Caffeine: Friend or Foe?

Abstract

The debate on the safety of and regulatory approaches for caffeine continues among various stakeholders and regulatory authorities. This decision-making process comes with significant challenges, particularly when considering the complexities of the available scientific data, making the formulation of clear science-based regulatory guidance more difficult. To allow for discussions of a number of key issues, the North American Branch of the International Life Sciences Institute (ILSI) convened a panel of subject matter experts for a caffeine-focused session entitled "Caffeine: Friend or Foe?," which was held during the 2015 ILSI Annual Meeting. The panelists' expertise covered topics ranging from the natural occurrence of caffeine in plants and interindividual metabolism of caffeine in humans to specific behavioral, reproductive, and cardiovascular effects related to caffeine consumption. Each presentation highlighted the potential risks, benefits, and challenges that inform whether caffeine exposure warrants concern. This paper aims to summarize the key topics discussed during the session.

Caffeine, a Risk Factor for Osteoarthritis and Longitudinal Bone Growth Inhibition

“…The biological effects of caffeine are heterogeneous ( Figure 3). On the one hand, it has been suggested that low doses of caffeine could exert beneficial activities on endothelial function [35,36], in inflammatory processes by reducing some pro-inflammatory cytokines [36,37], and in the improvement of cognitive faculties, as well as providing protection against dementia [35,38]. However, clinical trials conducted in humans have suggested that caffeine is not responsible for the certain beneficial properties observed in caffeinated beverages, like the anti-inflammatory effects of coffee [39,40].…”

Hold off on that shot of Java: more evidence that caffeine intake leads to false negative adenosine stress myocardial perfusion

“…In a recent study, Liu et al found that normal, infarcted, ischemic myocardium can be differentiated by native T1 mapping at rest and during adenosine stress because these tissues classes exhibit distinctive T1 profiles. Compared to resting conditions, myocardial T1 values during adenosine stress increased approximately 6 % both at 1.5 and 3.0T field strengths in of variation between individuals are frequency of caffeine intake, concurrent cigarette smoking and genetic variations in the adenosine receptors and downstream signaling cascade proteins [4]. As demonstrated by Kuijpers et al, native T1-mapping seems capable of detecting the blunting effects of caffeine consumption on adenosine-induced myocardial hyperaemia.…”

“…Caffeine (1,3,7-trimethylxanthine) is one of the most widely consumed stimulants worldwide with over 80 % of the US population reporting daily intake [4]. Individuals primarily consume caffeine for a variety of behavioral effects such as changes in mood, energy and alertness [5].…”

“…Caffeine is present in coffee, tea, a variety of different soft drinks, energy drinks as well as cacao products and many fruits and vegetables. In the US approximately 75 % of caffeine intake is attributable to coffee consumption with estimated mean intake of approximately 180 mg/day [4]. A number of studies have investigated the effect of caffeine on adenosine stress myocardial perfusion imaging, but there is no consensus on whether inadvertent intake should lead to postponement of a planned examination [6,7].…”

“…In humans, caffeine is metabolized in the liver by the cytochrome P450 (CYP) enzyme CYP1A2 and healthy adults the half-life of caffeine is approximately 4-5 h [4]. However, there is substantial variation between males and females and different age groups; other important sources evidence that native T1 mapping could potentially replace contrast-enhanced MR-MPI.…”