (303,887 individuals aged at least 55). years).
The researchers tested the cognition of MAP participants each year and collected hospitalization and death records from UKB participants. Researchers found that 266 MAP participants developed dementia at an average age of 89.8 ± 5.9 years, of whom 252 developed Alzheimer’s disease (AD) at an average age of 90.0 ± 5. 9 years.
MAP participants reported regular consumption of coffee, herbal tea, soda and chocolate at each annual clinical assessment, while UKB participants reported regular consumption of coffee and black/green tea during their initial visit.
Compared to MAP participants who consumed no more than 100 mg/d of caffeine, those who consumed more 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 consumption was inversely associated with postmortem Lewy bodies. Those who consumed more than 100 mg/d were more likely to have inferior neocortical Lewy bodies (OR 0.40 95% CI 0.21-0.75).
Caffeine consumption was not linked to cognitive decline.
Among UKB participants, those who consumed more caffeine per day were less likely to develop all-cause dementia than 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 > 400 mg/d), with similar results for AD.
Limitations of the study included possible misdiagnosis of dementia, long pre-symptomatic phases of dementia, possible reverse causation, and lack of information on other sources of caffeine in the UKB.
Caffeine consumption was found to be inconsistently associated with clinical dementia, possibly due to cohort differences in the underlying etiology of dementia, the researchers explained.
“Caffeine consumption was inversely associated with postmortem [Lewy bodies] LB but not associated with other neuropathologies. The inconsistencies in the broader epidemiological literature on caffeine and dementia may in part be due to differences between studies in the underlying etiology of dementia,” 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