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Inflammatory mediators and dual depression: Potential biomarkers in plasma of primary and substance-induced major depression in cocaine and alcohol use disorders.

ABSTRACT: Major depressive disorder (MDD) is the most prevalent comorbid mental disorder among people with substance use disorders. The MDD can be both primary and substance-induced and its accurate diagnosis represents a challenge for clinical practice and treatment response. Recent studies reported alterations in the circulating expression of inflammatory mediators in patients with psychiatric disorders, including those related to substance use. The aim of the study was to explore TNF-?, IL-1?, CXCL12, CCL2, CCL11 (eotaxin-1) and CX3CL1 (fractalkine) as potential biomarkers to identify comorbid MDD and to distinguish primary MDD from substance-induced MDD in patients with substance disorders. Patients diagnosed with cocaine (CUD, n = 64) or alcohol (AUD, n = 65) use disorders with/without MDD were recruited from outpatient treatment programs [CUD/non-MDD (n = 31); CUD/primary MDD (n = 18); CUD/cocaine-induced MDD (N = 15); AUD/non-MDD (n = 27); AUD/primary MDD (n = 16) and AUD/alcohol-induced MDD (n = 22)]. Sixty-two healthy subjects were also recruited as control group. Substance and mental disorders were assessed according to "Diagnostic and Statistical Manual of Mental Disorders, 4th edition, text revision" (DSM-IV-TR) and a blood sample was collected for determinations in the plasma. The cocaine group showed lower TNF-? (p<0.05) and CCL11 (p<0.05), and higher IL-1? (p<0.01) concentrations than the control group. In contrast, the alcohol group showed higher IL-1? (p<0.01) and lower CXCL12 (p<0.01) concentrations than the control group. Regarding MDD, we only observed alterations in the cocaine group. Thus, CUD/MDD patients showed lower IL-1? (p<0.05), CXCL12 (p<0.05) and CCL11 (p<0.05), and higher CXC3CL1 (p<0.05) concentrations than CUD/non-MDD patients. Moreover, while CUD/primary MDD patients showed higher CCL11 (p<0.01) concentrations than both CUD/non-MDD and CUD/cocaine-induced MDD patients, CUD/cocaine-induced MDD patients showed lower CXCL12 (p<0.05) concentrations than CUD/non-MDD patients. Finally, a logistic regression model in the cocaine group identified CXCL12, CCL11 and sex to distinguish primary MDD from cocaine-induced MDD providing a high discriminatory power. The present data suggest an association between changes in inflammatory mediators and the diagnosis of primary and substance-induced MDD, namely in CUD patients.

