Nutrition (14 page)
Deficiency
Vitamin D deficiency occurs in those who do not obtain or absorb enough from their diet and do not regularly expose their skin to sunlight – either because they are confined indoors or because they cover their skin with clothing or sunblock. Prolonged vitamin D deficiency in children results in rickets. In adults, vitamin D deficiency results in osteomalacia with softening of bones, skeletal pain, increased risk of fractures and muscle weakness. These changes are due to raised levels of parathyroid hormone, which leaches calcium from bones. Increased calcium in the circulation may become deposited in coronary artery walls and contribute to heart disease. Lack of vitamin D has recently been linked with reduced immunity and an increased risk of bacterial vaginosis in pregnancy, a common bacterial imbalance that increases the risk of miscarriage and premature labour.
Toxicity
Excess vitamin D can cause headache, loss of appetite, nausea, vomiting, diarrhoea or constipation, palpitations and fatigue.
Vitamin E
Vitamin E is the collective term for two groups of fat-soluble compounds: the tocopherols and tocotrienols. These consist of four tocopherols (alpha, beta, gamma and delta) and four tocotrienols (alpha, beta, gamma and delta). Recently, a ninth substance with vitamin E activity, delta-tocomonoenol, was identified in kiwi fruit. Of all of these, the most active form is natural source d-alpha-tocopherol. Synthetic d-alpha tocopherol is less biologically active due to the different molecular symmetries present. Total vitamin E activity is therefore usually expressed as d-alpha-tocopherol equivalents. Alpha-tocopherol is the main source of vitamin E in the European diet, while gamma-tocopherol is the most common form in the American diet.
Vitamin E mainly functions as an antioxidant in the lipid (fatty) parts of the body, maintaining the integrity of cell membranes, nerve sheaths, circulating cholesterol molecules, dietary fats and body fat stores. When it acts as an antioxidant it is itself converted into a free radical and other antioxidants, such as vitamin C, are needed to regenerate antioxidant vitamin E. Like vitamin A, vitamin E may also modify gene expression and transcription to strengthen muscle fibres and boost immunity. Interestingly, selenium and vitamin E appear to have a synergistic effect to increase antibody synthesis.
Dietary sources of vitamin E
These include: wheatgerm, soybean, corn and olive oils; avocado; butter and fortified margarine; wholegrain cereals; nuts and seeds; meat, poultry and dairy products.
Vitamin E is rapidly depleted on exposure to air. Processing cereals and grains, canning vegetables and freezing removes over 80 per cent of their vitamin E content. Heating destroys around 30 per cent of vitamin E content of foods, while frying or roasting destroys virtually all vitamin E present.
Vitamin E activity is sometimes expressed in International Units (IU) rather than milligrams, as nine different chemicals contribute towards vitamin E activity in the body. One IU = 0.67 mg alpha-tocopherol equivalents, or conversely: 1 mg =1.5 IU. The EU RDA for vitamin E of 12 mg is therefore equivalent to 18 IU. In general, the more polyunsaturated fats you eat, the more vitamin E you need.
Deficiency
Lack of vitamin E affects the integrity of cell membranes, muscle contraction and nerve transmission. As a result, lack of vitamin E has a harmful effect on the nervous system and can produce symptoms such as lack of energy, lethargy, poor concentration, irritability, muscle weakness and poor coordination. In severe, long-term lack (such as that incurred by malabsorption) serious effects such as blindness, dementia and abnormal heart rhythms can occur.
Toxicity
Vitamin E is relatively non-toxic. Very high intakes can cause headache, fatigue, double vision, muscle weakness, abdominal pain and diarrhoea. High doses may also interfere with the function of vitamin K.
Vitamin K
Vitamin K is the collective term for a group of four fat-soluble substances: phylloquinone (K1 made in plants), menaquinone (K2, made by Gram-positive bacteria in your small intestine) plus menadione (K3) and menadiol (K4), which are closely related synthetic substances found to have vitamin K activity (although they are not present in nature).
