Smoking, Obesity, and Post-Cessation Weight Gain: Neurobiological Intersection and Treatment Recommendations

In the US, 28.8 million adults currently smoke cigarettes, and approximately 1.25 billion people use tobacco globally. Unfortunately, post-cessation weight gain is a substantial barrier to smoking cessation and sustained abstinence. Among people who smoke, 36% meet the body mass index (BMI) criteria for obesity and over 50% meet the waist circumference criteria for central obesity. Despite this, primary care providers currently have limited guidance on how to best treat their patients who want to quit smoking without post-cessation weight gain. There are common neurobiologic and endocrine dysregulations in nicotine dependence and weight gain. For example, nicotine dependence and obesity are both associated with dysregulation in hypothalamic neuropeptide systems and dopaminergic pathways. Medications for nicotine dependence act on dopaminergic pathways and hypothalamic pro-opiomelanocortin (POMC) cells. Similarly, medications for obesity may increase dopamine and norepinephrine signaling and stimulate POMC activity. A unique medication, the fixed-dose extended-release combination of naltrexone and bupropion, supports both smoking cessation and weight loss by increasing dopamine and norepinephrine signaling and stimulating POMC-producing cells. This narrative review outlines neurobiologic mechanisms common to smoking and obesity and compares the effects of available pharmacotherapies on dopaminergic system and neuroendocrine dysregulation. Finally, this review outlines factors that primary care professionals should consider when treating people who want to stop smoking but are at risk of post-cessation weight gain.

Duke Scholars

Author James Davis Medicine, General Internal Medicine