Social inequalities and correlates of psychotropic drug use among young adults: a population-based questionnaire study

<p>Abstract</p> <p>Background</p> <p>Use of psychotropic drugs is widespread in Europe, and is markedly more common in France than elsewhere. Young adults often fare less well than adolescents on health indicators (injury, homicide, and substance use). This population-based study assessed disparities in psychotropic drug use among people aged 18–29 from different socio-occupational groups and determined whether they were mediated by educational level, health status, income, health-related behaviours, family support, personality traits, or disability.</p> <p>Methods</p> <p>A total of 1,257 people aged 18–29, randomly selected in north-eastern France completed a post-mailed questionnaire covering sex, date of birth, height, weight, educational level, occupation, smoking habit, alcohol abuse, income, health-status, diseases, reported disabilities, self-reported personality traits, family support, and frequent psychotropic medication for tiredness, nervousness/anxiety or insomnia. The data were analyzed using the adjusted odds ratios (ORa) computed with logistic models.</p> <p>Results</p> <p>Use of psychotropic drugs was common (33.2%). Compared with upper/intermediate professionals, markedly high odds ratios adjusted for sex were found for manual workers (2.57, 95% CI 1.02–6.44), employees (2.58, 1.11–5.98), farmers/craftsmen/tradesmen (4.97, 1.13–21.8), students (2.40, 1.06–5.40), and housewives (3.82, 1.39–10.5). Adjusting for all the confounders considered reduced the estimates to a pronounced degree for manual workers (adjusted OR 1.49, non-significant) but only slightly for the other socio-occupational groups. The odds ratio for unemployed people did not reach statistical significance. The significant confounders were: sex, not-good health status, musculoskeletal disorders and other diseases, being worried, nervous or sad, and lack of family support (adjusted odds ratios between 1.60 and 2.50).</p> <p>Conclusion</p> <p>There were marked disparities among young adults from different socio-occupational groups. Sex, health status, musculoskeletal diseases, family support, and personality traits were related to use of psychotropic drugs. These factors mediated the higher risk strongly among manual workers and slightly among the other groups.</p

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Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62838/1/nature02168.pd

Preoperative cerebrospinal fluid cytokine levels and the risk of postoperative delirium in elderly hip fracture patients

Aging and neurodegenerative disease predispose to delirium and are both associated with increased activity of the innate immune system resulting in an imbalance between pro- and anti-inflammatory mediators in the brain. We examined whether hip fracture patients who develop postoperative delirium have altered levels of inflammatory mediators in cerebrospinal fluid (CSF) prior to surgery. Patients were 75 years and older and admitted for surgical repair of an acute hip fracture. CSF samples were collected preoperatively. In an exploratory study, we measured 42 cytokines and chemokines by multiplex analysis. We compared CSF levels between patients with and without postoperative delirium and examined the association between CSF cytokine levels and delirium severity. Delirium was diagnosed with the Confusion Assessment Method; severity of delirium was measured with the Delirium Rating Scale Revised-98. Mann-Whitney U tests or Student t-tests were used for between-group comparisons and the Spearman correlation coefficient was used for correlation analyses. Sixty-one patients were included, of whom 23 patients (37.7%) developed postsurgical delirium. Concentrations of Fms-like tyrosine kinase-3 (P=0.021), Interleukin-1 receptor antagonist (P=0.032) and Interleukin-6 (P=0.005) were significantly lower in patients who developed delirium postoperatively. Our findings fit the hypothesis that delirium after surgery results from a dysfunctional neuroinflammatory response: stressing the role of reduced levels of anti-inflammatory mediators in this process. The Effect of Taurine on Morbidity and Mortality in the Elderly Hip Fracture Patient.Registration number: NCT00497978. Local ethical protocol number: NL16222.094.0

Inflammasome signaling affects anxiety- and depressive-like behavior and gut microbiome composition

The inflammasome is hypothesized to be a key mediator of the response to physiological and psychological stressors, and its dysregulation may be implicated in major depressive disorder. Inflammasome activation causes the maturation of caspase-1 and activation of interleukin (IL)-1β and IL-18, two proinflammatory cytokines involved in neuroimmunomodulation, neuroinflammation and neurodegeneration. In this study, C57BL/6 mice with genetic deficiency or pharmacological inhibition of caspase-1 were screened for anxiety- and depressive-like behaviors, and locomotion at baseline and after chronic stress. We found that genetic deficiency of caspase-1 decreased depressive- and anxiety-like behaviors, and conversely increased locomotor activity and skills. Caspase-1 deficiency also prevented the exacerbation of depressive-like behaviors following chronic stress. Furthermore, pharmacological caspase-1 antagonism with minocycline ameliorated stress-induced depressive-like behavior in wild-type mice. Interestingly, chronic stress or pharmacological inhibition of caspase-1 per se altered the fecal microbiome in a very similar manner. When stressed mice were treated with minocycline, the observed gut microbiota changes included increase in relative abundance of Akkermansia spp. and Blautia spp., which are compatible with beneficial effects of attenuated inflammation and rebalance of gut microbiota, respectively, and the increment in Lachnospiracea abundance was consistent with microbiota changes of caspase-1 deficiency. Our results suggest that the protective effect of caspase-1 inhibition involves the modulation of the relationship between stress and gut microbiota composition, and establishes the basis for a gut microbiota-inflammasome-brain axis, whereby the gut microbiota via inflammasome signaling modulate pathways that will alter brain function, and affect depressive- and anxiety-like behaviors. Our data also suggest that further elucidation of the gut microbiota-inflammasome-brain axis may offer novel therapeutic targets for psychiatric disorders