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[1] 2014, nationally representative sample: Results showed that 85% of the U.S. population consumes at least one caffeinated beverage per day. The mean (±SE) daily caffeine intake from all beverages was 165 ± 1 mg for all ages combined. Caffeine intake was highest in consumers aged 50–64 years (226 ± 2 mg/day). The 90th percentile intake was 380 mg/day for all ages combined. Coffee was the primary contributor to caffeine intakes in all age groups. Carbonated soft drinks and tea provided a greater percentage of caffeine in the younger (<18 years) age groups. The percentage of energy drink consumers across all age groups was low (⩽10%).
[2] https://www.democrats.senate.gov/newsroom/press-releases/majority-leader-schumer-demands-fda-investigate-prime-for-absurd-caffeine-content-and-marketing-targeting-kids-on-social-media-schumer-warns-parents-that-summers-hottest-drink-has-so-much-caffeine-that-it-puts-red-bull-to-shame
[3] https://www.documentcloud.org/documents/24075542-katz-v-panera?responsive=1&title=1
[4] https://loop.frontiersin.org/people/2183/bio
[5] Coffee (via caffeine and other components, mainly polyphenols) stimulates the secretion and production of gastrin and hydrochloric acid…Regular coffee and decaffeinated coffee stimulate the secretion of cholecystokinin (CCK), a hormone that stimulates gallbladder function and contractility, and increases the production of bile.
[6] https://pubmed.ncbi.nlm.nih.gov/2338272/ Subjects were positioned on their left sides and a multilumen manometric probe was inserted into the rectosigmoid using a rigid sigmoidoscope.
[7] In another similar study, “Caffeinated coffee stimulates colonie motor activity. Its magnitude is similar to a meal, 60% stronger than water and 23% stronger than decaffeinated coffee.”
[8] The speed at which the response occurs (within four minutes after drinking the coffee) suggests an indirect action on the colon as it seems unlikely that coffee would reach the colon in this time either via the intestinal lumen or the blood stream. We suspect that coffee may induce a 'gastrocolonic response' by acting on epithelial receptors in the stomach or small bowel. Such a mechanism could be mediated by neural mechanisms or by gastrointestinal hormones. Coffee has been shown to promote release of Gastrin' which can increase colonic spike and motor activity.7 Cholecystokinin is another putative mediator of the 'gastrocolonic response'8 but there are no data on the effect of coffee on CCK release.
[9] In ten men: The oral absorption was very rapid, reaching a peak (Tp) plasma concentration after 29.8±8.1 min (mean±SEM). [sci hub]
[10] According to human studies, nearly 99% of caffeine is absorbed across the wall of the gastrointestinal (GI) tract within approximately 30–45 minutes.
[11] After caffeine dosing, plasma caffeine levels peaked at an average concentration of 3.2 % 1.5 mg/L 75 minutes after 2 mg/kg and 7.5 2 1.0 mg/L 75 minutes after 4 mg/kg doses."
[12] Caffeine is lipophilic enough to cross all cellular membranes, including the blood-brain barrier. [sci hub]
[13] The association between increases in D2/D3 receptor availability in ventral striatum and alertness suggests that caffeine might enhance arousal, in part, by upregulating D2/D3 receptor
[14] The results showed that caffeine led to a more positive mood and improved performance on a number of tasks. [sci hub]
[15] The molecular structure of caffeine is similar to
that of adenosine, which allows caffeine to bind to
adenosine receptors, block adenosine, and inhibit
its effects ….
Accumulation of adenosine in the brain inhibits arousal and increases drowsiness. In moderate doses (40 to 300 mg), caffeine can antagonize
the effects of adenosine and reduce fatigue, increase
alertness, and reduce reaction time
[16] Caffeine —the most often consumed stimulant in the world—blocks adenosine receptors and normally attenuates the consequences of sleep deprivation on arousal, vigilance, and attention.
