**3.4 Factors affecting vitamin D production**

Vitamin D skin synthesis is negatively influenced by factors such as the following [6]:


#### **3.5 Clinical manifestation of vitamin D levels**

Calcidiol (25(OH)D) is the vitamin D metabolite that is estimated to identify a patient's vitamin D status [14]:


However, females are at 3 times higher risk of having vitamin D deficiency compared to males. There is no relationship between the age and vitamin D levels in males, but in females, those having an age between 30 and 40 are at higher risk for deficiency. But, children (10–20 years) are at highest risk for deficiency [15].

#### **3.6 Vitamin D transport**

#### *3.6.1 Transfer from chylomicrons to plasma*

Practically, all consumed vitamin D is held in a nonesterified structure, which is believed to be associated with the outside of chylomicrons (lipoprotein particles). Vitamin D that is not moved in the plasma is taken up with chylomicron remainders by the liver, where it is then transferred to the same binding protein and discharged to the plasma [4].

#### *3.6.2 Vitamin D–binding protein*

Vitamin D is transferred in the plasma to a great extent in association with protein, as other sterols, which is the vitamin D–binding protein (DBP) [4].

#### **3.7 Vitamin D storage**

Vitamin D storage in the liver is minimal, in contrary to other fat-soluble vitamins. Vitamin D levels do not go above 25 nmol per kg in the liver. Plasma calcidiol (25-hydroxyvitamin D) is the storage form of vitamin D, which has a half-life of 3 weeks [11]. Long-standing admission of vitamin D inside the physiological range induces storage in fat tissues and most likely in other tissues of clinical importance [16].

#### **3.8 Vitamin D toxicity**

Vitamin D toxicity is incredibly uncommon; however, it can occur by unplanned or purposeful ingestion of unreasonably high portions. Portions of more than 50,000 IU every day raise levels of 25-hydroxyvitamin D to more than 150 ng for each milliliter (374 nmol/L) as well as hypercalcemia and hyperphosphatemia. Portions of 10,000 IU of vitamin D3 every day for as long as 5 months do not cause toxicity [13]. Excessive exposure to sunlight represents no danger of toxicity through overproduction of endogenous cholecalciferol [8].

When calcium plasma concentrations reach 2.75–4.5 mmol/L, vitamin D toxicity causes several symptoms such as nausea, appetite loss, cramps, and diarrhea, and in more severe cases, it causes hypercalcemia. When plasma calcium levels exceed 3.75 mmol/L, hypertensive encephalopathy occurs due to the contraction of smooth muscles. Hypercalcemia and expanded vitamin D levels lead to soft tissue calcification (kidneys, heart, and lungs) [11].

## **4. Vitamin D deficiency**

The most popular and worldwide deficiency currently is vitamin D deficiency [17]. It is a worry for public health and has several acute and chronic impacts. It results from wrong lifestyle starting in predominance obesity and inadequate sun exposure [18].

#### **4.1 Vitamin deficiency**

Living with a lifestyle that is inadequate in any food group will result in a vitamin deficiency. A vitamin deficiency results in different diseases and disorders. The clinical signs and symptoms are the final stage in hypovitaminosis [4].

**83**

*4.3.1 Rickets*

*4.3.2 Osteomalacia*

*Nutritional Considerations of Vitamin D Deficiency and Strategies of Food Fortification*

During marginal deficiency, there is only depletion of vitamin stores and its effect on cells. This depletion cannot be recognized without chemical or biochemical testing, which shows the stores' concentrations. However, in observational deficiency, the signs and symptoms appear and morphological changes take place [4].

1.Decreased synthesis in the skin: due to creams, aging, and skin pigment, the

2.Decreased bioavailability: obesity and malabsorption diminish the availability

3.Breastfeeding: decreased amount of vitamin D in human milk can lead to vita-

4. 25-hydroxyvitamin D diminished synthesis: vitamin D malabsorption caused by liver failure results in 25-hydroxyvitamin D diminished synthesis.

5. 1,25 dihydroxy vitamin D diminished synthesis: decreased phosphorus excretion and decreased serum levels of 1,25-dihydroxyvitamin D are caused by

Vitamin D deficiency's first stages include rickets and osteomalacia, whereas the final and long-term stages include osteoporosis in which there are chronic changes [19].

Vitamin D deficiency in children leads to rickets. Rickets is classified by bone mineralization loss [8]. This occurs due to deficiency in both vitamin D and calcium [7]. Consequently, the bones twist due to their inability to hold the body, stand, or walk [3].

As rickets occur in children, osteomalacia occurs in adults [4]. Osteomalacia is the result of the demineralization of bones [7]. In the case of osteomalacia, nonmineralized bones are much more than mineralized bones. Consequently, the

*DOI: http://dx.doi.org/10.5772/intechopen.89612*

• Stage I—depletion of vitamin stores

• Stage II—cellular metabolic changes

• Stage IV—morphological changes

**4.2 Vitamin deficiency causes and effects**

vitamin D3 synthesis will be reduced.

of vitamin D3.

chronic kidney diseases.

**4.3 Manifestation of vitamin D deficiency**

Vitamin D deficiency is caused by the following [13]:

min D deficiency when the child is exclusively breastfed.

1.Marginal deficiency

2.Observable deficiency

• Stage III—clinical defects

Stages of vitamin deficiency are as follows:

*Nutritional Considerations of Vitamin D Deficiency and Strategies of Food Fortification DOI: http://dx.doi.org/10.5772/intechopen.89612*
