Vitamin D- Introduction , source, synthesis of vitamin D in body, absorption of vitamin D in the body , action of vitamin D, vitamin D deficiency & toxicity, Dietary reference value,

1. VITAMIN D
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Submitted By:
Alisha Nandan
M.Sc. Food Technology

2. Vitamin D:
Introduction:
• Considering vitamin D amongst the vitamins creates a problem, because:
The definition of vitamins states that they are substances that (generally) cannot be synthesized in the body and that a dietary intake
is required. However, vitamin D can be made in the skin from a provitamin under the influence of ultraviolet (UV-B) light of
wavelength between 290 and 320 nm. There has been considerable debate, therefore, whether vitamin D should continue to be
considered as a vitamin.
• However, there are circumstances when individuals may not be able to synthesize the vitamin, for example, owing to
insufficient exposure to UV light and most nutritionists agree that a dietary source is required.
• Consequently, synthesis that has taken place during the summer months has to provide the body’s vitamin D needs during the
winter.
• In addition, those who are housebound or those living in an environment with high levels of air pollution may have to depend on
a dietary source all year round.
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3. • There are two potential provitamins for vitamin D:
i. 7-dehydrocholesterol (vitamin D3) and,
ii. Ergosterol (vitamin D2).
• 7-dehydrocholesterol (Vitamin D3) is present in animal fats, including
the skin of humans, having been made in the body from cholesterol.
• Ergosterol (Vitamin D2) is found in yeast and fungi, and is used as a
source of commercial vitamin production.
• The principal physiological role of vitamin D is to maintain serum calcium
and phosphorus concentrations at a level appropriate for the formation of bone,
support of cellular processes, and functioning of nerves and muscles.
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4. Vitamin D in the diet:
• There are few sources of vitamin D that are consumed on a regular basis.
Butter, spreading fats (including margarine, low-fat spreads), eggs and milk are
the most regularly consumed sources. Levels in the dairy products vary with the
seasons and are higher in the summer months.
• Meat has relatively recently found to be a useful source of the vitamin D.
• Other sources include oily fish and liver, although these may occur rarely in
the diet.
• A number of manufactured foods may also be fortified with vitamin D, e.g.
breakfast cereals, evaporated milk, bedtime drinks, yoghurts and infant foods.
• Fish oil supplements are a rich source of vitamin D, and may be taken by
individuals as a prophylactic treatment for rheumatism or joint pains.
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5. • The main food groups contributing to dietary vitamin D are reported by DEFRA (2001) to be:
 Fats and oils- 31%
 Meat and meat products- 19%
 Fish- 16%
 Fortified breakfast cereals- 14%
 Milk and cheese- 8%
• Most people obtain vitamin D by skin synthesis during the summer months on exposure to UV light from the sun. The day does
not have to be sunny nor the skin completely uncovered for synthesis to occur, the light can penetrate thin cloud and light clothing.
• There is now greater awareness of the dangers of exposure to solar radiation with respect to skin cancer, with recommendations to
cover the skin with sun-screening creams or clothing.
• It is likely that this reduces the potential synthesis of vitamin D. A balance between the harmful (cancer risk) and beneficial
outcomes (vitamin D synthesis) is required; it has been suggested that about half an hour per day of exposure to sunlight (avoiding
the hottest part of the day) can achieve the beneficial synthesis, without riskingharmful consequences.
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6. Absorption of vitamin D:
• About 50 per cent of the dietary vitamin is found in the chylomicrons leaving the digestive tract in the lymph; most of this vitamin
finds its way to the liver with the remnants of the chylomicrons.
• Vitamin D synthesized in the skin diffuses into the blood and is picked up by a specific vitamin-D-binding protein (DBP), which
transports it to the liver, although some may remain free and be deposited in fat and muscle.
• The production of vitamin D3 from 7-dehydrocholesterol in
the epidermis.
• Sunlight (the ultraviolet B component) breaks the B ring of
the cholesterol structure to form pre- D3.
• Pre-D3 then undergoes a thermal induced rearrangement to
form D3.
• Continued irradiation of pre-D3 leads to the reversible
formation of lumisterol-3 and tachysterol-3 which can revert
back to pre-D3 in the dark.
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7. • Before the vitamin D can perform its functions in the body, two activation stages occur.
 In the liver, an –OH group is added at position 25 on the side-chain of cholecalciferol to form 25 hydroxycholecalciferol (25-OH
D3), by the enzyme 25-hydroxylase.
 The next stage occurs in the kidneys, where a second hydroxyl group is added at position 1 of 25 hydroxycholecalciferol to yield
