The blood pressure-elevating effect of Red Bull energy drink is mimicked by caffeine but through different hemodynamic pathways.
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ABSTRACT:
SUBMITTER: Miles-Chan JL
PROVIDER: S-EPMC4393199 | biostudies-other | 2015 Feb
REPOSITORIES: biostudies-other
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Project description:BackgroundThe purpose of this study was to examine if Red Bull® Energy Drink can counteract sleepiness and driving impairment during prolonged driving.MethodsTwenty-four healthy volunteers participated in this double-blind placebo-controlled crossover study. After 2 h of highway driving in the STISIM driving simulator, subjects had a 15-min break and consumed Red Bull® Energy Drink (250 ml) or placebo (Red Bull® Energy Drink without the functional ingredients: caffeine, taurine, glucuronolactone, B vitamins (niacin, pantothenic acid, B6, B12), and inositol) before driving for two additional hours. A third condition comprised 4 h of uninterrupted driving. Primary parameter was the standard deviation of lateral position (SDLP), i.e., the weaving of the car. Secondary parameters included SD speed, subjective driving quality, sleepiness, and mental effort to perform the test.ResultsNo significant differences were observed during the first 2 h of driving. Red Bull® Energy Drink significantly improved driving relative to placebo: SDLP was significantly reduced during the 3rd (p?<?0.046) and 4th hour of driving (p?<?0.011). Red Bull® Energy Drink significantly reduced the standard deviation of speed (p?<?0.004), improved subjective driving quality (p?<?0.0001), and reduced mental effort to perform the test (p?<?0.024) during the 3rd hour of driving. Subjective sleepiness was significantly decreased during both the 3rd and 4th hour of driving after Red Bull® Energy Drink (p?<?0.001 and p?<?0.009, respectively). Relative to uninterrupted driving, Red Bull® Energy Drink significantly improved each parameter.ConclusionRed Bull® Energy Drink significantly improves driving performance and reduces driver sleepiness during prolonged highway driving.
| S-EPMC3053448 | biostudies-literature
Project description:Objective: Studies report that acute consumption of energy drinks transiently increases blood pressure (BP). However, few studies report the effect of chronic energy drink consumption on BP. In this study, we investigated the effects of long-term energy drink ingestion on BP in C57BL/6J normotensive wild-type mice. Research Methods and Procedures: Groups of mice were randomized to no treatment (water) (Control group), or to Mother™ provided as a decarbonated 30% (v/v) drinking solution (Energy Drink group), sugar-free Mother™ at 30% (Sugar-free group), Coca Cola™ at 30% (Coke group) for a total intervention period of 13 weeks. Results: After 13 weeks of intervention, the control mice showed a modest increase in systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) by 7.1 ± 8.8, 5.8 ± 9.4, and 6.3 ± 9.1 mmHg, respectively. However, the Energy Drink significantly decreased the DBP and MAP by 18.8 ± 9.9 and 15.3 ± 9.8 mmHg, respectively. Similarly, Sugar-free group mice showed significant decrease of the SBP, DBP, and MAP by 10.85 ± 5.6, 18.7 ± 6.7, and 15.6 ± 6.1 mmHg, respectively. The SBP, DBP, and MAP in Coke mice showed no significant changes. The estimated cumulative intake of caffeine, taurine, and vitamin B3 and B5 was significantly higher in the mice of Energy Drink and Sugar-free groups compared to the Control and Coke mice. Conclusion: Collectively, the data suggest that the long-term chronic consumption of energy drinks may significantly lower the BP in normotensive mice through the actions of caffeine, taurine, and/or B-vitamins. The study findings do not support consideration of energy drinks for BP management, but rather demonstrate no long-term amplification of BP in normotensive preclinical models.
