Effects of acute and chronic caffeine on risk-taking behavior in children and adolescents

2017 ◽  
Vol 31 (5) ◽  
pp. 561-568 ◽  
Author(s):  
Jennifer L Temple ◽  
Amanda M Ziegler ◽  
Adam M Graczyk ◽  
Amanda Crandall

Consumption of caffeinated beverages is associated with increased risk-taking behavior. The purpose of this study was to determine if acute caffeine administration influences risk-taking behavior in a dose-dependent manner. Participants were pre- (ages 8–9) and post-pubertal (ages 15–17) children who visited the laboratory three times and consumed a beverage containing 0, 1, or 2 mg/kg of caffeine. Thirty minutes later, participants completed the balloon analogue risk task (BART), the Iowa gambling task (IGT), and a delay discounting task. The number of balloons exploded on the BART task was significantly increased after 2 mg/kg of caffeine in moderate caffeine consumers, but was decreased after 2 mg/kg of caffeine in high caffeine consumers. There were no main effects of caffeine dose on the delay discounting task or on the IGT. Post-pubertal participants showed reduced delay discounting compared with pre-pubertal participants. Finally, average daily caffeine use was significantly, positively correlated with scores on a risk-taking questionnaire. These data suggest that caffeine dose-dependently influences decision making and risk taking. More research is needed to determine the mechanism of this difference as well as the extent to which sex and pubertal phase influence these relationships.

F&S Reviews ◽  
2021 ◽  
Author(s):  
Nadia A. du Fossé ◽  
Marie-Louise P. van der Hoorn ◽  
Nina H. Buisman ◽  
Jan M.M. van Lith ◽  
S askia le Cessie ◽  
...  

2013 ◽  
Vol 19 (4) ◽  
pp. 474-482 ◽  
Author(s):  
Ceren Hıdıroğlu ◽  
Özlem Demirci Esen ◽  
Zeliha Tunca ◽  
Şehnaz Neslihan Gűrz Yalçìn ◽  
Lauren Lombardo ◽  
...  

AbstractRisk-taking behavior and impulsivity are core features of bipolar disorder. Whether they are part of the inherited aspect of the illness is not clear. We aimed to evaluate risk-taking behavior as a potential endophenotype for bipolar disorders, and its relationship with impulsivity and illness features. The Balloon Analogue Risk Task (BART) and Barratt Impulsiveness Scale-11 (BIS-11) were used to assess risk-taking behavior and impulsivity respectively in 30 euthymic bipolar I patients (BD), their 25 asymptomatic first-degree relatives (BD-R), and 30 healthy controls (HC). The primary BART outcome measure was the behavioral adjustment score (number of pumps after trials where the balloon did not pop minus the number of pumps after trials where the balloon popped). BD (p< .001) and BD-R (p= .001) had similar and significantly lower adjustment scores than HC. Only BD scored significantly higher on BIS-11 total (p= .01) and motor (p= .04) subscales than HC. Neither the BART, nor impulsivity scores associated with illness features. A limitation of this study is medicated patients and a heterogeneous BD-R were included. Riskiness may be a candidate endophenotype for bipolar disorder as it appears independently from illness features, presents similarly in BD and BD-R groups and differs from impulsivity. (JINS, 2013,19, 1–9)


2019 ◽  
Vol 72 (8) ◽  
pp. 1998-2017 ◽  
Author(s):  
Adam Bulley ◽  
Beyon Miloyan ◽  
Gillian V Pepper ◽  
Matthew J Gullo ◽  
Julie D Henry ◽  
...  

Humans frequently create mental models of the future, allowing outcomes to be inferred in advance of their occurrence. Recent evidence suggests that imagining positive future events reduces delay discounting (the devaluation of reward with time until its receipt), while imagining negative future events may increase it. Here, using a sample of 297 participants, we experimentally assess the effects of cued episodic simulation of positive and negative future scenarios on decision-making in the context of both delay discounting (monetary choice questionnaire) and risk-taking (balloon-analogue risk task). Participants discounted the future less when cued to imagine positive and negative future scenarios than they did when cued to engage in control neutral imagery. There were no effects of experimental condition on risk-taking. Thus, although these results replicate previous findings suggesting episodic future simulation can reduce delay discounting, they indicate that this effect is not dependent on the valence of the thoughts, and does not generalise to all other forms of “impulsive” decision-making. We discuss various interpretations of these results, and suggest avenues for further research on the role of prospection in decision-making.


