Author + information
- Jukka T. Salonen, MD, PhD, MSc∗ ( )()
- ↵∗Department of Public Health, Clinicum, Faculty of Medicine, University of Helsinki, Omenamäenkatu 23, 00990 Helsinki, Finland
Ko et al. conclude (1) that “high-density lipoprotein cholesterol (HDL-C) level is unlikely to represent a cardiovascular risk factor or a target for intervention.” As this has profound implications, I’d like to discuss possible explanations behind their findings. Alcohol intake increases total HDL-C, and therefore HDL-C is in part a measure of alcohol intake. High non–cardiovascular disease mortality at very high HDL-C levels may well be due to alcohol-induced non–cardiovascular disease mortality. I showed in a prospective population study (the KIHD [Kuopio Ischemic Heart Disease] study) in Finland that low HDL-C is associated with increased coronary, cardiovascular, and all-cause mortality only if alcohol intake, as measured by serum gamma–glutamyl transferase levels, is low (2). I suggested in my discussion that HDL elevation might be beneficial only if gamma–glutamyl transferase is low and promoted liver enzyme measurements in studies of HDL-C and mortality. Therefore, I question the validity of the authors’ conclusions, which were based on a study with no data on either alcohol intake or liver damage.
Please note: Dr. Salonen has reported that he has no relationships relevant to the contents of this paper to disclose.
- 2017 American College of Cardiology Foundation
- Ko D.T.,
- Alter D.A.,
- Guo H.,
- et al.
- Salonen J.T.