The gut in the brain: the effects of bariatric surgery on alcohol consumption

Abstract

Obesity represents a major medical and public health problem worldwide. Efforts have been made to develop novel treatments, and among them bariatric surgery is used as an effective treatment to achieve significant, long-term weight loss and alleviate medical problems related to obesity. Alcohol use disorder (AUD) is also a leading cause of morbidity and mortality worldwide. Recent clinical studies have revealed a concern for bariatric surgery patients developing an increased risk for alcohol consumption, raising concerns about development of AUD. A better understanding of the relationship between bariatric surgery and potential later development of AUD is important, given the critical need of identifying patients at high risk for AUD. This paper reviews current clinical and basic science research and discusses potential underlying mechanisms. Special emphasis in this review is given to recent work suggesting that, alterations in alcohol metabolism/pharmacokinetics resulting from bariatric surgery are unlikely to be the primary or at least the only explanation for increased alcohol use and development of AUD, as changes in brain reward processing are also likely to play an important role. Additional studies are needed to clarify the potential role and mechanisms of how bariatric surgery may increase alcohol use and lead to AUD development.

Alcohol and other substance use after bariatric surgery: prospective evidence from a U.S. multicenter cohort study

“…1 However, evidence is mounting that Roux-en-Y gastric bypass (RYGB) increases the risk of developing an alcohol use disorder (AUD). 2-5 Pharmacokinetic studies provide evidence that RYGB, but not laparoscopic adjustable gastric band (LAGB), is associated with higher peak blood alcohol concentration, which is reached more quickly compared to presurgery status or non-surgical controls. 2,5 Additionally, rodent models suggest that RYGB increases alcohol reward sensitivity via a neurobiological mechanism, independent of changes in alcohol absorption.…”

“…2-5 Pharmacokinetic studies provide evidence that RYGB, but not laparoscopic adjustable gastric band (LAGB), is associated with higher peak blood alcohol concentration, which is reached more quickly compared to presurgery status or non-surgical controls. 2,5 Additionally, rodent models suggest that RYGB increases alcohol reward sensitivity via a neurobiological mechanism, independent of changes in alcohol absorption. 2,5 Hypothesized pathways include changes to the ghrelin system and altered genetic expression in regions of the brain associated with reward circuitry.…”

“…2,5 Additionally, rodent models suggest that RYGB increases alcohol reward sensitivity via a neurobiological mechanism, independent of changes in alcohol absorption. 2,5 Hypothesized pathways include changes to the ghrelin system and altered genetic expression in regions of the brain associated with reward circuitry. 2,5 …”

“…2,5 Hypothesized pathways include changes to the ghrelin system and altered genetic expression in regions of the brain associated with reward circuitry. 2,5 …”

“…2,5,6 However, findings from longitudinal studies of AUD-related outcomes prior to and following bariatric surgery are inconsistent 3-5 and few studies have long-term follow-up or evaluation of non-alcohol SUD, 3,4 such that we have little understanding of whether the risk of AUD or non-alcohol SUD changes over time and the proportion of post-surgical patients that are ultimately affected. Recent literature reviews of AUD or SUD and bariatric surgery concluded there is a need for large, prospective, longitudinal studies that extend beyond two years, separate alcohol from other drug use, use standardized assessments, account for type of bariatric surgical procedure and identify risk factors for development of post-surgery AUD.…”