Caffeine is the most commonly ingested drug in the world. It is so frequently and ubiquitously used that the World Health Organization even recognised caffeine dependence as a disorder. In my profession, caffeine is most consumed in the form of coffee. But here’s a shocker: I am not a coffee drinker. I never really was EVER one – even in college and even now in medical school, coffee is not my poison. Honestly, I just don’t find the coffee taste very appealing. When I sip a cup, my taste buds register a gustatory sensation of musk and chalk. However, I know many in my profession and many patients I’ve treated are big coffee junkies.
It always fascinated me that a lot of us don’t realize that caffeine is a drug – a very socially and culturally accepted drug, a drug that helps us in many ways become productive – but it is still a drug with actual effects on our physiology and our brains.
When I rotated on the cardiology service, coffee took on a more academic interest for me given the effects of caffeine on heart rate, specifically caffeine’s ability to trigger arrhythmias, or irregular heart beats. We would often recommend that our patients with heart failure limit their caffeine intake, but is there research to back this up? An article recently published in the Journal of the American Medical Association by Zuchinali et al demonstrated that acute ingestion (defined in their study as 500 mg of caffeine intake over 5 hours) did not induce arrhythmias in patients with systolic heart failure and patients at high risk for ventricular arrhythmias BOTH at rest and during physical activity. The researchers also note that to date, there is “no solid evidence to support the recommendation to limit moderate caffeine consumptions in patients at risk for arrhythmias.” So what is a clinician to do?
For starters, the study has its limitations in terms of applicability. In reality, many patients ingest caffeine chronically and in varying degrees in the form of coffee, tea, sports drinks, chocolate and in unlikely sources like guarana berries, guayasa and yaupon holly. This study focuses on the effects of ACUTE caffeine ingestion and does not take into account the fact that the subjects may be chronic coffee drinkers, AND so there is the possibility that long-term caffeine may blunt the pro-arrhythmic effect of an acute ingestion. So while this study is valuable and fascinating, I would still personally recommend for patients to limit caffeine intake given what research has told us about the physiological effects of caffeine.
Physiologically, caffeine disinhibits (a fancy work for activates) the effect on endogenous adenosine on ascending dopamine and arousal systems. Normally, adenosine stimulates adenosine receptors, which in turn inhibit the state of physiological arousal characterized by alertness and psychomotor agitation. In organic chemistry terms, caffeine is a derivative of a purine called methylxanthine, a known psychostimulant. In animal models, methylxanthine induces a well-documented dose-response increase in locomotor activity. In humans, paraxanthine is the primary metabolite of caffeine. In terms of addictive potential, caffeine induces dopamine release in the shell of the nucleus accumbens, the same structure that is targeted by amphetamines and cocaine. So there is solid evidence that suggests that caffeine is legitimately addictive and that it can induce a chemical dependence in our brains.
It always fascinated me that a lot of us don’t realize that caffeine is a drug – a very socially and culturally accepted drug, a drug that helps us in many ways become productive – but it is still a drug with actual effects on our physiology and our brains. Whether or not you are a coffee drinker, what are your thoughts on caffeine? Do you partake in this socially acceptable practice? Do you shun it – as I do? Are you in the process of withdrawing from it (which interestingly is characterized by an upregulation of adenosine in our brains, which we interpret as annoying for those of us undergoing withdrawal)?