Skip Navigation LinksHome > October 2013 - Volume 45 - Issue 5 > In Praise of Coffee ... and Caffeine
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Journal of Neuroscience Nursing:
doi: 10.1097/JNN.0b013e3182a44aed
Editorial

In Praise of Coffee ... and Caffeine

Carroll, V. Susan Editor

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The Editor declares no conflicts of interest.

Although the title of this editorial suggests that it will be an unabashed paean to venti lattes, mochachinos of all sizes, and an enormous variety of sodas and energy drinks, the reality will unfold a bit differently. Truth be told, coffee—with caffeine at its core—has been one of the earth’s most popular and widely consumed beverages for thousands of years. Coffee drinkers attest to its ability to boost energy and provide a quick mental and physical stimulus when we’re flagging and to its often crucial role in social interactions. Coffee drinkers, and I am a lifelong, die-hard one, find it comforting, even soothing, and we look for evidence that bolsters our belief in its positive benefits.

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Good news! Recent research on several scientific fronts points to coffee’s notable health benefits. In a large-scale epidemiological study, the National Cancer Institute evaluated health data from more than 400,000 volunteers and found that men who reported drinking two or three cups of coffee each day were 10% less likely to have died during the 10+ year study than those who didn’t drink coffee; women fared even better, with a 13% lower risk of dying. Is there a direct link to coffee (and caffeine) intake? Maybe, maybe not, but the correlation looks suspiciously strong. Other research has linked moderate coffee drinking—three or four 5-ounce cups or a single venti-size cup—with a reduction in the risks for developing type 2 diabetes or basal cell, prostate, and oral cancers or the recurrence of breast cancer.

Perhaps most relevant to us as neuroscience nurses, and of the most potential consequence to our patients, are recent animal experiments and human studies that show how caffeine may actually reshape the biochemical world inside our brains in ways that could prevent dementia or alter the course of its progression. In October 2012, researchers at the University of Illinois published the results of an experiment in which mice that were briefly deprived of oxygen lost their ability to form new memories. Half of the mice were then given caffeine equivalent to several cups of coffee (a double-shot venti dose). When all of the mice were reoxygenated, the caffeinated mice regained their memory-forming abilities more than 33% faster than the uncaffeinated mice. The researchers hypothesize that caffeine disrupted the action of adenosine, a substance that plays a role in activating caspase and cytokine IL-1ß, which in turn cause cerebral inflammation. Caffeine apparently blocks inflammatory signaling and prevents memory impairment or loss.

Neuroscience researchers at the University of South Florida and the University of Miami examined the effects of high blood caffeine levels in individuals with mild cognitive impairment. Individuals with higher caffeine intake and consequent high blood levels of caffeine showed little, or slower, progression of cognitive losses than individuals with little or no caffeine in their bloodstreams. The uncaffeinated group was more likely to have progressed from mild cognitive impairment to moderate or moderately severe Alzheimer’s disease. This study in humans underscored the role caffeine may play in dementing disorders in which memory impairment is a key component,

Can we, or should we, chalk up the potential to preserve memory-forming functions or to limit cognitive decline to the effects of coffee and caffeine? Is it the coffee alone that accounts for changes in the brain’s biochemical foundation? Probably not. Many coffee drinkers regularly add sugar, artificial sweetener, dairy products, chocolate, or alcohol to their cups. Many of us ingest food with our coffee. These other substances also may contribute to actual or perceived benefits and confound the research results. And, no matter how rigorous the research design, mouse brains aren’t human brains, so we need to limit the degree to which we extrapolate evidence in mice to humans.

Me? Starbucks here I come and I’ll find some rodent companions to help me remember the way back to my office.

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© 2013 American Association of Neuroscience Nurses

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