| S-EPMC6663975 | biostudies-literature
Project description:Background Energy drinks have been linked to an increase in emergency room visits and deaths. We aim to determine the impact of energy drinks on electrocardiographic and hemodynamic parameters in young healthy volunteers. Methods and Results 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. The primary end point of QT c interval and secondary end points of QT interval, PR interval, QRS duration, heart rate, and brachial and central blood pressures were measured at baseline, and every 30 minutes for 240 minutes. A repeated-measures 2-way analysis of variance was performed with the main effects of intervention, time, and an interaction of intervention and time. Thirty-four participants were included (age 22.1±3.0 years). The interaction term of intervention and time was statistically significant for Bazett's corrected QT interval, Fridericia's corrected QT interval, QT , PR , QRS duration, heart rate, systolic blood pressure, diastolic blood pressure, central systolic blood pressure, and central diastolic blood pressure (all P<0.001). 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 ( P=0.005 for ANOVA ) ( P=0.04 and <0.01, respectively compared with placebo). Peripheral and central systolic and diastolic blood pressure were statistically significantly different compared with placebo (all P<0.001). Conclusion Energy drinks significantly prolong the QT c interval and raise blood pressure. Clinical Trial Registration URL : http://www.clinicaltrials.gov . Unique identifier: NCT03196908.
| S-EPMC6585360 | biostudies-literature
Project description:Energy drink consumption is increasing worldwide, especially among young adults, and has been associated with physical and mental health problems. In two experiments, we tested the prediction that energy drink consumption is in part driven by biased cognitive processing (attentional and approach biases), with a view to modifying these to reduce consumption. Young adults (18-25 years) who regularly consume energy drinks completed the dot probe (Exp.1; N = 116) or approach-avoidance task (Exp.2; N = 110) to measure attentional and approach bias for energy drink cues, respectively. They then underwent a cognitive bias modification protocol where they were trained to direct their attention away from pictures of energy drink cans (Exp.1), or to push a joystick away from themselves in response to these pictures (Exp.2). Following a post-training assessment of attentional (Exp.1) or approach bias (Exp.2), energy drink consumption was measured by an ostensible taste test. Regular energy drink consumers showed both an attentional and an approach bias for energy drink cues. Cognitive bias modification successfully reduced both biases. However, neither attentional nor approach bias modification significantly reduced energy drink intake. The results lend some support to incentive sensitisation theory which emphasises the role of biased decision-making processes related to addictive behaviours.
| S-EPMC6913920 | biostudies-literature
Project description:Phosphoinositide signaling lipids are essential for several cellular processes. The requirement for a phosphoinositide is conventionally studied by depleting the corresponding lipid kinase. However, there are very few reports on the impact of elevating phosphoinositides. That phosphoinositides are dynamically elevated in response to stimuli suggests that, in addition to being required, phosphoinositides drive downstream pathways. To test this hypothesis, we elevated the levels of phosphatidylinositol-3-phosphate (PI3P) by generating hyperactive alleles of the yeast phosphatidylinositol 3-kinase, Vps34. We find that hyperactive Vps34 drives certain pathways, including phosphatidylinositol-3,5-bisphosphate synthesis and retrograde transport from the vacuole. This demonstrates that PI3P is rate limiting in some pathways. Interestingly, hyperactive Vps34 does not affect endosomal sorting complexes required for transport (ESCRT) function. Thus, elevating PI3P does not always increase the rate of PI3P-dependent pathways. Elevating PI3P can also delay a pathway. Elevating PI3P slowed late steps in autophagy, in part by delaying the disassembly of autophagy proteins from mature autophagosomes as well as delaying fusion of autophagosomes with the vacuole. This latter defect is likely due to a more general defect in vacuole fusion, as assessed by changes in vacuole morphology. These studies suggest that stimulus-induced elevation of phosphoinositides provides a way for these stimuli to selectively regulate downstream processes.
