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Concentration-effect curves for caffeine at various potential sites of action. Caffeine markedly affects A1 and A2a receptors at low micromolar concentrations. To inhibit phosphodiesterase (PDE), concentrations 20 times as large are required. Approximate caffeine concentrations resulting from a single cup of coffee and toxic doses of caffeine are indicated. (Modified from Fredholm (1995) with permission from Elsevier.).
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Caffeine is consumed by over 80% of U.S. adults. This review examines the effects caffeine has on cognitive and physical function, since most real-world activities require complex decision making, motor processing and movement. Caffeine exerts its effects by blocking adenosine receptors. Following low (∼40mg or ∼0.5 mg·kg(-1)) to moderate (∼300mg o...
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Background:
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Objective:
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Citations
... Caffeine (1,3,7-trimethylxanthine) ( Fig. 1b the chemical structure), is the most widely consumed psychoactive compound globally [9,10]. It is naturally found in different quantities in the seeds, leaves, vegetables, cereals, coffee beans, tea leaves, cocoa beans, cola nuts, and fruits of various plants [10][11][12]. ...
... By using Eqs. (6)(7)(8)(9) to interpret absorption spectra, these features are crucial for comparing the strength of electron transitions in various solvents [26]. ...
In this research, the photophysical properties of metformin hydrochloride (MF-HCl) were studied using spectroscopic and molecular docking techniques. The interaction between metformin hydrochloride and caffeine is essential for understanding the pharmacokinetics of metformin, particularly in populations with high caffeine consumption. Metformin is a first-line medication for managing type 2 diabetes, while caffeine is a widely consumed dietary stimulant. Knowing how caffeine may affect the action of metformin is crucial for effective diabetes management. The spectroscopic techniques results showed that the photophysical properties (fluorescence quantum yields, lifetime, radiative, and non-radiative decay) of the drug are influenced by solvent polarity and drug concentration. The binding mechanism of metformin hydrochloride–caffeine (MF-HCl-CAF) was identified through the fluorescence quenching method. The quenching of drugs induced by caffeine is due to ground state complex formation. The binding occurs due to hydrogen bonds and Van der Waals forces in the reaction. The förster resonance energy transfer (FRET) between metformin hydrochloride and caffeine was also calculated using flourtools.com software. The threshold distance (R0), for 50% energy transfer from metformin hydrochloride to caffeine is 1.81 nm and the binding distance (r), between caffeine and the amino acid residue in metformin hydrochloride is 1.55 nm. Dynamic light scattering (DLS), Zeta potential, and Fourier transform infrared (FTIR) spectroscopy confirm the conformational change of the drugs, as the caffeine molecule binds to metformin hydrochloride molecules. The molecular docking of metformin hydrochloride with the amp-activated protein kinase receptor (PDB Id: 1z0n) is analyzed. Again the docking of both metformin hydrochloride and caffeine (two ligands) with the protein receptor (PDB Id: 1z0n) was also analyzed and the results agreed with the fluorescence quenching techniques.
... There is general agreement about the enhancement effects exerted by caffeine on "low-order" cognitive functions such as speed of processing, simple reaction times and choice reaction times, attention, and vigilance (i.e., the ability to sustain performance on prolonged, repetitive, or monotonous assignments). Sustained tasks needing vigilance seem to be the most sensitive to the behavioral effects of variable doses of caffeine ranging from 32 to 300 mg (McLellan et al., 2016). In both sleep-deprived and rested individuals, caffeine ingestion improves visual and auditory vigilance detection in several tasks (e.g., Lieberman et al., 2002). ...