[17] Almost all tests demonstrate significant effects of various doses of caffeine on attention performance. Three tests that have been extensively used, namely the repeat digit detection, simple reaction time and a focused attention choice reaction time test, shown consistent effects of a range of doses
[18]Caffeine exerts its most reliable beneficial effects on vigilance tasks. Caffeine’s positive effects are present in rested individuals (Lieberman et al., 2010, Lieberman et al., 1987b, Lieberman et al., 1987a, Smith, 2005) and in sleep-deprived individuals (Lieberman et al., 2002, Smith, 2011, Weiss and Laties, 1962, Wesensten et al., 2002, Wesensten et al., 2004), and likely occur because caffeine reverses decrements in alertness associated with prolonged maintenance of attention. Caffeine also reliably enhances the fundamental cognitive processes that underlie all types of performance such as reaction time (Nehlig, 2010, Smith, 2002) and attention (Einother and Giesbrecht, 2013, Smith, 2011). The acute effects of caffeine on memory are less consistent and appear, among other things, to be influenced by whether or not the task is boring or engaging (Amendola et al., 1998, Anderson and Revelle, 1983).
[19] Nighttime driving performance was similar to daytime performance (0 to 1 line crossing) for 75% of participants after coffee (0 or 1 line crossing), for 66% after the nap (P 0.66 vs. coffee), and for only 13% after placebo (P 0.041 vs. nap; P 0.014 vs. coffee). [sci hub]
[20] After adjustment for potential confounders, drivers who consumed caffeinated substances for this purpose had a 63% reduced likelihood of crashing (odds ratio 0.37, 95% confidence interval 0.27 to 0.50) compared with drivers who did not take caffeinated substances.
[21] An example of a visual cartoon item is shown in Figure 1. An example of a verbal headline item is as follows: Headline 1—“Veterinarian Investigates Failed Panda Mating;” Headline 2—“Panda
Mating Fails; Veterinarian Takes Over.” Participants made a forced choice for each pair, deciding whether the stimulus on the right was funnier, the one on the left was funnier, or whether the 2 stimuli
were equally funny…The modafinil 400-mg group (mean = 55.86, SD = 12.65) demonstrated significantly better performance on the cartoon items than both the placebo group (mean = 39.97, SD = 12.62, p = .004) and the caffeine 600 mg group (mean = 41.58, SD = 12.62, p = .011). None of the other groups differed significantly. [sci hub]
[22] https://profiles.ucsf.edu/gregory.marcus
[23] https://www.irhythmtech.com/providers/zio-service/zio-monitors
[24] The participants downloaded the Eureka app (developed and maintained by investigators at the University of California, San Francisco) to their smartphones to continuously monitor their geolocation in order to track visits made to coffee shops.
[25] Table S23
[26] When randomized to coffee, participants slept about a half-hour less per night (36 fewer minutes, 95% CI 25 to −47, p < .001, Figure 2), and every additional coffee drink was associated with 14 min less sleep per night (95% CI 10−18 fewer minutes, p < .001). Coffee notoriously disrupts sleep, but to our knowledge, the relationship had not previously been characterized, nor quantified, among ambulatory patients in a randomized trial. Of interest, there was a statistically significant interaction with caffeine metabolism-related genetic variants: slower caffeine metabolizers experienced almost an hour less sleep on average, whereas the fastest caffeine metabolizers had no detectable difference in sleep duration when exposed to coffee.
[27] The CYP1A2 variant is associated with the inducibility of CYP1A2, such that CYP1A2 C allele carriers (∼32% of the European population) metabolize caffeine less effectively than AA carriers
[28] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4388784/
[29] https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1002033
[30]Modeling based on twin studies reveals that genetics plays a role in individual variability in caffeine consumption and in the direct effects of caffeine."
[31]See Figure B https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2734709
[32]There is sound evidence that caffeine enhances endurance and provides a small but worthwhile enhancement of performance over a range of exercise protocols, with the traditional protocol involving a caffeine dose of ~6 mgkg–1 body mass taken 1 h pre-exercise.
