Chapter 9 - Minerals.docx

Chapter 9: Minerals Minerals are solid, naturally occurring, inorganic substances. They are found throughout nature, often bound to other minerals or substances, such as in rocks. The human body requires certain minerals to sustain life. While they do not provide energy, minerals are essential struc...

Chapter 9: Minerals Minerals are solid, naturally occurring, inorganic substances. They are found throughout nature, often bound to other minerals or substances, such as in rocks. The human body requires certain minerals to sustain life. While they do not provide energy, minerals are essential structural and functional nutrients. Accordingly, mineral deficiencies are asso- ciated with a range of complications. By the end of this chapter, you will be able to: List factors that affect mineral bioavailability. Outline the functions, sources and symptoms of deficiency and toxicity for each mineral. Explain how minerals are involved in bone health and the body’s electrical activity. Outline health-related considerations with respect to certain minerals. The periodic table shown in Figure 9.1 highlights the various elements necessary for human life. Carbon, oxygen, hydrogen and nitrogen are sometimes called the basic organic elements because they are found within the molecules that make up living things, such as carbohydrates, lipids and proteins. Conversely, minerals are elements that form solid compounds and are not bound to carbon. They are therefore inorganic (Box 9.1). Minerals are further classified based on how much of that mineral is required from the diet. Major minerals are those required in higher amounts, while minor minerals, also known as trace minerals, are needed in smaller amounts. Major minerals make up about 3% of the body’s weight and include calcium, phosphorus, potassium, sodium, chloride, sulfur and magnesium. Trace minerals make up about 0.15% of the body’s weight. They include iron, copper, zinc, molybdenum, manganese and selenium. Minerals typi- cally occur alone or bound to other inorganic elements. Box 9.1: An Indigenous Lens: Are minerals living things? Western science defines organic matter as that which contains carbon and comes from living things. Minerals do not contain carbon, which according to a Western science lens, makes them non-living, inorganic things. However, the use of an Indigenous lens may lead to a different conclusion. Wab Kinew, on Ojibway broadcaster and member of Manitoba’s legislative assembly, offers the following perspective: …the Indigenous world view thinks much more in terms of [things] being alive…If you talk about a rock in English, you are thinking about it being something static, something fixed…but in Ojibway, when you’re talking about asin or asiniig, you’re talking about something that is alive, something that has a spirit, some- thing that is in motion. And if you can start to conceive of things around you in a different way, I think it’s going to open up your worldview…such that you are going to be able to think about things in many different ways, in a plurality of fashions. And I think that benefits you because it helps you think laterally on occasion, while also thinking linearly. And if you could cultivate both of those…you can drive innovation, you can think of differ- ent ways to solve the problem, you can think of ways to think outside the box (Kinew, 2018). A Western science lens, like that used in this textbook, offers one way to see and engage with our world, but it is not the only perspective of value. An Indigenous view might offer a different understanding of how minerals and other nutrients fit into our food systems and lives, as well as the reciprocal relationship we might have with them. Using two- eyed seeing may accordingly provide a more holistic understanding of the natural world. The bioavailability of a mineral refers to its availability in food as well as its propensity to be absorbed and available for use within the body. Both plants and animals are a source of minerals. The quantity and diversity of min- erals found in plants depends on the mineral composition of the soil in which they are grown. The mineral content of animal products depends on what the animal consumes. The more an animal eats, the more concentrated in minerals they become. Taken together, animal products, especially larger animal products, are a better source of minerals than plant products. Plants are also more likely to contain substances that negatively impact mineral bioavailability. Plant compounds, such as phytates, oxalates, tannins and glucosinolates, can negatively affect mineral absorption (Figure 9.2). These substances are sometimes referred to as anti-nutrients because their presence in foods reduces the amount of minerals absorbed. Figure 9.2: Compounds that compromise mineral biovailability Phytates are found in