Epigenetic Effects of Childhood Adversity in the Brain and Suicide Risk

Author(s):  
Benoit Labonté ◽  
Gustavo Turecki
Molecules ◽  
2021 ◽  
Vol 26 (10) ◽  
pp. 2954
Author(s):  
Justyna Gorzkiewicz ◽  
Grzegorz Bartosz ◽  
Izabela Sadowska-Bartosz

Phytoestrogens are naturally occurring non-steroidal phenolic plant compounds. Their structure is similar to 17-β-estradiol, the main female sex hormone. This review offers a concise summary of the current literature on several potential health benefits of phytoestrogens, mainly their neuroprotective effect. Phytoestrogens lower the risk of menopausal symptoms and osteoporosis, as well as cardiovascular disease. They also reduce the risk of brain disease. The effects of phytoestrogens and their derivatives on cancer are mainly due to the inhibition of estrogen synthesis and metabolism, leading to antiangiogenic, antimetastatic, and epigenetic effects. The brain controls the secretion of estrogen (hypothalamus-pituitary-gonads axis). However, it has not been unequivocally established whether estrogen therapy has a neuroprotective effect on brain function. The neuroprotective effects of phytoestrogens seem to be related to both their antioxidant properties and interaction with the estrogen receptor. The possible effects of phytoestrogens on the thyroid cause some concern; nevertheless, generally, no serious side effects have been reported, and these compounds can be recommended as health-promoting food components or supplements.


2020 ◽  
Author(s):  
Brenda Cabrera-Mendoza

Despite individuals with substance use disorder (SUD) have a high suicide risk, most of gene expression studies in suicide have excluded individuals with this disorder. Thus, little is known about the gene expression profile in suicides with SUD. The identification of altered biological processes in the brain of suicides with SUD is crucial in the comprehension of the SUD and suicidal behavior comorbidity. This dissertation describes the evaluation of gene expression differences in the dorsolateral prefrontal cortex of suicides and non-suicides with and without SUD.Sixty-six brain tissue samples were collected and classified in the following groups: i) 23 suicides with SUD, ii) 20 suicides without SUD, iii) 9 non-suicides with SUD and iv) 14 non-suicides without SUD. The results of this study suggest that suicides with SUD have a gene expression profile in the prefrontal cortex different from that of individuals with only one of these conditions, presenting differences in the expression of genes involved in cell proliferation and glutamatergic neurotransmission.We performed a re-analysis of the gene expression data of 38 suicides focused on dual diagnosis and suicide. Dual diagnosis is the concurrence of at least one SUD and one or more mental disorders in a given individual. Although this comorbidity is highly prevalent and is associated with adverse clinical outcomes, its neurobiology has not been elucidated. In addition, patients with dual pathology have a higher suicide risk compared to patients with only one disorder.The objective of this re-analysis was to evaluate the differences in the gene expression profile in the prefrontal cortex of suicides with dual pathology compared to suicides with a single disorder. Our results suggest an alteration in the expression of genes involved in glutamatergic neurotransmission, GABAergic neurotransmission and neurogenesis in suicides with dual diagnosis compared to suicides with a single disorder and suicides without mental comorbidities.The observed differences in gene expression in the prefrontal cortex between suicides with and without SUD, as well as suicides with dual diagnosis and a single disorder may contribute to the phenotypic and clinical discrepancies observed among these patients. The identification of molecular characteristics in the brain of individuals with suicidal behavior and psychiatric comorbidities will allow the design of preventive and therapeutic measures aimed at the adequate treatment of each comorbidity.


2021 ◽  
Vol 9 (1) ◽  
pp. 43-51
Author(s):  
Alexander Shand

Children who experience adversity have increased risk for psychiatric disorders. However, little is known about the exact alterations that occur in the neural circuitry and how that information may help lead to early diagnosis or preventive medicine. Research has shown that there are specific changes in neurological functional connectivity in the brain associated with childhood adversity. This review will examine recent papers that have investigated the correlation between these changes in brain connectivity and specific psychiatric disorders. Understanding the changes may help with preventive medicine by ensuring clinicians monitor patients with more severe history of adversity who are therefore at higher risk for developing a psychiatric disorder. This paper will also address potential recommendations that could be implemented in the future as research offers more conclusive evidence. Research is now beginning to address the questions of whether these changes can be attenuated, either during childhood or as adults.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tiffany C. Ho ◽  
Lucy S. King

AbstractEarly exposure to psychosocial adversity is among the most potent predictors of depression. Because depression commonly emerges prior to adulthood, we must consider the fundamental principles of developmental neuroscience when examining how experiences of childhood adversity, including abuse and neglect, can lead to depression. Considering that both the environment and the brain are highly dynamic across the period spanning gestation through adolescence, the purpose of this review is to discuss and integrate stress-based models of depression that center developmental processes. We offer a general framework for understanding how psychosocial adversity in early life disrupts or calibrates the biobehavioral systems implicated in depression. Specifically, we propose that the sources and nature of the environmental input shaping the brain, and the mechanisms of neuroplasticity involved, change across development. We contend that the effects of adversity largely depend on the developmental stage of the organism. First, we summarize leading neurobiological models that focus on the effects of adversity on risk for mental disorders, including depression. In particular, we highlight models of allostatic load, acceleration maturation, dimensions of adversity, and sensitive or critical periods. Second, we expound on and review evidence for the formulation that distinct mechanisms of neuroplasticity are implicated depending on the timing of adverse experiences, and that inherent within certain windows of development are constraints on the sources and nature of these experiences. Finally, we consider other important facets of adverse experiences (e.g., environmental unpredictability, perceptions of one’s experiences) before discussing promising research directions for the future of the field.


