Analysing Fat Soluble Vitamins Biology Essay


Vitamins are essential organic nutrients our body needs in small amounts for various roles in the body. The "Vitamine" was first coined from the word vital plus amine, since the earliest identified one has amino group in their structure. Later it was found that amino acid are not common in most vitamin, therefore "e" was deleted. Vitamins are mainly divided into two groups: water soluble (Vitamin B and C) and fat-soluble (A, D, E and K). Unlike water-soluble vitamins that need regular replacement in the body, fat-soluble vitamins can be stored in the human body in liver and fatty tissues, and are eliminated much more slowly than water-soluble vitamins. The differences between the water soluble and fat soluble vitamins are given in Table 1.

When consumed in excess, fat-soluble vitamins can cause toxicity as they are stored for long periods, this is not true for the water soluble Vitamins, as these water soluble vitamins can easily get excreted from body and thus unlikely to have high concentration leading to adverse effects. Eating a normal, well-balanced diet will not lead to toxicity in otherwise healthy individuals. However, taking vitamin supplements that contain mega doses of vitamins A, D, E and K may lead to toxicity as the body only needs small amounts of any vitamin. The recommended dietary allowance (RDA) of Indian populations has been made and revised by ICMR in 1988 and are available for some vitamins but is infrequently used as it's not complete and it is not revised in recent times. The Table 2 presents the RDA of fat soluble vitamins according to different age groups.

Lady using a tablet
Lady using a tablet


Essay Writers

Lady Using Tablet

Get your grade
or your money back

using our Essay Writing Service!

Essay Writing Service

Vitamin A (retinol) is an essential nutrient, needed in small amounts by humans for the normal functioning of the visual system; growth and development; and maintenance of epithelial cellular integrity, immune function, and reproduction. Three different forms of Vitamin A are active in the body: retinol (alcohol form), retinal (aldehyde form) and retinoic acid (acid form) which are collectively called retinoids. The retinol is the active component of vitamin A associated with visual function. The vitamin A deficiency is one of the measure causes of severe visual impairment/ blindness, in a recent study 7.5% to 25% of blindness was reported to be due to Vitamin A deficiency.

Vitamin A metabolism:

Food derived from animals provide compound (retinyl esters) that are easily converted in intestine to retinol. Food derived from plants provides carotenoids, some of which may have vitamin A activity. There are more than 600 carotenoids in nature; β carotene is the most prevalent carotenoid with vitamin A activity, which can be split into intestine and liver to retinol. The β carotene absorption and conversion is less efficient than retinoids. The 12 µg of β carotene is equivalent to 1 µg of retinol.

The retinol binding protein (RBP) is the special transport protein which binds to retinol in blood and transports it to the appropriate cells that have specific protein receptors for their binding.

Vitamin A Biological Role:

The major role of vitamin A in body includes:

Supporting growth and reproduction.

Promoting vision

Maintenance and growth of epithelial cells of skin and mucus membrane.


The vitamin A retinol has the major role in transport in of vitamin A and in supporting growth and reproduction. In Men retinol participates in sperm development and in women it supports normal foetal development. Retinol also have major role in the normal growth and remodelling of bones. The retinal plays two major roles in normal vision. First it is required for maintenance of crystal clarity of cornea and secondly it participates in the conversion of light energy into nerve impulse in the retina. The rhodopsin pigment present in retina is composed of a molecule of retinal and a protein opsin. When light strikes the retina the rhodopsin pigment gets bleached and retinal shifts from cis to trans configuration. This trans retinal cannot bind to opsin leading to change in membrane potential of opsin and activation of electrical impulse, which transmits it to nerve cell and later to brain. Much of trans retinal is converted back to active cis form but small amount of it get converted to irreversible retinoic acid which has to be replaced with dietary intake.

Lady using a tablet
Lady using a tablet


Writing Services

Lady Using Tablet

Always on Time

Marked to Standard

Order Now

Retinoic acid-vitamin A has important role in promotion of cell differentiation and protein synthesis leading to normal development of epithelial cells of skin and mucus membrane integrity.