plant seeds and are abundant in nuts, legumes and grains. Plant foods can vary a lot in their phytate composition, with nuts and beans tending to contain especially high amounts (Schlemmer et al., 2009). Phytates impair iron and zinc absorption (Lopez et al., 2002). They also negatively affect calcium absorption, but to a lesser extent. Phytate levels can sometimes be reduced by soaking certain foods overnight (e.g., when preparing beans), or fermenting them (e.g., when making sourdough for bread) (Leenhardt et al., 2005). Oxalates are found in leafy green vegetables, nuts and seeds. Oxalates bind to minerals, forming compounds that cannot be absorbed. Specifically, oxalates decrease calcium and iron bioavailability (Heaney & Weaver, 1989). Boiling foods high in oxalates can significantly reduce their oxalate content (Chai & Liebman, 2005). Tannins are found in tea, coffee, red wine and legumes. Tannins interfere with iron absorption. Those prone to iron-deficiency are advised to avoid consuming tannin-rich foods and beverages with meals that contain iron. Interestingly, tannins have also been studied for a wide range of disease-re- ducing effects. Specifically, they have been shown to have anti-cancer, antioxidant, antimicrobial and anti-inflammatory properties (Chung et al., 1998). Glucosinolates are found in cruciferous vegetables such as broccoli, Brussels sprouts and cabbage. They compromise iodine absorption. Many minerals achieve their functions because they act as cofactors. Cofactors are inorganic metals that bind to enzymes, often activating them and thus improving the rate of reaction (Figure 9.3). Recall that enzymes are typically made from protein. However, these proteins may require an inorganic (cofactor) or organic (coenzyme) substance in their structure to become active. In other words, cofactors and coenzymes are needed to help enzymes do their work. That is one of the main reasons we require minerals and vitamins from our diet: to facilitate the enzymatic processes necessary for life. Figure 9.3: Mineral cofactors. Our daily mineral needs depend on our age and life stage. For instance, younger individuals often have a lower RDA/AI for the various minerals, while pregnancy and lactation typically increase mineral needs. In this chapter, we will list either the RDA or AI as well as the UL for each mineral based on the 18-50 year old age range. If there is a different recommendation for males and females, this will also be noted. If the mineral does not have a UL, there will be no UL listed. A more detailed breakdown of the recommendations for other age groups and life stages can be found at https:// ods.od.nih.gov/Health_Information/Dietary_Reference_Intakes.aspx. Calcium is the most abundant mineral in the human body, accounting for approximately 1.5% of the body’s weight. It is essential to the structure and function of our bodies. For instance, calcium is a key signalling molecule; it helps send nerve signals and is an important messenger within cells. It is also needed for muscle and heart contraction and for secreting substances from glands. Because it is so important, the body stores a lot of calcium. Indeed 99% of the body’s calcium is stored within the bones and teeth (Institute of Medicine, 2011). This, in turn, promotes their structure and stability. A constant dietary supply of calcium is needed, otherwise it will be taken from bones, negatively affecting bone density and health. Calcium has been studied for its effects on various chronic conditions. Studying this relationship is challenging, however, because it is difficult to separate the effects of calcium from those of dairy products, its main dietary source. With that in mind, a systematic review found that calcium supplementation may help moderately reduce the risk of col- orectal cancer (Weingarten et al., 2008). However, the quality of evidence was not high enough to suggest recommend- ing calcium supplementation to reduce cancer risk. Calcium supplementation has also been suggested for decreasing the risk of cardiovascular disease (CVD) and obesity. However, systematic reviews of randomized control trials have not supported these associations (Chen et al., 2012; Chung et al., 2016). Maintaining appropriate levels of calcium in the blood is of utmost importance. When calcium levels are too low, body processes that require calcium are compromised. Conversely, when blood calcium is too high, it can deposit in tissues, hardening and damaging them. When calcium levels drop, parathyroid hormone (PTH) is released. PTH restores calcium levels through three mechanisms (Figure 9.4). First, PTH promotes calcium release from bones by activating bone breaking cells called osteo- clasts. Second, PTH decreases calcium excretion at the kidneys, so more is kept within the blood and less is lost in urine. Third, PTH promotes the