Smoking and Body Weight: Is There Any Relation?

Abstract

Tobacco is a tall, green leafy plant, originally grown in South and Central America, but now cultivated throughout the world. The link between smoking and body weight is evident as early as adolescence. Nicotine acts on nicotinic cholinergic receptors in the brain and autonomic ganglia. The binding of nicotine to the nicotinic receptors opens ion channels, allowing entry of sodium and calcium, thereby; augment the release of various neurotransmitters. This process includes the systemic release of catecholamines in the central nervous system, release of dopamine, norepinephrine, serotonin, acetylcholine, glutamate and γ-amino butyric acid. To make best use of the health benefits of smoking cessation and notify behavioral and pharmacologic interventions to mitigate post-cessation weight gain, it is important to identify processes that account for overeating among smokers within the first six months after quitting. Smoking and obesity are cardiovascular risk factors and cause cardiovascular disease. Smoking causes endothelial dysfunction enhances thrombogenesis, cause insulin resistance and diabetes, and is associated with an atherogenic lipid profile. Leptin is released from adipose tissue inproportion to the amount of adipose and acts centrally to suppress food intake and increasemetabolic rate. Studies comparing leptin levels in smokers with those in nonsmokers showcontradictory results. The efficacy and safety of long-term nicotine medication for weight control remains investigated. Nicotine was conveyed to people through cigarette smoke, which is toxic. Considerate brain mechanisms of how nicotine affects body weight may lead to innovative approaches to pharmacotherapy.

Keywords: body weight, nicotine, smoking, tobacco