Human rights, human wrongs

There is little doubt that the overall burden of mental disorders weighs heavily on both patients and society. The editorial by Dakić (pp. 241–242) sketches this out elegantly. Loss of productivity, sickness absence, unemployment, physical comorbidity, increased hospital admissions and premature death are a few of our least favourite things that could be reversed through improved investment for research into mental disorders. Without evidence-based research, treatment options are few and far between for a population under-served by modern medicine. Over 430 million people globally live with depression, bipolar affective disorder, schizophrenia or dementia. It is argued that a ‘conscious’ capitalism of needs-based research should be driven both by justice and a longer-term saving for society in both overall health and years of life lost to disability.

Society is quick to judge individuals with a mental disorder. Such judgement carries with it the inevitable stigma that is mirrored by people living with these disorders. Guilt, self-blame and anomie may be outcomes from such self-judgement. But hope comes in the form of the HOP or Honest, Open, Proud programme that has shown promising results, as outlined in the editorial by Scior and colleagues (pp. 243–245). Reducing self-stigmatising beliefs, managing disclosure decisions and deciding what to share and with whom, are key components of the programme. Results from randomised controlled trials appear promising, with participants less likely to entertain negative stereotypes and conceal their experiences; as well as more likely to manage negative stereotypes from others.

Split genes

The field of genetics can often remain just another protein shake to psychiatrists, but we would do well to refresh and expand our knowledge in this area. Which is why the analysis by Schijven and colleagues (pp. 246–249) allows us to see the utility of genetic cross-disorder research unravel before us. There is also a new lexicon to master. The way many DNA sequences affect a few individuals or a single variation in a sequence affects many individuals allows us to examine the strength of associations for both individual mental disorders and the relationship between them. If we drill down still further, more refined methods can examine a more precise association between genotype and phenotype. But it is not just about diagnosis – these techniques may also hold the key to prognosis and treatment response.

Fishing in the gene pool

To view schizophrenia on a spectrum with other disorders such as autistic spectrum disorder is not new. But the paper by Foley and colleagues (pp. 275–279) brings the topic to life through the study of people with a diagnosis of schizophrenia who have either higher duplication or deletion rates or copy number variants (CNVs) in their DNA sequences compared with reference groups. Researchers found that the presence of schizophrenia CNVs was more likely in people with accompanying neurodevelopmental disorders. Benefits from the identification at these ‘at risk’ individuals remain to be seen.

A similar method was used by Legge and colleagues (pp. 259–266), as they examined how these CNVs were used to predict treatment-resistant psychosis. Premorbid social adjustment, younger age at onset of psychosis, younger paternal age at birth and cannabis use were all more likely in treatment-resistant psychosis. Read more about this paper in this month's Mental Elf blog by Dr Maria Bragado-Jimenez from Oxleas NHS Foundation Trust at: https://elfi.sh/bjp-me22. While still on the subject of psychotic disorders, Liu and colleagues observed that the cumulative effect of multiple genetic variants was found to have a strong association with both reduced hippocampal grey matter volume and reduced connectivity between the hippocampus and medial prefrontal cortex. It would appear that, as research that uses genetic markers progresses, we are diving for pearls and not dredging up the shopping trolleys and wellington boots of psychiatric research.

A state of flux

The role of calcium channel blockers (CCBs) in psychiatry enjoyed a renaissance in the 1990s, but further research has since all but disappeared. It is probably time for a revival. In their reappraisal of the evidence, Harrison and colleagues (pp. 250–253) seek neither to bury nor praise CCBs. They point out that CCBs affect voltage-gated calcium channels that modulate calcium flux across cell membranes. This is known to influence brain circuits that underlie cognition, mood and reward. They also note evidence that points to lower rates of psychiatric admission and self-harm for patients taking CCBs than those not treated with this class of drugs. But the potential cardiovascular effects of prescribing CCBs for mental disorders may be too risky, with the search for alternative isoforms with differential effects on the brain still some way in the distance.