Depression Outcomes in Smokers and Nonsmokers: Comparison of Collaborative Care Management Versus Usual Care

Akambase, Joseph; Miller, Nathaniel E.; Garrison, Gregory M.; Stadem, Paul S.; Talley, Heather Laine; Angstman, Kurt B.

doi:10.1177/2150132719861265

Cited by 9 publications

(4 citation statements)

References 37 publications

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“…For the relationship between smoking and depression, our results, using improved genetic instruments compared to prior studies, are consistent with previous evidence supporting a reciprocal association between these variables. Observational evidence has shown that depression can trigger smoking commencement and make its cessation more challenging [59][60][61][62][63] . Moreover, smoking has been shown to lead to depression, and smoking cessation has been associated with improved depressive outcomes and decreased depression symptomatology [63][64][65] .…”

Section: Smoking and Depressionmentioning

confidence: 99%

Applying Mendelian randomization to appraise causality in relationships between smoking, depression and inflammation

Galán

Perry

Warrier

et al. 2022

Sci Rep

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Smoking, inflammation and depression commonly co-occur and may be mechanistically linked. However, key questions remain around the direction of association and the influence of residual confounding. We aimed to characterize the association between lifetime smoking and depression, as well as to assess the role that genetically-predicted C-reactive protein (CRP) level, (an archetypal generalized inflammatory marker) and/or IL-6 activity, as a potential explanation for this association. We performed inverse variance weighted Mendelian randomization (MR) analyses using recently published summary-level GWAS data for lifetime smoking index, CRP levels, and depression. A subset of inflammatory-related genetic variants from the lifetime smoking GWAS were also used to assess the potential inflammatory causal pathways between smoking and depression. The analysis indicated reciprocal relationships of lifetime smoking with depression (ORSmk–Dep = 2.01, 95% CI 1.71–2.37, p < 0.001; ORDep–Smk = 1.09, 95% CI 1.06–1.13, p < 0.001), CRP levels and IL-6 activity (ORSmk–CRP = 1.40, 95% CI 1.21–1.55, p < 0.001; ORCRP–Smk = 1.03, 95% CI 1.02–1.05, p < 0.001, ORIL-6/CRP–Smk = 1.06 (1.03–1.09), p < 0.001). These associations were also supported by the majority of the robust MR methods performed. We did not find evidence for a reciprocal relationship between CRP levels (using > 500 genetic instruments for CRP) and depression (ORCRP–Dep = 1.01, 95% CI 0.99–1.04; ORDep–CRP = 1.03, 95% CI 0.99–1.07). We observed little variation in the IVW estimates between smoking and depression when we limited the genetic variants assessed to those related to measures of generalized inflammation, but we found evidence for an attenuation of the smoking-depression association in multivariable mendelian randomization when adjusting for IL-6 activity, suggesting that the IL-6 pathway may be at least in part responsible for the association of smoking and depression. Our study supports potential bidirectional causal associations between lifetime smoking and depression which may be at least in part explained by the IL-6 signalling pathway. The IL-6 pathway may represent a putative therapeutic target for smoking and to mitigate the effects of smoking on depression.

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Section: Smoking and Depressionmentioning

confidence: 99%

Applying Mendelian randomization to appraise causality in relationships between smoking, depression and inflammation

Galán

Perry

Warrier

et al. 2022

Sci Rep

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“…On the contrary, smoking also affects the outcome of depression 25 . Mendelian randomization study 26 found that there is a two-way causal relationship between depression and smoking, and the two interact, forming a vicious circle.…”

Section: Discussionmentioning

confidence: 99%

The impact of depression on cervical spondylosis is mediated by smoking and insomnia: Mendelian randomization study

