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Journal ArticleDOI

The Association of Cigarette Smoking with Depression and Anxiety: A Systematic Review

01 Jan 2017-Nicotine & Tobacco Research (Oxford University Press)-Vol. 19, Iss: 1, pp 3-13
TL;DR: The literature on the prospective association between smoking and depression and anxiety is inconsistent in terms of the direction of association most strongly supported, suggesting the need for future studies that employ different methodologies, such as Mendelian randomization (MR), which will allow for stronger causal inferences.
Abstract: Background Many studies report a positive association between smoking and mental illness. However, the literature remains mixed regarding the direction of this association. We therefore conducted a systematic review evaluating the association of smoking and depression and/or anxiety in longitudinal studies. Methods Studies were identified by searching PubMed, Scopus, and Web of Science and were included if they: (1) used human participants, (2) were longitudinal, (3) reported primary data, (4) had smoking as an exposure and depression and/or anxiety as an outcome, or (5) had depression and/or anxiety as the exposure and smoking as an outcome. Results Outcomes from 148 studies were categorized into: smoking onset, smoking status, smoking heaviness, tobacco dependence, and smoking trajectory. The results for each category varied substantially, with evidence for positive associations in both directions (smoking to later mental health and mental health to later smoking) as well as null findings. Overall, nearly half the studies reported that baseline depression/anxiety was associated with some type of later smoking behavior, while over a third found evidence that a smoking exposure was associated with later depression/anxiety. However, there were few studies directly supporting a bidirectional model of smoking and anxiety, and very few studies reporting null results. Conclusions The literature on the prospective association between smoking and depression and anxiety is inconsistent in terms of the direction of association most strongly supported. This suggests the need for future studies that employ different methodologies, such as Mendelian randomization (MR), which will allow us to draw stronger causal inferences. Implications We systematically reviewed longitudinal studies on the association of different aspects of smoking behavior with depression and anxiety. The results varied considerably, with evidence for smoking both associated with subsequent depression and anxiety, and vice versa. Few studies supported a bidirectional relationship, or reported null results, and no clear patterns by gender, ethnicity, clinical status, length to follow-up, or diagnostic test. Suggesting that despite advantages of longitudinal studies, they cannot alone provide strong evidence of causality. Therefore, future studies investigating this association should employ different methods allowing for stronger causal inferences to be made, such as MR.

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Journal ArticleDOI
TL;DR: In this paper, the authors report differences in genetic architecture between depression defined by minimal phenotyping and strictly defined major depressive disorder (MDD): the former has a lower genotype-derived heritability that cannot be explained by inclusion of milder cases and a higher proportion of the genome contributing to this shared genetic liability with other conditions than for strictly defined MDD.
Abstract: Minimal phenotyping refers to the reliance on the use of a small number of self-reported items for disease case identification, increasingly used in genome-wide association studies (GWAS). Here we report differences in genetic architecture between depression defined by minimal phenotyping and strictly defined major depressive disorder (MDD): the former has a lower genotype-derived heritability that cannot be explained by inclusion of milder cases and a higher proportion of the genome contributing to this shared genetic liability with other conditions than for strictly defined MDD. GWAS based on minimal phenotyping definitions preferentially identifies loci that are not specific to MDD, and, although it generates highly predictive polygenic risk scores, the predictive power can be explained entirely by large sample sizes rather than by specificity for MDD. Our results show that reliance on results from minimal phenotyping may bias views of the genetic architecture of MDD and impede the ability to identify pathways specific to MDD.

