Micronutrients Vitamins and Minerals
Micronutrients are comprised of vitamins and minerals, which are essential elements required in small quantities to enable a wide variety of metabolic and physiologic processes.
Given the ubiquitous commercial claims for the nutritional essentiality of these substances, it is no surprise that nearly 50% of Australian and American adults report taking vitamin and mineral supplements. Despite massive yearly spending on all types of vitamins and minerals, current evidence does not demonstrate general benefits of supplements for the prevention of disease not related to nutritional deficiency.
Routine micronutrient supplementation is not recommended for the majority of the population, however targeted supplementation may be warranted for particular subgroups (e.g. pregnant, vegans, people with osteoporosis) for whom nutritional requirements may be difficult to meet through diet alone.
Instead, some studies suggest that micronutrient supplementation in amounts that exceed the recommended dietary allowance (e.g. beta-Carotene, vitamin E, selenium, calcium) may have harmful effects, including increased risk of cancer, stroke and mortality.
A well-balanced diet made up of real foods provides an adequate supply of all micronutrients, and for most individuals, consuming extra vitamins and minerals does not generally offer any advantage – and instead is likely to make for expensive urine.
Can we really prevent cancer and reverse ageing by sprinkling chia seeds on our porridge, adding acai berries to our smoothies, or substituting brown rice with quinoa for our kale salads? Probably not.
Although tasty (and often expensive!), ‘superfoods’ are not a panacea for good health. Rather, the label is used as a clever marketing device; stories about superfoods sell magazines and makes for good morning television, and industry often sponsors research to show that their foods or supplements are the elixir for optimal health and long life.
But what exactly is a superfood? The Oxford Dictionary defines superfood as ‘a nutrient-rich food considered to be especially beneficial for health and well-being’. If that’s the case, shouldn’t every real, whole, unprocessed food be consider super? In fact, there is no official definition of a superfood in nutritional science, and as of 2007, the European Union has banned superfood health claims on packaging, unless supported by scientific evidence.
Vitamins are chemically unrelated families of organic substances that cannot be synthesised by humans and are essential for supporting normal metabolism. They have diverse biochemical functions, acting as enzyme cofactors, antioxidants and hormone-like regulators for the maintenance of cells, tissues and organs. Although most can be obtained from food alone, some require the help of bodily processes (e.g. Vitamin D is synthesised in the skin with exposure to sunlight). They are sensitive to destruction by light, heat, chemical agents and food processing.
The 13 recognised vitamins can be divided into two classes based on their relative solubility in water and fat. Each vitamin name (e.g. Vitamin ‘C’) refers to a collection of chemical compounds with similar molecular structures and activities.
Table 6.3 Categories of vitamins
|Fat-soluble vitamins||Water-soluble vitamins|
|B vitamins (8)
Vitamin A is a subclass of a family of lipid-soluble compounds referred to as retinoic acids. There are two main forms of vitamin A:
- provitamin A carotenoids (e.g. beta-Carotene)
- preformed vitamin A (e.g. retinol)
Vitamin A from animal sources or supplements is preformed. Vitamin A toxicity, while rarely seen, is more likely to occur when derived from animal sources due to increased bioavailability.
Vitamin A from food is stored in the liver until required by the body to support a variety of biological processes, such as maintaining the integrity of epithelial surfaces and cellular differentiation in the eye, which is essential for vision.
Vitamin A deficiency can lead to xerophthalmia (pathologic dryness of the conjunctiva and cornea), night blindness, poor bone growth, non-specific dermatological problems, and impaired immune function.
|Table 6.4 Food sources of vitamin A|
|Preformed vitamin A – liver, kidney, egg yolk, butter
Provitamin A – green leafy vegetables, orange-fleshed sweet potatoes, pumpkins and carrots
Vitamin D is a group of fat-soluble steroids responsible for increasing intestinal absorption of calcium, magnesium and phosphate. It plays an important role in muscle function, insulin resistance, immunity, and parathyroid hormone regulation, as well as bone growth, density and remodelling. Low levels of vitamin D increases bone turnover, which increases fracture risk. Additionally, unlike exogenous vitamin D supplementation, endogenously derived vitamin D (not from supplementation) is positively associated with reduced risk of all-cause mortality, cardiovascular mortality, and cancer mortality.
