Аспирин снижает риск депрессии у людей с повышенным уровнем гомоцистеина

High total plasma homocysteine (tHcy) is associated with increased risk of cardiovascular events and depression. Consumption of B-vitamins (B6, B9 and B12) reduces tHcy by about 15%, but has equivocal effects on these health outcomes, suggesting that this relationship is either not causal or is confounded by other factors. The results of recent randomized trials suggest that antiplatelet therapy may confound these associations. This cross-sectional study assessed 3687 men aged 69–87 years for history of clinically significant depression (Geriatric Depression Scale 15 items 7) or a recorded diagnosis of depression in the Western Australian Data Linkage System, and collected information on the use of aspirin, B-vitamins and antidepressant medication, along with age, education, living arrangements, smoking history and medical comorbidity as assessed by the Charlson index. Participants donated a blood sample for the measurement of tHcy, and concentrations15 μmol l−1 were considered high. Five hundred and thirteen (13.9%) men showed evidence of depression, and of those 31.4% had high tHcy, 41.5% were using aspirin, 6.8% were consuming B-vitamins. Multivariate logistic regression showed that high tHcy was associated with increased odds of depression (odds ratio (OR)=1.60, 95% confidence interval (CI)=1.20–2.14), as was the use of B-vitamins (OR=1.95, 95% CI=1.21–3.13). There was a significant interaction between high tHcy and aspirin use (OR=0.57, 95% CI=0.36–0.91), but not between high tHcy and B-vitamin use (OR=0.80, 95% CI=0.26–2.46). The analyses were adjusted for smoking status, Charlson index and use of antidepressants. The results of this study indicate that older men with high tHcy who use aspirin have lower risk of depression, and suggest that antiplatelet therapy may be an effective preventive or management strategy for these cases. Randomized trials are required to confirm the antidepressant effect of aspirin in people with high tHcy.

Aspirin decreases the risk of depression in older men with high plasma homocysteine

Перинатальные инфекции и риск шизофрении

These studies have yielded a series of intriguing associations (reviewed in Brown and Derkits)[2] and are briefly summarized here. Our group demonstrated that prenatal exposure to rubella was related to a greater than 5-fold increased risk of nonaffective psychosis during young adulthood[12] and in midadulthood over 20% of subjects who were exposed in utero to rubella were diagnosed with schizophrenia or a schizophrenia spectrum disorder.[13] Influenza exposure documented by quantification of maternal antibody titers during pregnancy was associated with a 3-fold increased risk of schizophrenia for exposure in mid to late gestation and a 7-fold elevation in risk of the disorder following first trimester exposure.[14] Elevated maternal IgG antibodies to Toxoplasma gondii, an intracellular parasite and a well-known infectious cause of central nervous system (CNS) congenital anomalies,[1,15] was related to greater than 2-fold increased risk of schizophrenia,[16] a finding which was essentially replicated in a Danish sample that capitalized on filter paper blood spots taken from the infant within the first week of birth.[17] In 3 studies, elevated maternal IgG antibody to (HSV-2) was related to an increased risk of psychotic disorders, including schizophrenia,[18,19,20] while the finding was not replicated in a different birth cohort.[21] Maternal genital/reproductive infections, broadly defined, were, however, associated with a 5-fold increased risk of schizophrenia when the exposure occurred during the periconceptional period.[22] Exposure to maternal respiratory infection was related to a 2-fold elevated schizophrenia risk,[23] as well as bacterial infections broadly defined.[24]

In summary, birth cohort studies have provided several key methodological advantages that have allowed for more rigorous testing of relationships between maternal infection and schizophrenia. Birth cohort studies conducted to date have provided further support for the hypothesis that maternal viral, protozoal, and bacterial infections increase the risk for schizophrenia in adult offspring.

Although cytokines represent a leading candidate agent for the effect of infection on schizophrenia risk, other possible mediators include hyperthermia, which is teratogenic to animals;[32] fetal hypoxia, which has been associated with schizophrenia;[33,34] and over the counter remedies taken for influenza such as aspirin, which has been associated with anomalies of the CNS.

Maternal Infection and Schizophrenia

Аспирин

If aspirin may be able to reduce schizophrenia symptoms, how might it do so? By correcting an imbalance in the production of pro-inflammatory and antiinflammatory cytokines by helper T cells, the researchers proposed. Other researchers have implicated such an imbalance in schizophrenia.

Aspirin Regimen May Help Counter Schizophrenia Symptoms

Аспирин при шизофрении

"Aspirin given as [an adjunct treatment] to regular antipsychotic treatment reduces the symptoms of schizophrenia spectrum disorders. The reduction is more pronounced in those with the more altered immune function. Inflammation may constitute a potential new target for antipsychotic drug development."

Aspirin for Schizophrenia?