182 citations

Journal ArticleDOI
TL;DR: Neurodevelopmental copy number variants appear to be associated with increases in the risk of depression in those without neurodevelopmental disorders, and no evidence was found of an association between measures of copy number variant burden and depression.
Abstract: Importance The role of large, rare copy number variants (CNVs) in neuropsychiatric disorders is well established, but their association with common psychiatric disorders, such as depression, remains unclear. Objective To examine the association of a group of 53 CNVs associated with neurodevelopmental disorders and burden of rare CNVs with risk of depression. Design, Setting, and Participants This case-control study used data from the UK Biobank study sample, which comprised 502 534 individuals living in the United Kingdom. Individuals with autism spectrum disorder, intellectual disability, attention-deficit/hyperactivity disorder, schizophrenia, or bipolar affective disorder diagnoses were excluded. Analyses were further restricted to individuals of European genetic ancestry (n = 407 074). The study was conducted from January 2017 to September 2018. Exposures CNV carrier status. Main Outcomes and Measures For the primary outcome, individuals who reported that a physician had told them they had a depression diagnosis were defined as cases. Analyses were repeated using 2 alternative depression definitions: self-reported lifetime depression with current antidepressant prescription at the time of visit 1, and hospital discharge diagnosis of depression. Results Copy number variants were identified in 488 366 individuals aged 37 to 73 years. In total, 407 074 individuals with European genetic ancestry (220 201 female [54.1%]; mean [SD] age of 56.9 [8.0] years) were included in the study. Of these individuals, 23 979 (5.9%) had self-reported lifetime depression and 383 095 (94.1%) reported no lifetime depression. The group of 53 neurodevelopmental CNVs was associated with self-reported depression (odds ratio [OR], 1.34; 95% CI, 1.19-1.49, uncorrectedP = 1.38 × 10−7), and these results were consistent when using 2 alternative definitions of depression. This association was partially explained by physical health, educational attainment, social deprivation, smoking status, and alcohol consumption. A strong independent association remained between the neurodevelopmental CNVs and depression in analyses that incorporated these other measures (OR, 1.26; 95% CI, 1.11-1.43;P = 2.87 × 10−4). Eight individual CNVs were nominally associated with risk of depression, and 3 of these 8 CNVs (1q21.1 duplication, Prader-Willi syndrome duplication, and 16p11.2 duplication) survived Bonferroni correction for the 53 CNVs tested. After the exclusion of carriers of neurodevelopmental CNVs, no association was found between measures of CNV burden and depression. Conclusions and Relevance Neurodevelopmental CNVs appear to be associated with depression, extending the spectrum of clinical phenotypes that are associated with CNV carrier status.

85 citations

Journal ArticleDOI
TL;DR: Evidence is provided that COPD and asthma are associated with depression in the community and complex underlying demographic, medical and psychosocial variables have been identified which may justify an integrative treatment approach.
Abstract: Medicated obstructive pulmonary disease (asthma or COPD) has been associated with depression. Yet, there is little knowledge of the interplay of contributing social, biological, behavioral and psychological factors in the community. The study was conducted: (1) To determine the prevalence of depression in participants with medicated COPD or asthma from the general population, (2) to identify underlying social, biological, behavioral and psychological factors and (3) to determine the contribution of obstructive pulmonary disease and depression to subjective health. The population-based sample of 15.010 study participants (35–74 years) from the Gutenberg Health Study (GHS) was queried according to a medical diagnosis of obstructive pulmonary disease, defined as medicated COPD or asthma, and comorbid disorders. Demographic, behavioral and psychological factors were assessed by self-report; lung function (FEV1; FCV) was measured by spirometry. 307 men (4.3%) and 396 women (5.6%) reported a medical diagnosis of COPD or asthma. The prevalence of depression (PHQ-9 > = 10) was twice as high (16.2% vs. 7.5%) compared to participants without obstructive pulmonary disease. Participants with obstructive pulmonary disease were older, had a lower SES, more comorbid diseases and cardiovascular risk factors, higher distress and took more psychotropic medication. In multivariable logistic regression analyses, obstructive pulmonary disease was associated with a 71% increase of depression (OR = 1.71; 95% CI = 1.30 to 2.24). Additional contributors were FEV1 (1.18; 95% CI = 1.05 to 1.32) and dyspnea (NYHA > = 1) (2.19; 1.82 to 2.64), sex (women) (OR = 1.73; 95% CI 1.41 to 2.12), lower SES (OR = 0.98; 95%CI = 0.96 to 0.99). Lack of active sports OR = 0.79; 95% CI 0.68 to 0.92), obesity (OR 1.27; 95% CI 1.07 to 1.50), smoking (OR = 1.26; 95% CI 1.06 to 1.49) and dyslipidemia (OR = 1.35; 95% CI 1.15 to 1.57) also increased the risk of depression. Additional psychological risks were social phobia, type D, low social support, loneliness and life events in the past 12 months. In multivariable linear regression analyses, obstructive pulmonary disease and depression independently contributed to reduced subjective health in addition to sedentary behavior, smoking and comorbid somatic and mental disorders. These findings provide evidence that COPD and asthma are associated with depression in the community. Complex underlying demographic, medical and psychosocial variables have been identified which may justify an integrative treatment approach. Promoting health behavior (smoking cessation, exercising, weight reduction) and social integration may not only improve the somatic course of the disease, but also mental health. Mental health treatment may also improve health behavior and subjective health.

