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Genetic Determinants of Cardiovascular Response to Coffee Drinking

Genetic Determinants of Cardiovascular Response to Coffee Drinking

Status
Completed
Phases
NA
Study type
Interventional
Source
ClinicalTrials.gov
Registry ID
NCT01330680
Enrollment
110
Registered
2011-04-07
Start date
2004-09-30
Completion date
2010-09-30
Last updated
2011-04-07

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Caffeine

Keywords

coffee, caffeine, blood pressure, nutrigenetics, gene polymorphisms, Acute Cardiovascular and Neuropsychologic Effects

Brief summary

Cardiovascular and neuropsychologic effects of coffee are still debated. The precise mechanism underlying the actions of caffeine on the cardiovascular and neuropsychologic systems is incompletely understood and a considerable variability in the response to coffee drinking was observed, in part ascribable to a genetic trait. The aim of the study is to evaluate acute cardiovascular and neuropsychologic effects of coffee and explore whether such effects are influenced by the genetic asset of caffeine metabolism (by a polymorphisms of cytochrome P450 1A2), adenosine metabolism (by polymorphisms of adenosine receptor and adenosine monophosphate deaminase) or catecholamine receptors (by polymorphisms of adrenergic receptors).

Detailed description

Coffee is among the most widely consumed beverages worldwide. Despite the relationship between coffee consumption and the incidence of cardiovascular disease has been studied extensively, the effects of this drink on the cardiovascular apparatus and its role as a risk factor for coronary heart disease are still debated. Moreover, the effect of coffee on attention, sleep changes, anxiety and panic disorders was studied but a great variability was observed. Many of the known or suspected cardiovascular and neuropsychologic effects of coffee have been attributed to caffeine. The main mechanism of action of caffeine is to antagonize adenosine receptors; a secondary effect is the inhibition of phosphodiesterases, with the subsequent accumulation of cyclic adenosine monophosphate and a intensification of the effects of catecholamines. It is also well known that there is a considerable variability in the cardiovascular and neuropsychologic response to coffee drinking, explaining the inconsistency between different effects observed in the various studies. This variability may have a genetic basis. The aim of the study is to evaluate acute cardiovascular and neuropsychologic effects of coffee and explore whether such effects are influenced by the genetic asset of caffeine metabolism (by a polymorphisms of cytochrome P450 1A2), adenosine metabolism (by polymorphisms of adenosine receptor and adenosine monophosphate deaminase) or catecholamine receptors (by polymorphisms of adrenergic receptors).

Interventions

DIETARY_SUPPLEMENTCoffee

40 mL dose of a decaffeinated preparation spiked with the addition of caffeine, at a dose of 3 mg/kg

DIETARY_SUPPLEMENTDecaffeinated coffee

40 mL dose of decaffeinated coffee

Sponsors

Institute for Scientific Information on Coffee
CollaboratorOTHER
Italian Istituto Nazionale Ricerche Cardiovascolari
CollaboratorUNKNOWN
G. d'Annunzio University
Lead SponsorOTHER

Study design

Allocation
RANDOMIZED
Intervention model
CROSSOVER
Masking
QUADRUPLE (Subject, Caregiver, Investigator, Outcomes Assessor)

Eligibility

Sex/Gender
MALE
Age
18 Years to 40 Years
Healthy volunteers
Yes

Inclusion criteria

* Age between 18 and 40 years * Males (to avoid variation due to female hormonal cycle) * No known active ongoing disease (apparent good health) * Non-smokers (to avoid contributory effects of nicotine or other tobacco alkaloids to caffeine effects or tolerance) * Average coffee intake (not less than one cup/day and not greater than three cups/day)

Exclusion criteria

* Treatment with any drug with known activity on the adrenergic system * Hypertension * Therapy with sympathomimetic drugs, theophylline, alpha- or beta-blockers, any antihypertensive therapy * Body mass index (BMI) \> 30 kg/m2 (obesity) * BMI \< 18.5 kg/m2

Design outcomes

Primary

MeasureTime frameDescription
Change in platelet aggregationFrom baseline to 30 minutes and 2 hours after coffee or decaffeinated alternativelyLight transmission aggregometry (LTA) induced by ADP and apinephrine. Platelet function analyzer (PFA) by collagen-ADP and collagen-epinephrine cartridges.
Change in cognitive tasks measuresFrom 30 minutes until 2 hours after coffee or decaffeinated alternativelyLow intensity task of focused attention and choice reaction times (Categorical Search Task). More demanding response interference tasks (Letter Flanker Task). Classic interference task (Stroop Test).
Change in blood pressureFrom baseline until 2 hours after coffee or decaffeinated alternatively
Change in heart rateFrom baseline until 2 hours after coffee or decaffeinated alternatively

Secondary

MeasureTime frame
Change in plasma caffeine concentrationFrom baseline to 30 minutes and 2 hours after coffee or decaffeinated alternatively
Change in plasma adrenaline and noradrenaline concentrationFrom baseline to 30 minutes and 2 hours after coffee or decaffeinated alternatively

Countries

Italy

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Mar 27, 2026