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A significant proportion of the global burden of disease can be attributed to mental illness. Despite important advances in identifying risk factors for mental health conditions, the biological processing underlying causal pathways to disease onset remain poorly understood. This represents a limitation to implement effective prevention and the development of novel pharmacological treatments. Epigenetic mechanisms have emerged as mediators of environmental and genetic risk factors which might play a role in disease onset, including childhood adversity (CA) and cannabis use (CU). Particularly, human research exploring DNA methylation has provided new and promising insights into the role of biological pathways implicated in the aetio-pathogenesis of psychiatric conditions, including: monoaminergic (Serotonin and Dopamine), GABAergic, glutamatergic, neurogenesis, inflammatory and immune response and oxidative stress. While these epigenetic changes have been often studied as disease-specific, similarly to the investigation of environmental risk factors, they are often transdiagnostic. Therefore, we aim to review the existing literature on DNA methylation from human studies of psychiatric diseases (i) to identify epigenetic modifications mapping onto biological pathways either transdiagnostically or specifically related to psychiatric diseases such as Eating Disorders, Post-traumatic Stress Disorder, Bipolar and Psychotic Disorder, Depression, Autism Spectrum Disorder and Anxiety Disorder, and (ii) to investigate a convergence between some of these epigenetic modifications and the exposure to known risk factors for psychiatric disorders such as CA and CU, as well as to other epigenetic confounders in psychiatry research.
We are almost into the fifth decade of the acquired immunodeficiency syndrome (AIDS) pandemic, and in that time the illness has gone from being a highly unpredictable series of life-threatening illnesses that is consequent upon being immune compromised with a high mortality rate to being a highly treatable one-tablet-a-day infection. This represents an enormous revolution in medical treatment. AIDS was first recognized in 1981 after early cases of kaposi sarcoma and pneumocystis carinii were reported in the USA in young immunocompromised homosexual men (David et al., 2012; Rosca et al., 2012). However, the disease has been thought to have existed since the mid-1970s (Des Jarlais et al., 1989). There then followed the AIDS pandemic of the early 1980s when the spread of the virus grew exponentially throughout the world. Since then, several breakthroughs have taken place. In 1983, a retrovirus, now called human immunodeficiency virus (HIV), was identified as the causative agent (Sharp and Hahn, 2011). This led to the synthesis of antiviral medication aimed at inhibiting enzymes unique to the virus, such as reverse transcriptase inhibitors, protease inhibitors, and most recently, integrase inhibitors. In 1996 it was shown that taking a combination of these medications called combination antiretroviral therapy (cART) provided significantly effective treatment and basically stopped viral replication and the ensuing damage to the immune system (Ghosn et al., 2018). Since the introduction of cART and with further advances in research, HIV and AIDS have become a chronic illness. There has been a significant reduction in mortality and morbidity as a result of increased viral suppression that markedly halts the disease progression and reduces the rate of human transmission, resulting in people living longer and healthier lives (Ghosn et al., 2018; David et al., 2012).
Daily use of high-potency cannabis has been reported to carry a high risk for developing a psychotic disorder. However, the evidence is mixed on whether any pattern of cannabis use is associated with a particular symptomatology in first-episode psychosis (FEP) patients.
We analysed data from 901 FEP patients and 1235 controls recruited across six countries, as part of the European Network of National Schizophrenia Networks Studying Gene-Environment Interactions (EU-GEI) study. We used item response modelling to estimate two bifactor models, which included general and specific dimensions of psychotic symptoms in patients and psychotic experiences in controls. The associations between these dimensions and cannabis use were evaluated using linear mixed-effects models analyses.
In patients, there was a linear relationship between the positive symptom dimension and the extent of lifetime exposure to cannabis, with daily users of high-potency cannabis having the highest score (B = 0.35; 95% CI 0.14–0.56). Moreover, negative symptoms were more common among patients who never used cannabis compared with those with any pattern of use (B = −0.22; 95% CI −0.37 to −0.07). In controls, psychotic experiences were associated with current use of cannabis but not with the extent of lifetime use. Neither patients nor controls presented differences in depressive dimension related to cannabis use.
Our findings provide the first large-scale evidence that FEP patients with a history of daily use of high-potency cannabis present with more positive and less negative symptoms, compared with those who never used cannabis or used low-potency types.
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