Metabolic and Addiction Indices in Patients on Opioid Agonist Medication-Assisted Treatment: A Comparison of Buprenorphine and Methadone

Abstract

Metabolic hormones stabilize brain reward and motivational circuits, whereas excessive opioid consumption counteracts this effect and may impair metabolic function. Here we addressed the role of metabolic processes in the course of the agonist medication-assisted treatment for opioid use disorder (OUD) with buprenorphine or methadone. Plasma lipids, hemoglobin A1C, body composition, the oral glucose tolerance test (oGtt) and the Sweet taste test (Stt) were measured in buprenorphine-(n = 26) or methadone (n = 32)-treated subjects with OUD. On the whole, the subjects in both groups were overweight or obese and insulin resistant; they displayed similar oGtt and Stt performance. As compared to methadone-treated subjects, those on buprenorphine had significantly lower rates of metabolic syndrome (MetS) along with better values of the high-density lipoproteins (HDL). Subjects with-vs. without MetS tended to have greater addiction severity. correlative analyses revealed that more buprenorphine exposure duration was associated with better HDL and opioid craving values. in contrast, more methadone exposure duration was associated with worse triglycerides-, HDL-, blood pressure-, fasting glucose-and hemoglobin A1C values. Buprenorphine appears to produce beneficial HDL-and craving effects and, contrary to methadone, its role in the metabolic derangements is not obvious. our data call for further research aimed at understanding the distinctive features of buprenorphine metabolic effects vis-à-vis those of methadone and their potential role in these drugs' unique therapeutic profiles. Opioid use disorder (OUD) is an ominous public health problem afflicting about 16 million people worldwide 1. In the US, OUD constitutes the seventh cause for disability-adjusted life-years 2-4 ; including opioids' propensity 5 for the excessive body weight gain (BWG) and its medical sequelae in the form of the 'Metabolic Syndrome' (MetS) 5-7 , that is to say, a cluster of interrelated cardiometabolic risk factors comprised of insulin resistance, impaired glucose tolerance, dyslipidemia, abdominal adiposity and hypertension 8-10. Consequently, even though medication-assisted treatment (MAT) via opioid agonist replacement with long-acting opioids namely, buprenorphine and methadone, usually yields positive clinical outcomes in terms of overdose mortality, infectious diseases, crime, and societal ties 11-14 concerns have been raised about further worsening of the metabolic status 5. There are several lines of evidence that link OUD to metabolic derangements. With regard to genetic antecedents, the TCF7L2 gene codes a transcription factor implicated 15,16 in non-insulin-dependent

Regulation of body weight and food intake by AGRP neurons during opioid dependence and abstinence in mice

“…The epidemiological data showing high co-incidence of these disorders – estimated at 37% of people with obesity ( Janssen et al, 2020 ), 1.89% of people with eating disorders ( Qian et al, 2021 ), and 4% of people who misuse opioid prescriptions, as well as many more who obtain substances through the illicit drug market ( Jannetto, 2021 ) – indicate a potential for a high degree of overlap. Recent work has demonstrated the critical importance of considering metabolic factors in selecting treatment for patients with opioid use disorder ( Elman et al, 2020 ). Moreover, during opioid dependence, the selection of foods for consumption becomes limited.…”

Multicenter Observational/Exploratory Study Addressed to the Evaluation of the Effectiveness and Safety of Pharmacological Therapy in Opioid-Dependent Patients in Maintenance Therapy in Southern Italy

“…This is reported to be superior with other drugs, rather than rac-methadone/levomethadone, as buprenorphine and diamorphine patients rated their physical functioning substantially higher than methadone patients [15]. Buprenorfine also showed more favorable metabolic effects vs. other drugs in these patients [44].…”

A Novel Precision Approach to Overcome the “Addiction Pandemic” by Incorporating Genetic Addiction Risk Severity (GARS) and Dopamine Homeostasis Restoration

“…We encourage clinicians to research and understand the importance of a molecular framework to explain the current underpinnings of endorphinergic/dopaminergic mechanisms related to opioid deficiency syndrome and a generalized reward processing deficiency [ 19 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 , 96 , 97 ]. Along these same lines, many RDS subtypes have also been linked to hypodopaminergia using sophisticated imaging techniques [ 98 , 99 , 100 , 101 , 102 , 103 , 104 , 105 , 106 , 107 , 108 , 109 , 110 , 111 , 112 ]. Can we better combat SUD through early genetic risk screening enable early intervention by the induction of dopamine homeostasis?…”