Source: https://www.ncbi.nlm.nih.gov/pubmed/18574092 WITHOUT PERMISSION
Vitamin D is found in a few naturally-occurring foods, but some food products (e.g. milk, cereals, margarine, orange juice) have vitamin D added to them.
For most individuals, the predominant source of vitamin D is cholecalciferol (vitamin D3), synthesised in the skin from cholesterol through a chemical reaction that is dependent on sunlight (UVB radiation) exposure.Vitamin D synthesis from sunlight is greatly influenced by season, time of day, latitude, altitude, air pollution, skin pigmentation, sunscreen use, glass and plastic filters, and aging. Whole body exposure of mid-day sun in summer for 10–15 minutes is comparable to taking 15 000 IU of vitamin D3 orally.
Vitamin D levels should be maintained above 80 nmol/L. The nutrient reference values (NRVs) for Australia and New Zealand are 200 IU (5 μg) a day for infants, children and adults below 50, 400 IU (10 μg) for those aged 50–70, and 600 IU (15 μg) for those over 70. The US Institute of Medicine’s recommended daily allowance (RDA) for vitamin D is 600 IU. However, many experts contend that these amounts are far too low, and some even recommend as much as a 10-fold increase.
Vitamin D insufficiencies are estimated to affect over one billion people worldwide. Insufficient vitamin D impairs bone metabolism and causes inadequate bone mineralisation, leading to osteomalacia (referred to as Rickets when present in children) and increased risk of fracture. For individuals with low vitamin D levels, vitamin D3supplementation may be required. Notably, daily supplementation of 700 IU or greater has been shown to significantly reduce the risk of falls in the elderly and subsequent fracture rates.
|Table 6.5Food sources of vitamin D|
|Portobello and crimini mushrooms
Dairy (e.g. milk, butter)
Vitamin E refers to a group of fat-soluble antioxidant compounds that are found in naturally-occurring foods (Table 6.6). Vitamin E helps stop the production of reactive oxygen species when fat undergoes oxidation and aids immune function via regulation of gene expression and cell proliferation.
Vitamin E deficiency is rare. Those at risk include individuals with Crohn’s disease or cystic fibrosis. Symptoms of deficiency include peripheral neuropathy, ataxia, skeletal myopathy, retinopathy, and impaired immune response. Notably,
High dose (≥400 IU/day) vitamin E supplements may increase all-cause mortality and should generally be avoided.
|Table 6.6Food sources of vitamin E|
Vitamin K refers to a group of fat-soluble compounds that are essential for protein synthesis, blood coagulation and bone metabolism. These compounds include:
- phylloquinone (vitamin K1)
- menaquinones (vitamin K2)
Vitamin K1is found primarily in green leafy vegetables and is the main dietary form of vitamin K. Vitamin K2, which is predominantly of intestinal bacterial origin is present in small amounts in various animal-based and fermented foods. VitaminK1serves as a cofactor in the clotting cascade, helping to maintain blood homeostasis. Vitamin K2is involved in calcium transport, preventing calcium deposition in the lining of arterial walls, and helps maintain the normal structure of bone.
It is postulated that phylloquinone can be converted to menaquinones in humans – a process which has been found to occur in chimeric studies– and it has been shown that menaquinonescan be produced for nutritional requirements by human intestinal microflora.
Vitamin K deficiency is rare. Newborns are at increased risk, as well as alcoholics and those with inflammatory bowel disease or cystic fibrosis. Deficiency results in coagulopathy, and common presenting symptoms include lethargy, easy bruising, nosebleeds and bleeding gums.
|Table 6.7Food sources of vitamin K|
|Vitamin K1 – collards, spinach, kale, broccoli, soybeans, pumpkin, pine nuts, kiwi fruit, blueberries
Vitamin K2 – natto, sauerkraut. hard cheeses, , egg yolk, butter, chicken, beef, bacon
B vitamins are a class of water-soluble vitamins that play essential roles in cell metabolism. It is beyond the scope of this chapter to explore each of the eight B vitamins in depth. Rather, we will discuss the clinical relevance of several important B vitamins.
