Caffeine – the psychoactive substance found in caffeinated beverages such as coffee, tea, and soda, as well as in chocolate – is a drug, although it’s a legal one in our society. It has multiple physiological effects. Among these are increased blood pressure, increased cortical activity and, possibly, protecting brain cells from damage and death.
There is huge individual variability in response to caffeine, partly determined by genetic predispositions and partly by an individual’s tolerance and expectations. Most people find that a mild dose of caffeine produces feelings of positive mood and arousal – which is why many people have a cup of coffee to help start the day, or a cup of tea to shrug off the mid-afternoon blues. Other people find that caffeine makes them irritable and restless, and still others seem mostly immune to the drug’s effects. High, chronic intake of caffeine can also lead to negative effects, not least of which is addiction followed by withdrawal symptoms if caffeine intake is stopped.
Caffeine can also affect performance on cognitive tests, including tests of memory. Usual findings are that a single mild dose of caffeine (similar to the amount in a cup of coffee) temporarily improves attention and vigilance. Thus, for example, a dose of caffeine may help people respond faster and more accurately on timed tasks. But caffeine may also cause a temporary reduction in memory function. For example, a mild dose of caffeine often produces a reduction in people’s ability to learn and remember lists of words. Similar attention and memory effects are often seen following caffeine administration in animals such as rats.
In addition to its short-term effects on attention and memory, caffeine temporarily blocks a chemical pathway in the brain (specifically, blocking adenosine A-2 receptors), and this may have positive effects – protecting brain cells and helping to attenuate the damage caused by beta-amyloid, the toxic protein that accumulates in the brain of patients with Alzheimer’s disease. In mice genetically bred to develop a rodent version of Alzheimer’s, long-term caffeine administration protects against accumulation of beta-amyloid and also reduces cognitive decline. This raises the possibility that long-term consumption of moderate amounts of caffeine may similarly protect against (or at least retard the development of) Alzheimer’s in humans.
Some recent evidence seems consistent with this hypothesis. A study by Ritchie and colleagues examined some 7,000 healthy elderly people from three French cities. On average, women with higher daily rates of caffeine consumption (equivalent to three or more cups of coffee or tea per day) showed less cognitive decline over a four-year period than women who drank one cup or less. The effect was particularly pronounced for verbal skills – such as the ability to learn and recall words. This protective effect of caffeine increased with age – so that older women seemed to benefit more. No such relationship between caffeine intake and cognitive decline was found in men – perhaps because, in this French sample, the men did not tend to consume as much caffeine as the women.
Another large-scale study assessed several thousand healthy elderly Canadians, and then tested them again five years later, by which time a few hundred had developed Alzheimer’s. One factor that seemed to be associated with reduced risk for Alzheimer’s was moderate caffeine consumption. (Other factors included moderate alcohol intake and regular physical activity.) In other words, healthy elderly people who consumed moderate amounts of coffee and tea (as well as those who consumed moderate amounts of wine and/or engaged in regular exercise) were less likely to develop Alzheimer’s over the five-year period.
These studies don’t definitively prove that caffeine prevents cognitive decline. For example, it’s possible that people in the early stages of Alzheimer’s simply reduce their coffee and tea intake, perhaps because they no longer like the taste, or because they can’t remember how to brew the beverages, in which case the correct conclusion would be that Alzheimer’s prevents caffeine consumption! Caffeine intake was also higher among non-smokers and highly-educated individuals in the French study, so it’s possible that not smoking, or having extra education – rather than caffeine intake per se – is what really produces the reduction in cognitive decline in these individuals.
Still, the data are suggestive, and it seems quite plausible that the same chemical effects of caffeine that produce short-term increases in blood flow and brain activity, as well as producing those subjective feelings of arousal, may also in the longer term help protect the brain from the effects of aging and disease.
So, if you enjoy a cup of coffee or tea, and if your caffeine intake is at moderate levels that don’t cause you unwanted physical or psychological side effects, sip away – in the hopes that, just maybe, you’re also striking a little blow in the fight against Alzheimer’s and age-related cognitive decline.
Further reading about caffeine, memory, and Alzheimer’s disease:
E. Childs, E. and H. de Wit (2006). “Subjective, behavioral, and physiological effects of acute caffeine in light, nondependent caffeine users.” In, Psychopharmacology, vol. 185, pp. 514-523.
J. Lindsay and others (2002). “Risk factors for Alzheimer’s disease: A prospective analysis from the Canadian Study of Health and Aging.” In, American Journal of Epidemiology, vol. 156, pp. 445-453.
K. Ritchie and others (2007). “The neuroprotective effects of caffeine: A prospective population study (The Three City Study).” In Neurology, vol. 69, pp. 536-645.
May 18, 2008 at 7:30 pm |
Resveratrol…
Education Affects Life Expectancy. Despite increased attention during the 1980s and 1990s to reducing disparities in life expectancy among the educationally disadvantaged, the educational gap in life expectancy is rising. Between the 1980s and 2000, li…
May 19, 2008 at 3:58 pm |
Education Affects Life Expectancy. Despite increased attention during the 1980s and 1990s to reducing disparities in life expectancy among the educationally disadvantaged, the educational gap in life expectancy is rising. Between the 1980s and 2000, life expectancy increases occurred nearly exclusively among highly educated groups, according to research from Ellen Meara , an assistant professor of health economics at Harvard Medical School, and colleagues.