**1. Introduction**

Vitamin D is an integral biological substance used to maintain bone health primarily, but it also plays its importance in several other biochemical pathways within the human body. Vitamin D, at the end of its metabolizing physiology, gets converted into an active hormone metabolite of vitamin D, i.e., calcitriol (1,25(OH)2 vitamin D), which binds to vitamin D receptors (VDR). Vitamin D enzymes present in the central nervous system are responsible for the regulation of cellular function in several tissues located in the body including brain neurons. Vitamin D comes in two main forms: the first form is vitamin D2 also known as ergocalciferol which is obtained from sources like mushrooms grown in UV light, dietary supplements, and fortified food, and the second form of vitamin D is vitamin D3 also known as cholecalciferol, obtained from oily fish and fish oil, liver, egg yolk, butter, and dietary supplements. Vitamin D2 and D3 are not equal when it comes to raising your vitamin D status. Both are effectively absorbed into the bloodstream. However, the liver metabolizes them differently. The liver metabolizes vitamin D2 into 25-hydroxy vitamin D2 and vitamin D3 into 25-hydroxy vitamin D3. These two compounds are collectively known as calcifediol. The main circulating form of vitamin D is Calcifediol. The amount of Calcifediol can be determined by checking its blood levels in the body. However, vitamin D2 seems to yield less calcifediol than an equal amount of vitamin D3 [1, 2].

Vitamin D deficiency is prevalent worldwide. The knowledge of the causes of vitamin D deficiency and community affected by the same causes are prominent, and hence, differentiation in the therapy and supplementation of these populations is focused upon accordingly. Further, in India, the prevalence of vitamin D deficiency ranges from 40–90% in all age groups and high-risk groups alike, with the majority of study responses reporting 80–90% prevalence as reported by the National Center for Biotechnology Information (NCBI), India [3]. Vitamin D deficiency contributes to a high disturbance in the health/disease ratio and adds to the disease burden of the country [4, 5]. The daily requirement of the human body for vitamin D is not fulfilled by the dietary pattern of the Indian population, and hence, fortification of various foods with vitamin D is emphasized under the initiatives of various national programs [2].

Vitamin D deficiency can be defined as circulating 25(OH) vitamin D levels below 20 ng/ml, while vitamin D insufficiency is defined by circulating levels below 32 ng/ml [3]. Vitamin D receptors are located in the bone, skeletal muscle, immune cells, and several other body tissues (including brain, prostate, breast, and colon). Deficiency of vitamin D hormone at its receptor site or the enzyme metabolizing site causes disturbed cell signalling, further indicating the increased risk of diseases like autoimmune diseases, cancer, tuberculosis, cardiovascular diseases, bone diseases, neurodegenerative diseases, and mood disorders, specifically discussed in this review. Low 25-hydroxyvitamin D levels less than 20 ng/ml are found to have a higher incidence of mood disorders consisting of premenstrual syndrome (PMS), seasonal affective disorder (SAD), non-specified mood disorder, and major depressive disorder (MDD) [1].

The physiology of vitamin D in the human body involves both synthesizing and catabolizing pathways. Vitamin D is either absorbed by dietary intake or is synthesized in the presence of ultraviolet B (UVB) rays ranging from 290 to 310 nm. In the epidermal layer of the skin, 7-dehydrocholesterol gets converted into pre-vitamin D3 in the presence of UVB rays, which further, under thermal reaction, forms vitamin D3 (also known as cholecalciferol). Vitamin D-binding proteins bind to vitamin D3, and by circulatory transport this protein-bound vitamin D3 reaches the liver, where it is further metabolized into 25(OH) vitamin D (calcifediol) and an inert form of vitamin D. Tightly regulated by parathyroid hormone (PTH), 25(OH) vitamin D converts into 1,25-dihydroxy vitamin D (also known as calcitriol), which is an active hormonal form of vitamin D in the kidneys and other extrarenal tissues. This active metabolite binds to vitamin D receptors to regulate the several tissue and cellular functions. When vitamin D deficiency occurs due to inadequate intake of vitamin D through diet or by application of excessive sun-protective agents, it causes dysfunctional regulation of glucocorticoid signalling which is known to be implicated in major depressive disorders and various other mood disorders, together with other body functioning disorders. It is reported to have elevated levels of glucocorticoid (a type of cortisol) for the patients of MDD [1, 6].

