Vitamins are defined as a group of complex organic compounds present in minute amounts in natural foodstuffs that are essential to normal metabolism and lack of which in the diet causes deficiency diseases and variety of other disorders. Among them, vitamin D is unique of its kind because of its synthesis in body through action of sunlight (UV rays) and action as steroid like pro-hormone. Vitamin D comprises a group of fat-soluble seco-sterols (type of sterols with "broken" ring) popularly known as sunshine vitamin or anti-ricketic factor or calciferol. Vitamin D known for its crucial role in calcium homeostasis and bone metabolism, recently been reported to have epidemiological linkages between vitamin D insufficiency and several diseases like hypertension, myopatic disorders, susceptibility to infections, cancer (Feldman et al., 2014) and autoimmune disorders i.e. multiple sclerosis (Munger et al., 2004), type 1 and type 2 diabetes mellitus (Alvarez and Ashraf, 2010).
Poor lifestyle choices, such as lack of physical activity, non exposure to sunlight, inadequate relief from chronic stress and poor diet are key contributors in the development and progression of preventable chronic diseases, including obesity, type 2 diabetes mellitus, hypertension, cardiovascular disease and several types of cancer in humans. In winter, northern and eastern parts of India are encountered with dense smog which restricts exposure to sunlight. Smog affects vitamin D synthesis in body negatively and it becomes nutritionally important in absence of sunlight. Supplementation of vitamin D through enrichment of later is a better way because vitamin D is considerably higher in eggs as compared to other terrestrial animal source food. Consumption of vitamin D enriched egg and meat by humans can act as preventive measure for aforementioned vitamin D deficiency diseases.
How Vitamin D metabolise in body?
Vitamin D is a group of complex vitamins that includes vitamin D2 – ergocalciferol, 25- hydroxycholecalciferol also referred to as calcidiol or calcifediol, vitamin D3 – cholecalciferol and 1, 25- dihydroxycholecalciferol (1,25 (OH)2 vitamin D) also referred to as calcitriol. Vitamin D is absorbed in lower parts of small intestine along with fat because of its fat soluble nature. Absorbed vitamin D is transported in portomicron to blood (unlike animals, wherein it is transported in chylomicron to lymph and then to venous blood).
Efficiency of vitamin D absorption is less i.e. approximately 50- 60% only. This low efficiency may be due to the fact of cutaneous vitamin D synthesis in presence of sunlight (Collins and Norman, 1991). Cholecalciferol is produced in outer skin layers of poultry birds by irradiation of 7-dehydrocholesterol (present in skin) with UV light either from the sun or an artificial source. In poultry, ergocalciferol (vitamin D2) has only about one-tenth the activity of cholecalciferol (vitamin D3), therefore vitamin D is expressed as international chick unit (ICU) unlike IU in other species. Low activity of vitamin D2 in chickens is due to the fact that they metabolize vitamin D2 rapidly as compared to other species. Hence, in this context unit for vitamin D expression is ICU (unless mentioned as other). One ICU or IU of vitamin D is defined as activity of 0.025 μg of vitamin D3 contained in the USP vitamin D reference standard.
Exposure of sunlight to epidermis causes high-energy UV rays (290–315 nm) to penetrate and photolyze 7-dehydrocholesterol (provitamin D3) to previtamin D3. Once formed, previtamin D3 undergoes thermal isomerisation at body temperature to vitamin D3. This isomerisation is a slow process i.e. it takes 2 to 3 days to produce Vitamin D3 from previtamin D3. Since, previtamin D3 is labile to sunlight; it begins to photolyze to additional photoproducts, principally luminsterol and tachysterol (Figure. 1). Therefore, it can be said that prolonged exposure to sunlight is not beneficial i.e. exposure of sunlight for 15-30 minutes a day is sufficient (for fair skinned humans).
Figure.1: Vitamin D metabolism
Source: Craig Aurand, (2018)
After absorption of vitamin D3 along-with portomicron in blood it reaches to liver wherein, microsomal enzyme i.e. 25, hydroxylase convert vitamin D3 to 25- hydroxy-vitamin D3. This 25- hydroxy-vitamin D3 is transported to kidney with the help of vitamin D binding protein (VDBP, also called transcalciferin). Here, it is converted to 1, 25- dihydroxy-vitamin D3 in presence of 1α hydroxylase. So formed 1, 25- dihydroxy-vitamin D3 [1, 25 (OH)2 vitamin D] is the most active form of vitamin D3, responsible for most of its biological activity. Excretion of vitamin D occurs through faeces with the help of bile salts and part of vitamin D is also excreted in urine.