[33] This 2020 review on caffeine and athletic performance says: “Synthesis of the currently available meta-analyses suggest that caffeine ingestion improves exercise performance in a broad range of exercise tasks. Ergogenic effects of caffeine on muscle endurance, muscle strength, anaerobic power and aerobic endurance were substantiated by moderate quality of evidence coming from moderate-to-high quality systematic reviews. For other outcomes, we found moderate quality reviews that presented evidence of very low or low quality. It seems that the magnitude of the effect of caffeine is generally greater for aerobic as compared with anaerobic exercise.” [sci hub]
[34] Aerobic endurance appears to be the form of exercise with the most consistent moderate-to-large benefits from caffeine use, although the magnitude of its effects differs between individuals.
[35] Synthesis of the currently available meta-analyses suggest that caffeine ingestion improves exercise performance in a broad range of exercise tasks. Ergogenic effects of caffeine on muscle endurance, muscle strength, anaerobic power and aerobic endurance were substantiated by moderate quality of evidence coming from moderate-to-high quality systematic reviews.
[36] A review published last year found that “The performance-enhancing effect of acute caffeine ingestion has been well established, with a number of meta-analysis demonstrating benefits for muscular strength and power [1,2,3,4], endurance performance [5,6,7,8], anaerobic power [9], sport-specific skills [10,11] and cognitive function [12].”
[37] Caffeine significantly improved squat (4.5 ± 1.9%, effect size [ES]: 0.25) and bench press 1RM (3.3 ± 1.4%, ES: 0.20), and squat (15.9 ± 17.9%, ES: 0.31) and bench press RTF (9.8 ± 13.6%, ES: 0.31), compared to placebo. MVC torque (4.6 ± 7.3%, ES: 0.26), CMJ height (7.6 ± 4.0%, ES: 0.50), and power (3.8 ± 2.2%, ES: 0.24) were also significantly increased with caffeine.
[38] https://pubmed.ncbi.nlm.nih.gov/7640644/
[39] The Panel notes that caffeine antagonises the vasodilator effect of adenosine and other A2A receptor agonists in the coronary arteries in a dose-dependent manner and this effect leads to a reduction of MBF and MFR during intense physical exercise, primarily in subjects with CAD, but also in healthy subjects to some degree. However, on the basis of the data available, the Panel considers that caffeine at doses of 200 mg consumed one to two hours prior to exercise does not induce clinically relevant reductions of the coronary flow reserve in healthy adult subjects under normal environmental conditions. The Panel notes that the effect of higher doses of caffeine has not been tested.
[40] Our findings indicate
Our findings indicate that acute caffeine supplementation in trained subjects has positive effects on several psychophysiological mood variables and psychological responses, and on performance.
[41] Of the papers reviewed in Supplementary Tables 2–4, almost 80% reported positive findings during endurance exercise, whereas two-thirds reported ergogenic effects for measures of muscle strength and associated tests of muscular endurance or high-intensity exercise. Except for very short duration anaerobic exercise, there was also a common thread throughout these studies, regardless of the type of exercise, that caffeine reduced perception of effort and lowered sensations of pain.
[42] Cochrane says “The addition of caffeine (≥ 100 mg) to a standard dose of commonly used analgesics provides a small but important increase in the proportion of participants who experience a good level of pain relief.”
[43] “There is some evidence that the effects of caffeine on physical performance could be related to the release of calcium from the sarcoplasmic reticulum and inhibition of its reuptake, which subsequently increases nitric oxide via the activation of endothelial nitric oxide synthase (see Cappelletti et al., 2015). These actions may be associated with changes in neuromuscular function and increased contractile force in skeletal muscles that could be ergogenic (Tarnopolsky, 2008).”
[44] Caffeine withdrawal is a clinically significant cluster of symptoms, behaviours and/or physiological features, varying in degree of severity and duration, that occurs upon cessation or reduction of use of caffeine.
[45] 55% of a sample of people fasting for Ramadan got a caffeine withdrawal headache; it was worse for people who typically drank more coffee.
[46] Caffeine withdrawal could potentially trigger a migraine in people who get migraines routinely.
