COVID-19 is a major health threat around the world causing hundreds of millions of infections and millions of deaths. There is a pressing global need for effective therapies. We hypothesized that leukotriene inhibitors (LTIs), that have been shown to lower IL6 and IL8 levels, may have a protective effect in patients with COVID-19.

In this retrospective controlled cohort study, we compared death rates in COVID-19 patients who were taking a LTI with those who were not taking an LTI. We used the Department of Veterans Affairs (VA) Corporate Data Warehouse (CDW) to create a cohort of COVID-19-positive patients and tracked their use of LTIs between November 1, 2019 and November 11, 2021.

Of the 1,677,595 cohort of patients tested for COVID-19, 189,195 patients tested positive for COVID-19. Forty thousand seven hundred one were admitted. 38,184 had an oxygen requirement and 1214 were taking an LTI. The use of dexamethasone plus a LTI in hospital showed a survival advantage of 13.5% (CI: 0.23%–26.7%; p < 0.01) in patients presenting with a minimal O2Sat of 50% or less. For patients with an O2Sat of <60 and <50% if they were on LTIs as outpatients, continuing the LTI led to a 14.4% and 22.25 survival advantage if they were continued on the medication as inpatients.

When combined dexamethasone and LTIs provided a mortality benefit in COVID-19 patients presenting with an O2 saturations <50%. The LTI cohort had lower markers of inflammation and cytokine storm.

Olanzapine (OL) represents one of the main chooses for the treatment of psychosis. However, OL increase the risk of metabolic syndrome (MS). Previous literature proposes the “Leptin resistance” as a possible hypothalamic pathogenesis of OL induced MS because of the occurrence of weight gain with increased Leptin blood level.

The aim of our study is to investigate in a murine model of full-MS phenotype induced by Olanzapine the hypothalamic gene expression of the pathways involved in Leptin receptor signalling to clarify if a Leptin resistance occurs.

For the experiment C57BL/6Jfemale mice are used.The OL group (n=15) received pure Olanzapine compounded into chow (54 mg/kg of diet). The vehicle group (n=15)is fed with the same chow without OL. Weight gain is measured every 5 days. After 4 weeks of treatment, mice are sacrificed by rapid cervical dislocation. Blood is collected for Glucose, Insulin and Leptin evaluation. Hypothalamus is dissected and RNA-seq is performed.

The OL group shows a significantweight gain compared to Control (p= 0.02). Likewise blood glucose, Insulin and Leptin levels appear increased (p= 0,0089, p= 0,01, p= 0,0012). From the analysis of RNA-seq hypothalamic differentially expressed genes the anorexigenic POMC pathway downstream to the Leptin Receptor shows a 4-fold increased compared to control.

In our study the “Leptin resistance” involvement in OL induced MS is not confirmed. In fact, although there is an increase in blood Leptin, the expression of Leptin receptor downstream pathways shows a significant increase. This could suggest a possible “POMC resistance” mechanism for OL induced MS.

No significant relationships.

Population-based research on mental disorders needs to keep pace with trends in general epidemiology. At present, this requirement is complicated by uncertainty within the parent discipline about its future development. The present study examines proposals for new directions in strategy and methods and considers their significance for psychiatric epidemiology.

Narrative review, cross-checked by search of English-language journals of epidemiology for new trends and developments reported in the years from 2000 onwards.

The proposals reviewed here are divided into three groups:

1. 1. A new research paradigm of ‘eco-epidemiology’, which includes both individual risk factors and macro-environmental systems that mediate population levels of health and sickness.

2. 2. Improved ‘translation’ of research findings – i.e. more rapid and effective implementation of epidemiological evidence into health policy and practice.

3. 3. Adaptation of epidemiology to a globalised economy, with firmer regulation of funding and resources.

Each of these proposals has implications for psychiatric epidemiology. Workers in this field, however, are still preoccupied by relatively specific problems of definition, measurement and classification, and so far the current debates in general epidemiology are scarcely reflected. The proposals outlined above call for:

• • a working model of eco-epidemiology as it relates to psychiatric disorders;

• • implementation strategies to encourage more active participation in epidemiological research by community health services and caregiver organisations;

• • international collaborative projects that offer practical benefits in training and service facilities for the countries taking part.