82 citations

Posted ContentDOI
04 Nov 2020
TL;DR: Viertiö et al. as mentioned in this paper proposed an approach to improve the quality of health care for women in Finland by using the National Institute for Health and Welfare (NICW).
Abstract: Satu Viertiö (  satu.viertio@thl. ) National Institute for Health and Welfare https://orcid.org/0000-0002-8894-2056 Olli Kiviruusu Finnish Institute for Health and Welfare Maarit Piirtola University of Helsinki Jaakko Kaprio University of Helsinki Tellervo Korhonen University of Helsinki Mauri Marttunen Finnish Institute for Health and Welfare Jaana Suvisaari Finnish Institute for Health and Welfare

81 citations


Cites result from "The Association of Cigarette Smokin..."

  • ...Consistent with a large body of previous research, smoking [59, 98, 99] and at-risk drinking [100, 101] were associated with more psychological distress; however, their effect was less prominent than that of social and work-related factors in our study....

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Journal ArticleDOI
TL;DR: The cardiovascular consequences of cortisol excess are outlined, the comprehensive overview of recent studies investigating the relationship of hair cortisol with CVD is provided, and clinical implications and limitations of the evidence are discussed.
Abstract: This review focuses on the concentration of cortisol in human hair as a biomarker of chronic stress in cardiovascular disease (CVD). We outline the cardiovascular consequences of cortisol excess and provide a comprehensive overview of recent studies investigating the relationship of hair cortisol with CVD. In addition, clinical implications and limitations of the evidence are discussed, together with directions for future research. Hair cortisol may be a reliable biomarker of chronic stress since it provides quantification of total cortisol secreted into hair over several weeks. A growing body of evidence suggests that elevated hair cortisol levels are associated with both the incidence of CVD and poorer recovery and treatment outcomes. Moreover, increased hair cortisol concentration has been linked with established cardiometabolic risk factors for CVD including high blood pressure, diabetes, and adiposity. Hair cortisol is a promising biomarker of chronic cortisol excess which may contribute to both the pathogenesis and prognosis of CVD. However, the current evidence relies on small-scale cross-sectional studies. Further research adopting longitudinal designs across larger samples of CVD patients and healthy participants is required to inform the development of novel evidence-based interventions.

79 citations

References
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Reference EntryDOI
11 Jun 2013