Qian,

Li,

Wang

et al. 2024

Preprint

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Patients with cervical spondylosis are often accompanied by a series of mental disorders, but there is no direct evidence of causal relationship and the mediation factors are not clear. Our purpose is to use the aggregated data of the large-scale genome-wide association study (GWAS) to explore the causal relationship between mental disorders and cervical spondylosis by using Mendelian randomization analysis, and further explore the mediation factors, to provide theoretical basis for the prevention and treatment of cervical spondylosis. Data on cervical spondylosis, mental disorders (depression, anxiety and schizophrenia), and living habits (smoking, insomnia, drinking, exercise, and time spent watching TV) were collected from the aggregated data of GWAS. In the univariable MR, inverse variance weighted (IVW) method was adopted as the main method, MR-Egger-based regression method, weighted median (WME) method, simple mode method, and weighted mode (WM) method were adopted as the complementary methods to evaluate the causal relationship between mental disorders and cervical spondylosis. Cochran's Q test, MR-Egger intercept test, and MR pleiotropy residual sum and outlier (MR-PRESSO)test were used to verify the reliability of the analysis results as sensitivity analysis. In the multivariable MR, IVW was used to analyze the causal relationship between the three mental disorders and cervical spondylosis after adjustment. In the mediation MR analysis, according to the steps of exposure to mediation and mediation to outcome, the qualified mediation factors in living habits were screened out, and the P-value of mediation effect was calculated by coefficient product test. The confidence interval was estimated by Delta method, and the proportion mediated was calculated. The univariable analysis (OR=1.398, 95%CI:1.085-1.803, P=0.010) indicated that depression was a risk factor for cervical spondylosis. The multivariable analysis showed that depression still has positive causal relationship with cervical spondylosis after adjustment for anxiety and schizophrenia (OR=1.343, 95%CI:1.06-1.70, P=0.013). The mediation MR analysis showed that from depression to living habits, “time spent watching TV” was excluded. From living habits to cervical spondylosis, “exercise” was excluded. Drinking was also excluded by the results of coefficient product test. The mediation MR analysis showed that the causal relationship between depression and cervical spondylosis was partly mediated by smoking and insomnia, and the proportion mediated was 15.98% and 41.70%. Our study shows that there is a positive causal relationship between depression and cervical spondylosis, which is partly mediated by smoking and insomnia, and the finding may be helpful for the prevention and treatment of cervical spondylosis.

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“…For the relationship between smoking and depression, our results, using improved genetic instruments compared to prior studies, are consistent with previous evidence supporting a reciprocal association between these variables. Observational evidence has shown that depression can trigger smoking commencement and make its cessation more challenging 50–54 . Moreover, smoking has been shown to lead to depression, and smoking cessation has been associated with improved depressive outcomes and decreased depression symptomatology 54–56 .…”

Section: Discussionmentioning

confidence: 99%

Is the Association Between Smoking and Depression Mediated by Inflammation? A Mendelian Randomization Study

Galán

Perry

Warrier

et al. 2021

Preprint

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Smoking, inflammation and depression commonly co-occur and may be mechanistically linked. However, key questions remain around the direction of association and the influence of residual confounding. We aimed to characterize the association between lifetime smoking and depression, as well as to assess the role that genetically-predicted C-reactive protein (CRP) level, an archetypal inflammatory marker, as a potential mediator for this association. We performed inverse variance weighted Mendelian randomization (MR) analyses using recently published summary-level GWAS data for lifetime smoking index, CRP levels, and depression. A subset of inflammatory-related genetic variants from the lifetime smoking GWAS were also used to assess the potential inflammatory causal pathways between smoking and depression. The analysis indicated significant reciprocal relationships between lifetime smoking and both depression (ORSmk-Dep = 2.01, 95% CI 1.71- 2.37, p < 0.001; O RDep-Smk = 1.09, 95% CI 1.06- 1.13, p < 0.001) and CRP levels (ORSmk-CRP = 1.40, 95% CI 1.21-1.55, p < 0.001; ORCRP-Smk = 1.03, 95% CI 1.02- 1.05, p < 0.001). These significant and positive associations were also supported by the majority of the robust MR methods performed. The reciprocal relationships between CRP levels (using >500 genetic instruments for CRP) and depression were not significant (ORCRP-Dep = 1.01, 95% CI 0.99-1.04; ORDep-CRP = 1.03, 95% CI 0.99-1.07). We observed little variation in the IVW estimates between smoking and depression when we limited the genetic variants assessed to those related to inflammation or when we adjusted the analysis by CRP-levels in multivariable analysis. Our study supports potential causal associations between lifetime smoking and depression, as well as between lifetime smoking and CRP levels, but not between CRP and depression. No evidence was found that CRP mediates the relationship between smoking and depression.

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Depression Outcomes in Smokers and Nonsmokers: Comparison of Collaborative Care Management Versus Usual Care

Cited by 9 publications

References 37 publications

Applying Mendelian randomization to appraise causality in relationships between smoking, depression and inflammation

Applying Mendelian randomization to appraise causality in relationships between smoking, depression and inflammation

The impact of depression on cervical spondylosis is mediated by smoking and insomnia: Mendelian randomization study

Is the Association Between Smoking and Depression Mediated by Inflammation? A Mendelian Randomization Study

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