[47] 2004 review: Of 49 symptom categories identified, the following 10 fulfilled validity criteria: headache, fatigue, decreased energy/ activeness, decreased alertness, drowsiness, decreased contentedness, depressed mood, difficulty concentrating, irritability, and foggy/not clearheaded. In addition, flu-like symptoms, nausea/vomiting, and muscle pain/stiffness were judged likely to represent valid symptom categories. In experimental studies, the incidence of headache was 50% and the incidence of clinically significant distress or functional impairment was 13%. Typically, onset of symptoms occurred 12–24 h after abstinence, with peak intensity at 20–51 h, and for a duration of 2–9 days. In general, the incidence or severity of symptoms increased with increases in daily dose; abstinence from doses as low as 100 mg/day produced symptoms.
[48] See Figure 1.
[49]Addiction is defined as a chronic, relapsing disorder characterized by compulsive drug seeking and use despite adverse consequences.
[50] Addiction is defined as not having control over doing, taking or using something to the point where it could be harmful to you.
[51] See table 2 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3777290/
[52] NHANES study finds people consume caffeine based on circadian rhythms and generally stay within healthy amount
[53] Tolerance to some subjective effects of caffeine, namely
anxiety, jitteriness/nervousness, activity/stimulation/
energy, and the potency of caffeine effects might occur
(Evans and Griffiths, 1992). Tolerance to caffeine-induced
alertness and wakefulness is debated (for review, see
Nehlig, 2004). These effects are paralleled by the lack of
tolerance of cerebral glucose metabolism and brain function to caffeine. As shown in rodents, the acute administration of a low dose of caffeine leads to similar metabolic
increases whether the animals have been exposed for
15 days to daily chronic treatment of caffeine or saline.
[54] Nevertheless, in drug-discrimination studies in users of prototypical psychostimulants, low to intermediate doses of caffeine produce a profile of positive subjective effects similar to those of amphetamine and cocaine, while with high doses of caffeine the subjects report aversive subjective feelings of anxiety and nervousness
[55] While more clinical research needs to be done to determine if caffeine use disorder can adhere to the general scheme of SUD and about the real contribution of arousal/withdrawal reversal in caffeine use, there is at present no reasonable doubt in the literature about the fact that a rising real societal danger of caffeine is its association with other drugs that fulfill the DSM-5 criteria for SUD. …..By blocking the A2A receptor, caffeine counteracts the remaining brake that endogenous adenosine imposes on D2 receptor signaling, which results in a maximal D2 and minimal A2A receptor signaling: a maximal psychostimulant effect (Fig. 3C).
[56] 1991: On the basis of available data, the working group concluded that coffee is possibly carcinogenic to the human urinary bladder.
[57] 2019: In summary, findings from this large meta-analysis of prospective studies suggest that coffee consumption was not significantly associated with long-term risk of bladder cancer.
[58] Habitual caffeine consumption up to 200 mg per day by pregnant women does not give rise to safety concerns for the fetus.
[59]Caffeine passes the placental barrier freely; the fetus does not express the main enzymes that inactivate it [4,5], and caffeine metabolites have been found to accumulate in the fetal brain.
[60] WHO recommendations for pregnant women with high daily caffeine intake (more than 300 mg per day), lowering daily caffeine intake during pregnancy is recommended to reduce the risk of pregnancy loss and low birth weight neonates.
[61] You can have caffeine, but no more than 200mg per day. Regularly drinking more than this amount can increase your risk of pregnancy complications, such as low birthweight, and even miscarriage.
[62]A linear dose-relationship for decreased PD risk with tea and caffeine consumption was found, whereas the strength of protection reached a maximum at approximately 3 cups/day for coffee consumption overall. https://pubmed.ncbi.nlm.nih.gov/23879665/
[63] https://journals.sagepub.com/doi/abs/10.1177/0004867415603131 Coffee and caffeine consumption were significantly associated with decreased risk of depression.
