The best-deﬁned function of vitamin C is its role in the synthesis of collagen, the principal connective tissue protein found in tendons, arteries, bone, skin, and muscle.
Vitamin C deﬁciency in animals leads to a reduction in the activity of liver enzymes (i.e. mixed function oxidases) involved in the metabolism of hormones, cholesterol, drugs, and carcinogens.
Fruits and vegetables are the major sources of vitamin C in the diet, contributing together upto 90% of the vitamin intake in countries like New Zealand and the United Kingdom Fruit juices and drinks fortiﬁed with vitamin C are the most signiﬁcant source in some groups, such as adolescents.
Vitamin C is readily absorbed in the small intestine by an energy-dependent mechanism, with 70–90% of average daily vitamin C intake (30–200mg) being absorbed. The absorption decreases to 20% when a single 5g dose of the vitamin is ingested and to 16% with a 12g dose. The bioavailability of vitamin C from foods is similar to that from supplements. The highest concentration of vitamin C in the body is found in pituitary and adrenal glands, eye lens, leukocytes, lymph glands, brain, and other internal organs. The lowest levels are found in plasma and saliva.
Vitamin C is not stored for long in the body. When a vitamin C free diet is consumed approximately 3% of the total body pool is lost per day, although this proportion decreases considerably with duration of the diet.
Factor affecting metabolism
Cigarette smokers have lower concentrations of ascorbic acid in plasma and leukocytes. These lower levels are partly, but not entirely, the result of reduced consumption of vitamin C. Isotopic studies have shown that the metabolic turnover of vitamin C in smokers is twice that in non-smokers. Acute and chronic infections and disease can reduce levels of vitamin C in plasma and leukocytes. However, in chronic disease the poor vitamin C status is often due to poor diet. There is some evidence that excretion of vitamin C increases under acute infections and stressful conditions.
Scurvy is uncommon in populations unless there is a prolonged shortage of fruits and vegetables together with an overall reduced food supply, as in the Irish Potato Famine of the nineteenth century. The supplementary foods, cereals, legumes, and oil, were almost completely deﬁcient in vitamin C. Accordingly, the World Health Organization (WHO) now advises that in this area of Africa vitamin C supplements be added to relief food at an early stage of a crisis. Symptoms such as weakness, fatigue, inﬂamed and bleeding gums, impaired wound healing, petechial and other skin haemorrhages, and depression have been observed after 3–6 months on the scorbutic diets.
A high enhancing effect can be attained with a vitaminC intake of roughly 100mg per meal. When body iron stores are low, the enhancing effect of vitaminC on non-haem iron absorption is markedly higher than when iron stores are high. Accordingly, it is common to recommend to vegetarians, many of whom have lower than average iron stores, that foods containing vitaminC be consumed with meals.
Higher dose effects
One of the most commonly ascribed beneﬁts of ingesting large doses of vitaminC (1–10g/day), in the form of supplements, relates to prevention of the common cold.
Toxicity of vitamin C is low, given the wide spread chronic and acute use of supplements and the lack of reported harmful effects. There is some concern that vitamin C can increase oxidant stress in those susceptible to iron overload (e.g. with haemochromatosis) by reducing ferritin bound iron from ferriciron(Fe3+) to ferrous iron(Fe2+)thereby promoting its release into the circulation.
Vitamin E is a powerful antioxidant which plays an essential role in protecting cell membranes and plasma lipoproteins from free radical damage. Free radicals contain an unpaired electron and react readily with polyunsaturated fatty acids, proteins, carbohydrates, and DNA. Vitamin E is able to ‘neutralize’ free radicals because the hydroxyl group on the chromanol ring readily gives up an electron or hydride group to the free radical.
Vitami E is absorbed in a manner similar to most other dietary lipids and requires that fat digestion be functioning normally.. Absorption is normally quite efﬁcient, ranging from 50% to 70% of usual vitamin E intake but decreases substantially at high doses. Lack of bile acids or fat digestive enzymes, damage to the gastrointestinal lining, or an inability to synthesize chylomicrons will decrease vitami E absorption. Diseases in which vitamin E absorption is reduced include: pancreatic diseases (e.g. cystic ﬁbrosis), biliary obstruction, coeliac disease, and a rare genetic inability to make chylomicrons. VitaminE is distributed throughout the body mainly associated with cell membranes, plasma lipoproteins, and adipose (i.e. triglyceride) deposits. Higher concentrations of the vitamin tend to be found in organs with a high fatty acid content.