1,25-dihydroxy vitamin D (1,25-(OH)2 D3, or calcitriol), by the enzyme1-alpha-hydroxylase. This is the biologically active form
of the vitamin D.
 Each of the above forms of vitamin D is hydrophobic, and is transported in blood bound to carrier proteins. The major carrier is
called, vitamin D-binding protein.
• The liver converts vitamin D to 25OHD.
• The kidney converts 25OHD to 1,25(OH)2D and 24,25(OH)2D.
• Other tissues contain these enzymes, but the liver is the main source for
25-hydroxylation, and the kidney is the main source for 1 hydroxylation.
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8. • The activity of the enzyme 1-alpha-hydroxylase, is determined by parathyroid hormone and low blood
calcium levels, which increase its activity.
• High levels of phosphate inhibit calcitriol production.
• When the body does not require calcitriol to be produced, the kidneys perform an alternative hydroxylation
at position 24, producing 24,25- dihydroxy vitamin D. The role of this metabolite is unclear,
but it may be a way of ‘switching off’ production of the active hormone.
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9. Action of vitamin D
Calcitriol, the biologically active form, has a number of target tissues containing specific receptors for the vitamin, the
most notable of which are the intestine, bone and kidney. In each case, the function of the vitamin is to cause an
increase in the plasma level of calcium.
• In the intestines, this is achieved by the vitamin-stimulated synthesis of calcium binding protein, required for
absorption of calcium.
• In the bone, calcium can be mobilized by the action of the osteoclasts and also made available for the osteoblasts to
resynthesize bone. Thus, calcitriol enables appropriate amounts of calcium (and phosphorus) to be available in the
bones for synthesis, while at the same time facilitating their release to maintain plasma levels.
• In the kidneys, calcium reabsorption is promoted by the action of vitamin D.
In summary, when plasma calcium levels fall, parathyroid hormone is released. This causes synthesis of calcitriol in
the kidneys. In response, more calcium is absorbed by the gut, some calcium is mobilized by the bone and less
calcium is lost at the kidneys.
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10. • If, however, the kidney is unable to respond to the original stimulus in this way (because there is insufficient 25-
OH vitamin D being brought to the kidney, or the kidneys themselves are diseased), more parathyroid hormone
will continue to be secreted. This can create a state of hyperparathyroidism, which may be a feature of vitamin D
deficiency.
• Before the role of the kidneys in vitamin D and bone metabolism was fully understood, patients with kidney
disease developed unexplained bone diseases. Treatment with active vitamin D can now prevent these problems
arising.
• In addition, recent work has discovered calcitriol receptors in other tissues, including placenta, gonads, skin and
cells of the immune system, suggesting roles that are not directly linked to calcium homeostasis.
• Potent effects on cell proliferation and cell differentiation both in normal and malignant cells have been described.
The vitamin may also be involved in downregulating the immune response, and vitamin D defects may be
involved in autoimmune reactions.
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11. Vitamin D deficiency:
• The lower cut off for adequate vitamin D status is taken as a plasma 25-OH vitamin D level of 10µg/L (25 nmol/L).
• Elevated parathyroid hormone levels may be an alternative indicator of poor vitamin D status, but at present accurate limits
have not been published.
• Rickets- is the softening and weakening of bones in children, usually because
of an extreme and prolonged vitamin D deficiency.
 the bones are poorly mineralized and soft, so that limb bones bend under the body
weight, the spine becomes curved and the pelvis and thorax may become deformed.
 the gait becomes waddling, with bowlegs or knock knees.
 the cartilage at the ends of the bones continues to grow and enlarge without becoming
mineralized.
 plasma 25-OH vitamin D concentrations may be below 8µg/L (20 nmol/L).
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• Osteomalacia- the comparable condition in adult is called osteomalacia.
 bone gradually becoming demineralized and soft, easy to fracture.
 there is likely to be bowing of the spine and difficulty in walking.
 depression, neuromuscular changes and generalized pain of uncertain origin may also be present.
 plasma 25-OH D3 levels are likely to be as low as 4µg/L (10 nmol/L).
• In both cases, there is muscular weakness and bone pain; plasma calcium, and phosphorus levels may be low and plasma alkaline
phosphatase is raised.
• There is an increased awareness that rickets may be returning in various parts of the world for a number of reasons.
These can be attributed to:
 reduced sunshine exposure, for example, owing to increased pollution, less playing outdoors, increased use of sun creams, the
darker skin pigmentation and highly covering clothing;
 reduced vitamin D intakes, as a result of longer breastfeeding (beyond 6 months), vegan/vegetarian diets, decreased use of milk
and replacement with non-vitamin D containing drinks.