Vitamin K was named after the German word
koagulation,
as it acts as an essential cofactor for the production of certain blood-clotting proteins in the liver: factors II (prothrombin), VII, IX, X, protein C, protein S and protein Z. It therefore acts as an antidote for the blood-thinning drug warfarin. Vitamin K is also needed for the synthesis of osteocalcin (a calcium-binding protein found in bone), and plays a role in the reabsorption of calcium in the kidneys. It is also thought to play a role in cell signalling, brain metabolism and cardiovascular health.
koagulation,
as it acts as an essential cofactor for the production of certain blood-clotting proteins in the liver: factors II (prothrombin), VII, IX, X, protein C, protein S and protein Z. It therefore acts as an antidote for the blood-thinning drug warfarin. Vitamin K is also needed for the synthesis of osteocalcin (a calcium-binding protein found in bone), and plays a role in the reabsorption of calcium in the kidneys. It is also thought to play a role in cell signalling, brain metabolism and cardiovascular health.
Dietary sources of vitamin K
Most of your vitamin K requirements are met by probiotic bacteria in your gut, which secrete absorbable vitamin K2. Dietary sources, of which 90 per cent are in the form of vitamin K1, include cauliflower (the richest source); dark green leafy vegetables; safflower, rapeseed, soybean and olive oils; fish-liver oils; yogurt; dairy products; meat and eggs.
Deficiency
As it is secreted by intestinal bacteria, deficiency is rare but can occur as a result of malabsorption or prolonged use of broad-spectrum antibiotics. Symptoms that may be due to lack of vitamin K include prolonged bleeding time, easy bruising, recurrent nosebleeds, heavy periods and diarrhoea. A single dose of vitamin K is offered to all newborn infants to prevent a condition known as haemorrhagic disease of the newborn.
High doses of vitamins A or E may interfere with vitamin K function.
Toxicity
Patients taking warfarin should avoid extreme changes to dietary intake of vitamin K from vegetables such as broccoli or cauliflower, which can affect blood-clotting control. However, as long as you maintain a fairly consistent intake of these foods, and your warfarin tests are stabilized to that intake, you do not need to avoid them altogether.
Essential minerals are metallic and non-metallic elements that play a vital role in body metabolism. Those needed in very tiny amounts are usually referred to as trace elements.
Despite the fact that you store over 3 kg of minerals within your skeleton, mineral deficiency is generally more common than vitamin deficiency. Unlike the vitamin content of a particular food, which is usually similar wherever it is harvested, the mineral content of your food depends on the soil in which its ingredients were grown or reared. This is because plant roots absorb vital nutrients from the soil for optimum growth and these, in turn, are eaten by livestock. Selenium, for example, was leached out of the soil throughout much of Europe during the last Ice Age. Exposure to acid rain, which can interact with minerals to form insoluble salts, and food processing can also significantly reduce the mineral content of foods.
Minerals have several different functions in the body. Some act as antioxidants (selenium, manganese, zinc), while others have structural roles (calcium, magnesium, phosphate). Some maintain electrical potentials across cell membranes (sodium, potassium, chloride), and are vital for electrical transmission in muscle and nerve cells and muscle contraction (calcium). Many act as cofactors for important enzymes (copper, iron, magnesium, manganese, molybdenum, selenium, zinc), or are important for hormone function (chromium, iodine). Perhaps the best known, however, is iron, which forms part of the proteins that bind oxygen in red blood cells (haemoglobin) and muscle cells (myoglobin).
As discussed at the beginning of the previous chapter, the EU Recommended Daily Amounts (EU RDA) estimate the intake of minerals and trace elements that are believed to supply the needs of most (97.5 per cent) of the adult population. These are shown in
Table 10
, together with the upper safe limits suggested by the UK Expert Group on Vitamins and Minerals (EVM) in 2003. To recap, the upper safe limits are the maximum daily amount of each mineral that is considered safe to take long term in the form of food supplements. These are in addition to the amounts typically obtained from your food, unless otherwise stated. Different RDA values are used in non-EU countries, and during pregnancy and breastfeeding.
Table 10
, together with the upper safe limits suggested by the UK Expert Group on Vitamins and Minerals (EVM) in 2003. To recap, the upper safe limits are the maximum daily amount of each mineral that is considered safe to take long term in the form of food supplements. These are in addition to the amounts typically obtained from your food, unless otherwise stated. Different RDA values are used in non-EU countries, and during pregnancy and breastfeeding.