In the patients with bipolar disorder, mood stabilizers would be used to diminish swings of the mood. Antipsychotics, lithium and anticonvulsants are used as mood stabilizers. The exact mechanisms of these drugs in controlling the mood swings are not clear specifically with regard to antipsychotics. These drugs have effects on dopamine receptors in the pathways related to motivation and emotion, in some parts of the brain like nucleus accumbens, amygdala and hippocampus. The mechanism of action of lithium is different from antipsychotics. Lithium protects neurons from insults and inhibits cellular apoptosis process by glycogen synthase kinase-3b inhibition or increasing anti-apoptotic protein BCL-2 production. Inhibiting the inositol-1-phosphatase by lithium, cause it to have effects on inositol phosphate second messengers production. Dentate gyrus new neurons growth, will be promoted by lithium either. Lithium also decreases the suicide risk in the patients.


2022 ◽  
pp. 1-9
Author(s):  
Cara Richardson ◽  
Kathryn A. Robb ◽  
Sally McManus ◽  
Rory C. O'Connor

Abstract Background Previous research has highlighted the importance of understanding which psychosocial factors distinguish between those with suicide thoughts compared to those who attempt suicide. This study aims to investigate these distinguishing factors further within an ideation-to-action framework and to explore sex differences in suicide risk. Methods Participants (n = 7546, aged 16+) were from the cross-sectional Adult Psychiatric Morbidity Survey (APMS; 2014) of England. Face-to-face and self-completion questionnaires assessed lifetime suicidal ideation, lifetime suicide attempts, demographic characteristics, life experiences, social support, health and mental illness. Multinomial logistic regression examined factors differentiating between those with suicidal ideation only and suicide attempt histories (with or without suicidal ideation) in men and women. Results Overall men were less likely to report suicidal thoughts and attempts, compared to females. More factors differentiated between suicidal thoughts and attempts in women compared to in men; these included hospital admission for mental illness, below degree level qualifications, being single and childhood adversity. In men, factors which significantly differentiated between suicidal thoughts and attempts included self-report of professional diagnosis of mental illness and childhood adversity. Higher levels of social support were associated with being in the suicidal thoughts group v. in the attempts group in men. Conclusion This study identified some key differences between men and women in factors associated with suicide attempts compared to suicidal thoughts. The findings support the use of the ideation-to-action framework to investigate sex differences in suicidal behaviour. Future research should examine the extent to which these factors are associated with suicide risk over time.


2007 ◽  
Vol 12 (11) ◽  
pp. 981-983 ◽  
Author(s):  
T Dawood ◽  
J Anderson ◽  
D Barton ◽  
E Lambert ◽  
M Esler ◽  
...  

2020 ◽  
Vol 33 (3) ◽  
pp. 299-327
Author(s):  
Stephanie Lloyd ◽  
Alexandre Larivée

ArgumentIn this article, we trace shifting narratives of trauma within psychiatric, neuroscience, and environmental epigenetics research. We argue that two contemporary narratives of trauma – each of which concerns questions of time and psychopathology, of the past invading the present – had to be stabilized in order for environmental epigenetics models of suicide risk to be posited. Through an examination of these narratives, we consider how early trauma came to be understood as playing an etiologically significant role in the development of suicide risk. Suicide, in these models, has come to be seen as a behavior that has no significant precipitating event, but rather an exceptional precipitating neurochemical state, whose origins are identified in experiences of early traumatic events. We suggest that this is a part of a broader move within contemporary neurosciences and biopsychiatry to see life as post: seeing life as specific form of post-traumatic subjectivity.


2019 ◽  
Author(s):  
Delia A. Gheorghe ◽  
Chenlu Li ◽  
John Gallacher ◽  
Sarah Bauermeister

AbstractBackgroundExperiences of chronic stress and trauma are major risk factors for psychiatric illness. Evidence suggests that adversity-related changes in brain structure and function accelerate this vulnerability. It is yet to be determined whether neuroendocrine effects on the brain are a result of the interference with neural development during sensitive periods or a consequence of cumulative lifetime adversity. To address this question, the present study investigated the associations between brain structure and self-reported data of childhood and adult adversity using machine learning techniques and structural equation models (SEM).MethodsThe UK Biobank resource was used to access Imaging Derived Phenotypes (IDPs) of grey matter and white matter tract integrity of 7003 participants, together with selected childhood and adult adversity data. Latent measures of adversity and imaging phenotypes were estimated to evaluate their associations using SEM.ResultsWe demonstrated that increased incidence of childhood adversity events may be associated with smaller grey matter in frontal, insular, subcallosal and cerebellar regions of the brain. There were no significant associations between brain phenotypes and negative experiences during adulthood.ConclusionsUsing a large population cohort dataset, this study contributes to the suggestion that childhood adversity may determine grey matter reductions in brain regions, which are putatively sensitive to the neurotoxic effects of chronic stress. Furthermore, it provides novel evidence to support the “sensitive periods” model though which adversity affects the brain.


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