Role of Vitamin D
Classic functions of vitamin D (hormonal form of vitamin D i.e. 1,25 (OH)2 vitamin D) involve calcium binding protein synthesis responsible for absorption of calcium from intestine and other tissues, bone matrix calcification and osteoblast differentiation. Effect of this hormonal form of vitamin D is observed only after binding to the vitamin D receptor (VDR). This complex dimerizes with the retinoid X receptor (RXR) and so formed, 1,25D-VDR-RXR heterodimer translocates to the nucleus. Here, it binds vitamin D responsive elements (VDRE) in the promoter regions of vitamin D responsive genes and induces expression of these vitamin D responsive genes.
VDR have been reported to be expressed on nephritic, intestinal tissue, bone marrow stem cells, pancreatic β cells, brain cells, breast cells, malignant cells and immune cells suggesting that vitamin D may have functions other than calcium and bone homeostasis (Bikle, 2009). Presence of VDR on these cells suggest that 1,25 (OH)2 vitamin D act in paracrine or autocrine fashion. Active form of vitamin D3 is also synthesized in extrarenal tissues i.e. in macrophages and other immunologic cells by action of 1α hydroxylase. The extra-renal 1-α-hydroxylase enzyme in macrophages is not regulated by PTH however, it is dependent upon circulating levels of 25- hydroxyl vitamin D or it may be induced by cytokines such as IFN-γ, IL-1 or TNF-α (Van et al., 2008). Vitamin D act like steroid hormone and help in transcription and thereby synthesis of bactericidal agents (i.e. defensins and cathelocidin) in macrophages, these bactericidal agents kill pathogenic microbes. This activity is observed after stimulation 1-α-hydroxylase activity and VDR which in turn is activated by reorganization of infectious organisms through toll like receptors.
Vitamin D status worldwide?
Majority of world’s population is vitamin D deficient and similar is the condition for Indians despite their residence in tropical region (Figure.2). Vitamin D deficiency is affecting the global population in these modern days because of sedentary and poor lifestyle.
Figure.2: Vitamin D deficiency status in the world and India
Source: Lucas et al. (2015)
Epidemiological linkages have been found that vitamin D deficiency causes inhibition of B cells proliferation, differentiation and antibody (i.e. immunoglobulin) production (Lemire et al., 1984). Additionally, it is also found to have role in T cells proliferation (Bhalla et al., 1984). Considering the above facts given by several researchers on vitamin D nutrition of body systems, prevention of infectious, autoimmune diseases it can be assured by vitamin D supplementation.
Deficiency of vitamin D
Vitamin D and its metabolites are the most extensively studied nutrients with respect to bone development in poultry. The outstanding disease of vitamin D deficiency is rickets, generally characterized by a decreased concentration of calcium and phosphorus in the organic matrices of cartilage and bone. A deficiency of vitamin D results in clinical signs similar to those of a lack of calcium or phosphorus or both, as all three are concerned with proper bone formation. Also, excess of vitamin A and E may lead to deficiency of vitamin D due to sharing of absorption mechanism. In the adult, osteomalacia is the counterpart of rickets and, since cartilage growth has ceased, is characterized by a decreased concentration of calcium and phosphorus in the bone matrix.
Outward signs of rickets include
Weak bones causing curving and bending of bones,
Enlarged hock and knee joints,
Tendency to drag hind legs, and
Beaded ribs and deformed thorax.
Clinical signs in all poultry species would be rickets and-
Lowered growth rate, egg production and hatchability.
Beaks and claws become soft, rubbery and pliable usually between two and three weeks of age.
Thin and misshapen eggshells.
Vitamin D nutrition of the hen also influences its content in egg yolk and the subsequent need for this vitamin by the chick.
Malpositions due to reduced embryonic bone and muscular development.
Embryos often show a short upper mandible or incomplete formation at the base of the beak.
During periods of extreme leg weakness, hens show a characteristic posture that has been described as a “penguin-like squat”.
Natural sources of Vitamin D
As mentioned earlier in this context, marine animals are able to store high amount of vitamin D in liver and body so, they are rich sources as compared to terrestrial animal liver and their products (Table.1). Supplementation of below mentioned sources to humans and poultry birds in absence of sunlight is very much essential for preventing health problems.
Table.1: sources of vitamin D and their concentration
Source: Scott et al. (1982)
Requirement of Vitamin D
Diversity in poultry bird’s species makes it difficult to cite requirement of Vitamin D for all poultry birds. Therefore, requirement for chicken, few other poultry birds is mentioned here (Table.2) and requirement for humans too. Looking at recent vitamin D concentration (Table.1) and recommendation of ICMR, 2009 for egg and consumption of prior one, we need to focus on improving the concentration of vitamin D in egg. This can commendably be done by enrichment of layer birds diet with vitamin D. Supplementation of Vitamin D has been reported to improve the concentration of vitamin D in egg by three to four fold (Manttila et al., 2004).