[64] https://www.sciencedirect.com/science/article/abs/pii/S0165032719301442
Regardless of psychiatric problems such as depression or sleep problems, regular and moderate caffeine intake likely reduces suicide risk as well as depression in women.
[65] Available evidence indicates that coffee consumption is inversely associated with risk of T2D.
[66]"Prospective epidemiological studies concur in an association between habitual coffee consumption and a lower risk of type 2 diabetes." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8066601/
[67] Moderate coffee consumption was inversely significantly associated with CVD risk, with the lowest CVD risk at 3 to 5 cups per day, and heavy coffee consumption was not associated with elevated CVD risk.
[68] Findings consistently indicate that consumption of up to 6 standard cups of filtered, caffeinated coffee per day, as compared with no coffee consumption, is not associated with an increased risk of these cardiovascular outcomes in the general population. [sci hub]
[69] In this large, prospective, population-based community cohort study of more than 300 000 participants, each additional daily cup of coffee was associated with a 3% reduced risk of developing an arrhythmia.
[70] Compared with no coffee consumption, the relative risks of stroke were 0.86 (95% confidence interval (95% CI): 0.78, 0.94) for 2 cups of coffee per day, 0.83 (95% CI: 0.74, 0.92) for 3−4 cups/day, 0.87 (95% CI: 0.77, 0.97) for 6 cups/day, and 0.93 (95% CI: 0.79, 1.08) for 8 cups/day.
[71] Coffee consumption is significantly associated with a decreased risk of colorectal cancer at ≥ 5 cups per day of coffee consumption.
[72] The EC risk decreased by 5% for every 1 cup per day of coffee intake, 7% for every 1 cup per day of caffeinated coffee intake, 4% for every 1 cup per day of decaffeinated intake of coffee and 4% for every 100 mg of caffeine intake per day.
[73] https://pubmed.ncbi.nlm.nih.gov/33431520/
[74] From this meta-analysis, the risk of HCC is reduced by 40% for any coffee consumption vs no consumption.
[75] Indeed, systematic reviews have found a protective effect of coffee on liver, hepatocellular, and breast cancers. However, coffee seems to increase the risk for lung cancer development, whereas the association of coffee with other cancers such as those of the pancreas, bladder, ovaries, and prostate is controversial.
[76] This large prospective cohort study of a half million people found inverse associations for coffee drinking with mortality, including among participants drinking 1 up to 8 or more cups per day.
[77] Consumption of caffeinated coffee and consumption of decaffeinated coffee were similarly associated with a reduced risk of death from any cause. [sci hub]
[78]These results confirm prior findings on the reduced risk of mortality associated with coffee drinking but additionally show that this relationship does not vary by country where coffee preparation and drinking habits may differ. The study also reports novel inverse relationships between coffee drinking and digestive disease mortality.
[79] In the very large UK Biobank cohort, coffee drinking was associated inversely with all-cause mortality, including in those drinking at least 8 cups per day, in both slow and fast metabolizers of caffeine, and in consumers of ground, instant, and decaffeinated coffee.
[80]Green and black tea: Relative to no tea drinking, the hazard ratios (95% CIs) for participants drinking 1 or fewer, 2 to 3, 4 to 5, 6 to 7, 8 to 9, and 10 or more cups per day were 0.95 (95% CI, 0.91 to 1.00), 0.87 (CI, 0.84 to 0.91), 0.88 (CI, 0.84 to 0.92), 0.88 (CI, 0.84 to 0.92), 0.91 (CI, 0.86 to 0.97), a https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10623338/
[81]Green tea consumption was associated with lower risk of mortality from all causes, CVD and other causes but not from cancer. The association of drinking green tea with CVD-specific mortality was particularly strong, with HRs (95% CIs) of 0.79 (0.68, 0.91) for men and 0.78 (0.68, 0.90) for women who drank at least five cups per day of green tea compared with non-drinkers. The association between black tea consumption and mortality was weak, with no clear trends noted across the categories of consumption.
