Chronic Caffeine Intake in Adult Rat Inhibits Carotid Body Sensitization Produced by Chronic Sustained Hypoxia but Maintains Intact Chemoreflex Output

2012 ◽  
Vol 82 (6) ◽  
pp. 1056-1065 ◽  
Author(s):  
Silvia V. Conde ◽  
Maria J. Ribeiro ◽  
Ana Obeso ◽  
Ricardo Rigual ◽  
Emilia C. Monteiro ◽  
...  
Keyword(s):  
Carotid Body ◽  
Caffeine Intake ◽  
Adult Rat ◽  
Chronic Caffeine ◽  
Sustained Hypoxia

Caffeine-Induced Psychosis

CNS Spectrums ◽  
2009 ◽  
Vol 14 (3) ◽  
pp. 127-131 ◽  
Author(s):  
Dawson W. Hedges ◽  
Fu Lye Woon ◽  
Scott P. Hoopes
Keyword(s):  
Antipsychotic Medication ◽  
Healthy People ◽  
Caffeine Intake ◽  
Adenosine Antagonist ◽  
Dopamine Transmission ◽  
Chronic Caffeine ◽  
Chronic Psychosis

ABSTRACTAs a competitive adenosine antagonist, caffeine affects dopamine transmission and has been reported to worsen psychosis in people with schizophrenia and to cause psychosis in otherwise healthy people. We report of case of apparent chronic caffeine-induced psychosis characterized by delusions and paranoia in a 47-year-old man with high caffeine intake. The psychosis resolved within 7 weeks after lowering caffeine intake without use of antipsychotic medication. Clinicians might consider the possibility of caffeinism when evaluating chronic psychosis.

Caffeine intake reduces incident atrial fibrillation at a population level

2018 ◽  
Vol 25 (10) ◽  
pp. 1055-1062 ◽  
Author(s):  
Edoardo Casiglia ◽  
Valérie Tikhonoff ◽  
Federica Albertini ◽  
Federica Gasparotti ◽  
Alberto Mazza ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
General Population ◽  
Univariate Analysis ◽  
Population Level ◽  
Caffeine Intake ◽  
General Belief ◽  
The Third ◽  
Chronic Caffeine ◽  
Artery Disease ◽  
Cox Analysis

Background The general belief is that caffeine increases the risk of hyperkinetic arrhythmias, including atrial fibrillation. The aim of this study is to investigate the effect of chronic caffeine intake on incident atrial fibrillation in general population. Design and methods A population cohort of 1475 unselected men and women observed for 12 years and left free to intake food or beverages containing caffeine was studied. Subjects were stratified into tertiles of caffeine intake both in the whole cohort and after genotyping for the –163C > A polymorphism of the CYP1A2 gene, regulating caffeine metabolism. Results In the whole cohort, the 12-year incidence of atrial fibrillation was significantly lower in the third (2.2%) than in the first (10.2%) or second (5.7%) tertile of caffeine intake ( P < 0.001). The same trend was observed in all genotypes; the apparently steeper reduction of atrial fibrillation in slow caffeine metabolisers found at univariate analysis was proved wrong by multivariate Cox analysis. Age, chronic pulmonary disease, history of heart failure and of coronary artery disease, and systolic blood pressure − but not the genotype or the caffeine ×  CYP1A2 interaction term − were significant confounders of the association between incident atrial fibrillation and being in the third tertile of caffeine intake (hazard ratio 0.249, 95% confidence intervals 0.161–0.458, P < 0.01). Conclusions A higher caffeine intake (>165 mmol/day or > 320 mg/day) is associated with a lower incidence of atrial fibrillation in the 12-year epidemiological prospective setting based on the general population.

scholarly journals Chronic caffeine intake decreases circulating catecholamines and prevents diet-induced insulin resistance and hypertension in rats

2011 ◽  
Vol 107 (1) ◽  
pp. 86-95 ◽  
Author(s):  
Silvia V. Conde ◽  
Tiago Nunes da Silva ◽  
Constancio Gonzalez ◽  
Miguel Mota Carmo ◽  
Emilia C. Monteiro ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Visceral Fat ◽  
Tolerance Test ◽  
Caffeine Intake ◽  
Insulin Tolerance ◽  
Hepatic Glutathione ◽  
Chronic Caffeine ◽  
High Sucrose