113,134 citations

Journal ArticleDOI
TL;DR: An issue concerning the criteria for tic disorders is highlighted, and how this might affect classification of dyskinesias in psychotic spectrum disorders.
Abstract: Given the recent attention to movement abnormalities in psychosis spectrum disorders (e.g., prodromal/high-risk syndromes, schizophrenia) (Mittal et al., 2008; Pappa and Dazzan, 2009), and an ongoing discussion pertaining to revisions of the Diagnostic and Statistical Manuel of Mental Disorders (DSM) for the upcoming 5th edition, we would like to take this opportunity to highlight an issue concerning the criteria for tic disorders, and how this might affect classification of dyskinesias in psychotic spectrum disorders. Rapid, non-rhythmic, abnormal movements can appear in psychosis spectrum disorders, as well as in a host of commonly co-occurring conditions, including Tourette’s Syndrome and Transient Tic Disorder (Kerbeshian et al., 2009). Confusion can arise when it becomes necessary to determine whether an observed movement (e.g., a sudden head jerk) represents a spontaneous dyskinesia (i.e., spontaneous transient chorea, athetosis, dystonia, ballismus involving muscle groups of the arms, legs, trunk, face, and/or neck) or a tic (i.e., stereotypic or patterned movements defined by the relationship to voluntary movement, acute and chronic time course, and sensory urges). Indeed, dyskinetic movements such as dystonia (i.e., sustained muscle contractions, usually producing twisting and repetitive movements or abnormal postures or positions) closely resemble tics in a patterned appearance, and may only be visually discernable by attending to timing differences (Gilbert, 2006). When turning to the current DSM-IV TR for clarification, the description reads: “Tic Disorders must be distinguished from other types of abnormal movements that may accompany general medical conditions (e.g., Huntington’s disease, stroke, Lesch-Nyhan syndrome, Wilson’s disease, Sydenham’s chorea, multiple sclerosis, postviral encephalitis, head injury) and from abnormal movements that are due to the direct effects of a substance (e.g., a neuroleptic medication)”. However, as it is written, it is unclear if psychosis falls under one such exclusionary medical disorder. The “direct effects of a substance” criteria, referencing neuroleptic medications, further contributes to the uncertainty around this issue. As a result, ruling-out or differentiating tics in psychosis spectrum disorders is at best, a murky endeavor. Historically, the advent of antipsychotic medication in the 1950s has contributed to the confusion about movement signs in psychiatric populations. Because neuroleptic medications produce characteristic movement disorder in some patients (i.e. extrapyramidal side effects), drug-induced movement disturbances have been the focus of research attention in psychotic disorders. However, accumulating data have documented that spontaneous dyskinesias, including choreoathetodic movements, can occur in medication naive adults with schizophrenia spectrum disorders (Pappa and Dazzan, 2009), as well as healthy first-degree relatives of chronically ill schizophrenia patients (McCreadie et al., 2003). Taken together, this suggests that movement abnormalities may reflect pathogenic processes underlying some psychotic disorders (Mittal et al., 2008; Pappa and Dazzan, 2009). More specifically, because spontaneous hyperkinetic movements are believed to reflect abnormal striatal dopamine activity (DeLong and Wichmann, 2007), and dysfunction in this same circuit is also proposed to contribute to psychosis, it is possible that spontaneous dyskinesias serve as an outward manifestation of circuit dysfunction underlying some schizophrenia-spectrum symptoms (Walker, 1994). Further, because these movements precede the clinical onset of psychotic symptoms, sometimes occurring in early childhood (Walker, 1994), and may steadily increase during adolescence among populations at high-risk for schizophrenia (Mittal et al., 2008), observable dyskinesias could reflect a susceptibility that later interacts with environmental and neurodevelopmental factors, in the genesis of psychosis. In adolescents who meet criteria for a prodromal syndrome (i.e., the period preceding formal onset of psychotic disorders characterized by subtle attenuated positive symptoms coupled with a decline in functioning), there is sometimes a history of childhood conditions which are also characterized by suppressible tics or tic like movements (Niendam et al., 2009). On the other hand, differentiating between tics and dyskinesias has also complicated research on childhood disorders such as Tourette syndrome (Kompoliti and Goetz, 1998; Gilbert, 2006). We propose consideration of more explicit and operationalized criteria for differentiating tics and dyskinesias, based on empirically derived understanding of neural mechanisms. Further, revisions of the DSM should allow for the possibility that movement abnormalities might reflect neuropathologic processes underlying the etiology of psychosis for a subgroup of patients. Psychotic disorders might also be included among the medical disorders that are considered a rule-out for tics. Related to this, the reliability of movement assessment needs to be improved, and this may require more training for mental health professionals in movement symptoms. Although standardized assessment of movement and neurological abnormalities is common in research settings, it has been proposed that an examination of neuromotor signs should figure in the assessment of any patient, and be as much a part of the patient assessment as the mental state examination (Picchioni and Dazzan, 2009). To this end it is important for researchers and clinicians to be aware of differentiating characteristics for these two classes of abnormal movement. For example, tics tend to be more complex than myoclonic twitches, and less flowing than choreoathetodic movements (Kompoliti and Goetz, 1998). Patients with tics often describe a sensory premonition or urge to perform a tic, and the ability to postpone tics at the cost of rising inner tension (Gilbert, 2006). For example, one study showed that patients with tic disorders could accurately distinguish tics from other movement abnormalities based on the subjective experience of some voluntary control of tics (Lang, 1991). Another differentiating factor derives from the relationship of the movement in question to other voluntary movements. Tics in one body area rarely occur during purposeful and voluntary movements in that same body area whereas dyskinesia are often exacerbated by voluntary movement (Gilbert, 2006). Finally, it is noteworthy that tics wax and wane in frequency and intensity and migrate in location over time, often becoming more complex and peaking between the ages of 9 and 14 years (Gilbert, 2006). In the case of dyskinesias among youth at-risk for psychosis, there is evidence that the movements tend to increase in severity and frequency as the individual approaches the mean age of conversion to schizophrenia spectrum disorders (Mittal et al., 2008). As revisions to the DSM are currently underway in preparation for the new edition (DSM V), we encourage greater attention to the important, though often subtle, distinctions among subtypes of movement abnormalities and their association with psychiatric syndromes.