[82] https://pubs.acs.org/doi/abs/10.1021/jf804025c
[83] In this report, we examined the effects of caffeine and other well-known coffee components, such as quercetin, flavone, and chlorogenic acids (CGAs), on neuroinflammation and neurotoxicity mediated by toxic factors from activated microglia and astrocytes…..We found that CGA, flavone, quercetin, and caffeine reduced the release of proinflammatory cytokines such as tumor necrosis factor-α (TNFα) and interleukin-6 (IL-6) from lipopolysaccharide/interferon-γ (LPS/IFNγ)-stimulated microglia and THP-1 cells, as well as from IFNγ-stimulated astrocytes and U373 cells.
[84] Lower circulating levels of inflammatory markers among coffee drinkers may partially mediate previously observed associations of coffee with cancer and other chronic diseases.
[85] Black, green, and red tea are rich in polyphenols and flavonoids, namely catechins and their oxidated products. These and other bioactive compounds in tea have the potential to reduce oxidative stress and inflammation, which may promote carcinogenesis, and improve endothelial function
[86] Senate Majority Leader Chuck Schumer (D-NY) sent the following letter to FDA Commissioner, Dr. Robert Califf, regarding Prime Energy drink – a product marketed to kids and teens to quench thirst – which contains an eye-popping 200mg of caffeine.
[87] https://drinkprime.com/products/original-energy
[88] Ninety-seven espresso samples in Australia were analysed. The mean (±SD) quantity of caffeine was 106 ± 38
[89]Starbucks says 75 mg per shot of its espresso. Literature says 63 mg per ounce of espresso, and 12 oz brewed coffee is 235 mg.
[90] https://academic.oup.com/nutritionreviews/article/72/suppl_1/23/1929608
"In general, a serving of espresso (about 1 oz or 30 mL) provides 64 mg of caffeine, and an 8-oz cup (237 mL) of automatic drip coffee provides 145 mg of caffeine.41"
[91] Review of Caffeine-Related Fatalities along with Postmortem Blood Concentrations in 51 Poisoning Deaths
[92] Caffeine is a mild central nervous stimulant that occurs naturally in coffee beans, cocoa beans and tea leaves. In large doses, it can be profoundly toxic, resulting in arrhythmia, tachycardia, vomiting, convulsions, coma and death.
[93] Toxic effects (including tachycardia, ventricular arrhythmia, and seizures) are observed at approximately 1200 mg, or 1.2 grams (0.15 tablespoons of caffeine) (Ref 2, 3, 4, 5, 6). A life threatening dose of caffeine is typically estimated at between 10,000 and 14,000 mg, or 10 and 14 grams (g) (1.2 – 1.7 tablespoons of caffeine), although smaller doses can be life-threatening in certain individuals (such as children or other sensitive populations) (Ref 5, 14, 15, 16, 17).
[94]Prior to cardiac arrest [a 22-year old female] patient consumed six cans of a caffeinated energy drink within 4 hours."
[95] “An otherwise healthy 28-year-old man had a cardiac arrest after a day of motocross racing… he had consumed 7–8 cans of a caffeinated “energy drink” between 8 am and his collapse 7 hours later.
[96] We present the case of a 22-year-old male attended in the emergency department of a general hospital…he ingested 20 cans of 250 cc of an energy drink in 24 hours.
[97] In 2007, a man in Australia was reported to have suffered cardiac arrest after consuming seven to eight cans of an energy drink while taking part in vigorous physical activity (36). A Swedish study in 2006 identified a number of cases with severe symptoms and a number of deaths possibly linked to energy drinks (37). Iyadurai and Chung (38) reported on four cases in the US, where patients presented at emergency rooms after suffering new, adult-onset seizures and the only common finding was that all the patients had consumed large amounts of energy drinks. Once the patients abstained from consuming energy drinks, no further seizures were reported. Avci et al. (39) reported another case from the United States where a 28-year-old man consumed three 250 ml energy drink cans, 5 h before a basketball match. After playing for 30 min, he lost consciousness, suffered from cardiac arrest, and died 3 days later.
