Quitting smoking does not increase the risk of major depressive episodes among users of Internet smoking cessation interventions.

BACKGROUND: Limited evidence has suggested that quitting smoking increases the incidence of major depressive episodes (MDEs), particularly for smokers with a history of depression. Further evidence for this increase would have important implications for guiding smoking cessation. METHOD: Spanish- and English-speaking smokers without a current MDE (n=3056) from an international, online smoking cessation trial were assessed for abstinence 1 month after their initial quit date and followed for a total of 12 months. Incidence of screened MDE was examined as a function of abstinence and depression history. RESULTS: Continued smoking, not abstinence, predicted MDE screened at 1 month [smoking 11.5% v. abstinence 7.8%, odds ratio (OR) 1.36, 95% confidence interval (CI) 1.04-1.78, p=0.02] but not afterwards (smoking 11.1% v. abstinence 9.8%, OR 1.05, 95% CI 0.77-1.45, p=0.74). Depression history predicted MDE screened at 1 month (history 17.1% v. no history 8.6%, OR 1.71, 95% CI 1.29-2.27, p<0.001) and afterwards (history 21.7% v. no history 8.3%, OR 3.87, 95% CI 2.25-6.65, p<0.001), although the interaction between history and abstinence did not. CONCLUSIONS: Quitting smoking was not associated with increased MDE, even for smokers with a history of depression, although a history of depression was. Instead, not quitting was associated with increased MDE shortly following a quit attempt. Results from this online, large, international sample of smokers converge with similar findings from smaller, clinic-based samples, suggesting that in general, quitting smoking does not increase the incidence of MDEs.

The effect of catecholamines and adenosine on the induction of morphological alterations and depigmentation of newt iris epithelial cells in vitro.

Catecholamines and adenosine have a stimulating effect on the process of dedifferentiation of cultured iris epithelial cells (IECs) from the adult newt Notophthalmus viridescens. Micromolar concentrations of adrenergic ligands such as isoproterenol, norepinephrine, and epinephrine induced marked morphological alterations culminating in the stellate configuration and depigmentation of IECs. Dopamine at 100 microM or higher induced the morphological response, while serotonin was ineffective. The morphological change was transient, requiring 80-90 min for maximum induction, and only a fraction of the cells was responsive. The response was blocked by beta-adrenergic antagonists, such as propranolol and alprenolol, but not by alpha-adrenergic blockers. Adenosine at 10 microM, or higher, also induced morphological alterations of IECs. The effect of adenosine was partially blocked by various adenosine receptor antagonists. The effect of isoproterenol and norepinephrine on the induction of morphological alterations was potentiated by adenosine. The release of melanosomes from IECs was increased in the presence of catecholamines and adenosine. Catecholamines and adenosine at 10 microM increased the intracellular levels of cAMP of dedifferentiating dorsal irides. The increase in cAMP levels induced by isoproterenol was inhibited by propranolol and the adenosine receptor antagonist 5'-deoxy-5'-methyl thioadenosine (MTA) partially blocked the effect of adenosine. Our results suggest that adrenergic hormones may be coupled to a beta-adrenergic adenylate cyclase system. The presence of an adenosine receptor is also suggested by the results. Our data strongly support previous work in which cAMP and substances related to it induced morphological alterations and depigmentation of IECs. It is proposed that catecholamines and adenosine may participate in the regulation of dedifferentiation during the transdifferentiation of IECs into lens cells.