Adolescent smoking and depression: Which comes first?

Steuber, Traci L.; Danner, Fred

doi:10.1016/j.addbeh.2005.04.010

Cited by 162 publications

(123 citation statements)

References 6 publications

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“…These observations are entirely consistent with the view that the brain adaptations to addictive stimuli do not simply regress to normal after discontinuing drug exposure, but rather are kept in balance through lasting adjustments in synaptic activity, as postulated by the sensitization-homeostasis theory of nicotine addiction (DiFranza and Wellman, 2005). Accordingly, there are long-term sequelae that persist beyond the stage of smoking or abstinence, including enhanced susceptibility to relapse, and as found recently, emergence of depression as a consequence of adolescent smoking (Steuber and Danner, 2006). The current results, combined with earlier work on the prenatal + adolescent exposure model, permit the formulation of a hypothesis as to how smoking behaviors can be transmitted across generations (Figure 6).…”

Section: Resultssupporting

confidence: 86%

Permanent, Sex-Selective Effects of Prenatal or Adolescent Nicotine Exposure, Separately or Sequentially, in Rat Brain Regions: Indices of Cholinergic and Serotonergic Synaptic Function, Cell Signaling, and Neural Cell Number and Size at 6 Months of Age

Slotkin

MacKillop

Rudder

et al. 2006

Neuropsychopharmacol

146

116

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Nicotine is a neuroteratogen that disrupts neurodevelopment and synaptic function, with vulnerability extending into adolescence. We assessed the permanence of effects in rats on indices of neural cell number and size, and on acetylcholine and serotonin (5HT) systems, conducting assessments at 6 months of age, after prenatal nicotine exposure, adolescent exposure, or sequential exposure in both periods. For prenatal nicotine, indices of cell number and size showed few abnormalities by 6 months, but there were persistent deficits in cerebrocortical choline acetyltransferase activity and hemicholinium-3 binding to the presynaptic choline transporter, a pattern consistent with cholinergic hypoactivity; these effects were more prominent in males than females. The expression of 5HT receptors also showed permanent effects in males, with suppression of the 5HT 1A subtype and upregulation of 5HT 2 receptors. In addition, cell signaling through adenylyl cyclase showed heterologous uncoupling of neurotransmitter responses. Nicotine exposure in adolescence produced lasting effects that were similar to those of prenatal nicotine. However, when animals were exposed to prenatal nicotine and received nicotine subsequently in adolescence, the adverse effects then extended to females, whereas the net effect in males was similar to that of prenatal nicotine by itself. Our results indicate that prenatal or adolescent nicotine exposure evoke permanent changes in synaptic function that transcend the recovery of less-sensitive indices of structural damage; further, prenatal exposure sensitizes females to the subsequent adverse effects of adolescent nicotine, thus creating a population that may be especially vulnerable to the lasting behavioral consequences of nicotine intake in adolescence.

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Section: Resultssupporting

confidence: 86%

Permanent, Sex-Selective Effects of Prenatal or Adolescent Nicotine Exposure, Separately or Sequentially, in Rat Brain Regions: Indices of Cholinergic and Serotonergic Synaptic Function, Cell Signaling, and Neural Cell Number and Size at 6 Months of Age

Slotkin

MacKillop

Rudder

et al. 2006

Neuropsychopharmacol

146

116

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“…Indeed, epidemiological (Grant, Hasin, Chou, Stinson, & Dawson, 2004;Lasser, et al, 2000), community (Hayward, Killen, & Taylor, 1989) and clinical (Himle, Thyer, & Fischer, 1988;McCabe et al, 2004;Pohl, Yeragani, Balon, Lycaki, & McBride, 1992) studies have found that daily cigarette smoking is more common among those with anxiety and depressive psychopathology compared to those without such problems. Other studies have found that smoking, particularly at higher rates, increases the risk for developing and maintaining clinically significant anxiety and depressive symptoms (Breslau & Klein, 1999;Breslau, Novak, & Kessler, 2004;Goodwin, Lewinsohn, & Seeley, 2005;Isensee, Wittchen, Stein, Höfler, & Lieb, 2003;Johnson et al, 2000;Korhonen, et al, 2007;McLeish, Zvolensky, & Bucossi, 2007;Steuber & Banner, 2006). There is also evidence to suggest daily smokers experiencing high levels of anxiety and/or depressive symptoms tend to experience more severe withdrawal sensations (Breslau, Kilbey, & Andreski, 1992), resulting in more difficult and less successful quit attempts (Anda et al, 1999; Zvolensky, Gibson et al, in press).…”