Vitamin B1 (Thiamine) [D]
Thiamine along with necessary coenzymes serves as a catalyst in the conversion of pyruvate to acetyl coenzyme A (CoA). It is involved in many cellular metabolic activities, including the tricarboxylic acid cycle and participates in nerve impulse propagation. Thiamine deficiency causes beriberi and Wernicke-Korsakoff syndrome.
Thiamine is primarily found in foods such as yeast, legumes, pork, brown rice, and cereals made from whole grains. Thiamine is very low in white “polished” rice or milled white cereals including wheat flour. Cooking, baking, canning of some foods and pasteurization can destroy thiamine which is denatured at high pH and high temperatures. Milk products, fruits, and vegetables are poor sources of thiamine. Thiamine deficiency is most commonly reported in populations in which the diet consists mainly of polished rice or milled white cereals.
Thiamine’s biologic half-life is approximately 10 to 20 days and continuous intake is required. Thiamine deficiency may cause either Beriberi or Wernicke-Korsakoff syndrome. Beriberi may occur in infants, mainly in those whose are breastfed by women with a thiamine-deficient diet. Clinical features may include cardiomegaly, tachycardia, cyanosis, dyspnoea, and vomiting. Neurological symptoms may be seen in older infants. Beriberi in adults has two clinical phenotypes, classically described as “dry” or “wet.” Dry beriberi is characterised by a symmetrical peripheral neuropathy with both sensory and motor impairments. Wet beriberi includes signs of cardiac involvement with cardiomegaly, cardiomyopathy, heart failure, peripheral oedema, and tachycardia. Adult beriberi is treated with thiamine replacement.
Wernicke-Korsakoff syndrome refers to two different syndromes representing a spectrum of neurological signs and symptoms. Wernicke’s encephalopathy is an acute syndrome that without urgent treatment may result in death or neurologic morbidity. Korsakoff syndrome is a chronic neurologic condition that may result from Wernicke’s encephalopathy, characterised by short term memory impairment and confabulation. Wernicke’s encephalopathy classically occurs in alcoholics however it is increasingly being seen following weight loss surgery. Wernicke’s encephalopathy is treated with large dose thiamine supplementation. Administration of dextrose to alcoholic patients is often delayed until after thiamine supplementation due to fears of precipitating Wernicke’s encephalopathy. Thiamine toxicity has not been described, likely due to rapid renal clearance and lack of storage mechanisms.
Vitamin B3 (Niacin) [D]
Vitamin B3 is composed of nicotinic acid and nicotinamide, and plays an important role in energy transfer reactions in the metabolism of glucose, fat and alcohol. In other words, vitamin B3 is required to help turn food into energy. Excessive vitamin B3 from foods is not known to cause toxicity, however excessive supplemental Vitamin B3 has been associated with serious multisystem organ failure and fulminant hepatic failure.
Vitamin B3 deficiency, and/or deficiency of its precursor tryptophan (an essential amino acid), leads to pellagra, which is characterised by dermatitis, dementia, and diarrhoea.
Vitamin B9 (Folate) [D]
Vitamin B9 or as it is more commonly known folate or folic acid, acts as a coenzyme or co-substrate in the synthesis of DNA and RNA, and in the metabolism of amino acids. It is essential for the production and maintenance of new cells and is particularly important during periods of cell division and growth (e.g. pregnancy).
Folate and folic acid are often used interchangeably when referring to vitamin B9. Folate is the bioavailable, natural form of Vitamin B9 that is found in food, while folic acid is the synthetic form, primarily found in supplements and fortified food (e.g. bread, cereal, pasta).
Folic acid is substantially more bioavailable compared to naturally occurring food folates at equivalent intake levels
As folate deficiency impairs nucleic acid synthesis and cell division, haematopoietic and cancer cells are particularly affected due to their greater frequency of cell division. Limited cell division leads to impaired production of erythrocytes, which results in megaloblastic anaemia (seen in conditions such as inflammatory bowel disease, coeliac disease and other malabsorption disorders).
