Assistance of Gut Microbiota in Depression

The association between gut microbiota and mental health is a relatively new research topic that has gained traction in recent years. Depression is a serious mental illness and a leading cause of disability, morbidity, and mortality worldwide. Based on the WHO reports, there are approximately 350 million people affected by depression globally. Currently available treatments can temporarily alleviate the symptoms of depressive illness, but these management plans are unable to completely reverse the multifactorial pathology of depression, and the antidepressant medications may produce side effects and adverse drug reactions which may turn down the quality of life of patients. Research has shown that the gut microflora interacts with the brain through various mechanisms, and this leads to the recognition of the microbiome in managing mental health. By unveiling the complexities involved in this area can help to develop novel strategies to treat the depressed patients and to prevent the public from falling to depressive disorder. Keywords: Gut microbiome, depression, neurotransmitters

Childhood urbanicity interacts with polygenic risk for depression to affect stress-related medial prefrontal function

Urbanization is increasing globally, and is associated with stress and increased mental health risks, including for depression. However, it remains unclear, especially at the level of brain function, how urbanicity, social threat stressors, and psychiatric risk may be linked. Here, we aim to define the structural and functional MRI neural correlates of social stress, childhood urbanicity, and their putative mechanistic relevance to depressive illness risk, in terms of behavioral traits and genetics. We studied a sample of healthy adults with divergent urban and rural childhoods. We examined childhood urbanicity effects on brain structure as suggested by MRI, and its functional relevance to depression risk, through interactions between urbanicity and trait anxiety-depression, as well as between urbanicity and polygenic risk for depression, during stress-related medial prefrontal cortex (mPFC) engagement. Subjects with divergent rural and urban childhoods were similar in adult socioeconomic status and were genetically homogeneous. Urban childhood was associated with relatively reduced mPFC gray matter volumes as suggested by MRI. MPFC engagement under social status threat correlated with the higher trait anxiety-depression in subjects with urban childhoods, but not in their rural counterparts, implicating an exaggerated physiological response to the threat context with urbanicity, in association with behavioral risk for depression. Stress-associated mPFC engagement also interacted with polygenic risk for depression, significantly predicting a differential mPFC response in individuals with urban but not rural childhoods. Developmental urbanicity, therefore, appears to interact with genetic and behavioral risk for depression on the mPFC neural response to a threat context.

Psychosocial impairment in children with Celiac disease.

Objective: To determine the frequency of psychosocial impairment in patients with celiac disease. Study Design: Descriptive Cross Sectional study. Setting: Children Hospital Complex and Institute of Child Health, (CHICH) Multan. Period: August 2019 to August 2020. Material & Methods: A total number of 177 patients having age 4-16 years with diagnosis of CD were included in this study. In children with CD depressive illness were assessed by using Pediatric symptoms checklist (PSC) form and this PSC form was filled by asking questions from parents then filling of form by doctor. Outcome variable was calculated on the basis of Pediatric symptoms checklist (PSC), whether patient has psychosocial illness or not. Results: Mean age of patients was 8.91±3.50 years. Mean duration of celiac disease of patients was 4.27±2.00 months. There were 135 (76.27%) female patients and 42 (23.73%) male patients. Mean serum anti-tissue transglutaminase IgA (tTG-IgA) level of patients was 122.73±24.31 µg/ml. The socioeconomic status of 115 (64.97%) patients was poor, 31 (17.51%) was middle, 18 (10.17%) patient was upper middle and 13 (7.34%) patients was high. Psychosocial illness was present in 35 (19.77%) patients. Conclusion: Psychosocial illness was diagnosed in 19.77% children having CD. So the children with celiac disease should be monitored for symptoms of anxiety and depression and a thorough counselling of the children to reduce the risk of psychosocial illness.

The PPARg System in Major Depression: Pathophysiologic and Therapeutic Implications

To an exceptional degree, and through multiple mechanisms, the PPARg system rapidly senses cellular stress, and functions in the CNS in glial cells, neurons, and cerebrovascular endothelial cell in multiple anti-inflammatory and neuroprotective ways. We now know that depression is associated with neurodegeneration in the subgenual prefrontal cortex and hippocampus, decreased neuroplasticity, and defective neurogenesis. Brain-derived neurotrophic factor (BDNF) is markedly depleted in these areas, and is thought to contribute to the neurodegeneration of the subgenual prefrontal cortex and the hippocampus. The PPARg system strongly increases BDNF levels and activity in these brain areas. The PPARg system promotes both neuroplasticity and neurogenesis, both via effects on BDNF, and through other mechanisms. Ample evidence exists that these brain areas transduce many of the cardinal features of depression, directly or through their projections to sites such as the amygdala and nucleus accumbens. Behaviorally, these include feelings of worthlessness, anxiety, dread of the future, and significant reductions in the capacity to anticipate and experience pleasure. Physiologically, these include activation of the CRH and noradrenergic system in brain and the sympathetic nervous system and hypothalamic–pituitary–adrenal axis in the periphery. Patients with depression are also insulin-resistant. The PPARg system influences each of these behavioral and physiological in ways that would ameliorate the manifestations of depressive illness. In addition to the cognitive and behavioral manifestations of depression, depressive illness is associated with the premature onsets of coronary artery disease, stroke, diabetes, and osteoporosis. As a consequence, patients with depressive illness lose approximately seven years of life. Inflammation and insulin resistance are two of the predominant processes that set into motion these somatic manifestations. PPARg agonists significantly ameliorate both pathological processes. In summary, PPARg augmentation can impact positively on multiple significant pathological processes in depression. These include loss of brain tissue, defective neuroplasticity and neurogenesis, widespread inflammation in the central nervous system and periphery, and insulin resistance. Thus, PPARg agonists could potentially have significant antidepressant effects.