activation of vitamin D at the kidneys. Vitamin D then promotes calcium absorption at the small intestine. Conversely, when blood calcium is high, the hormone calcitonin is released. Calcitonin opposes the actions of PTH leading to a decrease in blood calcium. Indeed, calcitonin impairs osteoclast activity in bone, leading to less being released into blood. Further, it promotes calcium excretion at the kidneys and a decrease in calcium absorption at the small intestines. Figure 9.4: Parathyroid hormone maintains adequate blood calcium levels. The main sources of calcium are dairy prod- ucts (Figure 9.5). It can also be found in eggs, canned fish with bones, fortified milk alternatives and leafy green vegetables. Figure 9.5: Sources of calcium. Minor fluctuations in calcium are normal and parathyroid and vitamin D help maintain blood calcium at adequate levels. However, if we are consistently at a calcium deficit, our ability to achieve peak bone mass decreases, and our risk of osteoporosis increases. Peak bone mass is typically achieved within our 20s, after which it decreases over time (Figure 9.6). A systematic review and position statement from the American National Osteoporosis Foundation found that life- style factors, such as calcium intake and physical activity levels, are strongly associated with achieving a higher peak bone mass (Weaver et al., 2016). They also found good evidence to support the role of vitamin D and dairy consumption in achieving this higher bone density. Achieving a higher peak bone mass and maintaining bone density throughout life are key to reducing our risk of osteoporosis. Figure 9.6: Bone mass decreases after peak bone mass is achieved. Osteoporosis (Figure 9.7) is a lack of bone mineralization and density and is the main cause of bone fractures in older adults. It is caused by an imbalance in bone remodelling favouring the breakdown of bone by osteoclasts. Peak bone mass influences risk for osteoporosis, as do factors that negatively effect bone mineralization. Women are at higher risk for osteoporosis since their peak bone mass is not as high as males Also, hormonal changes around menopause further promote decreases in bone density, further increasing risk for osteoporosis. Low calcium and vitamin D intake are the two most critical nutritional factors that increase risk of both osteoporosis and bone fractures (Abrahamsen et al., 2014). Other modifiable risk factors include physical inactivity, smoking, alcohol consumption and a lower body weight. Non-modifiable risk factors include female gender, age and family history. In addition to its affects on bones, severe calci- um deficiency can lead to numbness, muscle spasms, seizures and confusion. Figure 9.7: Progression towards osteoporosis. Minor increases in blood calcium often present no symptoms. However, chronically elevated levels or a quick increase in calcium levels may be evidenced by abdominal pain, bone pain and mental confusion. Consistently high levels of calcium can be fatal as they can lead to the calcification, or hardening, of the tissues. In the heart this can lead to car- diac arrest. Luckily, high dietary calcium intake rarely leads to these conditions. Calcification of the tissues is typically due to other conditions such as an overactive parathyroid gland or cancer. Phosphorus is the second most abundant dietary mineral in the human body and has both structural and func- tional roles (Figure 9.8). Phosphorus is found within hydroxyapatite – a crystal that contains both calcium and phospho- rus. This crystal mineralizes bones and teeth, hardening them and promoting their strong structure. Phosphorus is also a critical component of all cells, as it is needed to form the phospholipids that make up the cell membrane. It is also part of the key physiological molecule ATP (adenosine triphosphate) as well as DNA and RNA, which have a sugar-phosphate backbone. Figure 9.8: Functions of phosphorus. Figure 9.9: Sources of phosphorus. Phosphorus is abundant in animal products such as salmon, cheese, milk, eggs and beef (Figure 9.9). Plant sources include boiled lentils, cashews, potatoes, kidney beans, rice and oatmeal. Since phosphorus is abundant in many foods, dietary deficiency is rare; it typically occurs with severe malnutri- tion. Phosphorus deficiency can increase the risk for osteoporosis, seizures and coma. Symptoms of deficiency include anorexia, muscle weakness, anemia and an increased risk of infection (Harnack et al., 2017). Phosphorus toxicity is rare in healthy individuals. High levels can lead to the hardening of the tissues. Sodium, potassium and chloride are collectively known as the electrolytes, meaning they are involved in the body’s electrical activity (Figure 9.10). Calcium and magnesium are also electrolytes, though this is not their main func- tion. In water, the electrolytes become ions – atoms