Sources of vitamin A

The vitamin A recommendations are expressed in retinol activity equivalent (RAE). 1 RAE equals to1 µg of retinol; 12 µg of β carotene; 3.33 IU of vitamin A. Vitamin A recommendation used to be given in international units (IU) in past but it is now expressed in µg and the same will be used in this chapter. Table 2 summarizes the estimated mean requirements for vitamin A and the recommended safe intakes, taking into account the age and sex differences in mean body weights.

Preformed vitamin A is found almost exclusively in animal products, such as human milk, glandular meats, liver and fish liver oils (especially), egg yolk, whole milk, and other dairy products. Preformed vitamin A is also used to fortify processed foods, which may include sugar, cereals, condiments, fats, and oils. Provitamin A carotenoids are found in green leafy vegetables (e.g. spinach, amaranth, and young leaves from various sources), yellow vegetables (e.g. pumpkins, squash, and carrots), and yellow and orange non-citrus fruits (e.g. mangoes, apricots, and papayas).

Foods containing provitamin A carotenoids tend to have less biologically available vitamin A but are more affordable than animal products. It is mainly for this reason that carotenoids provide most of the vitamin A activity in the diets of economically deprived populations.

Vitamin A deficiency (VAD):

Vitamin A deficiency is a major health problem of developing countries. WHO estimates that more than 100 million children's have some degree of deficiency. In a recent study from India, the prevalence of Bitot's spots and night blindness in schoolchildren was found to be around 5% while prevalence of night blindness in pregnant female was found to be as high as 20% in few centres. The ocular manifestation due to vitamin A deficiency is known as xerophthalmia. The night blindness is the earliest manifestation of the deficiency in which there is lack of vitamin A in back of eye (retina), in later stages of xerophthalmia there may be total blindness due to involvement of front of eye (cornea). The corneal involvement starts with dryness and hardening (xerosis) and later followed by softening, ulceration and necrosis (keratomalacia).

The normal range of serum vitamin A (retinol) is between 30-100µg/dL. The other methods used to diagnose normal levels are blood spot retinol, tests for dark adaptation and liver biopsy to estimate the vitamin A reservoir. The serum level below 20µg/dL is regarded as vitamin a deficiency. The clinical and subclinical infections can lower serum levels of vitamin A on an average by as much as 25%, independently of vitamin A intake.

Management of Vitamin A deficiency:

Any stage of xerophthalmia should be treated with three 60 mg of vitamin A soft gel capsule given on day 0, day 1 and day 14. The dose should be half (30 mg) for the children's in age group of 6 months to 11 months. Pregnant mothers with deficiency should be a treated with 7.5 mg/ week for 3 months. Patients with malabsorption should be treated with 15 mg/day of water soluble vitamin A and this should be followed by maintenance dose according to serum retinol levels.

Prophylactic vitamin A dose of 60 mg every 6 months is recommended in high risk individuals and similarly children's suffering from measles should be given two capsules of 60 mg for two consecutive days.

Vitamin A Toxicity

Routine consumption of large amounts of vitamin A over a period of time can result in toxic symptoms, including liver damage, bone abnormalities and joint pain, alopecia, headaches, vomiting, and skin desquamation. Hypervitaminosis A appears to be due to abnormal transport and distribution of vitamin A and retinoids caused by overloading of the plasma transport mechanisms. Very high single doses can also cause transient acute toxic symptoms that may include bulging fontanelles in infants; headaches in older children and adults; and vomiting, diarrhoea, loss of appetite, and irritability in all age groups.


Vitamin D (calciferol) is the only vitamin which can be synthesized in human body. It is required to maintain normal blood levels of calcium and phosphate, which are in turn needed for the normal mineralization of bone, muscle contraction, nerve conduction, and general cellular function in all cells of the body. Vitamin D achieves this after its conversion to the active form 1,25-dihydroxyvitamin D [1,25-(OH)2D], or calcitriol. This active form regulates the transcription of a number of vitamin D-dependent genes which code for calcium-transporting proteins and bone matrix proteins. Vitamin D also have important role of cell differentiation and immunomodulation.

