## 1 Introduction  
Caffeine is consumed worldwide in various forms such as coffee, chocolate, beverages, and pharmaceuticals [1]. The caffeine content varies by form, with approximately 17 mg/oz in coffee, 0.8 mg/oz in cocoa and hot chocolate, and 30-100 mg in medications [2]. Most caffeine intake occurs through coffee, which is consumed at various times throughout the day, such as after waking up or during meals [1,3]. Globally, since 2002, the coffee consumption per capita has increased by 37% over the last 20 years [4], resulting in a paralleled increase in caffeine intake. Currently, the U.S. FDA recommends a maximum daily caffeine intake of 400 mg for healthy adults. Similarly, Health Canada recommends maximum daily doses of 45-85 mg/day for children aged <12, 2.5 mg/kg/day for adolescents aged >12 years, 400 mg/day for adults, and 300 mg/day for pregnant women [5]. The European Food Safety Authority (EFSA) recommends daily caffeine intake limits of 0.2-2.0 mg/kg body weight (bw)/day for children (3-10 years), 0.4-1.4 mg/kg bw/day for adolescents (10-18 years), 400 mg/day for adults, and 200 mg/day for pregnant women. The Ministry of Food and Drug Safety of South Korea recommends maximum daily intakes of 2.5 mg/kg bw/day for children and adolescents, 400 mg/day for adults, and 300 mg/day for pregnant women [6; 7]. Despite these guidelines, public awareness remains low, resulting in excessive caffeine consumption without consideration of the recommended limits. The primary driver of this consumption is the stimulatory effect of caffeine. Caffeine exerts its stimulatory effects through multiple mechanisms. Its structural similarity to adenosine allows it to act as an antagonist, with stimulatory effects being a key outcome [8]. Adenosine typically binds to the A1 and A2A receptors in the brain, thereby reducing the release of glutamate and dopamine and inducing drowsiness and sleepiness [9]. However, caffeine binds to these receptors non-selectively, blocking adenosine-mediated signaling and enhancing neurotransmitter release. This results in reduced drowsiness, improved brain function, and sympathetic nervous system activation, which increases catecholamine release and alertness [8; 10; 11]. Additionally, caffeine induces vasoconstriction, elevates blood pressure (BP) [8; 12; 13], increases renal blood flow, and inhibits ion and fluid reabsorption, leading to diuretic effects [8]. After exerting these effects, caffeine is metabolized by the liver and excreted by the kidneys through the urine [14; 15]. Its half-life in the body averages 3-5 h and varies according to physiological and environmental factors [8; 16; 17]. The positive effects of caffeine extend beyond its stimulatory effects. It activates lipase, promotes fat breakdown [14; 15; 18], enhances muscle strength by affecting muscle contraction [8; 15; 19], and aids in digestion by stimulating gastrin release and gastric acid secretion in the stomach and duodenum [20; 21]. However, excessive caffeine intake can cause dehydration due to excessive diuresis, gastritis, or ulcers due to the overproduction of gastric acid [8; 21], in addition to psychological side effects such as anxiety, tension, and insomnia [22]. High accessibility to caffeine also affects adolescent consumption, potentially causing electrolyte imbalances that impair growth and development, with potentially adverse effects on mental health during critical periods of physical and emotional change [23; 24]. In pregnant women, excessive caffeine intake may result in caffeine crossing the placental barrier owing to its lipid solubility, potentially causing miscarriages or other complications [25]. The effects of caffeine, both in terms of dosage and duration, are well documented. While small doses of caffeine may improve cognitive function and vascular health, excessive amounts can lead to reduced blood flow, an increased heart rate (HR), and impaired cognitive performance [18; 19; 20].