that carry a positive or negative charge. Their movement therefore leads to the creation of an electrical current, which facilitates the electrical activity and function of our nerves, heart and muscles. Figure 9.10: Electrolytes are responsible for the body’s electrical activity. Sodium’s main function in the body is as an electrolyte. It is the primary cation (positively charged ion) found in the extracellular space. The movement of sodium into a cell is part of what leads to the transmission of an electrical signal. Sodium also plays an important role in regulating fluid balance in the body. Water moves across a semi-permeable membrane to equal out concen- tration differences. For example, if there is a lot of sodium on one side of a membrane compared to the other side, water will move towards that so- dium to even out this difference in concentration (Figure 9.11). Without this fluid balance, water can build up in a tissue, causing it to swell. Sodium is found naturally in many foods and is also added during food processing (Figure 9.12). Almost three quarters of the sodium we consume comes from the sodium added to processed foods (Harnack et al., 2017). Smoked, cured and salted animal products, as well as canned entrees, salted nuts and many prepackaged foods are all high in sodium. Table salt, or simply salt, is sodium chloride (NaCl). The salt we add to our food at the dinner table contributes only about 5% to our sodium intake. Figure 9.12: Proportion of sodium intake from different sources. Sodium deficiency is called hyponatremia, which typically arises due to excessive vomiting, sweating or diarrhea – situations in which the body loses a large number of electrolytes, including sodium. Symptoms of hyponatremia include nausea, vomiting, irritability, fatigue, loss of appetite, confusion, muscle weakness and spasm. In more extreme cases, it can lead to loss of consciousness and coma. High blood sodium is typically caused by the excessive loss of body water, which concentrates the amount of sodium in the blood. It is more common in elderly people, who might have an impaired thirst sensation, restricted access to water or disease conditions that promote water loss. Mild cases result in thirst, weakness, nausea and loss of appetite. At higher and chronic levels, sodium toxicity can lead to confusion, muscle twitching and brain hemorrhages. People who regularly consume high levels of sodium may also be at higher risk for hypertension, or high blood pressure. The exact cause of hypertension is not fully understood, but sodium reduction may help manage the condition (Box 9.2). Box 9.2: Hypertension, sodium and the DASH diet. Our blood must be pressurized to have enough force to transport itself. An ideal blood pressure is 120/80 mmHg. At values significantly lower than this, there is a higher risk for feeling lightheaded or faint- ing. The real risk, however, is when blood pressure is chronically elevated – especially above values of 140/90 mmHg, which are considered hypertensive. Hypertension is a main risk factor for CVD since it in- creases the risk for heart attacks and strokes. The causes of hypertension are not fully clear. Some people are otherwise healthy but still develop high blood pressure. However, certain factors, such as older age, African heritage, family history as well as chronic conditions like kidney disease and diabetes, are associated with a higher risk. Modifiable risk factors, such as obesity, physical inactivity, stress, alcohol use and tobacco smoke, also increase risk. In addition, diet is believed to play a role. For instance, diets that are high in whole foods, potassium and fibre, moderate in calories and low in sodium are associated with a decreased risk. These are the foundations of the Dietary Approaches to Stop Hypertension (DASH) eating plan, which is recommended to reduce the risk for, as well as in the management of, hypertension. DASH is promoted by the Heart and Stroke Foundation of Canada, as well as by the National Heart, Lung and Blood Institute in the USA (Heat and Stroke Foundation of Canada, n.d.; National Heart, Lung, and Blood Institute, n.d.).The DASH eating plan emphasizes whole foods, particularly fruits, vegetables, whole grains, low-fat dairy, poultry, fish and nuts and is high in fibre, potassium, magnesium, calcium and protein. It is also lower in red meat and sweets compared to a typical American diet, leading to lower total fat, satu- rated fat, cholesterol and sugar intake. The DASH eating plan has been exten- sively studied. Multicentre randomized control trials found that compared to controls who followed a typical American diet, individuals following the DASH eating plan had lower systolic and diastolic blood pressure. They further found that reductions in sodium led to decreases in blood pressure for those consum- ing both the DASH and