Metabolism vitamin D:

Lady using a tablet
Lady using a tablet

This Essay is

a Student's Work

Lady Using Tablet

This essay has been submitted by a student. This is not an example of the work written by our professional essay writers.

Examples of our work

Vitamin D, a seco-steroid, can either be made in the skin from as cholesterol like precursor (7-dehydrocholesterol) by exposure to sunlight or can be provided pre-formed in the diet. The version made in the skin is referred to as vitamin D3 or cholecalciferol whereas the dietary form known as vitamin D2 or ergocalciferol. The vitamin D is also known as prohormone because it can be synthesized in human body and acts like a hormone at distant target cells.

The vitamin D3 is metabolized first in the liver to 25-hydroxyvitamin D (calcidiol) and subsequently in the kidneys to1, 25-(OH)2D (calcitriol) to produce a biologically active hormone. The calcitriol and other vitamin D metabolites are complexed to Vitamin D-binding protein (globulin) in the blood. Calcitriol is believed to act on intracellular receptors similar to steroid hormones.

Recently there has been rising interest in the discovery of vitamin D receptors in more than 20 different cells of the body which includes brain, bone marrow cells, skin, lymphocytes etc. The exact role of these receptors is still unknown but it is speculated that this may have some important functions of immunomodulation and cell differentiation.

Sources of vitamin D

The most efficient and physiologically relevant endogenous synthesize of vitamin D from skin is maximum in the world in a broad band around the equator (between latitudes42°N and 42°S). Approximately 30 minutes of adequate exposure of arms and face to sunlight can provide the daily adequate requirement of an individual. However, skin synthesis of vitamin D is negatively influenced by the following factors: latitudes > 42°N or >42°S , winter months, thinned skin of elderly, dark pigmented skin (Asian and Africans), clothing and sunscreens use. It is reported that in winter months persons living in latitudes higher than 420 have zero vitamin D synthesize.

Vitamin D recommendation is usually given in international units (IU) and the conversion used is 1IU=0.025µg cholecalciferol. The RDA for vitamin D is given in Table 2. The food sources rich in vitamin D are fortified dairy products, fortified margarine, fish oils and egg yolk

Vitamin D deficiency

Vitamin D deficiencies is widely prevalent in India and in recent studies up to 90% of Indians are found to be having hypovitaminosis D, which may be due to dark skin complexion, poor sun exposure, vegetarian food habits and lack of vitamin D in food fortification program. The vitamin D acts on intestinal cells to increase calcium absorption from gut therefore in its deficiency serum ionized calcium level decreases leading to rickets in children's and osteomalacia and osteoporosis in adults. Optimal vitamin D level of 25(OH) D is >25 ng/mL (37 nmol/L) but the level at which the parathyroid hormone (PTH) increases and bone density decreases is < 15ng/mL of vitamin D.

Rickets: is very common in developing countries like India. The low levels of calcium lead to failure of bone calcification leading to growth retardation and skeletal abnormalities like saber tibia.

Osteomalacia: It is the adult form of rickets. It is associated with soft brittle bone, with or without deformity. The patients also commonly present with nonspecific musculoskeletal pain and aches and on radiology there may be presence of pseudo fractures or "looser zone".

Osteoporosis: In adults due to defective mineralization of bones there develops a condition of weak bones with decreased bone mineral density. These patients if not treated properly may develop recurrent fractures of vertebral spine and hip bone.

Management of vitamin D deficiency

Recommended daily intake of 800IU of vitamin D is associated with decrease in risk of hip fracture in elderly. The cause of vitamin D deficiency should be treated first before vitamin D and calcium correction. In patient with chronic renal function or 1α-hydroxylation defect the treatment should be with 0.25-0.5µg/day of calcitriol [1, 25(OH)2D3]. Patients with intact vitamin d hydroxylation should be treated with 60,000 IU of cholecalciferol sachet/ week for 4-12 weeks followed by maintenance therapy of once monthly sachet or 800 IU daily. In patients with fat malabsorption intramuscular vitamin D should be used in the dose of 2.4 lac IU/ 6 months.

