smoking cessation

8 interactions related to smoking cessation

smoking + clozapine

Polycyclic aromatic hydrocarbons in tobacco smoke (not nicotine) potently induce CYP1A2, the enzyme responsible for roughly 70% of clozapine metabolism, lowering clozapine plasma levels by up to 50% in smokers. Sudden smoking cessation can cause clozapine levels to rise 50-72% within 3-5 days, risking sedation, seizures, and toxicity.

high
smokingclozapinecyp1a2antipsychoticdrug interactiontobaccoschizophreniasmoking cessationplasma levels

smoking + olanzapine

Polycyclic aromatic hydrocarbons in cigarette smoke induce CYP1A2, the primary enzyme that metabolizes olanzapine, increasing olanzapine clearance by roughly 37-48% in smokers. Meta-analysis data suggest olanzapine doses should be 30% lower in non-smokers than in smokers to reach the same plasma levels.

high
smokingolanzapinecyp1a2antipsychoticdrug interactiontobaccozyprexasmoking cessationschizophrenia

smoking + theophylline

Polycyclic aromatic hydrocarbons in tobacco smoke induce CYP1A2, increasing theophylline clearance by 58-100% and shortening its half-life by roughly 63%. Smokers often need 1.5-2 times the usual theophylline dose, and abrupt cessation can rapidly produce toxic levels.

high
smokingtheophyllinecyp1a2asthmacopddrug interactiontobaccosmoking cessationnarrow therapeutic window

smoking + propranolol

Cigarette smoking induces hepatic metabolism of propranolol via CYP1A2 and accelerated glucuronidation, increasing apparent oral clearance and reducing propranolol plasma concentrations in smokers compared with non-smokers. Nicotine also independently raises heart rate, blood pressure, and circulating catecholamines, partially counteracting propranolol's beta-blocking effect.

moderate
smokingpropranololbeta-blockercyp1a2hypertensiontobaccodrug interactionheart ratesmoking cessation

smoking + caffeine

Polycyclic aromatic hydrocarbons in tobacco smoke induce CYP1A2, the enzyme that performs about 95% of caffeine demethylation, raising caffeine clearance by 40-65% and shortening its half-life from roughly 6 hours to 3.5 hours in smokers. Quitting smoking can cause caffeine levels to rise sharply, contributing to jitters, anxiety, palpitations, and insomnia.

moderate
smokingcaffeinecyp1a2coffeetobaccosmoking cessationanxietyinsomniadrug interaction

smoking + insulin

Smoking reduces subcutaneous insulin absorption through vasoconstriction and worsens insulin resistance through nicotine-driven catecholamine release, oxidative stress, and inflammation, with HbA1c rising progressively with cigarettes per day. Diabetic smokers typically need 15-30% more insulin than non-smokers to achieve the same glycemic control.

high
smokinginsulindiabetestobaccoinsulin resistancehba1cdrug interactionsmoking cessationblood sugar

smoking + varenicline

Varenicline (Chantix) is a partial agonist at the alpha4-beta2 nicotinic acetylcholine receptor; continued smoking or concurrent nicotine replacement therapy can increase side effects such as nausea, headache, vomiting, dizziness, and fatigue. Varenicline blocks much of nicotine's rewarding effect.

moderate
smokingvareniclinechantixsmoking cessationnicotine receptorpartial agonistnauseaside effectsquit smokingnrt

bupropion + st. john's wort

Bupropion lowers the seizure threshold and St. John's wort may compound that risk, and the herb's induction of CYP enzymes (particularly the role of CYP2B6 and downstream pathways) can also alter bupropion exposure. Both also influence monoamine signaling, raising the risk of additive CNS effects.

high
bupropionwellbutrinst johns wortseizure thresholdantidepressant interactionherbal interactionsmoking cessationdepression