Smoking induces weight loss through complicated and poorly understood mechanisms. The majority of cigarette smoking’s effects on body weight are caused by nicotine, and smoking can be used as a behavioral substitute for eating, which reduces food intake. Nicotinic cholinergic receptors in the brain and autonomic ganglia are affected by nicotine.
Nicotine binds to nicotinic receptors, opening them so that calcium and salt can enter and increase the release of other neurotransmitters. Dopamine, norepinephrine, serotonin, acetylcholine, glutamate, -aminobutyric acid, and other neurotransmitters are released in the central nervous system in addition to the systemic release of catecholamines.
The processes via which smoking cigarettes results in weight reduction. By increasing energy expenditure and reducing the resulting compensatory increase in calorie intake, smoking helps people lose weight. Nicotine increases energy expenditure via indirect effects on neuroendocrine circuits in the central nervous system as well as direct effects on peripheral tissues (mediated mostly by catecholamines).
Smoking can be used as a behavioral alternative for eating because nicotine’s effects on the brain also lower appetite. The acronyms AgRP (Agouti-related peptide), CART (cocaine amphetamine-regulated transcript), DA (dopamine), Epi (epinephrine), GABA (gamma-aminobutyric acid), NEpi (norepinephrine), NPY (neuropeptide Y), and POMC (proopiomelanocortin) are used to denote several neurotransmitters.
Body weight is a function of the equilibrium between caloric intake and daily energy expenditure. Daily energy expenditure is influenced by a variety of factors, including resting metabolic rate, physical activity, and thermic effects of food. By raising the resting metabolic rate and reducing the anticipated gain in calorie intake as a result of the metabolic rate increase, nicotine reduces body weight.
Nicotine is a sympathomimetic drug, just like many other anti-obesity treatments. Sympathomimetic drugs increase energy expenditure through modulating brain metabolism and peripheral tissue function. Both local norepinephrine release in body tissues and systemic epinephrine release from the adrenal glands are stimulated by nicotine.
Nicotine increases lipolysis and fatty acid recycling into triglycerides, which in turn boosts thermogenesis in adipose tissue. Smoking boosts energy expenditure by 10% over a 24-hour period, and it does so more during exercise and right after eating than it does at rest.
It may seem small that a 10% increase in metabolic rate, or an additional 200 kcal per day, would result in a weight reduction of 10 kg over the course of a year, providing there is no change in calorie intake.
The central nervous system’s regulation of eating and energy expenditure may be impacted by nicotine in a number of different ways. Both eating behavior and metabolic rate are governed by the hypothalamus, which combines brain motivational and affective impulses with peripheral indications of satiety and adiposity.
The hormone leptin, which is produced in proportion to the body’s fat tissue, has central effects on appetite suppression and metabolic rate. Leptin levels in smokers and nonsmokers have been compared in several research, with varied results. However, it has been suggested that nicotine may intensify leptin’s effects in the brain by enhancing leptin binding or increasing the sensitivity of downstream transduction cascades.
Brain chemicals that suppress eating and increase up metabolism (like pro-opiomelanocortin and cocaine-amphetamine-regulated transcript) as well as those that suppress eating and slow down metabolism (like pro-opiomelanocortin and cocaine-amphetamine-regulated transcript) are both influenced by the central nervous system’s release of hormones like norepinephrine, dopamine, serotonin, and -aminobutyric acid (such as neuropeptide Y, Agouti-related peptide, melanin-concentrating hormone, and orexin).
These hormones are subject to the complicated effects of nicotine; the acute response is consistent with the activation of systems that reduce appetite and increase body metabolism, but the chronic changes are associated with the activation of systems that increase appetite and slow metabolic rate. Similar to nicotine, substances like phentermine, sibutramine, and bupropion that raise norepinephrine, dopamine, and/or serotonin levels in the brain help people lose weight.
Other metabolic effects of nicotine on body weight and composition include insulin resistance, which is probably related to the release of catecholamines. Smokers have lower levels than non-smokers of the adiponectin, an adipocyte-derived protein that regulates insulin sensitivity and has anti-inflammatory characteristics.
The development of visceral fat is one increase in body composition that is correlated with insulin resistance. Smokers have a higher amount of visceral fat compared to overall fat, which results in a higher waist-to-hip ratio than nonsmokers.
Although the reason for the link between smoking and increased visceral fat is uncertain, nicotine’s effects, which increase cortisol production and alter the ratio of male to female sex hormones, may be to blame. A high waist-to-hip ratio is associated with an increased risk of atherosclerotic cardiovascular disease and is thought to be related to both the frequency of smoking and the daily/yearly cigarette consumption.