Individuals with alcohol dependence are at high risk of deficiency, as chronic alcohol consumption impairs folate absorption and these individuals are also likely to have poor quality diets that do not provide adequate amounts of folate. Importantly, folate deficiency during pregnancy leads to neural tube defects in the foetus, and so supplementation, which has shown to be preventive, is widely encouraged.
Vitamin B12 (Cobalamins) [D]
Vitamin B12 is a water-soluble vitamin that functions as a co-factor in DNA synthesis, fatty acid and amino acid metabolism, myelin formation and maturation of erythrocytes. Vitamin B12 from ingested protein is cleaved from the amino acids through the action of digestive proteases in the stomach and small intestine. It is then bound to intrinsic factor, produced by gastric parietal cells, and absorbed in the terminal ileum. Given that absorption of vitamin B12 is dependent on intrinsic factor, conditions which decrease the secretion of intrinsic factor (e.g. pernicious anaemia, atrophic gastritis) or interrupt cleavage of the binding proteins (e.g. pancreatic insufficiency) can result in malabsorption and subsequent anaemia.
Vitamin B12 is not made by plants or animals, but by certain microbes, such as resident gut bacteria in ruminants. Animals store the vitamin in their livers and muscle tissue, and some pass the vitamin into their eggs and milk. Although most individuals obtain adequate dietary vitamin B12 by eating animal products, the vitamin can also be found in fortified foods and obtained through supplementation.
Individuals who eat a predominantly plant-based diet (e.g. vegetarians or vegans) are at high risk for deficiency, and so supplementation is critical for those who are not obtaining adequate amounts from fortified foods.
Although vitamin B12 deficiency can take years to develop, it can have severe consequences including paralysis, psychosis, blindness and death. Deficiency characteristically leads to megaloblastic anaemia, fatigue, weakness, constipation, weight loss and potentially irreversible nerve damage. Proton pump inhibitor (PPI) medication has been associated with an increased risk of vitamin B12 deficiency, as well impairing vitamin C, calcium, iron and magnesium metabolism.
When megaloblastic anaemia is detected, it is crucial to first rule out vitamin B12 deficiency before initiation of folic acid therapy, as folic acid may aggravate neurologic manifestations of underlying vitamin B12 deficiency. In severe megaloblastic anaemia, where therapy must be initiated immediately, concomitant folic acid and vitamin B12 should be given.
|Table 6.8Food sources of B vitamins|
|Vitamin B3– turkey, chicken breast, liver, tuna, peanuts, mushrooms, , green peas, sunflower seeds, avocado
Vitamin B9– dark leafy greens, liver, Brussels sprouts, asparagus, broccoli, citrus fruits, beans, peas, lentils, avocado, seeds and nuts
Vitamin B12 – liver, sardines, lamb, salmon, eggs, milk, cheese, nutritional yeast
Vitamin C, or ascorbic acid, is an essential water-soluble vitamin that functions as a co-factor in the synthesis of collagen, carnitine and some neurotransmitters. It is a naturally occurring micronutrient that is a potent antioxidant and must be consumed for survival.
Vitamin C deficiency leads to scurvy, which is characterised by lethargy, gum disease, painful limbs, bleeding from the skin and poor wound healing. More than 250 years since James Lind showed that citrus fruit were a cure for scurvy when testing his hypothesis on sailors in a prospective controlled therapeutic trial, the disease is now most commonly found in individuals with mental health disorders and alcohol dependence.
Vitamin C for the prevention and treatment of the common cold has been the subject of much controversy in previous years. Vitamin C supplementation does not reduce the incidence of the common cold in the general population but may be beneficial for individuals undergoing intense physical activity. Supplementation may reduce the duration of the common cold, however further research is needed.
Vitamin C can help improve absorption of non-haeme iron, which is present in plant-based foods. However, its influence on absorption may be less substantial in meals of high iron availability, such as those containing haeme iron found in meat or fish.
|Table 6.9Food sources of vitamin C|
Red capsicum (pepper)
The word ‘mineral’ is in fact a misnomer, as dietary minerals are chemical elements required to carry out metabolic functions necessary for life. Like vitamins, they cannot be synthesised by humans and are essential nutrients that must be ingested. Some function as electrolytes, while others plays a role in biological processes such as hormone synthesis, antioxidant activity, cell signalling, and energy production.