67,017 citations

Journal ArticleDOI
TL;DR: It is shown that the average statistical power of studies in the neurosciences is very low, and the consequences include overestimates of effect size and low reproducibility of results.
Abstract: A study with low statistical power has a reduced chance of detecting a true effect, but it is less well appreciated that low power also reduces the likelihood that a statistically significant result reflects a true effect. Here, we show that the average statistical power of studies in the neurosciences is very low. The consequences of this include overestimates of effect size and low reproducibility of results. There are also ethical dimensions to this problem, as unreliable research is inefficient and wasteful. Improving reproducibility in neuroscience is a key priority and requires attention to well-established but often ignored methodological principles.

5,683 citations

Journal ArticleDOI
Stephan Ripke1, Naomi R. Wray2, Cathryn M. Lewis3, Steven P. Hamilton4, Myrna M. Weissman5, Gerome Breen3, Enda M. Byrne2, Douglas Blackwood6, Dorret I. Boomsma7, Sven Cichon8, Andrew C. Heath9, Florian Holsboer, Susanne Lucae4, Pamela A. F. Madden9, Nicholas G. Martin2, Peter McGuffin3, Pierandrea Muglia8, Markus M. Noethen10, Brenda P Penninx7, Michele L. Pergadia9, James B. Potash11, Marcella Rietschel10, Danyu Lin12, Bertram Müller-Myhsok8, Jianxin Shi13, Stacy Steinberg8, Hans J. Grabe, Paul Lichtenstein14, Patrik K. E. Magnusson14, Roy H. Perlis7, Martin Preisig15, Jordan W. Smoller16, Kari Stefansson, Rudolf Uher3, Zoltán Kutalik17, Katherine E. Tansey3, Alexander Teumer, Alexander Viktorin14, Michael R. Barnes11, Thomas Bettecken18, Elisabeth B. Binder19, René Breuer10, Victor M. Castro20, Susanne Churchill13, William Coryell11, Nicholas John Craddock, Ian W. Craig3, Darina Czamara6, Eco J. C. de Geus7, Franziska Degenhardt8, Anne Farmer3, Maurizio Fava16, Josef Frank10, Vivian S. Gainer, Patience J. Gallagher16, Scott D. Gordon2, Sergey Goryachev, Magdalena Gross8, Michel Guipponi21, Anjali K. Henders2, Stefan Herms8, Ian B. Hickie22, Susanne Hoefels8, Witte J.G. Hoogendijk3, Jouke-Jan Hottenga7, Dan V. Iosifescu16, Marcus Ising9, Ian Jones2, Lisa Jones22, Tzeng Jung-Ying15, James A. Knowles18, Isaac S. Kohane16, Martin A. Kohli2, Ania Korszun9, Mikael Landén5, William Lawson19, Glyn Lewis23, Donald J. MacIntyre6, Wolfgang Maier8, Manuel Mattheisen8, Patrick J. McGrath5, Andrew M. McIntosh6, Alan W. McLean6, Christel M. Middeldorp7, Lefkos T. Middleton23, G. M. Montgomery2, Shawn N. Murphy16, Matthias Nauck, Willem A. Nolen, Dale R. Nyholt2, Michael Conlon O'Donovan24, Hogni Oskarsson, Nancy L. Pedersen14, William A. Scheftner20, Andrea Schulz, Thomas G Schulze16, Stanley I. Shyn9, Engilbert Sigurdsson, Susan L. Slager25, Johannes H. Smit7, Hreinn Stefansson17, Michael Steffens8, Thorgeir E. Thorgeirsson, Federica Tozzi, Jens Treutlein10, Manfred Uhr, Edwin J. C. G. van den Oord26, Gerard van Grootheest7, Henry Völzke14, Jeffrey B. Weilburg16, Gonneke Willemsen7, Frans G. Zitman27, Benjamin M. Neale, Mark J. Daly1, Douglas F. Levinson28, Patrick F. Sullivan12 
TL;DR: This article conducted a genome-wide association studies (GWAS) mega-analysis for major depressive disorder (MDD) using more than 1.2 million autosomal and X chromosome single-nucleotide polymorphisms (SNPs) in 18,759 independent and unrelated subjects of recent European ancestry.