Mineral for which an EU RDA has been set | EU RDA | Average dietary intakes from food | EVM upper safe level for long-term use from supplements |
Minerals | |||
Calcium | 800 mg | 830 mg per day from food; up to 600 mg from water | 1,500 mg |
Chloride | 800 mg | up to 6,000 mg | Not suggested |
Chromium | 40 mcg | 100 mcg per day | 10 mg 1 |
Copper | 1 mg | 1.4 mg per day from food, and up to 6 mg per day from water | 10 mg 1 |
Iodine | 150 mcg | 250 mcg per day | 500 mcg |
Iron | 14 mg | 12 mg per day | 17 mg |
Magnesium | 375 mg | 380 mg per day | 400 mg |
Manganese | 2 mg | 5 mg | 4 mg |
Phosphorus | 700 mg | 1,260 mg per day | 250 mg |
Potassium | 2,000 mg | 2,800 mg per day | 3,700 mg |
Selenium | 55 mcg | 39 mcg per day | 350 mcg |
Zinc | 10 mg | 9.8 mg per day from food, and up to 10 mg per day from water | 25 mg |
1
This upper safe level refers to total intakes from both diet and supplements
This upper safe level refers to total intakes from both diet and supplements
A word on bioavailability
Vitamins and minerals are absorbed from the small intestine, mainly within the jejunum. Their bioavailability refers to the fraction that is ingested and absorbed to become available for your body to use or store. The proportion of vitamins and minerals in the diet that is absorbed varies from person to person, and can also change over time. The absorption of many minerals in particular (e.g. chromium) is inefficient and highly variable, while for others efficiency can be high. For example, as much as 98 per cent of the selenium present in some food sources is absorbed.
Once ingested, minerals are mainly absorbed into intestinal lining cells (enterocytes) via passive diffusion. Some minerals also enter intestinal cells by following the movement of water (solvent drag) by squeezing between intestinal cells (e.g. magnesium) or by a process called cell drinking (pinocytosis) in which part of the cell encloses and engulfs a small droplet of fluid (e.g. calcium). These processes are unregulated, and you absorb the nutrients whether you need them or not.
Important minerals such as phosphorus, magnesium and zinc are also absorbed by a regulated process called active transport, which boosts uptake when intake is low or demand is high.
The absorption of many minerals depends on acidity (pH), and low levels of stomach acid (achlorhydria), which becomes increasingly common as you get older, can lead to a number of nutritional deficiencies, especially of zinc and of calcium, which also depends on the presence of vitamin D.
The chemical form in which minerals are presented to intestinal lining cells also affects their uptake. Most dietary iron is in the form of inorganic ferrous iron (Fe
2+
) or ferric iron (Fe
3+
), for example. Ferrous iron has a relatively inefficient uptake mechanism but when vitamin C (ascorbic acid) is present, it is converted into ferric iron, which is better absorbed due to its higher solubility. In contrast, the iron present in meat (haem iron) is ‘body ready’, as it is bound to porphyrin which is absorbed via a specific haem receptor, that is two to three times more efficient. Even so, only around 10 to 15 per cent of the iron present in a varied diet is usually absorbed.
2+
) or ferric iron (Fe
3+
), for example. Ferrous iron has a relatively inefficient uptake mechanism but when vitamin C (ascorbic acid) is present, it is converted into ferric iron, which is better absorbed due to its higher solubility. In contrast, the iron present in meat (haem iron) is ‘body ready’, as it is bound to porphyrin which is absorbed via a specific haem receptor, that is two to three times more efficient. Even so, only around 10 to 15 per cent of the iron present in a varied diet is usually absorbed.
Previous intake and body status
Mineral absorption may depend on previous intakes and how much is stored in the body (tissue saturation). Iron, for example, is initially stored within intestinal lining cells bound to a protein called ferritin, which releases it as needed. Once a cell’s ferritin is saturated with iron, it does not absorb more iron from food within the gut. Iron can only leave enterocytes and enter the circulation by binding to a blood protein called transferrin. If circulating transferrin saturation is high, iron remains within the enterocytes and is lost when the intestinal cell is shed (which occurs, on average, after a lifespan of three days). As absorption is inversely related to body iron stores, those with iron deficiency absorb more. This mechanism helps to prevent absorption of excess iron, which can be harmful. Similarly, movement of zinc depends on a protein, metallothionein, which ‘traps’ zinc within intestinal lining cells when body stores are high.
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