typical American diets. Those who consumed the lowest amount of sodium reduced their blood pressure most dramatically (Sacks et al., 2001). In addition, those consuming a DASH diet showed a reduc- tion in low-density lipoprotein cholesterol and body weight, other CVD risk factors. Accord- ingly, this eating plan is often recommended for reductions in blood pressure as well as improvements in overall health. Like sodium, the main role of potassium is as an electrolyte (Figure 9.10). In water, potassium also becomes a positively charged ion. While sodium is the main ion found in the extracellular space, potassium is the main ion found in the intracellular space – that is, within the cytoplasm of a cell. Together, potassium and sodium are the two most im- portant ions involved in the body’s electrical activity. Moreover, potassium and sodium also share the role of maintaining fluid balance (Figure 9.11). In addition to their sodium-related findings, the DASH randomized control trials showed that diets higher in po- tassium promoted lower blood pressure (Sacks et al., 2001). Potassium from both dietary and supplemental sources may reduce risk. Indeed, a meta-analysis of 25 randomized control trials found significant reductions in blood pressure with potassium supplementation (Filippini et al., 2017). Accordingly, the government of Canada allows health claims on food labels stating, “A healthy diet containing foods high in potassium and low in sodium may reduce the risk of high blood pressure, a risk factor for stroke and heart disease” (Government of Canada, 2014). Potassium intake has also been stud- ied for its potential to improve bone density and regulate blood glucose. However, more evidence, including randomized control trials, is needed before recommendations can be made (National Institutes of Health, n.d.-b). Figure 9.13: Sources of potassium. Potassium is abundant in many whole foods but is often removed during food process- ing. Dried apricots, lentils, squash, potatoes, kid- ney beans, bananas, dairy products and salmon are all naturally high in potassium (Figure 9.13). Potassium deficiency typically has no obvious symptoms. If individuals do show symptoms, they may feel tired, have weakness or experience cramps. Low blood potassium can further increase the risk of an irregular heart rhythm, promoting a slower heartrate that can lead to cardiac arrest. Clinical potassium deficiency is typically caused by excessive vomiting, diarrhea or certain medications. The kidneys can eliminate extra potassium, so higher intakes do not pose a health risk in healthy individuals. Those with impaired kidney function, who are on certain medications, or who have type 1 diabetes may have limited potassium excretion potential, increasing their risk for toxicity. Symptoms of potassium toxicity are rarely evidenced, but in severe cases it can promote muscle weakness, heart irregularities and paralysis. Though uncommon, those taking potassium supplements may also exhibit mild digestive tract issues. Chloride is another mineral that functions as an electrolyte (Figure 9.10). In water, or when bound to another element, chlorine becomes a negatively charged ion called chloride. Like sodium and potassium, chloride is essential for the body’s electrical activity as well as for maintaining fluid balance. It is also part of hydrochloric acid, which is secreted by the stomach and contributes to protein digestion. Table salt – sodium chloride – is our main dietary source of chloride (Figure 9.14). It can also be found in a va- riety of vegetables including seaweed, tomatoes, lettuce and celery. Since table salt is used to cure meats, these processed animal products are a source of both chloride and sodium. Figure 9.14: Table salt is our main source of chloride. Because salt is so abundant in the North American diet, chloride deficiency is rarely due to low dietary intake. Conversely, respiratory issues, vomiting and kidney malfunction are the main causes of chloride deficiency. Chloride deficiency often shows no symptoms, though in some individuals it can promote weakness, difficulty breathing, diarrhea and vomiting. Chloride toxicity is also typically asymptomatic. Since it can accompany other electrolyte toxicities, similar symp- toms such as tiredness and muscle weakness may occur. Again, this electrolyte imbalance is not typically due to dietary excess, but to irregular fluid balance in the body, which can concentrate chloride. Magnesium is found throughout the body and has a wide range of important roles. Magnesium is a cofactor for more than 600 enzymes, promoting many physiological activities (Bairoch, 2000; de Baaij et al., 2015). It is involved in enzymatic reactions including energy metabolism and protein synthesis. Magnesium also helps DNA and RNA form their three-dimensional structure. Furthermore, it is critical for