Abstract: Prior genome-wide association studies (GWAS) of major depressive disorder (MDD) have met with limited success. We sought to increase statistical power to detect disease loci by conducting a GWAS mega-analysis for MDD. In the MDD discovery phase, we analyzed more than 1.2 million autosomal and X chromosome single-nucleotide polymorphisms (SNPs) in 18 759 independent and unrelated subjects of recent European ancestry (9240 MDD cases and 9519 controls). In the MDD replication phase, we evaluated 554 SNPs in independent samples (6783 MDD cases and 50 695 controls). We also conducted a cross-disorder meta-analysis using 819 autosomal SNPs with P<0.0001 for either MDD or the Psychiatric GWAS Consortium bipolar disorder (BIP) mega-analysis (9238 MDD cases/8039 controls and 6998 BIP cases/7775 controls). No SNPs achieved genome-wide significance in the MDD discovery phase, the MDD replication phase or in pre-planned secondary analyses (by sex, recurrent MDD, recurrent early-onset MDD, age of onset, pre-pubertal onset MDD or typical-like MDD from a latent class analyses of the MDD criteria). In the MDD-bipolar cross-disorder analysis, 15 SNPs exceeded genome-wide significance (P<5 × 10(-8)), and all were in a 248 kb interval of high LD on 3p21.1 (chr3:52 425 083-53 822 102, minimum P=5.9 × 10(-9) at rs2535629). Although this is the largest genome-wide analysis of MDD yet conducted, its high prevalence means that the sample is still underpowered to detect genetic effects typical for complex traits. Therefore, we were unable to identify robust and replicable findings. We discuss what this means for genetic research for MDD. The 3p21.1 MDD-BIP finding should be interpreted with caution as the most significant SNP did not replicate in MDD samples, and genotyping in independent samples will be needed to resolve its status.

989 citations

Journal ArticleDOI
TL;DR: Findings suggest that adolescents with anxiety disorders are at an increased risk of subsequent anxiety, depression, illicit drug dependence, and educational underachievement as young adults.
Abstract: Objective This study examined associations between the extent of anxiety disorder in adolescence (14–16 years) and young people's later risks of a range of mental health, educational, and social role outcomes (16–21 years). Method Data were gathered over the course of a 21-year longitudinal study of a birth cohort of 1,265 New Zealand children. Measures collected included (1) an assessment of DSM-III-R anxiety disorders between the ages of 14 and 16 years; (2) assessments of mental health, educational achievement, and social functioning between the ages of 16 and 21 years; and (3) measures of potentially confounding social, family, and individual factors. Results Significant linear associations were found between the number of anxiety disorders reported in adolescence and later risks of anxiety disorder; major depression; nicotine, alcohol, and illicit drug dependence; suicidal behavior; educational underachievement; and early parenthood. Associations between the extent of adolescent anxiety disorder and later risks of anxiety disorder, depression, illicit drug dependence, and failure to attend university were shown to persist after statistical control for the confounding effects of sociofamilial and individual factors. Conclusions Findings suggest that adolescents with anxiety disorders are at an increased risk of subsequent anxiety, depression, illicit drug dependence, and educational underachievement as young adults. Clinical and research implications are considered.

928 citations