Immune and metabolic disturbance as a function of genetic risk and phase of illness in major depression
Why is this work in the frame?
A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.
No Canadian affiliation. An affiliation-only frame — the usual design — would never have seen this work. It is one of the works that make the case for inverting the frame.
The three-model screen
all 1,000 screened works →All three models called this out of scope.
Biobank study of inflammation and metabolic dysfunction in major depression.
The study examines biological and clinical features of depression rather than research itself.
Clinical epidemiology of inflammation and metabolism in depression, not research methods.
Abstract
Immune and metabolic factors are important in the pathophysiology of major depressive disorder (MDD) but we know little about how these factors manifest in relation to the status of depressive illness-from genetic risk for MDD, to a depressive episode, to depression in remission. Using genetic, diagnostic, biometric, and blood-bioassay data from the UK Biobank, we examined measures of pro-inflammatory signaling (C-reactive protein) and metabolic dysfunction (metabolic syndrome symptomatology) in females (N = 37,806) and males (N = 17,946) as a function of polygenic load for MDD (high versus low) interacting with depression status (never depressed, currently depressed, or depression in remission). We examined socioeconomic status (SES) as an exploratory factor in this design. Groups were matched for several confounders using a propensity-matching algorithm (females: n = 6301 per group for N = 37,806; n = 2991 per group for N = 17,946). In females we found increased inflammation and metabolic dysfunction in the higher-versus-lower PRS quartile, in those below-versus-above the median SES, and in those suffering currently from depression relative to their remitted depressed and healthy counterparts. This association remained when considering only non-psychotropic-medicated persons. Nonetheless, we also saw in both male and female samples that measures of immunological and metabolic dysfunction increased with increasing anti-depressant medication load. We discuss these findings in terms of the epidemiological significance of immune and metabolic functioning in depression and their paradoxical relation with antidepressant treatment.
Stored with the screening record, where it is evidence for the labels above.
The record
- Venue
- Brain Behavior & Immunity - Health
- Topic
- Tryptophan and brain disorders
- Field
- Neuroscience
- Canadian institutions
- —
- Funders
- Medicinska ForskningsrådetWellcome TrustMedical Research CouncilOffice of Research and DevelopmentHealth Services Research and DevelopmentRegion ÖstergötlandAlberta Law Foundation
- Keywords
- Depression (economics)Major depressive disorderConfoundingImmune systemRisk factorAntidepressantEpidemiologyImmune DysfunctionInflammation
- Has abstract in OpenAlex
- yes