The majority of chemical elements that are ingested by organisms are in the form of simple compounds. Plants absorb elements found in soil, which are subsequently ingested by animals that eat the plants, and again by animals who eat other animals (as well as plants). Minerals may also be obtained from the water we drink, which, like plants, vary based on location. The major (macro) minerals in humans are calcium, chloride, magnesium, phosphate, potassium, sodium and sulphur. The remaining elements found in humans are known as ‘trace elements’, all of which can be classified based on their estimated adult daily requirements (Table 6.10).
Table 6.10 Categories of minerals
|Macro minerals (>100mg/day)||Trace elements (1-100mg/day)|
As a major structural constituent of bones, calcium is the most abundant mineral found in the human body. Calcium concentration in blood and extracellular fluid must be tightly controlled to enable normal physiological function, so much so that the body will stimulate bone resorption when calcium intake is inadequate. Increased secretion of parathyroid hormone will also stimulate bone resorption. In addition to helping maintain a healthy skeleton, calcium plays an important role in mediating vasoconstriction and vasodilation, nerve impulse transmission, muscle contraction, coagulation and secretion of hormones.
Serum calcium levels are strictly regulated and do not necessarily reflect the calcium stores in bone.
Although dairy may be the first thing that comes to mind when thinking about calcium, the mineral can be found in a variety of foods (Table 6.11), such as dark green leafy vegetables, legumes, nuts and seeds. Calcium is mostly absorbed in the jejunum and its absorption is favoured by a low pH. Cow’s milk is the best-absorbed source of calcium, while other foods show high concentrations but varied bioavailability due to the actions of phytic acid and oxalates.
Importantly, vitamin D increases calcium absorption in the intestine(190), and helps maintain serum calcium and phosphate concentrations to enable normal bone mineralisation (along with vitamin K2).
Both hyper- and hypocalcaemia can have serious consequences. The most common cause of hypocalcaemia likely to seen by clinicians is vitamin D deficiency, although it may also be seen in people with reduced parathyroid hormone function or malabsorption disorders. Classic symptoms of hypocalcaemia are muscle twitching, spasms, paraesthesia and anaesthesia – and in severe cases, tetany, seizures and cardiac arrhythmias. Hypercalcaemia, on the other hand, can lead to agitation, bone and/or abdominal pain, gastrointestinal disturbances, kidney stones, and neurological dysfunction.
Calcium (alongside vitamin D) is routinely supplemented to mitigate the risk of developing or slow the progression of osteoporosis, and for the subsequent prevention of fractures. However, a 2015 meta-analysis found that calcium supplements have small, inconsistent benefits of fracture prevention and that dietary calcium intake is not associated with risk of fracture. In fact, in a cohort study that examined milk consumption in over 100 000 people for over 20 years, high milk intake was associated with higher mortality in men and women, and with higher fracture incidence in women. Of course, observational study designs make it difficult to control for confounding factors, yet it raises the question whether we should look at other methods or dietary sources for reducing risk of fractures.
Furthermore, isolated calcium supplementation may be associated with increased risk of cardiovascular events, as it may increase the risk of coronary artery calcification.
|Table 6.11Food sources of calcium|
Magnesium is a co-factor in over 300 enzymatic reactions, involved in physiological pathways that are responsible for nucleic acid and protein synthesis, ion transport, cell signalling and energy production among other processes(196). Notably, magnesium is thought to play a role in insulin secretion, owing to the altered insulin secretion and sensitivity observed in magnesium-deficient animals.
Magnesium is part of chlorophyll (the green pigment in plants), and so most green leafy vegetables are rich in magnesium. Other food sources are listed in Table 6.12.
Magnesium deficiency is common in the Western world due to poor diet and soil depletion. Modern agricultural methods have depleted soil of many nutrients, resulting in lower micronutrient content in the food we eat. Deficiency may impair vitamin D and calcium homeostasis, raise blood pressure and reduce insulin sensitivity. Chronic latent magnesium deficiency has been associated with atherosclerosis, myocardial infarction, malignant tumours, kidney stones, premenstrual syndrome and psychiatric disorders.