the health of various organs. It is associated with healthy brain development and maintaining a healthy heart. It also contributes to bone density by supporting the formation of hy- droxyapatite crystals (Salimi et al., 1985). Indeed, approximately half of the body’s magnesium content is stored in bone. Due to its wide-ranging effects, magnesium is a popular dietary supplement. For instance, magnesium may help prevent migraine headaches. Randomized control trials have found modest reduction in migraine occurrence with a 600 mg/day magnesium supplement (Sun-Edelstein & Mauskop, 2009). Accordingly, the Canadian Headache Society lists magnesium supplementation as an evidence-based way to reduce the risk for migraine headaches (Pringsheim et al., 2012). Magnesium supplements have also been touted for their potential to support heart health and manage blood glu- cose levels. Meta-analyses of prospective epidemiological studies support these claims (Del Gobbo et al., 2013; Dong et al., 2011). However, large, well-designed randomized control trials are required to fully understand magnesium’s effects and to support possible recommendations. Magnesium is plentiful in many foods including nuts, spinach, soymilk, black beans, edamame, bananas and avoca- do (Figure 9.15). Figure 9.15: Sources of magnesium. Since the kidneys tightly regulate magnesium levels, dietary magnesium deficiency is rare. However, individu- als with kidney malfunction, chronic alcoholism or who consistently consume low levels of magnesium may experience certain symptoms. Loss of appetite, nausea, vomiting, fatigue and weakness are early signs of magnesium deficiency. Symptoms can progress to more severe ones such as cramping, numbness, tingling, heart irregularities and seizures. The kidneys regulate magnesium levels so that they do not reach toxic states. Accordingly, dietary toxicity is rare in healthy individuals. Excessive magnesium levels due to dietary supplements or medications can lead to gastrointestinal issues such as diarrhea, nausea and abdominal cramping. Magnesium is found in many laxatives and antacids, and high doses from these sources can induce high blood levels of magnesium, which has potentially fatal side effects. Magnesium toxicity can promote low blood pressure, depression, muscle weakness and tiredness. It can progress to heartbeat irreg- ularity, difficulty breathing and heart failure (Musso, 2009). Supplement intake should accordingly be closely monitored. Sulfur is the third most abundant mineral in the human body. It is critical for the synthesis of the amino acids methionine and cysteine, whose side chains contain sulfur atoms. The presence of sulfur in these amino acids is critical to the three-dimensional structure of proteins, as bonds between sulfur groups help the amino acid chain fold into a functional protein. Sulfur is also needed for the formation of the enzyme glutathione peroxidase, an important antioxi- dant that can decrease cellular damage (Figure 9.16). Other minerals and vitamins also promote glutathione peroxidase function by acting as cofactors and coenzymes. Figure 9.16: Glutathione peroxidase neutralizes the free radical hydrogen peroxide. Figure 9.17: Sources of sulfur. Protein-rich foods supply the body with ample sulfur through the sulfur-containing amino acids methionine and cysteine (Figure 9.17). These ami- no acids are found in complete proteins like animal products. Eating a variety of plant products can also meet needs. Cruciferous vegetables like cauliflower, cabbage, kale, broccoli as well as leafy vegetables are naturally high in sulfur. Tap water and other beverages may also help us meet sulfur needs. Most Canadians consume adequate protein, which is our main source of sulfur, so sulfur deficiency is rare. In populations with inadequate protein intake, sulfur deficiency can contribute to protein-energy malnutrition, which was discussed in Chapter 7. Sulfur toxicity from dietary consumption is rare. However, excessive supplementation, consuming tap water with high sulfate levels or kidney malfunction can increase risk. Excess sulfur can promote diarrhea and perhaps colitis, though more research into this potential risk is needed (Nimni et al., 2007). Compared to the major minerals, minor minerals are required in much smaller amounts. For instance, the RDAs for the major minerals are often expressed in milligrams, while those for the minor minerals are typically expressed in micrograms, which are 1000 times smaller than milligrams. However, that does not mean that the minor minerals are unimportant. Like the major minerals, they are critical for the proper structure and function of the human body. Iron is essential for the structure and function of many proteins and enzymes. It is particularly critical for the formation of functional hemoglobin – the oxygen-carrying protein found in