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• Vitamin D deficiency had largely been eradicated by the use of fortified infant milks and supplementation with cod liver oil.
• Often plasma vitamin D levels are very low, with reports suggesting that 30–40 per cent of the over-75 age group have levels
below 5µg/L.
• Even when the individual is not totally housebound, exposure to sunlight may be brief and inadequate to raise plasma vitamin D
levels.
• The efficiency of vitamin D synthesis in skin may decline with age, as the skin becomes thinner and contains less of the vitamin
D precursor.
• Supplementation with 10µg vitamin D/day seems to be an appropriate prophylactic measure in this group, recommended by the
Department of Health.
• Vitamin D deficiency in pre-term infants may be linked to inadequate phosphorus supplies in the milk and resultant under -
mineralization of bone.
• There are high requirements for vitamin D and feeds should provide 20–25µg/day.

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• Various malabsorption conditions interfere with both calcium and vitamin D absorption and may deprive the body of both. This
is most likely to occur in coeliac disease, but can also be a consequence of gastrectomy and intestinal bypass surgery. Failure of
the various stages in the activation of the vitamin associated with liver or renal disease, or its excessive breakdown may also
result in deficiency. Anticonvulsants and alcohol both induce the enzymes that increase the loss of vitamin D in bile and may
deplete the body.
Vitamin D toxicity
• Excess cholecalciferol can be toxic.
• This is most likely to occur in children by accidental ingestion of vitamin supplements.
• It causes a loss of appetite, thirst and increased urine output.
• The blood calcium may rise and calcium deposits may be laid down in soft tissues.
• The margin of safety with vitamin D is not great and raised blood calcium may occur with regular intake of 50µg/day.

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Dietary reference value:
• This is difficult to establish for vitamin D because, for the majority of the population with a normal lifestyle who are able to
synthesize the vitamin in the skin, a dietary source is unnecessary.
• However, children under the age of 3 years have high needs to sustain rapid growth, which may not be met readily from the
diet or by exposure to sunlight and, therefore, an RNI value of 8.5µg/day up to 6 months and 7µg/day from 6 months to 3
years is given.
• Pregnant or lactating women may also benefit from a regular intake of vitamin D to sustain calcium metabolism.
• Older adults, who may have a reduced ability to synthesize the vitamin, or who are less likely to spend time outside may
also benefit from a dietary source of the vitamin. For both of these groups, the RNI is given as 10µg/day.
• It should be noted that an intake of 10µg/day is difficult to achieve through dietary means, and a supplement may be
needed.

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REFERENCE:
Nutrition & Health Book.

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