Addiction is a complex condition characterized by persistent drug-seeking behavior despite negative consequences.
Nicotine is highlighted as a potent and highly addictive chemical found in tobacco.
Over 1.3 billion global tobacco users.
Tobacco-related deaths approximate 5 million annually.
Limited success in quitting: fewer than 20% of users quit after their first attempt.
Addictive behaviors are developed through chemicals acting as positive reinforcers in the brain.
Physical and psychological dependencies are formed.
Nicotine enhances dopamine release in the brain's reward centers.
Creates pleasurable sensations that are associated with social aspects of smoking.
Smokers may experience lethargy, hunger, irritability, and other withdrawal symptoms when trying to quit.
Influenced by environmental factors, metabolism, age, sex, genetic predisposition, and psychiatric disorders.
Nicotine affects neurotransmitter release in the mesolimbic system.
Enhances performance, mood modulation, lower body weight, and acts as self-medication.
Successful quitting often involves combination of behavioral strategies and pharmacological treatments.
Nicotine Replacement Therapy (NRT) includes skins patches, gums, lozenges, and sprays.
Bupropion (inhibits reuptake of monoamines) mimics nicotine effects.
Varenicline selectively binds to nAChRs affecting nicotine addiction.
Chronic exposure to nicotine leads to increased numbers of receptors (up-regulation) contrary to usual down-regulation responses.
Continuous ACh exposure can desensitize cells; speculation on how this contributes to receptor up-regulation in smokers.
Noticeable increase in vaping among high school students (1.5% to 19.6% from 2011 to 2020).
Long-term effects of nicotine exposure are not fully understood.
Potential negative impacts on cardiovascular health and adolescent brain development.
Shanika’s journey exemplifies the struggle of nicotine addiction and the importance of support and treatment options.
Continued research is essential to better understand addiction and develop effective cessation methods.
When nicotine binds to nicotinic acetylcholine receptors (nAChRs) on a postsynaptic cell instead of acetylcholine (ACh), it leads to receptor activation, similar to the effects of ACh. However, nicotine typically causes prolonged activation of nAChRs. This can result in enhanced neurotransmitter release due to increased cation conductance, leading to depolarization of the postsynaptic membrane. Over time, chronic exposure to nicotine can cause up-regulation of nAChRs, meaning that the number of receptors can increase, compared to the normal response to ACh which usually leads to down-regulation in sustained exposure.