Table.2: Vitamin D requirement
Source: NRC, (1994) and ICMR, (2009)
Supplementation of Vitamin D to Humans
Animal source foods (Milk and Meat) are poor sources of vitamin D unlike marine animals who can store high amount of vitamin D in liver. However, egg from poultry birds is rich source of vitamin D as compared to milk and meat (Scott et al., 1982). Due to fat soluble nature of vitamin D, it is concentrated in egg yolk (majority of egg yolk is fat). Two approaches are prevailing nowadays for improving Vitamin D levels in egg and meat of poultry birds mentioned elsewhere in this context. Exposure of adequate sunlight to poultry birds is very necessary for cutaneous vitamin D synthesis that will ultimately be deposited in egg yolk or intramuscular fat of birds. Consumption of this vitamin D enriched eggs can at as primary preventive measure for aforementioned chronic disorders.
Approaches to Enrich Egg and Meat with Vitamin D
Feeding of birds with vitamin D enriched diets
This is the most efficient and beneficial way wherein, Layer birds fed with vitamin D enriched diet. Layer birds then laid eggs having three to four times higher vitamin D concentration as compared to control (Mantill ., 2004).
Exposure of UV rays from sunlight or artificial UV light to the poultry birds
It can easily be done in backyard farming of tropical countries wherein, the birds are allowed to take sufficient sun bath and synthesize enough of vitamin D in body. So formed vitamin D will ultimately be deposited in egg and meat used for human consumption.
Feeding of irradiated feeds
Irradiatation of feed causes conversion of ergosterol to ergocalciferol (vitamin D2), this is the case observed in sun cured feed grains, other ingredients. Feeding of this sun cured feed ingredients may be helpful in improving vitamin D level in egg and meat. But, this is of least importance .
Eggs and meat produced by feeding of birds with vitamin D enriched diet can be sold under the label “Vitamin D Enriched Eggs/ Meat” thereby providing profit to poultry farmers. Consumption of eggs or meat from birds fed on vitamin D enriched diet and exposed to sunlight by humans suffering from vitamin D deficiency disorders can be a preventive measure to treat the later. Also, it can help to prevent incidence of autoimmune diseases, cancer, hypertension and diseases of modern era caused due to change in lifestyle and increase in air pollution.
1, 3, 4. PhD Scholar, ICAR- Indian Veterinary Research Institute, Izatnagar, Bareilly- 243122
2. M.V.Sc Scholar, Bombay Veterinary College, Mumbai
For further readings
Alvarez, J. A., & Ashraf, A. (2010). Role of vitamin D in insulin secretion and insulin sensitivity for glucose homeostasis. International journal of endocrinology, 2010.
Bhalla, A. K., Amento, E. P., Serog, B., & Glimcher, L. H. (1984). 1, 25-Dihydroxyvitamin D3 inhibits antigen-induced T cell activation. The Journal of Immunology, 133(4), 1748-1754.
Bikle, D. (2009). Nonclassic actions of vitamin D. The Journal of Clinical Endocrinology & Metabolism, 94(1), 26-34.
Collins, E.D., and Norman, A.W. (1991). In Handbook of Vitamins (L. Machlin, ed.) p. 59. Marcel Dekker, New York.
Feldman, D., Krishnan, A. V., Swami, S., Giovannucci, E., & Feldman, B. J. (2014). The role of vitamin D in reducing cancer risk and progression. Nature reviews cancer, 14(5), 342-357.
ICMR, 2009, Vitamin D requirement in Allowances, R. D. Nutrient Requirements and Recommended Dietary Allowances For Indians. p 303
Lemire, J. M., Adams, J. S., Sakai, R., & Jordan, S. C. (1984). 1 alpha, 25-dihydroxyvitamin D3 suppresses proliferation and immunoglobulin production by normal human peripheral blood mononuclear cells. Journal of Clinical Investigation, 74(2), 657.
Mattila, P., Valaja, J., Rossow, L., Venäläinen, E., & Tupasela, T. (2004). Effect of vitamin D2-and D3-enriched diets on egg vitamin D content, production, and bird condition during an entire production period. Poultry science, 83(3), 433-440.
Munger, K. L., Zhang, S. M., O’reilly, E., Hernan, M. A., Olek, M. J., Willett, W. C., & Ascherio, A. (2004). Vitamin D intake and incidence of multiple sclerosis. Neurology, 62(1), 60-65.
Scott, M.L., Nesheim, M.C., and Young, R.J. (1982). Nutrition of the Chicken, p. 119. Scott, Ithaca, New York.
Van Etten, E., Stoffels, K., Gysemans, C., Mathieu, C., & Overbergh, L. (2008). Regulation of vitamin D homeostasis: implications for the immune system. Nutrition Reviews, 66(suppl_2), S125-S134.