Supplementation is being explored in the management of hypertension, cardiovascular disease, type 2 diabetes, migraines and asthma. As magnesium plays a role in neuromuscular transmission and muscle cramps, it is hypothesised that deficiency may predispose to muscle cramps, however magnesium does not appear to be effective in the treatment of nocturnal leg cramps. For women experiencing ‘pregnancy-associated rest cramps’, the literature is conflicting and further research in this patient population is needed.
|Table 6.12Food sources of magnesium|
Most people recognise potassium as an electrolyte that can be obtained from bananas (which surprisingly are not particularly rich in potassium relative to other foods (Table 6.13)). The term ‘electrolyte’ refers to a substance that dissociates into ions in solution, making it capable of conducting electricity. Potassium is the principal cation in intracellular fluid, while sodium is the principal cation in extracellular fluid. The concentration differences between potassium and sodium across cell membranes give rise to a membrane potential.
Potassium is required for the activation of sodium/potassium-ATPase and for the activity of pyruvate kinase, which is essential for carbohydrate metabolism. Evidence is also accumulating of the protective effect of dietary potassium on age-related bone loss and reduction of kidney stones.
Modern Western diets have led to a decrease in potassium intake due to reduced consumption of fruits and vegetables, with a concomitant increased consumption of processed foods. Acute potassium deficiency, which may present with fatigue, muscle cramps and/or intestinal paralysis, is most commonly seen with prolonged vomiting, diuretic use, and kidney disease.
Some international organisations discourage the use of potassium supplements or potassium-rich salt replacers due to the risk of hyperkalaemia, particularly for people with kidney disease. However, recent data suggests a moderate increase in potassium intake using supplements could be safe and void of risk of hazardous hyperkalaemia or renal deterioration in people with normal kidney function.
Large doses of potassium, consumed in supplemental forms that can be rapidly absorbed, can pose a risk for hyperkalaemia and subsequent cardiac arrhythmias.
Magnesium deficiency can exacerbate potassium deficiency and aggravate the adverse effects of hypokalaemia(208). Recognition of concomitant magnesium deficiency and early treatment with magnesium are crucial for prevention and treatment of complications of hypokalaemia.
|Table 6.13Food sources of potassium|
Sweet potato, white potato and squash
Sodium and chloride are the major electrolytes present in extracellular fluid. They work in tandem to control extracellular volume and blood pressure. Various mechanisms (e.g. renin-angiotensin-aldosterone system) act on the kidneys to ensure that the amount of sodium lost via renal excretion compensates for the amount of sodium consumed to maintain homeostasis.
For decades, policy makers, organisations and clinicians have advised people to limit sodium consumption to reduce blood pressure and subsequent risk of cardiovascular events. However, proposed benefits of dietary sodium restriction are generally based on extrapolation from anticipated reductions in blood pressure in concert with other epidemiological data. Some observational studiesand a meta-analysishave actually reported an increase in cardiovascular disease and mortality among those who consume the lowest levels of sodium, suggestinga U or J-shaped curve of sodium and health outcomes.
One large study found increased levels of all-cause mortality with daily urinary sodium excretions less than 3,000mg or greater than 6,000mg (O’Donnell 2014). This is inconsistent with current Australian Dietary Guidelines which recommend a population target (suggested dietary target -SDT) of 2000mg of sodium daily, with the stated goal of reducing the average blood pressure of Australian adults by 2mmHg. Interestingly however, the recommended upper limit of sodium intake for individuals has been removed given an inability to identify a threshold level of sodium intake, below which represents reduced risk. These contradictory targets within the same dietary guideline are no doubt a source of confusion for those seeking guidance.
Substantially lowering or restricting salt intake has not shown much benefit in clinical trials. Arguably, the majority of individuals would benefit more from a consuming a diet that consists of unprocessed foods than they would from micromanaging their salt intake.
Iodine is essential for the normal function of the thyroid gland. Iodine binds to tyrosine within the thyroid gland to form monoiodothyronine (MIT), diiodothyronine (DIT), triiodothyronine (T3), and thyroxine (T4). These thyroid hormones regulate the metabolic pattern of most cells and play a vital role in early growth and development of most organs (especially the brain).
