Hepatic, lipid and genetic factors associated with obesity: crosstalk with alcohol dependence?

Abstract

Objectives: Alcohol dependence represents a leading cause of mortality and morbidity. Understanding the variables that contribute to this diagnosis and its severity is critical. An overlap between factors that may predispose people to become obese and those that may increase the risk of alcohol dependence may exist. However, data in the literature are not conclusive. Therefore, this study aimed to identify the association between alcohol dependence and obesity-related factors, including biochemical and genetic factors.

Methods: In a case–control study with 829 participants, factors involved with metabolism and obesity were assessed, including biochemical lipid and liver markers, and the fat mass and obesity-associated (FTO) single nucleotide polymorphism (SNP) rs8050136.

Results: Increased triglycerides, having one or two minor A alleles for rs8050136 and being a smoker were associated with increased risk of alcohol dependence, while increased low-density lipoprotein cholesterol was associated with decreased risk. In addition, having abnormal gamma-glutamyl transferase and being female were factors associated with an increased severity of alcohol dependence.

Conclusions: Our preliminary findings suggest a link between alcohol dependence and obesity-related biochemical and genetic factors. Future studies are needed to better understand if these factors may play a predictive role and/or may act as biomarkers for treatment response.

Keywords:

• Obesity
• alcohol dependence
• FTO
• genetics
• metabolism

Acknowledgments

The authors would like to express their gratitude to the NIAAA and Clinical Center clinical and research staff members involved in data collection support at the National Institutes of Health Intramural Research Program. The authors would also like to thank Sean Andrew Aston, Allison Daurio, Matthew Rohn and Jamie Temko (joint NIAAA/NIDA Section on Clinical Psychoneuroendocrinology and Neuropsychopharmacology) for their assistance with data management of this study. Finally, the authors would like to thank Karen Smith, NIH Library for bibliographic assistance.

Statement of interest

None to declare.

Additional information

Funding

This work was supported by NIH intramural funding ZIA-AA000218 (Section on Clinical Psychoneuroendocrinology and Neuropsychopharmacology; PI: Leggio), jointly supported by the Division of Intramural Clinical and Biological Research of the National Institute on Alcohol Abuse and Alcoholism (NIAAA) and the Intramural Research Program of the National Institute on Drug Abuse (NIDA).