Caffeine—the principal active ingredient in coffee, tea, and energy drinks—is found in more than 60 plants globally. Experts believe that these plants evolved over millions of years to produce caffeine as a natural pesticide against destructive insects.
The Canon of Medicine, written by the Persian physician-philosopher Avicenna in 1025 CE, was the first medical text to acknowledge coffee as a potential therapeutic agent. At that time, coffee was largely used to clean the skin and improve body odor. Today, most people use it and other caffeinated beverages to keep awake and alert—but caffeine has a slew of other health benefits.
Researchers have shown that caffeine can boost alertness and wakefulness in some consumers. In one study involving 9,003 British adults, caffeine was linked to dose-dependent improvements in visuospatial reasoning, simple reaction time, choice reaction time, and incidental verbal memory. These results were durable and more prevalent in older vs younger adults, which indicated that tolerance to caffeine’s cognitive benefits may be incomplete. Moreover, a muted response was observed in tea drinkers in which researchers observed improvement only in simple reaction time and visuospatial reasoning. Of note, caffeine can cause anxiety in some consumers.
Caffeine changes the body’s preferred metabolic substrate from glycogen to fat, thus increasing lipolysis; it stimulates hormone-sensitive lipase. At very high doses—as in those who binge on energy drinks—caffeine kicks protein kinase A into action, an enzyme key to lipid and glucose metabolism.
Intense exercise burns off loads of glycogen. Caffeine promotes glycogen resynthesis, which is needed for recovery. In well-trained athletes, when paired with carbohydrate intake, post-exercise caffeine consumption stimulates glycogen build-up.
Before we look at caffeine’s potential benefit in those with atrial fibrillation, let’s unpack more general effects of caffeine on the heart. Caffeine increases heart rate and contractility, inhibits the negative inotropic and chronotropic actions of adenosine, and acts as both a positive inotrope and chronotrope by inducing β1-receptor activation—thus setting off the sympathetic nervous system.
In high-power studies involving healthy adults, coffee intake was not linked to atrial arrhythmias. Other researchers have shown that caffeine does not increase the risk of atrial fibrillation. Drinking 9 cups of coffee a day, however, was linked to a two-fold increased risk of premature ventricular contractions. Moreover, drinking 10 cups of coffee a day has been linked to increased risk of sudden death in patients with coronary artery disease who previously experienced cardiac arrest. Of note, experts have shown that in habitual coffee drinkers, the adrenergic and proarrhythmic effects of caffeine are reduced.
"drinking 10 cups of coffee a day has been linked to increased risk of sudden death in patients with coronary artery disease who previously experienced cardiac arrest. "
So, the reason why caffeine could possibly help people with atrial fibrillation is that it has antifibrotic actions, and atrial fibrosis is important in the pathogenesis of atrial fibrillation.
In observational studies, caffeine intake has been linked to a lower risk of Parkinson disease. According to the authors of an editorial published in Neurology discussing this association:
“The protective effect of caffeine (found not only in coffee, but also in tea, and some sodas) has been demonstrated in large prospectively followed populations of men, with a dramatic reduction in risk (up to fivefold for persons who drank more than 4 cups of coffee a day). Decaffeinated coffee afforded no protection, pointing to caffeine rather than other substances in coffee or tea as the underlying pharmacologic agent. No such linear relationship is found in women, in whom the protective effects are either nonexistent or U-shaped.”
Furthermore, although caffeine does not reduce excessive daytime somnolence in patients with Parkinson disease, some researchers have shown that it may improve motor function in this population.
In one study of the association between coffee and/or tea consumption at midlife and the risk of dementia or Alzheimer disease risk in late-life (mean follow-up period: 21 years), researchers found that compared with coffee abstainers, coffee drinkers had a decreased risk of dementia/Alzheimer disease. Interestingly, the lowest risk—65% decreased—occurred in those who drank 3-5 cups of java a day.
In a review article published in Current Neuropharmacology, researchers offered one potential explanation for the neuroprotective effects of caffeine:
“Recent experimental evidence suggests that the primary target of the neuroprotective effects of caffeine is either the activation or the inhibition of the A1 and A2A adenosine receptor subtypes. The use of adenosine receptor antagonists, such as caffeine, has shown its usefulness not only in the treatment, but also in the protection against [Alzheimer disease and Parkinson disease]. Experimental evidence supports the use of caffeine and other adenosine receptor antagonists, as well as adenosine receptor agonists, in the reduction of hyperalgesia, excitotoxicity, inflammatory response, dyskinesia, akinesia, sensory and motor deficits, and neuronal cell death related to the pathophysiology of the discussed neurodegenerative diseases.”