**3.2 Vitamin D needs and normal levels**

The Food and Nutrition Board has set an adequate intake (AI) for vitamin D due to the inability to set a more precise RDA level because of the variability in sun exposure among individuals [9]. Recommendations for vitamin D instructed an AI for vitamin D of at least 500 IU/day (12.5 μg) and more than 1000 IU/day (25 μg) for those not exposed to enough sunlight [8].

International units are used to quantify vitamin D. 1 IU is equal to 25 metric weight unit of cholecalciferol, and 1 g of cholecalciferol is equal to 40 IU [7].

#### **3.3 Metabolism and regulation**

Metabolism of vitamin D occurs through different stages that includes hydroxylation. Through these stages, vitamin ingested is transformed into its active form (**Figure 2**) [4].

Vitamin D synthesis starts when 7-dehydrocholesterol (cholesterol precursor found on skin) is visible to sunlight and then transformed to previtamin D [9, 10]. 7-Dehydrocholesterol is an intermediate precursor for vitamin D, it is found throughout the epidermis and dermis, and thus has the most elevated limit with respect to cholecalciferol synthesis [11].

The first step occurs when 7-dehydrocholesterol absorbs the UVB photons to convert them into previtamin D3. Then, photoisomerization occurs in order to covert previtamin D3 into vitamin D3 (cholecalciferol). However, it is not a problem since during delayed sun exposure previtamin D3 is converted into its inactive forms (lumisterol and tachysterol) [12].

Large portion of vitamin D reaches liver from lipoproteins or vitamin D–binding protein and is then transformed by hydroxylation to yield 25-OH-D3 [4]. 25-OH-D3 is the major circulating type of vitamin D used by clinicians to evaluate vitamin D level, though it is latent and must be transformed to its active form (1α,25 dihydroxyvitamin D) in the kidneys [13].

When calcium decreases in the body, parathyroid hormone is released leading to calcitriol synthesis increase (vitamin D active form: 1α,25(OH)2D) (**Figure 3**). Because of the hypocalcemia (declined blood calcium), PTH is released from parathyroid gland resulting in an increase in the hydroxylation of 25(OH)D3 to calcitriol. Then, calcitriol plays its role with PTH or by itself on its target tissues leading to an increase in serum calcium levels. Kidneys, bones, and intestines are the primary target tissues [8]:

#### **Figure 2.**

*Sources, sites, and processing of vitamin D metabolites [10].*

**81**

deficiency [15].

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

Increasing calcium and phosphorus absorption is the major role of calcitriol in the intestines. It works by the participation of calcitriol with cell membrane recep-

Calcitriol with the help of PTH increases calcium reabsorption in the distal renal tubule into the blood. Phosphorus released by the kidney is boosted and can result

Regarding the bone, PTH plays its role with calcitriol for reabsorption increase

Osteoclasts catalyze calcium and phosphorus from bone. The net impact of this is to

• Season: winter season decreases the quantity of ultraviolet light reaching the

• Skin pigmentation: dark pigments interfere with UV light entering the needed

Calcidiol (25(OH)D) is the vitamin D metabolite that is estimated to identify a

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

of calcium and phosphorus from bone to reach normal blood calcium level.

Vitamin D skin synthesis is negatively influenced by factors such as the

• Clothing: covering the skin leads to inadequate sunlight skin exposure.

• Vitamin D deficiency: 25(OH)D between 21 and 29 ng/mL

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

tors to improve calcium absorption [8].

in lower serum phosphorus levels [8].

raise blood calcium and phosphorus levels [8].

**3.4 Factors affecting vitamin D production**

skin, while summer season increases it.

**3.5 Clinical manifestation of vitamin D levels**

• Vitamin D lack: 25(OH)D < 20 ng/mL

• Normal vitamin D status: 25(OH)D > 30 ng/mL

• Vitamin D toxicity: 25(OH)D > 150 ng/mL

• Vitamin D overproduction: 25(OH)D > 40–60 ng/mL

risk for deficiency. But, children (10–20 years) are at highest risk for

*3.3.1 Intestine*

*3.3.2 Kidney*

*3.3.3 Bone*

following [6]:

skin layer.

patient's vitamin D status [14]:

#### **Figure 3.** *Calcitriol, 1,25 (OH)2 D3, synthesis and actions with parathyroid hormone (PTH) [8].*

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