| S-EPMC8120694 | biostudies-literature
Project description:Each year over 90 million units of blood are transfused worldwide. Our dependence on this blood supply mandates optimized blood management and storage. During storage, red blood cells undergo degenerative processes resulting in altered metabolic characteristics which may make blood less viable for transfusion. However, not all stored blood spoils at the same rate, a difference that has been attributed to variable rates of energy usage and metabolism in red blood cells. Specific metabolite abundances are heritable traits; however, the link between heritability of energy metabolism and red blood cell storage profiles is unclear. Herein we performed a comprehensive metabolomics and proteomics study of red blood cells from 18 mono- and di-zygotic twin pairs to measure heritability and identify correlations with ATP and other molecular indices of energy metabolism. Without using affinity-based hemoglobin depletion, our work afforded the deepest multi-omic characterization of red blood cell membranes to date (1280 membrane proteins and 330 metabolites), with 119 membrane protein and 148 metabolite concentrations found to be over 30% heritable. We demonstrate a high degree of heritability in the concentration of energy metabolism metabolites, especially glycolytic metabolites. In addition to being heritable, proteins and metabolites involved in glycolysis and redox metabolism are highly correlated, suggesting that crucial energy metabolism pathways are inherited en bloc at distinct levels. We conclude that individuals can inherit a phenotype composed of higher or lower concentrations of these proteins together. This can result in vastly different red blood cells storage profiles which may need to be considered to develop precise and individualized storage options. Beyond guiding proper blood storage, this intimate link in heritability between energy and redox metabolism pathways may someday prove useful in determining the predisposition of an individual toward metabolic diseases.
| S-EPMC5141275 | biostudies-literature
Project description:Epidemiologic study has suggested that arsenic exposure is positively related to increased blood pressure. However, the underlying mechanism concerning interaction between genetic polymorphisms and arsenic exposure remains unclear. In present study, within 395 Chinese, the effects of interaction between arsenic exposure and CCM3 gene polymorphisms on elevation of blood pressure were probed by multiple Logistic regression models after adjusting for confounding factors. Firstly, we found that serum arsenic was positively associated with blood pressure, cholesterol, glucose and C-reactive protein. Then, adjusted for confounding factors of age, gender, smoking, alcohol consumption, BMI and degree of education, arsenic exposure incurred the hazard of increased systolic pressure and diastolic pressure, with odds ratios (ORs) being 1.725 and 1.425, respectively. Distinctly, we found that interactions between rs3804610* rs9818496, rs6784267*rs9818496, and rs3804610* rs6784267 variant genotype can increase significantly risks of SBP. Additionally, interactions between rs9818496, rs3804610 and rs6784267 genotypic variantions and arsenic exposure boosted the hazard of increased systolic pressure, with ORs being 1.496, 1.496 and 1.312. In conclusion, our fingdings suggest that As exposure of population can assist CCM3 polymorphism in elevating SBP.
| S-EPMC5797022 | biostudies-literature
Project description:AIMS:Alcohol mixed with energy drink (AmED) use is associated with negative consequences including hazardous alcohol use and driving under the influence. While many studies have focused on correlates of AmED use among college samples, very few have examined patterns of AmED use during adolescence and young adulthood within the general population. Accordingly, the purpose of this study is to assess age differences in AmED use among a national sample of respondents aged 18 to 30. METHODS:The data for this study come from the Monitoring the Future panel study from 2012 to 2015. The sample consists of 2222 respondents between the ages of 18 and 30. Multiple logistic regression using generalized estimating equations (GEE) was used to model past-year AmED prevalence across age and other covariates. RESULTS:Nearly half (45.0%) of respondents indicated past-year AmED use at some point during the study period. The lowest prevalence rates were found at age 18 (25.9%) and the highest prevalence rates at age 21/22 (43.5%). GEE analyses indicated a statistically significant positive linear and negative quadratic trend with respect to the association between age of respondent and past-year AmED use. Namely, peak use occurred in early young adulthood (age 21/22 and 23/24) and then declined, reaching 32.0% by age 29/30. College attendance and several substance use behaviors at age 18 moderated these linear and quadratic age trends. CONCLUSIONS:AmED use peaked rapidly in early young adulthood and declined into later young adulthood. Substance use during adolescence was associated with a higher incidence of AmED use across all young adult ages and a slower decline of AmED use after age 21/22. Several sociodemographic factors were associated with AmED use, particularly college attendance at the age of 21/22.
