The Daily Telegraph has reported that scientists have discovered a molecule that may explain “why moderate drinking might be good for you”.
This was a study of cells and mice in the laboratory. The researchers found that alcohol inhibits the growth of “smooth muscle cells”, a type of cell known to have a role in atherosclerosis.
Previous studies have found that light to moderate alcohol consumption is associated with a reduced cardiovascular risk, but it is difficult to say whether the effect of alcohol seen in this study is the reason. Much more research will be needed to fully understand these effects and how they relate to cardiovascular risk.
The NHS says there is evidence to suggest that “a regular pattern of drinking small amounts of alcohol can reduce the risk of heart disease in men over the age of 40 and post-menopausal women. No more than one to two units a day is needed”.
The study was carried out by researchers from the University of Rochester Medical Center and Dublin City University. It was funded by the National Institutes of Health and the American Heart Association.
The research was published in the peer-reviewed medical journal Arteriosclerosis, Thrombosis and Vascular Biology . The Daily Telegraph provides balanced coverage of this study.
The researchers say that previous studies have suggested that moderate alcohol intake is associated with a reduced risk of cardiovascular disease, but it is not understood why. One theory is that alcohol’s effects on smooth muscle cells (SMCs) might be involved. SMCs are involved in the development of atherosclerosis by forming a fibrous covering over the fatty plaques that build up in blood vessels. Laboratory research has shown that one effect of alcohol is to reduce the proliferation of SMCs.
SMCs also proliferate as part of the healing process for injured blood vessels. A protein called Notch 1 is known to be involved in controlling the proliferation of SMCs, and the researchers wanted to test whether alcohol might affect SMCs by modifying Notch 1 signalling in the cells.
This type of study is an appropriate way to work out exactly how a compound such as alcohol might have an effect on cells in the body.
The researchers treated human coronary artery SMCs with alcohol (ethanol), and examined the effect this had on the activity of the genes that produce the Notch 1 protein, and on a gene that the Notch 1 protein usually switches on in the cells. They also looked at the effect that alcohol had on the proliferation of the SMCs.
The researchers then studied how alcohol affected human coronary artery SMCs that had been genetically engineered always to have an active form of the Notch 1 protein.
The researchers then looked at the effect of alcohol on SMCs in live mice. They reduced blood flow through the mice’s left coronary arteries by partially tying them off. This procedure leads to thickening of the artery walls caused by proliferation of SMCs. This vessel wall thickening is similar to what happens in the vessels in human cardiovascular disease. Some of the mice were given a moderate amount of alcohol daily, and vessel healing was compared between these mice and mice that were not given alcohol.
The researchers found that alcohol reduced the activity of the gene that produces the Notch 1 protein in human coronary artery SMCs, and also the activity of a gene that Notch 1 usually switches on in the cells. At the same time, alcohol also reduced the proliferation of the SMCs. Cells that were genetically engineered so that the Notch 1 protein was always active were not affected by alcohol: they did not show reduced proliferation when treated with alcohol.
In mice with partially tied off carotid arteries, drinking a moderate amount of alcohol reduced the proliferation of the SMCs in the vessel walls. It also reduced the normal thickening of the vessel wall that was seen in mice not drinking alcohol. The mice that drank alcohol also had a reduced activity in the gene that produces Notch 1 and in a gene that the Notch 1 protein usually switches on in the cells.
The researchers conclude that alcohol inhibits Notch 1 signalling and therefore SMC proliferation both in the laboratory and in mice. They say that this effect may be relevant to the effects of moderate alcohol consumption on cardiovascular health that has been suggested in epidemiological studies.
This study has identified one way that alcohol affects smooth muscle cells. It is difficult to say whether this contributes to the effects of moderate alcohol consumption on cardiovascular risk.
The mice used had surgically created vessel injuries rather than atherosclerosis, and therefore may not be fully representative of the disease process in humans. It has also not been clearly established exactly what dose of alcohol is needed for a protective cardiovascular effect in humans, and therefore it is not possible to say how well this corresponds to the amount of alcohol given to the mice in this study.
It is important to keep the tentative conclusions of this study in context. The effects of alcohol on the cells in the body are likely to be complex, and much more research will be needed to understand them fully.
The NHS recommends no more than one to two units a day are needed for a protective effect, saying there is evidence that “a regular pattern of drinking small amounts of alcohol can reduce the risk of heart disease in men over the age of 40 and post-menopausal women”.
One unit is the amount of pure alcohol in a 25ml single measure of spirits (ABV 40%), a third of a pint of beer (ABV 5 to 6%) or half a 175ml ‘standard’ glass of red wine (ABV 12%).