2015 ◽  
Vol 1596 ◽  
pp. 88-98 ◽  
Author(s):  
Arathi Radhakrishnan ◽  
B.S. Aswathy ◽  
Velayudhan Mohan Kumar ◽  
Kamalesh K. Gulia

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 2942-2942
Author(s):  
Aditya Chaubey ◽  
Shane Hormon ◽  
Chinavenmeni S. Velu ◽  
Tristan Bourdeau ◽  
Jinfang Zhu ◽  
...  

Abstract In severe congenital neutropenia (SCN) patients and mice with Growth factor independent-1 (Gfi1) loss of function, arrested progenitors are suspended in a hyperproliferative state while terminal granulpoiesis is blocked. SCN patients are at increased risk for the development of acute myeloid leukemia. We demonstrate that Gfi1 directly targets HoxA9, Pbx1 and Meis1 during normal myelopoiesis. Gfi1−/− progenitors exhibit elevated levels of HoxA9, Pbx1 and Meis1, exaggerated HoxA9-Pbx1-Meis1 activity, and increased persistence in vivo and in vitro. Limiting HoxA9 alleles corrects, in a dose dependent manner, in vivo and in vitro phenotypes observed with loss of Gfi1. Moreover, in a manner conserved in Drosophila anterior/posterior patterning, we demonstrate that these factors can compete for occupancy of DNA sequences encoding composite Gfi1-HoxA9-Pbx1-Meis1 binding sites. Finally, the expression of Gfi1 and HoxA9 are inverse and stratify human myeloid leukemias, suggesting a role for HoxA9- Gfi1 antagonism in human AML. In agreement with this, a myeloproliferative disorder progresses into a rapid, lethal and transplantable myeloid leukemia in a Gfi1−/− setting. We conclude that the lifespan and oncogenic transformation of hematopoietic progenitor cells is regulated through a conserved competition between Gfi1 and HoxA9-Pbx1-Meis1.


2017 ◽  
Vol 35 (4_suppl) ◽  
pp. 477-477 ◽  
Author(s):  
Arjun Gupta ◽  
Avash Das ◽  
Nivedita Arora ◽  
Kaustav Majumder ◽  
Preet Paul Singh ◽  
...  

477 Background: Excess body weight is associated with increased risk of developing hepatocellular cancer (HCC), but its effect on HCC mortality remains unclear. We performed a systematic review and meta-analysis to assess the association between premorbid body mass index (BMI) and HCC mortality. Methods: Through a systematic search of major databases and conference proceedings, up to March 2016, we identified observational studies reporting the association between premorbid BMI, and HCC-related mortality. We estimated summary adjusted hazard ratio (aHR) with 95% confidence intervals (CI), comparing obese (BMI > 30 kg/m2) and overweight (BMI 25-29.9 kg/m2) categories with reference category using random effects model; heterogeneity was measured using the inconsistency index (I2). Results: 9 studies were included in which 6,052 HCC deaths occurred in 1,599,453 cancer-free individuals at cohort inception. 5 studies reported data as obese vs. overweight vs. normal BMI, and 4 reported data as obese + overweight combined (BMI > 25 kg/m2). On meta-analysis, pre-morbid obesity was associated with higher HCC-related mortality, as compared to individuals with normal BMI (obese: aHR, 1.96; 95% CI, 1.46-2.46, I2= 37%; overweight: aHR, 1.08; 95% CI, 0.97-1.21, I2= 0%), in dose-dependent manner. This effect was stronger in males [3 studies, aHR, 2.50; 95% CI, 2.02-3.09] vs. females [2 studies, aHR, 1.45; 95% CI, 1.08-1.97]. This effect was seen primarily in Western populations [4 studies, aHR, 2.10; 95% CI, 1.77-2.48], but not in Asian population [1 study, aHR, 1.10; 95% CI, 0.63-1.92]. Conclusions: In this meta-analysis, there was a dose-dependent increase in HCC-related mortality with pre-morbid obesity, particularly in men, and in Western populations. Strategies targeting obesity-induced metabolic abnormalities may provide novel pathways for HCC therapy.


2014 ◽  
Vol 22 (5) ◽  
pp. 444-452 ◽  
Author(s):  
Kelly S. DeMartini ◽  
Robert F. Leeman ◽  
William R. Corbin ◽  
Benjamin A. Toll ◽  
Lisa M. Fucito ◽  
...  

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