... Such functions include, among others, the ability to plan, conceptualize, manage, and sustain behaviors toward objectives, response shifting and flexibility, inhibition, and working memory (Diamond, 2013). Caffeine impact on executive functions is still under debate due to both a relatively small number of published studies and the wide-ranging employing of materials and methods (McLellan et al., 2016), which lead to conflicting findings. In fact, while some studies have been found caffeine enhancement effects in several cognitive domains, such as task switching and anticipatory control processes (Tieges et al., 2006), monitoring of ongoing cognitive processes (Tieges et al., 2004), executive updating (Lanini et al., 2016), executive and inhibitory control (e.g., Einöther & Giesbrecht, 2013), others failed to find any effects (e.g., Tieges et al., 2009) or just revealed influences in light caffeine consumers after the ingestion of a relatively large dose (e.g., Lyvers et al., 2004). ...
Coffee and caffeinated products have a remarkable potential to beneficially influence different psychomotor variables. The main neuropharmacological mechanisms underlying caffeine’s psychostimulant action involve an antagonist role on the adenosine receptor, which enables an increase of brain catecholamine levels. These mechanisms also encompass dependence and withdrawal effects. Concerning the impact on mood, caffeine increases attention, alertness, hedonic tone, vigor, and motivation, whereas it decreases apathy, irritability, anxiety, and tiredness. The effects on cognition are featured by a positive influence on low-order cognitive functions such as processing speed (reaction times) or prolonged vigilance, whereas the ones on higher-order cognitive functions such as planning, conceptualizing, managing, and working memory are still under debate although with positive promises. Caffeine exerts also clear positive effects on physical activity, where it provides an ergogenic gain for endurance exercise and to a lesser degree also for short intense exercise. Dose dependence of the effects as well as the influence of contextual and subjective variables on caffeine’s psychomotor effects is discussed.
... Caffeine is one of the most widely consumed pharmacological substances globally, exerting several significant effects, including central nervous system stimulation, diuresis, and a positive impact on the cardiovascular scheme. (McLellan et al., 2016) Nonetheless, an enormous intake of CFE can lead to adverse impacts, like cardiovascular symptoms, depression symptoms, and hyperactivity illness. Consequently, there is a need for a precise, rapid, easy, and economically-saving method for determining CFE content in popular consumption products. ...
The RSCD-modified electrode has excellent catalytic electrochemistry properties to CFE with a well-defined electrochemical peak, at 1.26 V. The linear correlation of the peak current, Ip of CFE and the concentration range (0.2 µM – 1.4 µM) give a small LOD value of 0.095 M and LOQ value of 0.313 M. This illustrates good sensitivity and the ability to apply the modified electrode to detect CFE in several practical matrix samples.
... Additionally, caffeine has been shown to positively influence mental alertness/vigilance [102][103][104][105]. It is important to note that the effects of caffeine on "higher" cognitive functions, such as problem-solving and decision-making, remain uncertain [106,107]. Some research indicates that caffeine can improve executive functions, such as task switching and visual selective attention, though these effects are more variable and dose-dependent [108][109][110]. ...
Energy drinks are a commonly consumed beverage, and studies suggest a possible performance-enhancing effect. A Google Scholar search using the keywords “energy drinks” and “exercise” yields numerous results, underscoring the voluminous research on this topic. However, there are questions regarding the effectiveness and safety of energy drinks. These questions include, but are not limited to: (1) What are the main active ingredients in energy drinks? (2) Do energy drinks assist in weight management? (3) Do energy drinks enhance aerobic performance? (4) Do energy drinks enhance athletic speed? (5) Do energy drinks improve reaction time? (6) Do energy drinks enhance lean tissue mass? (7) Can energy drinks improve cognitive performance? (8) Does the acute consumption of energy drinks elevate resting energy expenditure? (9) Is there any evidence to suggest that energy drinks are more effective than an identical serving of caffeine alone? (10) Are there sex differences in the response to energy drink consumption? (11) Do energy drinks affect sleep or sleepiness? (12) Should pregnant women avoid energy drinks? (13) Do energy drinks adversely affect cardiovascular function? (14) Does consuming energy drinks cause brain damage? (15) What are other safety considerations regarding energy drinks? (16) Is there any evidence to suggest that energy drinks are more effective than an identical serving of caffeine alone? (17) If caffeine is the main active ingredient in energy drinks and coffee, why is there a discrepancy in the adverse events reported for each? To address these questions, we performed an evidence-based scientific evaluation of the literature on energy drink supplementation.
