**2. Vitamin D status**

*Vitamin D Deficiency*

amount of vitamin D3 [1, 2].

tives of various national programs [2].

sive disorder (MDD) [1].

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

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 initia-

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 depres-

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].

syndrome to the ladies on the onset of their menses.

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

**110**

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

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].