Understanding of “Feeling” and “Self-Consciousness” on the Border of the XIX–XX Centuries and M. Loewy’s Concept of Depersonalization

The aim was to review the understanding of the phenomena of “feeling” and “self-consciousness” in the concepts of the leading European scientists at the second half of XIX — beginning of the XX centuries.Method: H.R. Lotze, I.M. Sechenov, A. Bain, W. Wundt, G. Stoerring, Th. Lipps, K. Oesterreich, E. Kraepelin and some others are analyzed.Conclusion: while Th. Lipps, H.R. Lotze, W. Wundt and K. Oesterreich were striving for strict differentiation of the notions of “sensations” and “feelings”, A. Bain, I.M. Sechenov, G. Stoerring were not following an effi cient distinction of these phenomena. H.R. Lotze, I.M. Sechenov, A. Bain distinguished in the consciousness and self-consciousness the affective and intellectual components; Th. Lipps considered as the core of self-consciousness the feelings that were very manifold and accompanied different mental acts including the act of perception: “perceptions feeling”. G. Stoerring paid attention to the lack of the feeling of activity by depersonalization, and the Austrian psychiatrist and neurologist M. Loewy elaborated the concept of “ubiquitous” “action feelings” (Actionsgefuehle) that exist outside of “pleasure — displeasure” modality. According to M. Loewy’s concept every mental act is accompanied normally by two “feelings of act”: general and specifi c, in the abnormal case one or both of them may disappear. The clinical description of weakening or loss of the action feelings: impulse feeling, perception feeling of vital sensation, perception feelings of sensations from organs of sense, “feelings of the feeling process”, “thinking feeling”, M. Loewy accomplished by “personalizing” approach to the account of one of his patient, Russian female student. M. Loewy considered the depersonalization disorders in this case as a symbolic neurosis according to S. Freud and as a psychasthenia according to P. Janet. Although E. Kraepelin defi ned selfconsciousness as merely cognitive phenomenon he interpreted depersonalization as a kind of emotional disturbance including the disorders on the level of sensations in the frames of light depressive phase of the manic-depressive illness. The M. Loewy’s concept of the “action feelings” can be applied not only for the understanding of “neurotic” depersonalization but also for depersonalization cases on the ground of depressive and mixed phase affective states.

Lateralised attentional disruption and resource conservation in persistent depression and anhedonia

Anhedonia – a pervasive loss of interest or enjoyment in relation to previously valued stimuli - is a central feature of clinical depression. A series of studies investigated alterations in perceptual sensitivity and attention, and their relation to anhedonia, in participants with persistent depressive illness in comparison to healthy controls. Study 1 measured perceptual sensitivity in the somatic and auditory modalities while minimising attentional influences. Study 2 maximised attentional influences to assess their impact on perceptual sensitivity in the same modalities. Perceptual sensitivity did not differ between groups in either study. Both studies found evidence of lateralised attentional deficits suggestive of subtle left-sided neglect in the depressed samples. In both studies, lateralised attentional deficits were associated with anhedonia above and beyond depression severity. Study 3 demonstrated through simulation that a single lateralised attentional lapse model could predict the key outcomes in both empirical studies, and additionally demonstrated the plausibility of a resource conservation strategy as a data-generating process among depressed participants. In conclusion, the studies support the novel insight that anhedonia may be related to disruptions in brain networks subserving stimulus-driven attention, with a potential contribution of resource conservation strategies that reduce access to precise sensory information.

A Systematic Review of the Evidence on Inflammation in Depressive Illness and Symptoms, in Chronic and End Stage Kidney Disease

BackgroundDepressive illness and symptoms are known to be common in physical health problems and are present in at least a third of people with chronic kidney disease and end stage renalfailure (CKD/ESKD). Depressive illness and symptoms in CKD/ESKD complicates care, is associated with a shorter life expectancy, and may arise in response to inflammation.MethodsWe undertook a systematic review of studies including measures of depression and inflammatory markers in CKD/ESKD. The protocol was pre-registered with PROSPERO: CRD42019141305. Data base searches were completed in 2019 and repeated in May 2020. We assessed study quality, and undertook a narrative synthesis as well as meta-analyses of cross-sectional and longitudinal studies, examining associations between depressive states and inflammatory markers.ResultsThere was significant heterogeneity in study quality, comorbidities, samples, depression measures, and study design, as well as in the specific measured inflammatory markers.Overall, there is some evidence for associations of IL6 and CRP with depressive illness and symptoms, with inconclusive or contradictory evidence for other inflammatory markers. There were few intervention studies. Studies of samples with physical comorbidity and higher rated quality were more likely to show positive associations. There were few longitudinal studies.ConclusionsThere is some evidence of inflammation being an important correlate of depressive illness and symptoms in the presence of physical health comorbidities. Better research designs areneeded including a range of inflammatory markers.