... Last, but not least, another neurotransmitter that is influenced by caffeine exposure is acetylcholine, coffee beverages increasing its level, that can improve cognitive performance [28,31]. The relationship between coffee consumption and brain health is benefic in moderate consumption, thanks to the potential neuroprotective effects of caffeine. ...
Coffee, a habitual drinking nowadays, starts to be explored more in medical research. Moreover, in the last decade, it represented a main preoccupation for some groups of the researchers, the medical literature being improved with many science articles about its positive and negative effects, starting with the organs benefits and damage, the knowledge about its involvement progressing till molecular mechanism and establish influences in metabolic processes. The current state-of-the-art review related the last eleven years (2014-2024) medical concepts about this topic, focusing on the triad of coffee, neurotransmitters and obesity interplay, an incomplete discovered axis and few debated one, in spite of the coffee effects and its actions on human body.
... Although caffeine provides immediate energy after consumption, some longer-lasting effects consequences alter sleep patterns for many hours after intake, including prolonged sleep latency, reduced total sleep time, sleep inefficiency, worsened perceived sleep quality, and REM sleep behavior disorder. 15,41,42 The linkage between sleep characteristics and evening sugar intake hasn't been largely studied, but findings from the existing literature indicate that consuming lower-quality carbohydrates negatively impacts sleep quality. Higher intakes of dietary added sugars, starch, and nonwhole/refined grains were each associated with higher odds of incident insomnia among postmenopausal women from the Women's Health Initiative Observational Study. ...
Objective To examine the association of evening eating clock time, its elapsed time to the midpoint of sleep (TEM), consumption of caffeine and sugary foods, and reporting dinner as the largest meal with sleep quality indicators and insomnia.
Methods Participants ( n = 2,050;18–65y) were part of population-based research, with virtual data collection. Logistic regression models were fitted to assess differences in the ORs(95%CI) of sleep duration < 7 hours, sleep latency > 30 minutes, poor sleep quality, and insomnia (outcomes) with the evening diet-related variables. Linear regression analyses evaluated differences in sleep duration and latency associated with the same variables. Restricted cubic splines were used to study the shape of the association of eating event clock time and TEM with sleep duration and latency.
Results Each additional hour of evening eating clock time and of the TEM, respectively increased and decreased, the odds of sleep duration < 7/h [OR(95%CI):1.30(1.20,1.40); OR(95%CI):0.51(0.47,0.56)], sleep latency > 30min [OR(95%CI):1.14(1.07,1.22); 0.88(0.83,0.94)], poor sleep quality [OR(95%CI):1.21(1.13,1.30); 0.80(0.76,0.85)] and insomnia [OR(95%CI):1.12(1.04,1.20); 0.89(0.84,0.95)]. We found a dose-response association between evening eating (clock time and TEM) and sleep duration. The shortest latency was seen when evening eating was ∼20:00 and ∼7–8 hours before the midpoint of sleep. Participants who reported dinner as the largest meal and consumed caffeine and sugary foods/beverages after 18:00 presented higher odds of sleep duration < 7 hours, poor quality, and insomnia.
Conclusions Our findings indicate that an early-eating schedule has beneficial sleep effects and that it will be necessary to consider evening eating patterns and timing, along with the existing sleep and circadian hygiene, to improve sleep quality and circadian health.
... Following low (∼40 mg or ∼0.5 mg kg−1) to moderate (∼300 mg or 4 mg kg−1) caffeine doses, alertness, vigilance, attention, reaction time and attention improve, but less consistent effects are observed on memory and higher-order executive function, such as judgment and decision making. Effects on physical performance on a vast array of physical performance metrics such as time-toexhaustion, time-trial, muscle strength and endurance, and high-intensity sprints typical of team sports are evident following doses that exceed about 200 mg (∼3 mg kg−1) (. (Meng Yang, 2020), and improve sleep quality (McLellan, Caldwell & Lieberman, 2016). Both sleep loss and daily caffeine intake can induce changes in grey matter (GM). ...