Vitamin D Toxicity

The safety margin of vitamin D is very large and the toxicity is only seen at very large doses in the range of 40,000 IU/day. It may lead to hypercalcemia and hypercalciuria, leading to nephrolithiasis if urinary calcium is >250mg/ 24 hour.


Vitamin E consists of family of eight naturally occurring isomers of tocopherol and trocotrienols that are synthesized by plant homogentisic acid. It is the major lipid-soluble antioxidant in the cell antioxidant defence system and is exclusively obtained from the diet. The major biological role of vitamin E is to protect polyunsaturated fatty acids (PUFAs) and other components of cell membranes and low-density lipoprotein (LDL) from oxidation by free radicals. The recent studies do not document the beneficial role of vitamin E as antioxidant to prevent heart disease and cancer as previously thought.

Vitamin E Metabolism:

Absorption of vitamin E from the intestine depends on adequate pancreatic function, biliary secretion, and micelle formation. Conditions for absorption are like those for dietary lipid, that is, efficient emulsification, solubilisation within mixed bile salt micelles, uptake by enterocytes, and secretion into the circulation via the lymphatic system. After absorption of tocopherol (vitamin E), it is incorporated into the chylomicrons in the enterocyte and secreted into the lymphatic's and blood stream. The chylomicrons carry tocopherols to the liver parenchymal cells as well as in systemic circulations they are acted upon by lipoprotein lipase and get incorporated inside the LDL, VLDL and LDL. The tocopherol is mainly delivered to the peripheral tissue by the LDL through LDL receptor mechanism.

Dietary source of Vitamin E:

Vitamin E is naturally present in plant based diets and animal products. The vegetable oils and their products are the major source (60%) of vitamin E in human diet. The other important sources of vitamin E are animal fats, vegetables, meats, fruit, nuts, cereals and dairy products. Small amount of vitamin E is also present in eggs, fish, and pulses. The RDA for vitamin A is 15 mg/day for all adults.

Vitamin E Deficiency:

The dietary deficiency of vitamin E does not exist. This suggests that diets contain sufficient vitamin E to satisfy nutritional needs. The deficiency in humans is usually seen in infants and adults with fat-malabsorption syndromes or liver disease, in individuals with genetic anomalies in transport or binding proteins (e.g. abetalipoproteinemia), and possibly in premature infants. The deficiency may precipitate in the community at times of ecological disaster and famine. Disorders provoked by traces of peroxidised PUFAs in the diets of animals with low vitamin E status include cardiac or skeletal myopathies, neuropathies, and liver necrosis. The blood levels of α tocopherol < 5 µg/mL is suggestive of vitamin E deficiency.

Management of vitamin E deficiency

In deficient states vitamin E is required to be given in doses of 800-1200mg/day. In patients with abetalipoproteinemia the dose recommended is 5000-7000 mg/day of α tocopherol. In children with fat malabsorption with vitamin E deficiency should be treated with water soluble form of α tocopherol as well as by intramuscular injections.

Vitamin E Toxicity

Vitamin E appears to have very low toxicity, evidence of pro-oxidant damage has been associated with the feeding of supplements but usually only at very high doses of >1000mg/day. High doses can also interfere with platelet aggregation and vitamin K metabolism leading to bleeding tendency. Other common symptoms of toxicity include nausea, vomiting and flatulence.


Vitamin K has essential role in maintenance normal blood coagulation in the human body by acting as a cofactor in post translational modification of vitamin K dependent proteins or G1a proteins. The vitamin K dependent coagulation proteins are synthesized in the liver and comprises of factors II, VII, IX, and X, which have a haemostatic role and proteins C and S, which have an anticoagulant role. Nutritional deficiency of vitamin K leads to bleeding tendency. Vitamin K-dependent proteins synthesized by other tissues include the bone protein osteocalcin and matrix Gla protein, though their functions remain to be clarified.

Vitamin K Biological role

There are two types of naturally occurring vitamin K, the phylloquinone (vitamin K1) is synthesized by plants and menaquinones (vitamin K2) is synthesised by bacteria. Vitamin K1 can be converted to Vitamin K2 in some specific organs.

The biological role of vitamin K is to act as a cofactor for a specific carboxylation reaction that transforms selective glutamate (Glu) residues to γ-carboxyglutamate (Gla) residues.