Widespread food supply supplementation with iodine (e.g. table salt) has seen significant reduction of iodine deficiency in industrialised countries. However, deficiency still remains a major public health problem in developing countries (and some developed countries) due to poor diet and use of non-iodised salt. Iodine deficiency classically presents as an enlargement of the thyroid gland, known as a goitre, and can lead to hypothyroidism as well as stunting of physical growth and brain development in infants. Populations at particular risk of deficiency include pregnant women, lactating mothers, and young infants(214).
Supplementation of high doses of iodine in otherwise healthy people generally does not offer any benefits, as iodine is readily excreted and normalised by the body.
|Table 6.14Food sources of iodine|
|Seaweed (and other sea vegetables)
Iron is an essential structural and functional component of a multitude of proteins and enzymes that support essential biological processes such as oxygen transport, energy production, and DNA synthesis. Although Iron is essential, it can be harmful to cells because intracellular free iron can lead to the generation of free radicals which cause oxidative stress, and so concentrations must be tightly regulated. Hepcidin, a peptide hormone primarily synthesised by hepatocytes, is the primary regulator of systemic iron homeostasis and can be a helpful measure fordiagnosing iron-refractory iron deficiency anaemia.
Dietary iron is present in two main forms: haeme and non-haeme iron. Haeme iron is found in meat, poultry, and fish, and is well-absorbed. Non-haeme iron is found in vegetables and fruit (Table 6.15), as well as iron-fortified food products. Absorption and bioavailability of non-haeme iron is inferior to that of haeme, but can be improved with concurrent ingestion of vitamin C. The poor bioavailability of plant-based sources of iron is thought to be due to the presence of phytate, which chelates iron and prevents its absorption. Tannins present in tea and coffee can also impair absorption acutely, and so it may be recommended to drink tea or coffee between meals, rather than during.
Iron deficiency is the single most prevalent nutritional deficiency worldwide. Insufficient iron intake or uptake, and iron loss through prolonged bleeding can cause iron deficiency anaemia, characterised by symptoms of fatigue, shortness of breath, dizziness, agitation, brittle nails and hair loss. Iron deficiency, or at least iron depletion,is common in women of all ages, particularly in pregnant women and in those who are menstruating. Iron deficiency anaemia in womenis defined as a haemoglobin level of less than 120g/L. Iron depletion is indicated by a normal haemoglobin level (>120 g/L) but serum ferritin level (an indicator of iron stores) of less than 30 μg/ml.
In cases of deficiency, increased oral intake, supplementation and/or transfusion may be required. Other than in deficiency states, iron supplementation is not generally recommended as it can instead lead to iron poisoning.
An increased requirement for iron is seen in pregnancy, lactation and heavy menstruations, as well as in those who donate blood, perform strenuous exercise or follow a vegetarian or vegan diet.
|Table 6.15 Food sources of iron|
|Haeme iron – liver, grass-fed beef, sardines, turkey
Non-haeme iron – spirulina, lentils, tofu, beans, dark chocolate, spinach, pistachios, raisins, quinoa
Zinc is an essential mineral that plays important roles in catalysing enzymatic reactions, providing structural support for proteins and cell membranes, and regulating gene expression. It is a key element that is required for growth and development, immunity, neurological function, and reproduction.
Meat such as lamb, beef and chicken is rich in zinc, as are some nuts and legumes (Table 6.16). Zinc can also be found fortified in food products, such as breakfast cereals and bread.
Mild dietary zinc deficiency has been shown to impair growth velocity, while severe deficiency has been found to cause growth retardation(219). Other clinical manifestations of zinc deficiency include delayed sexual maturation, impotence, hypogonadism, oligospermia, alopecia, impaired taste, immune dysfunction, night blindness and impaired wound healing. In addition to malnutrition, causes of deficiency include alcoholism, pregnancy, prolonged parenteral nutrition, malabsorption disorders, and extensive burns.
Zinc is lost through sweat, and so supplementation may be important for athletes who do not obtain adequate amounts of zinc through diet alone.
Notably, taking large quantities of zinc over a period of weeks can interfere with copper bioavailability and cause copper deficiency.
|Table 6.16Food sources of zinc|