To evaluate the effects of various interventions on anaerobic power, fatigue index, and overall performance in college students. Participants were 30 college students aged 18-22 years from Sichuan Vocational College of Health. Their height, weight, and anaerobic capacity were measured using the running-based anaerobic sprint test (RAST). We divided the students into three groups of 10 participants each, consisting of 3 males and 7 females, based on their RAST test scores. Group 1 received a placebo (500 mg) combined with 4 weeks of athletic training; Group 2 received a single dose of 500 mg of green tea extract with exercise; and Group 3 received 500 mg of green tea extract combined with 4 weeks of athletic training. Before-and-after-experimental data research designs were compared using a t-test analysis, while differences between groups were assessed. The results showed that statistically significant were not differences in anaerobic capacity for Group 1, while Group 2 displayed significant improvements in anaerobic capacity and mean power among female students (p<.05). Group 3: students’ exercise training on anaerobic power, fatigue index, and mean power variables are differences, significant for both male and female students (p<.05). Confirmation of the effect of green tea extract in conjunction with exercise prices of training on anaerobic performance in college students’ outcomes between each paired-group using one-way ANOVA, the results revealed that the four variables are differences, significant in anaerobic power, average power, and fatigue index across the groups, and Group 3 indicating the most notable improvements. Suggestions that, combining green tea extract with prolonged athletic training significantly improves anaerobic capacity, particularly in female participants. These results highlight the potential benefits of green tea extract in enhancing athletic performance, warranting further research to explore its long-term effects and optimize exercise interventions.
... Moreover, excessive intake of coffee may increase the risk of DN. This review suggests that this is because caffeine, as an adenosine receptor antagonist, binds to adenosine receptors upon intake (76), influencing adenosine's antiinflammatory properties and glomerular hemodynamics, leading to glomerular remodeling, sclerosis, and the occurrence of proteinuria (77). ...
Diabetic nephropathy (DN), as the most serious minor vascular complication of diabetes, imposes a significant socioeconomic and medical cost around the world, and its prevention and treatment are a major challenge in the current medical community. Observational studies and randomized controlled trials have revealed protective and risk factors for some DN. However, the conclusions of these researches may be influenced by several types of confounding. Mendelian randomization is a new epidemiological method mainly used to infer the causal relationship between exposure and outcome. Many Mendelian randomization studies have found potential causal relationships between DN and some diseases and lifestyle habits, thus providing valuable data for future mechanistic studies as well as the development and implementation of clinical prevention strategies. As a result, the purpose of this review is to evaluate the published Mendelian randomization study of DN, using the bibliometric research method, analyze the current research status and hot spots, and further summarize the genetic evidence about the potential protection of DN and risk factors to provide new inspiration for the etiology of DN and as a reference for clinical intervention.
... Packed with a volatile cocktail of stimulants caffeine, sugar, taurine, ginseng, and guarana these drinks deliver a powerful neurochemical punch, with caffeine levels ranging from a mild 50 to a heart-racing 500 mg per can (Heckman et al., 2010). This primary ingredient acts like a molecular maestro, swiftly infiltrating the body and brain, antagonizing adenosine receptors and amplifying dopamine transmission to create an electrifying surge of energy (McLellan et al., 2016). Beyond basic stimulation, high doses of caffeine trigger a biochemical cascade, promoting catecholamine release, dilating blood vessels, and accelerating fat metabolism (Bühler et al., 2014). ...