Apart from the coagulation proteins, several other vitamin K-dependent proteins have been isolated from bone, cartilage, kidney, lungs, and other tissues. Only two, osteocalcin and matrix Gla protein (MGP), have been well characterized. Both are found in bone but MGP also occurs in cartilage, blood vessel walls, and other soft tissues. Evidence of a possible association of a suboptimal vitamin K status with increased fracture risk remains to be confirmed

Sources of vitamin K

The highest values of phylloquinone (normally in the range 400-700mg/100g) are found in green leafy vegetables (turnip greens, spinach, cauliflower, cabbage and broccoli etc). The next best sources are certain vegetable oils (e.g. soybean, rapeseed, and olive), which contain 50-200mg/100g. The animal food is generally poor source of vitamin K. The average daily requirement in adult is 100µg/day.

Animals and humans obtain a significant fraction of their vitamin K requirement from direct absorption of menaquinones produced by bacterial microflora present in the gut. The most promising site of absorption is the terminal ileum, but due to tight binding of menaquinone to the bacterial cytoplasmic membrane, the percentage of absorption is not confirmed.

Vitamin K Deficiency

Infants up to around age of 6 months are prone to vitamin K deficiency due to low levels of vitamin K in breast milk, low fat store, gut sterility, liver immaturity and poor placental transfer of vitamin K. The deficiency syndrome has been termed vitamin K deficiency bleeding (VKDB) disorder.

In adults, primary vitamin K-deficient states that manifest as bleeding are almost unknown except when the absorption of the vitamin K is impaired as a result of an underlying chronic small intestinal disease (e.g. celiac sprue) or intestinal resections.

Diagnosis of Vitamin K can be made by direct measurement or by prolonged prothrombin time.

Management of vitamin K deficiency

Vitamin K deficiency should be treated with 10 mg of parentral dose. In chronic malabsorption states the vitamin K dose required is 1-2 mg/ day orally or 1-2 mg/ week parentrally.

Vitamin K toxicity

When taken orally, natural K vitamins seem free of toxic side effects. However, synthetic preparations of menadione or its salts may be associated with neonatal haemolysis and liver damage. High doses of vitamin K can impair the actions of oral anticoagulants.


WHO. Vitamin and mineral requirements in human nutrition. Second edition; 2004.

Whitney EN, Cataldo CB and Rolfes SR. The Fat- Soluble Vitamins: A, D, E and K. In: Understanding Normal and Clinical Nutrition. 6th Edition.355.73. Wadsworth/ Thompson Learning Belmont USA. 2002.

Russell RM, Suter PM. Vitamin and Trace Mineral Deficiency and Excess. In: Harrison's, Principles of Internal Medicine, 17th Edition. Edi: Fauci, Braunwauld, Kasper, Hauser, Longo, Jameson et al. New York. McGraw Hill. 441-49.

Table 1: Differences between Fat soluble Vitamin and water soluble Vitamin.


Fat soluble vitamins

Water soluble vitamins

Major vitamin

A, D, E, K

Vitamin B complex &C


Fat soluble

Water soluble


Along with lipids, requires bile secretion

Simple absorption


Mainly liver and sometime fatty tissue (large amount)

Ussually no storage


Not excreted



Late manifestation

Early manifestation




Treatment of deficiency

Single dose may be effective

Regular dietary supplementation is required

Table 2: The recommended dietary allowances (RDA)/ adequate intake of fat soluble vitamins for individuals.

Life stage

Vitamin A (RAE*)

Vitamin D** (µg/d)

Vitamin E (µg/d)

Vitamin K (µg/d)







(1-13 yrs)






(>14 yrs)






(>14 yrs)















Note; *as retinol acid equivalent. 1RAE=1µg retinol, 12 µg β carotene

** As calciferol. 1 µg calciferol=40 IU vitamin D.

Source: Adapted from Food & Nutrition Board, Institute of Medicine-National Academy of Sciences: Dietary Reference Intake, 2002. National academy press, Washington, DC.

Figure 1. Flow chart showing synthesise of vitamin D in humans