red blood cells. This protein has four iron ions in its structure, making it a bonding site for oxygen molecules (Figure 9.18). Myoglobin, also known as myohemoglobin, is another oxygen-transporting compound that requires iron. It is found in muscle cells and contributes to their energy metabolism. In addition to its oxygen-transporting functions, iron is further involved in growth, neurological develop- ment and hormone synthesis. Figure 9.18: Red blood cell showing hemoglobin protein and iron-dependent heme group. Figure 9.19: Sources of iron. Iron is found in both animal and plant products (Figure 9.19). Dietary sources of iron are divided into two categories: sources of heme iron and sources of nonheme iron. Heme iron is the form that exists in blood and is accord- ingly only found in animal products such as red meat, poultry and seafood. Nonheme iron is found in plant products, but also in animal products, making animal products a source of both heme and nonheme iron. Plant sources of nonheme iron include lentils, beans, chickpeas, tofu, cashews and chia seeds. A fraction of dietary iron is available for use in the body. Iron bioavailability is approximately 14–18% for mixed diets and 5–12% for vegetarian diets (Hurrell & Egli, 2010). Animal-rich diets are thus more likely to promote adequate iron levels. This is partly because heme iron is absorbed better than nonheme iron and is thus more bioavailable. Also, the oxalates, phytates and tannins found in certain plant sources of nonheme iron negatively impact iron absorption. Other dietary factors can also impact iron bioavailability. For instance, caffeine and calcium negatively impact iron absorption. Conversely, vitamin C competes with the negative effects of iron inhibitors, promoting absorption (Lynch & Cook, 1980). Consuming heme or nonheme iron sources with foods rich in vitamin C, such as red peppers and citrus fruits, is thus recommended to improve bioavailability. Iron deficiency is one of the most common dietary deficiencies in the world. Its most serious outcome is iron-deficiency anemia (Figure 9.20). Iron-deficiency anemia occurs when there are not enough functional red blood cells due to low iron status, negatively impacting oxygen delivery to the tissues. There are several stages of iron deficiency and symptoms progress at higher levels of deficiency. Milder cases oc- cur when iron levels in the blood and bone marrow are low. This is known as mild iron deficiency. Marginal iron deficien- cy occurs when blood levels as well as stores in the liver, muscle, spleen and bone marrow become depleted. Iron-defi- ciency anemia is the final stage and negatively impacts the iron levels in hemoglobin and the production of healthy red blood cells. Earlier stages may show no symptoms, but symptoms can progress to lethargy, tiredness, weakness, hair loss and thinning, and pale-coloured skin. At more severe levels, iron-deficiency anemia can lead to an irregular heartbeat and delayed growth in infants and children. Since women lose blood due to menstruation, they are at a higher risk for iron-deficiency anemia, especially if they are consuming less iron due to a vegetarian diet or have higher iron needs. Athletes are at a higher risk of iron de- ficiency as they lose iron through sweat and urine and have a higher degree of hemolysis – the breakdown of red blood cells due to physical impact. Pregnancy also increases the risk for iron-deficiency anemia, as iron requirements increase to support blood volume development in the fetus. Indeed, researchers at St. Michael’s Hospital in Toronto analyzed the blood of 1830 pregnant women and found that 90% were iron deficient and half had severe iron deficiency (Tang et al., 2019). Iron can be very toxic at higher levels. Accordingly, the body controls iron intake by regulating its absorption in the digestive tract. Hepcidin, the body’s iron-regulatory hormone, is responsible for keeping iron stores in balance. Its main function is to suppress the absorption of iron when levels are high (Steinbicker & Muckenthaler, 2013). Converse- ly, when iron levels are low, hepcidin activity decreases, facilitating iron absorption. Accordingly, iron overload is rare in those who consume iron solely from dietary sources. Iron toxicity is typically due to genetic conditions or the overcon- sumption of iron supplements. Supplemental iron of more than twice the RDA can promote faintness as well as gastrointestinal issues such as nausea, vomiting and constipation. Excessive iron supplementation can also reduce zinc absorption and bioavailability (Solomons, 1986). In severe cases, a one-time consumption of 60 mg/kg of iron or more can lead to iron poisoning, which can cause organ failure, coma and death. Children are at highest risk for iron poisoning, as they may mistake their caregivers’ iron supplements for candies. In the