They develop reduced tendon reﬂexes by three to four years of age and more disabling cerebrospinal symptoms such as unsteadiness of gait, loss of touch and pain sense, limb ataxia (lack of coordination), ptosis, dysarthria, and impaired eye movements by early adolescence. Children often develop the clinical symptoms of ataxia, areﬂexia or hyporeﬂexia (absent or low/slow reﬂexes), loss of proprioception (position sense) within two to three years of the onset of fat malabsorption, whereas symptoms in adults may take up to 20 years to manifest. In some cases, there can be yellow/white pigment deposits in the retina.
Reports of vitamin E toxicity are rare. Intakes of 100–800mg/day appear to be well tolerated. Thus, vitamin E is one of the exceptions to the earlier belief that high doses of fat-soluble vitamins are toxic while high doses of water soluble vitamins are not.
Foods high in fat, particularly polyunsaturated fat, are the best food sources of vitaminE (Wheat germ oil is the richest source. Tocopherols comprise the bulk of vitaminE in plant foods with the exception of palm oil which contains more tocotrienols.
Recommended nutrient intakes IN healthy populations because clinical deﬁciency symptoms are rare, and there is no sensitive and speciﬁc biochemical measure of vitamin E status. Animal experiments conﬁrm the theoretical prediction that vitamin E requirements. Intakes of 50–200mg/day appear in prospective epidemiological studies to be associated with a reduced risk of coronary heart disease. But intakes as high as this cannot be achieved by ordinary diets, they require vitamin E supplements. The association between taking vitamin E supplements and reduced risk of coronary disease may be due to other confounding factors (i.e. the lifestyle of people who take vitamin supplements is likely to differ in other ways from people who do not take supplements).
In the tropical and subtropical regions of the world, enough vitami D is made in the skin to meet the body’s needs (unless people are housebound or completely covered). Since cholecalciferol is formed in one organ of the body (the skin) and transported by the blood to act on other organs (the bones, gut, kidneys) it can be called a hormone.
But when people live in high latitudes, are covered with clothes, spend nearly all their time indoors and the sky is polluted with smoke there is insufﬁcient UV exposure in the winter to make enough vitamin D in the skin. Dietary intake is required, so that the cholecalciferol present in a few foods and the ergocalciferol in fortiﬁed foods assume the role of a vitamin.
Inside the body, vitamin D itself is not active until it has been chemically modiﬁed (hydroxylated) twice. Vitamin D, whether of cutaneous origin or absorbed (D3 or D2), is carried in the plasma on a speciﬁc α2-globulin, vitamin D-binding protein. In liver microsomes, the end of the side chain is hydroxylated to form 25(OH)vitamin D. This compound has a more stable concentration in the blood than that of vitamin D which rises temporarily as some is absorbed or synthesized in the skin.
Rickets only occurs in young people, whose bones are still growing. Osteomalacia is the corresponding decalcifying bone disease in adults, whose epiphyses have fused so that the bones are no longer growing. Rickets and osteomalacia can also occur in the tropics in children and women usually staying indoors and fully covered when outdoors. In chronic kidney failure, 1α-hydroxylation is impaired. Renal osteomalacia does not respond to vitamin D (or sunlight), only to 1, 25(OH)2D (pharmaceutical name ‘calcitriol’) or to 1α(OH)D (pharmaceutical name ‘alphacalcidol’).
Fish liver oils (e.g. cod and halibut) and some ﬁsh and marine animal’s livers are rich sources. Moderate sources are fatty ﬁsh (sardine, tuna, salmon, etc.),margarines(which in most countries are fortiﬁed with vitamin D), infant milk formulas, eggs and beef or lamb liver. Milk is fortiﬁed with vitamin D in North America and Scandinavia.
Recommended nutrient intake
The US Institute of Medicine estimates ‘adequate intakes’ (AI) of vitamin D for those with no sun-mediated synthesis in the skin. For ages 0–50 years (including pregnancy and lactation) the AI is 5µg/day, for 51–70 years 10µg/day and over 70 years of age 15µg/day. Older people make less vitamin D in their skin and also tend to avoid sun exposure and use UV light blocking sunscreen.
Exposure of the skin to sunlight if excessive causes sunburn and brings up the plasma 25(OH)D if it was low but does not lead to vitamin D toxicity because with excessive UVlight,previtaminD3 (7-dehydrocholesterol) is converted to biologically inert products
Vitamin D3 is also photodegraded if it is not taken inside the body by vitamin D-binding protein. Vitamin D is one of the vitamins that should not be sold over the counter. Overdosage causes raised plasma calcium (hypercalcaemia),with thirst, anorexia, raised plasma levels of 25(OH) D,and risk of calciﬁcation of soft tissues and of urinary calcium stones. Infants are most at risk of hypervitaminosis D; some children have developed hypercalcaemia on intakes of only 50µg/day (ﬁve times the recommended nutrient intake).