SUBMITTER: Garcia-Marchena N

PROVIDER: S-EPMC6417778 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Project description:ImportanceTobacco use is highly concentrated in persons with mental illness.ObjectivesTo assess trends in past-month prevalence of cigarette smoking among adults with vs without past-year depression, substance use disorders (SUDs), or both, using nationally representative data.Design, setting, and participantsExploratory, serial, cross-sectional study based on data from 558 960 individuals aged 18 years or older who participated in the 2006-2019 US National Surveys on Drug Use and Health.ExposurePast-year major depressive episode (MDE) and SUD using Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition, Text Revision) criteria.Main outcomes and measuresPast-month self-reported cigarette use, adjusted for sociodemographic characteristics.ResultsOf the sampled 558 960 adults, 41.4% (unweighted) were aged 18 to 25 years, 29.8% (unweighted) were aged 26 to 49 years, and 53.4% (unweighted) were women. From 2006 to 2019, the past-month self-reported cigarette smoking prevalence declined significantly among adults with MDE from 37.3% to 24.2% for an average annual percent change of -3.2 (95% CI, -3.5 to -2.8; P < .001), adults with SUD from 46.5% to 35.8% for an average annual percent change of -1.7 (95% CI, -2.8 to -0.6; P = .002), and adults with co-occurring MDE and SUD from 50.7% to 37.0% for an annual average annual percent change of -2.1 (95% CI, -3.1 to -1.2; P < .001). The prevalence declined significantly for each examined age, sex, and racial and ethnic subgroup with MDE and with SUD (all P < .05), except for no significant changes in American Indian or Alaska Native adults with MDE (P = .98) or with SUD (P = .46). Differences in prevalence of cigarette smoking between adults with vs without MDE declined significantly for adults overall from 11.5% to 6.6%, for an average annual percent change of -3.4 (95% CI, -4.1 to -2.7; P < .001); significant average annual percent change declines were also seen for men (-5.1 [95% CI, -7.2 to -2.9]; P < .001); for women (-2.7 [95% CI, -3.9 to -1.5]; P < .001); for those aged 18 through 25 years (-5.2 [95% CI, -7.6 to -2.8]; P < .001); for those aged 50 years or older (-4.7 [95% CI, -8.0 to -1.2]; P = .01); for Hispanic individuals (-4.4 [95% CI, -8.0 to -0.5]; P = .03), and for White individuals (-3.6 [95% CI, -4.5 to -2.7]; P < .001). For American Indian or Alaska Native adults, prevalence did not significantly differ between those with vs without MDE during 2006-2012 but was significantly higher for those with MDE during 2013-2019 (difference, 11.3%; 95% CI, 0.9 to 21.7; P = .04). Differences among those with vs without SUD declined for women for an average annual percent change of -1.8 (95% CI, -2.8 to -0.9; P = .001).Conclusions and relevanceIn this exploratory, serial, cross-sectional study, there were significant reductions in the prevalence of self-reported cigarette smoking among US adults with major depressive episode, substance use disorder, or both, between 2006 and 2019. However, continued efforts are needed to reduce the prevalence further.

Project description:Recent studies have identified biomarkers related to the severity and pathogenesis of cocaine addiction and common comorbid psychiatric disorders. Monitoring these plasma mediators may improve the stratification of cocaine users seeking treatment. Because the neurotrophic factors are involved in neural plasticity, neurogenesis and neuronal survival, we have determined plasma concentrations of brain-derived neurotrophic factor (BDNF), insulin-like growth factor 1 (IGF-1) and IGF-1 binding protein 3 (IGFBP-3) in a cross-sectional study with abstinent cocaine users who sought outpatient treatment for cocaine (n = 100) and age/body mass matched controls (n = 85). Participants were assessed with the diagnostic interview 'Psychiatric Research Interview for Substance and Mental Disorders'. Plasma concentrations of these peptides were not different in cocaine users and controls. They were not associated with length of abstinence, duration of cocaine use or cocaine symptom severity. The pathological use of cocaine did not influence the association of IGF-1 with age observed in healthy subjects, but the correlation between IGF-1 and IGFBP-3 was not significantly detected. Correlation analyses were performed between these peptides and other molecules sensitive to addiction: BDNF concentrations were not associated with inflammatory mediators, lipid derivatives or IGF-1 in cocaine users, but correlated with chemokines (fractalkine/CX3CL1 and SDF-1/CXCL12) and N-acyl-ethanolamines (N-palmitoyl-, N-oleoyl-, N-arachidonoyl-, N-linoleoyl- and N-dihomo-γ-linolenoyl-ethanolamine) in controls; IGF-1 concentrations only showed association with IGFBP-3 concentrations in controls; and IGFBP-3 was only correlated with N-stearoyl-ethanolamine concentrations in cocaine users. Multiple substance use disorders and life-time comorbid psychopathologies were common in abstinent cocaine users. Interestingly, plasma BDNF concentrations were exclusively found to be decreased in users diagnosed with both primary and cocaine-induced disorders for mood and anxiety disorders. In summary, BDNF, IGF-1 and IGFBP-3 were not affected by a history of pathological use of cocaine supported by the absence of associations with other molecules sensitive to cocaine addiction. However, BDNF was affected by comorbid mood disorders. Further research is necessary to elucidate the role of BDNF and IGF-1 in the transition to cocaine addiction and associated psychiatric comorbidity.

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Inflammatory mediators and dual depression: Potential biomarkers in plasma of primary and substance-induced major depression in cocaine and alcohol use disorders.

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