Pathogenesis (development of disease)
Cigarette smoke contains more than 4,000 substances that have very different modes of action. Nicotine mediates neurobiological effects; for example, it has stimulating, appetite-reducing, rewarding, vigilance-increasing, and sedative effects. The psychotropic effects are manifold and are due to the nicotine-mediated release of dopamine, serotonin, norepinephrine or beta-endorphin. Physical dependence results from regular smoking through adaptation of the dopaminergic system and proliferation of nicotinic alpha-4-beta-2-acetylcholine receptors. This leads to the occurrence of withdrawal symptoms when smoking is discontinued due to nicotine withdrawal (e.g., smoking cessation). Further effects of cigarette smoking lead to suppression of the immune system, which in turn promotes infections and mutations (→ malignant neoplasms).
Etiology (causes)
- Genetic load
- Genetic risk depending on gene polymorphisms:
- Genes/SNPs (single nucleotide polymorphism):
- Genes: CHRNA4, CHRNA5
- SNP: rs16969968 in gene CHRNA4
- Allele constellation: AG (slightly increased risk of nicotine abuse).
- Allele constellation: AA (increased risk for nicotine abuse).
- SNP: rs1044396 in the CHRNA5 gene.
- Allele constellation: CC (increased risk of nicotine abuse).
- Genes/SNPs (single nucleotide polymorphism):
- Genetic risk depending on gene polymorphisms:
Behavioral causes
- Psycho-social situation
- Curiosity
- Stress
- Social reinforcement such as integration into groups
Causes related to disease
- Attention-deficit/hyperactivity disorder (ADHD); proportion of smokers among young ADHD patients is two to three times higher than among other peers
