Nicotine is an alkaloid compound naturally found in plants belonging to the nightshade family, predominantly the tobacco plant. It is widely used in various products, including traditional combustible cigarettes, electronic cigarettes, and nicotine replacement therapies such as patches, gum, lozenges, inhalers, and nasal sprays.
The Mechanism of Nicotine in the Body
Upon entering the body, nicotine rapidly travels into the bloodstream and reaches the brain. Once in the brain, it interacts with specific proteins called nicotinic acetylcholine receptors (nAChRs), activating them.
The activation of nAChRs leads to the release of several neurotransmitters. This includes dopamine in brain regions associated with pleasure and reward, contributing to rewarding sensations. Nicotine also prompts the release of adrenaline and norepinephrine, which heighten arousal and increase alertness. Over time, repeated nicotine exposure can cause these receptors to become less responsive, a process known as desensitization. The brain may then increase the number of nAChRs to compensate, contributing to tolerance.
Cardiovascular and Systemic Impact
Nicotine influences the cardiovascular system by stimulating the sympathetic nervous system. This results in an immediate increase in heart rate and elevates blood pressure. It also enhances the heart’s contractility, increasing the workload on the heart muscle.
Beyond these immediate effects, nicotine causes systemic vasoconstriction, narrowing blood vessels. Prolonged exposure can impair the function of the inner lining of blood vessels, potentially contributing to atherosclerosis, a condition where plaque builds up in arteries. This can increase the risk for serious cardiovascular events such as heart attacks and strokes. Nicotine has also been linked to the development of cardiac arrhythmias.
Nicotine also affects metabolism and can contribute to insulin resistance, where the body’s cells become less responsive to insulin, leading to higher blood glucose levels. This can worsen existing diabetes or increase the likelihood of developing type 2 diabetes. The substance can also trigger the body to produce more triglycerides, a type of fat linked to insulin resistance, and raise levels of hormones that counteract insulin. Nicotine can inhibit hypothalamic AMP-activated protein kinase activity, influence fat breakdown (lipolysis), and, with chronic use, impair mitochondrial fat oxidation, potentially leading to fat cell enlargement.
Neurological and Cognitive Consequences
The repeated release of dopamine in the brain’s reward pathways is a central factor in the development of nicotine dependence. This consistent stimulation effectively rewires these pathways, leading to a compulsive drive to seek and use nicotine. As the brain adapts to regular nicotine exposure, tolerance develops, and the increase in nicotinic acetylcholine receptors contributes to the intense cravings and discomfort experienced during withdrawal.
The developing adolescent brain is particularly susceptible to nicotine’s effects due to ongoing significant reorganization. Nicotine exposure during this sensitive period can interfere with brain maturation, potentially affecting cognitive functions such as attention, learning, and impulse control. Studies indicate that smoking during adolescence can increase the risk of cognitive impairment later in life. Furthermore, adolescent brains show heightened sensitivity to nicotine-induced changes in neuronal activity and synaptic plasticity.
Carcinogenicity and Tobacco Products
It is important to understand that nicotine itself is not generally considered a direct carcinogen, meaning it does not directly cause cancer. The primary cancer-causing agents associated with tobacco use are the thousands of other chemicals, including over 70 known carcinogens, found in tobacco smoke. These harmful compounds are produced during the combustion of tobacco.
Despite not being a direct carcinogen, some research suggests that nicotine may play a role as a “tumor promoter.” It has been observed to speed up cell growth, promote processes like epithelial-mesenchymal transition (EMT) which is involved in malignant cell development, and potentially decrease the effectiveness of tumor suppressor mechanisms. These actions could potentially accelerate the growth of existing cancer cells in tissues such as the breast, colon, and lung. Therefore, while combustible tobacco products are dangerous due to their numerous carcinogens, the long-term effects of nicotine from products like e-cigarettes or nicotine replacement therapies, which deliver nicotine without combustion, continue to be a subject of ongoing study.
Nicotine Withdrawal and Cessation
When individuals stop or significantly reduce their nicotine intake after prolonged use, they experience a range of physical, mental, and emotional symptoms collectively known as nicotine withdrawal. This occurs as the brain and body readjust to the absence of the substance they have become accustomed to. Common symptoms include intense cravings for nicotine, irritability, anxiety, and a depressed mood. Many individuals also report difficulty concentrating, trouble sleeping (insomnia), and an increased appetite, which can sometimes lead to weight gain.
Less common, but still possible, symptoms include headaches, nausea, nightmares, dizziness, constipation, coughing, a sore throat, and dry mouth. These symptoms generally begin within 4 to 24 hours after the last nicotine use and typically peak in intensity around the second or third day of abstinence. While physical discomfort often subsides within a few weeks, psychological and cognitive symptoms, such as mood swings and difficulty focusing, can sometimes persist for a longer duration.