Nicotine is highly addictive, more capable of compelling irrational behavior than alcohol or heroin. Nicotine’s action on the central nervous system is different than most other drugs of addiction because it bypasses all sensory centers and directly releases gratification producing neurotransmitters in the brain. Long term use of nicotine produces changes in brain function and structure that make it difficult for the patient to forego smoking in the face of predictable triggers such as stress. These structural changes, hard-wired connections between the motivation and emotion centers of the brain, are formed early in response to high concentration nicotine exposures that can only be produced using smoke as the delivery device. The cigarette is an “optimized” device, delivering free-base nicotine to the brain to create its impact. These structural changes don’t resolve easily upon abstinence, placing the newly “quit” smoker at elevated risk for relapse for several years. In this manner, smoking can be conceived of as the behavioral manifestation of a chronic biologic disturbance.
The impact of nicotine on the brain is not a function of background venous concentrations, but rather a function of the enormously high concentrations in arterial blood produced when nicotine is absorbed in the lung and returned to the left ventricle prior to redistribution or first pass metabolism.
Nicotine is highly addictive, more capable of compelling irrational behavior than alcohol or heroin. Nicotine’s action on the central nervous system is different than most other drugs of addiction because it bypasses all sensory centers and directly releases gratification producing neurotransmitters in the brain. Long term use of nicotine produces changes in brain function and structure that make it difficult for the patient to forego smoking in the face of predictable triggers such as stress. These structural changes, hard-wired connections between the motivation and emotion centers of the brain, are formed early in response to high concentration nicotine exposures that can only be produced using smoke as the delivery device. The cigarette is an “optimized” device, delivering free-base nicotine to the brain to create its impact. These structural changes don’t resolve easily upon abstinence, placing the newly “quit” smoker at elevated risk for relapse for several years. In this manner, smoking can be conceived of as the behavioral manifestation of a chronic biologic disturbance.
The impact of nicotine on the brain is not a function of background venous concentrations, but rather a function of the enormously high concentrations in arterial blood produced when nicotine is absorbed in the lung and returned to the left ventricle prior to redistribution or first pass metabolism.
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