Literature DB >> 23425242

Habitual alcohol consumption is associated with lower cardiovascular stress responses--a novel explanation for the known cardiovascular benefits of alcohol?

Alexander Jones1, Merlin R McMillan, Russell W Jones, Grzegorz T Kowalik, Jennifer A Steeden, Jens C Pruessner, Andrew M Taylor, John E Deanfield, Vivek Muthurangu.   

Abstract

In contrast to heavy alcohol consumption, which is harmful, light to moderate drinking has been linked to reduced cardiovascular morbidity and mortality. Effects on lipid status or clotting do not fully explain these benefits. Exaggerated cardiovascular responses to mental stress are detrimental to cardiovascular health. We hypothesized that habitual alcohol consumption might reduce these responses, with potential benefits. Advanced magnetic resonance techniques were used to accurately measure cardiovascular responses to an acute mental stressor (Montreal Imaging Stress Task) in 88 healthy adults (∼1:1 male:female). Salivary cortisol and task performance measures were used to assess endocrine and cognitive responses. Habitual alcohol consumption and confounding factors were assessed by questionnaire. Alcohol consumption was inversely related to responses of heart rate (HR) (r = -0.31, p = 0.01), cardiac output (CO) (r = -0.32, p = 0.01), vascular resistance (r = 0.25, p = 0.04) and mean blood pressure (r = -0.31, p = 0.01) provoked by stress, but not to stroke volume (SV), or arterial compliance changes. However, high alcohol consumers had greater cortisol stress responses, compared to moderate consumers (3.5 versus 0.7 nmol/L, p = 0.04). Cognitive measures did not differ. Findings were not explained by variations in age, sex, social class, ethnicity, physical activity, adrenocortical activity, adiposity, smoking, menstrual phase and chronic stress. Habitual alcohol consumption is associated with reduced cardiac responsiveness during mental stress, which has been linked to lower risk of hypertension and vascular disease. Consistent with established evidence, our findings suggest a mechanism by which moderate alcohol consumption might reduce cardiovascular disease, but not high consumption, where effects such as greater cortisol stress responses may negate any benefits.

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Year:  2013        PMID: 23425242     DOI: 10.3109/10253890.2013.777833

Source DB:  PubMed          Journal:  Stress        ISSN: 1025-3890            Impact factor:   3.493


  6 in total

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5.  Alcohol intake and long-term mortality risk after myocardial infarction in the Alpha Omega Cohort.

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6.  Role of neuronal nitric oxide synthase (nNOS) at medulla in tachycardia induced by repeated administration of ethanol in conscious rats.

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  6 in total

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