The J-shaped curve: An evolving perspective
6 December 2010
Ruidavets et al(1) confirm that consumption of low levels of alcohol is associated with reduced cardiovascular mortality, but importantly, also suggest that this effect only results in those with regular moderate consumption, and that the effect is probably through an anti-thrombotic action(2). Yet in spite of this, and much other evidence, there is still a lot of resistance to this idea in the clinical and research community(3). Perhaps it is difficult to understand why alcohol, a substance that clearly causes harm in excess, could be beneficial in low doses.
A population genetics perspective may help. In the evolution of thrombosis, a balance is to be achieved between the risk of early death from traumatic haemmorhage, and the risk of later death from intramural thrombosis of a critical artery. Whereas our species evolved in an environment where there was a significant risk of trauma, that is no longer true, and so the regular intake of an anti-thrombotic agent will adjust our thrombotic tendency to the adaptive peak of our current milieu.
Low dose alcohol may not be much different to taking aspirin or warfarin in adjusting our physiology to the new adaptive peak, but alcohol may have fewer side-effects. Given the complexities of promoting sensible consumption of alcohol in its currently available forms, should we not be exploring the potential benefits of a low-dose ethanol pill for widespread human consumption?
Mahmood Bhutta Research Fellow, University of Oxford
1.Ruidavets JB, Ducimetiere P, Evans Aet al. Patterns of alcohol consumption and ischaemic heart disease in culturally divergent countries: the Prospective Epidemiological Study of Myocardial Infarction (PRIME). BMJ (Clinical research ed;341:c6077. 2.Salem RO, Laposata M. Effects of alcohol on hemostasis. Am J Clin Pathol 2005;123 Suppl:S96-105. 3.Fillmore KM, Stockwell T, Chikritzhs T, Bostrom A, Kerr W. Moderate alcohol use and reduced mortality risk: systematic error in prospective studies and new hypotheses. Ann Epidemiol 2007;17:S16-23.
Competing interests: None declared
University of Oxford
Click to like: