**10.7 Schizophrenia**

*Vitamin D Deficiency*

symptom production [20, 38].

**10.5 Aging depressive symptoms**

D3 can accelerate aging symptoms [19, 24, 31].

of aging and related diseases [19].

and postpartum depression may have different pathogenesis; the first is found to be dejected with hyperactivity in the HPA axis and the second being atypical. The activity of the HPA axis is usually reduced in seasonal affective disorder, atypical depression, and PPD, which could point to a similar pathologic mechanism in all the three conditions mentioned. Furthermore, the physiological excess production of CRH at the end of pregnancy leads to a transient downregulation of hypothalamic CRH postpartum, which could possibly lead to an elevated risk for depression. Indeed, the hypothesis of PPD being related to hypoactivation of the HPA axis has been substantiated by a number of studies where women with PPD display lower baseline or reduced HPA responsiveness than controls, although conflicting data are available. In addition, women with a history of PPD appear to have increased levels of corticotropin-releasing hormone which further stimulates the dependent cortisol response in the experimental conditions of pregnancy. PPD can also be predicted by

Together with SAD, PPD has also been classified, under the depressive states characterized by hypoactivation of the HPA axis. Increased serum concentrations of biomarkers detecting the inflammatory response, for example, IL-6, a proinflammatory cytokine with a variety of endocrine and metabolic actions, have been observed in major depressive conditions. In this, IL-6 interacts with the HPA axis, and the interacted complex has significant higher serum levels in women with postpartum depressive symptomatology. Conclusively, vitamin D affects monoamine functional groups, the HPA axis, and immune responses to stress and

Aging depressive symptoms are noticed for both hypervitaminosis D3 and hypovitaminosis D3, which leads to premature aging of fibroblast growth factor 23 (FGF-23) that is emerging as a significant mediator/hormone for early aging symptoms, and its FGF-23 effects are dominated by vitamin D-mediated excess of calcitriol. The early aging phenotypic features include thin skin, intestinal atrophy, spleen atrophy, muscle atrophy, weight loss, short life prognosis, osteoporosis, and atherosclerosis. There is a tight physiological regulation of 24-hydroxylase, the hormonal form of vitamin D3, which can be modulated by physiological serum concentrations of calcidiol. This regulation of hormonal form of vitamin D3 explains the development of aging depressive symptoms [31]. However, some intoxications occur during the early period of synthesis and distribution of vitamin D3 with its substitution/ fortification. After the Second World War, the children in many parts of Europe were administered with extremely high oral doses of vitamin D3 and suffered from hypercalcemia, nephrocalcinosis, early aging, cardiovascular complications, and early death, supporting the possibility of hypothesizing that the hypervitaminosis

Calciferol hormone insufficiency may accelerate the risk of diseases of CNS. A

The hypothesis of the role of vitamin D in aging is considered based on three axial parameters, namely, calciferol hormone serum concentrations, risk of disease,

recent study postulated that the hypovitaminosis D3, also famously known as vitamin D deficiency, may cause premature or immature aging of cognitive functions. Thus, both a lack and an excess of calciferol hormones enhance aging in major dependency [32]. Initial events affect the genome, causing telomere shortening or accumulation of DNA damages, which are modulated by the tumor suppressor protein, p53. Hormonal forms of vitamin D3 appear to control the basic mechanisms

increased stress-induced cortisol levels or CRH levels [6, 20].

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A study conducted in the year 2006 on the psychiatric population to understand the association between lower plasma levels of 25(OH) vitamin D3 and mood disorders revealed that all 82 subjects were suffering from psychiatric disorders. Further, 53 patients were suffering from mood disorders, and the remaining 29 patients were diagnosed with schizophrenia. All these patients were found to have low vitamin D3 plasma concentration which confirms the significant association of low vitamin D3 plasma concentration with mood disorders and related disease symptoms. Additionally, significant hypovitaminosis D was also witnessed in mood disorders like major depression, bipolar disorder, and dysthymia than with schizophrenia [37]. Also, according to one of the neurodevelopmental hypothesis of schizophrenia, it was revealed that the prenatal vitamin D deficiency in a mother could be a high-risk factor for schizophrenia in an offspring [24].
