It is a good time to be an alcoholic. The condition is far better understood than it once was, and more treatment than ever is available. The social understanding of the condition is beginning to shift away from it entirely dark and disreputable. In the western world at least, is more and more recognised as an addiction that needs treatment than a self-indulgence that should attract censure. It is less enigmatic, less sphynx-like. Furthermore, there is declining shame for taking the treatment for it. The damage alcoholism can do, and the damage it and its effects have, both physical and social, can be healed more easily than once they could.

This is tremendously promising for the furtherance of a social cause, and thus for improving a social problem. However, with respect to the medical problem, this impressive cultural change offers little help for the molecular or cellular effects of alcoholism. What is required for that is a scientific and data-driven approach. The first glimmers of a fresh angle to treating alcohol-related damage to humans has been published in the last month, through two (unconnected) papers.

Reichel et al. [1] used lipidomics techniques to investigate what impact alcoholism, and subsequent detoxification, had on the lipid profile of blood plasma. They found that the concentration of several lipids was higher in alcoholic individuals than in healthy controls. This included phosphatidylcholine and phosphatidylinositol. What they also found was that some lipids increased in concentration during detoxification. This included sphingomyelin, a lipid named after the enigmatic sphynx.

On its own, this is an interesting observation, from a sound study with a straightforward hypothesis. The observation gains momentum in the context of another study, by Yang and Subbaiah [2]. They found that an enzyme that clears fats from the bloodstream, particularly from the much maligned high-density lipoproteins (HDLs), is affected by the concentration of sphingomyelin.

This enzyme is called hepatic lipase. The name indicates that it has a close association with the liver (hepatocytes are liver cells) and that it catalyses a reaction that degrades lipids. What this enzyme does is hydrolyse both phospholipids and fats, releasing fatty acids. The activity of this enzyme correlates with a reduction in HDLs.

A reduction in HDLs might therefore be regarded as evidence of detoxification. This might in turn indicate that a patient has made it through the withdrawal stage and is making steps to recovery. However, HDLs have been identified as important in another medical arena.

HDLs are fat-carrying modules that are understood to be a factor in coronary heart disease. Where the levels of HDLs are low, the risk of heart disease is expected to be higher. A number of studies have investigated this link [3,4,5], some of them in an effort to distinguish between the lighter counterpart to HDLs, Low-density lipoproteins (LDLs) [5].

These two sets of studies are therefore an interesting comparison: on one hand, we have an increase in sphingomyelin that we would expect to lower HDLs, and on the other that lower HDLs increases heart disease. We might therefore conclude, on this basis, that for coronary heart disease at least, giving up alcohol is a bad idea.

Of course I am not about to tell you that. It would be naïve because the time interval is so short—we know that a short time where the HDL count is low on detoxification is not going to suddenly result in a coronary. However, what interests me about this, is that had this not been in the context of alcoholism and chronic illness, and the intuitive notion that a short term lowering of HDLs is probably not that bad, we might not have noticed. Had this relationship between sphingomyelin levels and the activity of hepatic lipase and detoxification been a purely cultural or purely molecular relationship, the same alarm bells may not have rung. We might just as easily conclude that ‘that sounds plausible’ and think no more of it. No enigma, no nagging doubt.

This indicates the value of complete evidence, and of testing things both ways. A passing relationship between two studies is exciting and may be relevant, and is good for bloggers, but human judgement is a crucial factor in making sense of it. And of that, we are all capable. Except, perhaps, before we have sobered up.


[1] M. Reichela, S. Hönig, G. Liebisch, A, Lüth, B, Kleuser, E, Gulbins, G. Schmitz, J. Kornhuber, Biochimica et Biophysica Acta, 2015, 1851, 1501-1510. DOI: 10.1016/j.bbalip.2015.08.005

[2] P. Yang, P. V. Subbaiah, Biochimica et Biophysica Acta, 2015, 1851, 1327–1336. DOI: 10.1016/j.bbalip.2015.07.003

[3] D. J. Rader, G. K. Hovingh, The Lancet, 2014, 384, 618.

[4] K. M. Ali, A. Wonnerth, K. Huber, J. Wojta, British Journal of Pharmacology, 2012, 167, 1177–1194. DOI:10.1111/j.1476-5381.2012.02081.x

[5] J. P. Després , I. Lemieux, G. R. Dagenaisa, B. Cantin, B. Lamarche, Atherosclerosis, 2000, 153, 263–272.