Energy drink consumption, particularly among teenagers and young adults, has experienced a significant rise in recent years. However, mounting research points to the potential for chronic energy drink use to cause biochemical and histological abnormalities in vital organs such as the liver, kidneys, and reproductive system. To investigate whether pomegranate peel extract could offer protection against these toxic effects, this study was conducted on adult male albino rats divided into five groups: a control group, a pomegranate peel extract group, an energy drink group administered Red Bull ® , a group pre-treated with pomegranate peel extract before energy drink consumption, and a group given energy drink followed by pomegranate peel extract. Over a 12-week treatment period, serum and tissue samples were collected to analyze liver and kidney function markers, lipid profile, oxidative stress levels, and histological changes. Rats those consumed energy drinks for 12 weeks exhibited elevated liver enzymes, impaired kidney function, disrupted lipid profiles, increased oxidative stress, and noticeable morphological changes in liver, kidney, and testicular tissues. In contrast, rats those received pomegranate peel extract either before or after energy drink consumption showed significant improvements in these parameters, demonstrating the protective effects of pomegranate peel extract in attenuating biochemical abnormalities and restoring tissue histology. These findings suggest that pomegranate peel extract has both therapeutic and preventive potential against the toxicity induced by chronic energy drink consumption, offering valuable insights that could inform strategies to reduce the adverse health effects associated with the regular use of energy drinks.
... Caffeine is the most widely consumed psychoactive substance and among the most promising cognitive function enhancers (Cappelletti et al., 2015;James, 2014). Acute caffeine intake is shown to enhance simple cognitive functions such as attention and reaction time but less consistent effects are observed for complex functions such as decision making (McLellan et al., 2016). There are also data showing a positive relationship between habitual caffeine consumption with memory and executive function, but there is limited evidence for an association with simple cognitive functions (Johnson-Kozlow et al., 2002). ...
... Participants A sample size of 131 was calculated using G*Power 3.1 (Faul et al., 2009) for a medium effect size (f 2 = 0.15) at 80% power and an alpha level of 5% for 13 influencers of cognitive function: (1) age, (2) sex, (3) body mass index (BMI), (4) habitual caffeine intake, (5) genetic variants in genes involved in caffeine metabolism (AHR rs6968554 and CYP1A2 rs2472297) and response (ADORA2A rs5751876), (6) physical activity, (7) level of education, (8) subjective sleep quality and (9) subjective sleepiness prior to tasks, (10) tobacco, (11) alcohol use, (12) ADA rs73598374 and (13) APOE ε4−/ε4+ genes (Campos et al., 2016;Erickson et al., 2019;Harada et al., 2013;McLellan et al., 2016;Michaud et al., 2018;Wang et al., 2022). The ADA rs73598374 and APOE ε4+/ε4− were used as proxies of sleep quality and risk of cognitive impairment, respectively (Gharbi-Meliani et al., 2021;Tartar et al., 2021). ...
Background
Research on caffeine and cognitive performance remains controversial. Variations in genes associated with caffeine metabolism and response such as CYP1A2, AHR and ADORA2A may account for variable findings.
Aim
To investigate caffeine × gene interactions on cognitive performance in all key domains of cognition in healthy individuals.
Methods
Participants completed a lifestyle and food frequency questionnaire and a cognitive test battery including validated tasks to assess the domains of social cognition, memory, attention and executive function. Genotyping was performed for AHR rs6968554, CYP1A2 rs2472297, ADORA2A rs5751876, ADA rs73598374 and APOE rs429358 and rs7412.
Results
Significant gene × caffeine interactions were observed for the domains of social cognition, ( F 2, 123 = 5.848, p = 0.004) and executive function ( F 2, 109 = 3.690, p = 0.028). ‘Slow’ metabolisers had a higher performance in social cognition compared with ‘fast’ metabolisers among high-caffeine consumers ( p = 0.004), while ‘fast’ metabolisers had a higher performance in executive function compared with ‘slow’ metabolisers among moderate caffeine consumers ( p = 0.002).
Conclusions
The present findings suggest an association between genetic caffeine metabolism, habitual caffeine intake and cognitive function in the domains of social cognition and executive function. More research in naturalistic environments using larger cohorts is needed to confirm these findings to add to our understanding of how habitual caffeine may influence cognitive function based on individual genotype.