We tested the hypothesis that long-term caffeine intake prevents the development of insulin resistance and hypertension in two pathological animal models: the high-fat (HF) and the high-sucrose (HSu) diet rat. We used six groups of animals: control; caffeine-treated (Caff; 1 g/l in drinking water during 15 d); HF; caffeine-treated HF (HFCaff); HSu; caffeine-treated HSu (HSuCaff). Insulin sensitivity was assessed using the insulin tolerance test. Blood pressure, weight gain, visceral fat, hepatic glutathione, plasma caffeine, insulin and NO, and serum NEFA and catecholamines were measured. Caffeine reversed insulin resistance and hypertension induced by both the HF and HSu diets. In the HF-fed animals caffeine treatment restored fasting insulin levels to control values and reversed increased weight gain and visceral fat mass. In the HSu group, caffeine reversed fasting hyperglycaemia and restored NEFA to control values. There were no changes either in plasma NO or in hepatic glutathione levels. In contrast, caffeine totally prevented the increase in serum catecholamines induced by HF and HSu diets. To test the hypothesis that inhibition of the sympathetic nervous system prevents the development of diet-induced insulin resistance we administered carvedilol, an antagonist of β1, β2 and also α1 adrenoceptors, to HF and HSu rats. Carvedilol treatment fully prevented diet-induced insulin resistance and hypertension, mimicking the effect of caffeine. We concluded that long-term caffeine intake prevented the development of insulin resistance and hypertension in HF and HSu models and that this effect was related to a decrease in circulating catecholamines.

Influence of reduced carotid body drive during sustained hypoxia on hypoxic depression of ventilation in humans

1996 ◽  
Vol 81 (2) ◽  
pp. 565-572 ◽  
Author(s):  
A. Dahan ◽  
D. Ward ◽  
M. van den Elsen ◽  
J. Temp ◽  
A. Berkenbosch
Keyword(s):  
Carotid Body ◽  
Hypoxic Exposure ◽  
Hypoxic Response ◽  
Air Breathing ◽  
Carotid Bodies ◽  
Delayed Recovery ◽  
End Tidal ◽  
Second Period ◽  
Sustained Hypoxia

To evaluate whether the intact hypoxic drive from the carotid bodies during sustained hypoxia is required for the generation of hypoxic depression of ventilation (VE), 16 volunteers were exposed to two consecutive periods of isocapnic hypoxia (first period 20 min; second period 5 min; end-tidal PO2 45 Torr) separated by 6 min of normoxia. In study A, saline was given. In study B, 3 micrograms.kg-1.min-1 i.v. dopamine (DA), a carotid body inhibitor, was given during the first hypoxic exposure followed by saline during normoxia and the second hypoxic exposure. In study C, 20 min of normoxia with DA preceded 6 min of normoxia and 5 min of hypoxia without DA. The first peak hypoxic VE (PHV) in study A was approximately 100% above normoxic VE. After 20 min of hypoxia, VE declined to 60% above normoxic VE. The second PHV in study A was only 60% of the first PHV. We relate this delayed recovery from hypoxia to "ongoing" effects of hypoxic depression. During DA infusion, the changes in VE due to sustained hypoxia were insignificant (study B). The second PHV in study B was not different from the PHV after air breathing in studies A and C. This indicates that the recovery from sustained hypoxia with a suppressed carotid body drive was complete within 6 min. Our results show that despite central hypoxia the absence of ventilatory changes during 20 min of isocapnic hypoxia due to intravenous DA prevented the generation of central hypoxic depression and the depression of a subsequent hypoxic response.

scholarly journals Chronic caffeine intake reverses age-induced insulin resistance in the rat: effect on skeletal muscle Glut4 transporters and AMPK activity

AGE ◽  
2012 ◽  
Vol 35 (5) ◽  
pp. 1755-1765 ◽  
Author(s):  
Maria P. Guarino ◽  
Maria J. Ribeiro ◽  
Joana F. Sacramento ◽  
Sílvia V. Conde
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Caffeine Intake ◽  
Ampk Activity ◽  
Chronic Caffeine

Chronic Caffeine Intake by Rat Dams during Gestation and Lactation Affects Various Parts of the Neonatal Brain

Neonatology ◽  
1986 ◽  
Vol 49 (5) ◽  
pp. 277-283 ◽  
Author(s):  
Tetsuo Nakamoto ◽  
Arthur D. Hartman ◽  
Harvey I. Miller ◽  
Thomas E. Temples ◽  
Griffith E. Quinby, Jr.
Keyword(s):  
Caffeine Intake ◽  
Neonatal Brain ◽  
Chronic Caffeine
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