This review discusses sources of vitamin D, its association with different types of mood disorders in a different population, and its disease processes, together with the possible downstream molecular and genetic pathways associated with vitamin D deficiency and mood disorders. Further, this review focusses on the vitamin D deficiency causing mood disorders to the childbearing mothers and premenstrual syndrome to the ladies on the onset of their menses.

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including brain neurons [1].

*Association of Vitamin D Deficiency and Mood Disorders: A Systematic Review*

Vitamin D status is determined by assessing serum levels of 25(OH) vitamin D after 3 months of a stable regimen of vitamin D intake. Serum 25(OH) vitamin D is used to measure vitamin D status because it is the major circulating form of vitamin D and the most stable form of vitamin D. The National Health and Nutrition Examination Survey (NHANES) III data 8, which used a conservative measure of vitamin D deficiency {25(OH) vitamin D} levels <15 ng/mL, has reported 42.4% of African American women and 4.2% of white women are deficient in vitamin D

Toxic states (hypervitaminosis D) may occur when 25(OH) vitamin D levels supersede 100 ng/ml; however, in a study involving individuals diagnosed with multiple sclerosis treated with high doses of vitamin D, there was no evidence of toxicity found in individuals with 25(OH) vitamin D levels above 200 ng/ml [1].

The dietary recommendations are largely based on bone health and assuming a minimal sun exposure of an individual under study. While the safe upper limit is set at 4000 international unit/day (IU/d) for healthy adults, for pregnant women, doses are higher than 6000 IU/d. Based on limited data from randomized controlled trials, some authors suggest that pregnant women can be supplemented with 1000–2000 IU/d during the second and third trimesters, and a deficiency during

Vitamin D is a secosteroid hormone that is either absorbed by dietary intake or manufactured by the ultraviolet beam (UVB) rays ranging from 290 to 310 nm reaching the epidermis of the skin. In the presence of epidermal 7-dehydrocholesterol, the absorbed vitamin D gets converted into pre-vitamin D3. Within the epidermis, a thermal reaction occurs to convert the pre-vitamin D3 into vitamin D3 also known as cholecalciferol [10, 11]. Vitamin D3 further, in process, moves to bind to the vitamin D-binding plasma proteins. Vitamin D3 is transported via vitamin D-binding proteins to the liver where it is metabolized into 25(OH) vitamin D (calcifediol) and an inert form of vitamin D. Calcifediol is tightly regulated by parathyroid hormone and converts it into 1,25-dihydroxy vitamin D also known as calcitriol [1]. Calcitriol is the active form of vitamin D, which binds to VDRs in the intestines, bones, and kidney and other extrarenal tissues to enhance the absorption of calcium from the intestines, promotes calcium deposition in bones, and decreases parathyroid hormone concentrations (PTH) [3, 6]. In the process, calcitriol binds to vitamin D receptors, the receptors from the nuclear receptor superfamily that regulates the cellular function in several tissues located in the body

The estimation of calcitriol is very challenging as calcitriol (1,25(OH)2 vitamin D) has very short t1/2 and thus does not reflect long-term vitamin D status. Also, it is observed that the total 25(OH) vitamin D is the most reliable marker for vitamin D

*DOI: http://dx.doi.org/10.5772/intechopen.90617*

during their childbearing years [2, 8, 9].

**3. Dietary recommendations of vitamin D**

pregnancy can be treated with daily doses of 4000 IU [5].

**4. Synthesizing and metabolizing physiology of vitamin D**

**5. Challenges for estimation of serum vitamin D level**

**2. Vitamin D status**