[98] Fourteen-year-old Anais Fournier downed two 24-ounce energy drinks on one December day, while hanging out with her friends at the mall. The next day, the Maryland teenager went into cardiac arrest -- and just six days later, she was dead.
[99] A South Carolina teenager who collapsed in a high school classroom last month died because he drank several highly caffeinated drinks too quickly, a coroner said on Monday…Davis Allen Cripe, 16, drank a latte from McDonald's, a large Mountain Dew soda, and a highly caffeinated energy drink in just under two hours, said Gary Watts, the coroner of Richland County, South Carolina.
[100] See Table 1 – estimated caffeine content from various case reports not at toxic level
[101] Typically, caffeine toxicity–related adverse events have only been observed in case studies where doses far exceed 400 mg.
[102] As for the constituents of the energy drinks themselves, the concentrations of caffeine seem to be comparable or even lower than many popular coffee drinks making the amount of caffeine itself an unlikely reason to not consume the products.
[103] Shah et al 2019. A randomized, double‐masked, placebo‐controlled, crossover study was conducted in healthy volunteers. Participants consumed 32 oz of either energy drink A, energy drink B, or placebo within 60 minutes on 3 study days with a 6‐day washout period in between.
[104] This 2023 review attempts to look at all the negative effects & some mechanisms. In particular, the analysis identified nine cases of cardiac arrest, three of which were fatal.
[105] Overall, the AERs indicate that the FDA received 276 reports of adverse events involving energy drinks between January 1, 2004, and March 10, 2014. Excluding a suicide, thirty-four of the incidents involved death, often as a result of heart failure.
[106] Acute consumption of ED can alter the ECG in certain risk populations, posing a risk whose magnitude is yet to be determined.
[107] QT interval represents the duration of ventricular electrical systole, which includes ventricular activation and recovery.
[108] The danger inherent in a prolonged QT is that excessive QT prolongation carries a risk of sudden cardiac death (SCD) due to polymorphic tachycardia, also known as TdP…. Irrespective of the mechanism, TdP usually does not sustain long and terminates spontaneously. However, if it happens successively, it can degenerate into ventricular fibrillation and SCD
[109] An arrhythmia that starts in your ventricle is called ventricular fibrillation. This occurs when the electrical signals that tell your heart muscle to pump cause your ventricles to quiver (fibrillate) instead.
[110] The change in corrected QT interval from baseline in the energy drink arm was significantly higher than the caffeine arm at 2 hours (0.44±18.4 ms versus −10.4±14.8 ms, respectively; P=0.02).
[111] The maximum change from baseline in Bazett's corrected QT interval for drinks A, B, and placebo were +17.9±13.9, +19.6±15.8, and +11.9±11.1 ms, respectively
[112] Drugs such as ranolazine and terfenadine carry warnings, or have been removed from the market because of prolongation of the mean QT/QTc by 6 ms.
[113] In a large sample representative of the general US population, we found no association between QT interval duration and coffee or tea intake, cigarette smoking, physical activity, or total alcohol intake, although binge drinking was associated with an increased QT duration particularly in men.
[114] https://nutritionj.biomedcentral.com/articles/10.1186/1475-2891-10-15 The QT interval corrected for heart rate did not significantly change following CC or DC ingestion.
[115] Fletcher et al 2017 is the one that had caffeinated placebo
[116] Caffeinated energy drinks have significant haemodynamic effects in patients with LQTS, specifically an acute increase in blood pressure. [sci hub]
[117] The QTc interval was shortened after 1 h compared to baseline by the administration of CP + C + T and CP + G (both P < 0.05). Compared to the CP, CP + C and CP + C + T induced increased BP parameters. CP + C + T and CP + G caused a shortened QTc interval compared to CP (both P < 0.05) and CP + C + T reduced HR compared to CP (P < 0.05).
[118] So far, these effects caused by ED cannot be explained by any of the tested components caffeine, taurine, or glucuronolactone. We assume that other ED ingredients, for example, niacin or inositol could contribute to the cardiovascular effects, but this was not investigated in this study.
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