| S-EPMC5975232 | biostudies-literature
Project description:BACKGROUND:Thermogenic fitness drink formulas (TFD) have been shown to increase energy expenditure and markers of lipid metabolism. The purpose of the current study was to compare TFD formulas containing different caffeine concentrations versus a placebo drink on energy expenditure and lipid metabolism at rest and during exercise. METHODS:Thirty-two recreationally active participants (22.9?±?0.7 y, 167.1?±?1.4?cm, 68.8?±?2.0?kg, 24.0?±?1.2% fat) who were regular caffeine consumers, participated in this randomized, double-blind, crossover design study. Participants reported to the laboratory on three occasions, each of which required consumption of either a TFD containing 140?mg or 100?mg of caffeine or a placebo. Baseline measurements of resting energy expenditure (REE) and resting fat oxidation (RFO) were assessed using indirect calorimetry as well as measurements of serum glycerol concentration. Measurements were repeated at 30, 60, 90?min post-ingestion. Following resting measures, participants completed a graded exercise test to determine maximal oxygen uptake (V?O2max), maximal fat oxidation (MFO) and the exercise intensity that elicits MFO (Fatmax), and total energy expenditure (EE). RESULTS:A significant interaction was shown for REE (p <?0.01) and RFO (p <?0.01). Area under the curve analysis showed an increased REE for the 140?mg compared to the 100?mg formula (p =?0.02) and placebo (p <?0.01) and an increased REE for the 100?mg formula compared to placebo (p =?0.02). RFO significantly decreased for caffeinated formulas at 30?min post ingestion compared to placebo and baseline (p <?0.01) and significantly increased for the 140?mg formula at 60?min post-ingestion (p =?0.03). A main effect was shown for serum glycerol concentrations over time (p <?0.01). No significant differences were shown for V?O2max (p =?0.12), Fatmax (p =?0.22), and MFO (p =?0.05), and EE (p =?0.08) across drinks. CONCLUSIONS:Our results suggest that TFD formulas containing 100 and 140?mg of caffeine are effective in increasing REE and that a 40?mg of caffeine difference between the tested formulas may impact REE and RFO in healthy individuals within 60?min of ingestion.
| S-EPMC7020555 | biostudies-literature
Project description:Nesfatin-1 is a novel anorexic peptide hormone that also exerts cardiovascular protective effects in rodent models. However, nesfatin-1 treatment at high doses also exerts vasopressor effects, which potentially limits its therapeutic application. Here, we evaluated the vasoprotective and vasopressor effects of nesfatin-1 at different doses in mouse models. Wild-type mice and those with the transgene nucleobindin-2, a precursor of nesfatin-1, were employed. Wild-type mice were randomly assigned to treatment with vehicle or nesfatin-1 at 0.2, 2.0 or 10 μg/kg/day (Nes-0.2, Nes-2, Nes-10, respectively). Subsequently, mice underwent femoral artery wire injury to induce arterial remodeling. After 4 weeks, injured arteries were collected for morphometric analysis. Compared with vehicle, nesfatin-1 treatments at 2.0 and 10 μg/kg/day decreased body weights and elevated plasma nesfatin-1 levels with no changes in systolic blood pressure. Furthermore, these treatments reduced neointimal hyperplasia without inducing undesirable remodeling in injured arteries. However, nesfatin-1 treatment at 0.2 μg/kg/day was insufficient to elevate plasma nesfatin-1 levels and showed no vascular effects. In nucleobindin-2-transgenic mice, blood pressure was slightly higher but neointimal area was lower than those observed in littermate controls. In cultured human vascular endothelial cells, nesfatin-1 concentration-dependently increased nitric oxide production. Additionally, nesfatin-1 increased AMP-activated protein kinase phosphorylation, which was abolished by inhibiting liver kinase B1. We thus demonstrated that nesfatin-1 treatment at appropriate doses suppressed arterial remodeling without affecting blood pressure. Our findings indicate that nesfatin-1 can be a therapeutic target for improved treatment of peripheral artery disease.
| S-EPMC6499920 | biostudies-literature