Section: Introductionmentioning

confidence: 99%

Linkages between cigarette smoking outcome expectancies and negative emotional vulnerability

Johnson¹,

Zvolensky²,

Marshall³

et al. 2008

Addictive Behaviors

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The present investigation examined whether smoking outcome expectancies, as measured by the Smoking Consequences Questionnaire (SCQ; Brandon & Baker, 1991), were incrementally related to emotional vulnerability factors among an adult sample of 202 daily cigarette smokers (44.6% women; M age = 23.78 years, SD = 9.69 years). After controlling for cigarettes smoked per day, past 30-day marijuana use, current alcohol consumption, and coping style, negative reinforcement/ negative affect reduction outcome expectancies were significantly associated with greater levels of negative affectivity, emotional dysregulation, and anxiety sensitivity. The observed effects for negative reinforcement/negative affect reduction also were independent of shared variance with other outcome expectancies. Negative personal consequences outcome expectancies were significantly and incrementally related to anxiety sensitivity, but not negative affectivity or emotional dysregulation. Findings are discussed in terms of the role of negative reinforcement/negative affect reduction smoking outcome expectancies and clinically-relevant negative emotional vulnerability for better understanding cigarette smoking-negative mood problems.Correspondence concerning this article should be addressed to Michael J. Zvolensky, Ph.D., Dr. Zvolensky can be contacted at The University of Vermont, Department of Psychology, 2, Colchester Avenue, John Dewey Hall, Burlington,. Electronic mail may be sent to Michael.Zvolensky@uvm.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. 2 Although not a primary aim of the current study, exploratory analyses focused on positive affectivity were completed for comparative purposes. These analyses were completed in an identical fashion to those reported in the paper except positive affectivity was employed as the dependent variable. Here, predictor variables accounted for 22.1% of the overall variance for positive affectivity [F(9, 198) = 5.95, p < .001]. Level one of the model accounted for 17.1% of the variance, with significant contributions by the emotional processing and emotional expression subscales (β = .30, p < .001 and β = .16, p < .05, respectively). Level two of the model accounted for an additional 5% of the variance, with the appetite control subscale being the only significant predictor (β = −.16, p < .05). There is a recent and increasingly well-documented association between cigarette smoking and depressive and anxiety symptoms and disorders (Morrell & Cohen, 2006;Morissette, Tull, Gulliver, Kamholz, & Zimering, 2007;Patton, Carlin, Coffey, Wolfe, Hibbert, & ...

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“…Empirical investigations in the United States have shown that higher levels of depression are observed among adolescents who are current smokers, compared to levels of depression among adolescents who have never smoked and those who are former smokers (Martini, Wagner, & Anthony, 2002), but the exact mechanisms for this association have yet to be uncovered. For example, using longitudinal data from the United States National Longitudinal Study of Adolescent Health, Steuber and Danner (2006) found that current smokers were more likely to experience depressive symptoms, even after controlling for prior level of depression (Munafò et al, 2008;Steuber & Danner, 2006). For the past two decades, a considerable amount of empirical attention has been devoted to understanding the genetic factors associated with cigarette smoking.…”

Section: Comorbidity Of Depression and Cigarettes Use: Etiological Comentioning

confidence: 99%

Adolescent Cigarette Use in the Americas: The Link with Depression

Bares¹,

Delva²,

Hynes³

et al. 2012

Essential Notes in Psychiatry

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Adolescent smoking and depression: Which comes first?

Cited by 162 publications

References 6 publications

Permanent, Sex-Selective Effects of Prenatal or Adolescent Nicotine Exposure, Separately or Sequentially, in Rat Brain Regions: Indices of Cholinergic and Serotonergic Synaptic Function, Cell Signaling, and Neural Cell Number and Size at 6 Months of Age

Permanent, Sex-Selective Effects of Prenatal or Adolescent Nicotine Exposure, Separately or Sequentially, in Rat Brain Regions: Indices of Cholinergic and Serotonergic Synaptic Function, Cell Signaling, and Neural Cell Number and Size at 6 Months of Age

Linkages between cigarette smoking outcome expectancies and negative emotional vulnerability

Adolescent Cigarette Use in the Americas: The Link with Depression

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