Increased Admission for Alcohol Dependence After Gastric Bypass Surgery Compared With Restrictive Bariatric Surgery.
ABSTRACT IMPORTANCE We demonstrate that patients who have undergone gastric bypass surgery (GBS) have a higher risk of inpatient care for alcohol dependence than those who have undergone restrictive surgery. This highlights a need for health care providers to be aware of this so that early detection and treatment can be put in place. OBJECTIVE To evaluate inpatient care for alcohol abuse before and after GBS compared with restrictive surgery (vertical banded gastroplasty and gastric banding). DESIGN Retrospective population-based cohort study including all patients who underwent GBS, vertical banded gastroplasty, and gastric banding in Sweden from 1980 through 2006. The relative risk of inpatient care for alcohol abuse was studied before and after surgery. SETTING All hospitals in Sweden performing bariatric surgery. PARTICIPANTS A total of 11 115 patients older than 18 years (mean [SD] age, 40.0 [10.3] years; 77% women) who underwent a primary gastric bypass procedure, vertical banded gastroplasty, and gastric banding during the study period. MAIN OUTCOME MEASURES Inpatient care for alcohol abuse, substance abuse, depression, and attempted suicide. RESULTS Mean follow-up time was 8.6 years. Before surgery, there was no difference in inpatient treatment of alcohol abuse among patients who underwent gastric bypass or a restrictive procedure (incidence rate ratio, 1.1; 95% CI, 0.8-1.4). After surgery, there was a 2-fold increased risk of inpatient care for alcohol abuse among patients who had GBS compared with those who had restrictive surgery (hazard ratio, 2.3; 95% CI, 1.7-3.2). CONCLUSIONS AND RELEVANCE Patients who had undergone GBS had more than double the risk of inpatient care for alcohol abuse postoperatively compared with patients undergoing a restrictive procedure, highlighting a need for healthcare professionals to be aware of this for early detection and treatment.
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ABSTRACT: Recent insights into the neural circuits controlling energy balance and glucose homeostasis have rekindled the hope for development of novel treatments for obesity and diabetes. However, many therapies contribute relatively modest beneficial gains with accompanying side effects, and the mechanisms of action for other interventions remain undefined. This Review summarizes current knowledge linking the neural circuits regulating energy and glucose balance with current and potential pharmacotherapeutic and surgical interventions for the treatment of obesity and diabetes. Copyright © 2015 Elsevier Inc. All rights reserved.Cell 03/2015; 161(1):133-145. DOI:10.1016/j.cell.2015.02.023 · 33.12 Impact Factor
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ABSTRACT: In patients with chronic liver disease, portal hypertension is driven by progressive fibrosis and intrahepatic vasoconstriction. Interruption of the initiating and perpetuating etiology-mostly leading to necroinflammation-is possible for several underlying causes, such as autoimmune hepatitis, hepatitis B virus (HBV) infection, and most recently hepatitis C virus (HCV) infection. Thus, in the long run, lifestyle-related liver damage due to chronic alcoholism or morbid obesity will remain the main factor leading to portal hypertension. Both causes are probably more easily countered by socioeconomic measures than by individual approaches. If chronic liver injury supporting fibrogenesis and portal hypertension cannot be interrupted, a wide variety of tools are available to modulate and reduce intrahepatic resistance and therewith portal hypertension. Many of these have been evaluated in animal models. Also, some well-established drugs, which are used in humans for other indications (for example, statins), are promising if applied early and concomitantly to standard therapy. In the future, more individually tailored strategies must also be considered in line with the spectrum of portal hypertensive complications and risk factors defined by high-throughput analysis of the patient's genome, transcriptome, metabolome, or microbiome.10/2014; 6:95. DOI:10.12703/P6-95
Article: Response to Letter to the EditorJournal of Psychosomatic Research 01/2015; 78(3). DOI:10.1016/j.jpsychores.2015.01.005 · 2.84 Impact Factor