case of acute iron poisoning, it is imperative that the individual seek immediate medical treatment. In both Canada and the USA, iron is now sold in child safe packages with clear warning statements to reduce the risk of iron poisoning. Individuals with a rare genetic condition called hemochromatosis have dysregulated iron absorption and high levels of internal iron. They are at higher risk for liver cirrhosis, liver cancer and heart disease if they do not regulate their iron intake. They are accordingly recommended to avoid iron and vitamin C supplements (Bacon et al., 2011). Zinc is a ubiquitous mineral that acts as a cofactor for more than 100 different enzymes (Zastrow & Pecoraro, 2014). It plays many vital roles in the body including in gene expression, enzyme and immune function, protein and DNA synthesis, wound healing, and growth and development. It is also included in the structure of the antioxidants superoxide dismutase and glutathione peroxidase. It is present in every cell of the body and is the second-most abun- dant trace mineral after iron. Figure 9.21: Sources of zinc. Zinc is abundant in the diet as it is found in a wide variety of foods (Figure 9.21). Good sources of zinc include shellfish, animal products, legumes, dairy products, whole grains and certain vegetables like mushrooms, kale, peas, spinach and asparagus. Absorption of zinc from plant sources is more difficult because plant compounds such as phytates can inhibit absorption. Many foods are also fortified with zinc, including breakfast cereals and baking flours. Zinc deficiency is rare due to dietary insufficiency but may occur due to certain genetic mutations or in individu- als with alcoholism who are malnourished. Vegetarians and vegans are also at higher risk, though this can be mitigated with a well-planned and varied diet. Mild zinc deficiency can promote slowed growth, erectile dysfunction, diarrhea, thinning hair and impaired immunity (Saper & Rash, 2009) Zinc toxicity may occur due to excessive supplementation but is rare from dietary sources. Symptoms include nausea and vomiting, a metallic taste in the mouth, loss of appetite, diarrhea, abdominal cramps and headaches. High dietary intake of zinc can also limit the absorption of copper and iron and promote their deficiency. Manganese – not to be confused with magnesium – is a cofactor for several enzymes in the body. It facilitates enzymatic reactions involved in carbohydrate, protein and lipid metabolism, bone development and wound healing. It is also part of the antioxidant superoxide dismutase. Manganese is abundant in shellfish and plant products. Good sources include mussels, oysters, nuts, beans, chickpeas, whole wheat bread and leafy green vegetables. Foods that are higher in iron can slow its absorption. Manganese deficiency rarely results from dietary insufficiency. Conditions such as epilepsy, osteoporosis and di- abetes may increase risk (Institute of Medicine, 2001). Deficient individuals may experience poor growth, compromised fertility and abnormal carbohydrate and lipid metabolism. There are no established side effects of excessive manganese intake from food. Toxic levels can result from ex- cessive supplementation, occupational inhalation (welders and smelters) or if tap water has excessively high manganese levels. Toxicity promotes neurological symptoms including tremors, muscle spasms, muscular weakness and hearing loss. Copper plays a key role in red blood cell production, is involved in iron absorption and is a cofactor for many enzymatic reactions. Enzymes involved in energy metabolism, DNA synthesis and connective tissues synthesis all require copper. It is also part of the antioxidant superoxide dismutase. Furthermore, copper is required for iron absorption. Magnetic therapy bracelets, which often contain copper, have long been promoted as a wearable treatment for arthritic pain (Figure 9.22). However, their use is not fully supported by evidence. For in- stance, a randomized control trial in patients with rheumatoid arthritis assessed the effects of these bracelets on arthritis symptoms. There was no significant difference in pain, inflammation or physical ability with their use. Furthermore, several study participants experienced skin irritation from the bracelets (Richmond et al., 2013). Copper has also been studied for its potentially beneficial effects on CVD and Alz- heimer’s disease. However, the evidence base is insufficient to support the use of supplements in the prevention or management of these diseases (National Institutes of Health, n.d.-a). Figure 9.22: Magnetic bracelets often contain copper. Figure 9.23: Sources of copper. Copper is found in a wide variety of animal and plant products (Figure 9.23). Beef liver, oysters, crab and salmon are all high in copper. Plant products, such as potatoes, mushrooms, cashew nuts and sunflower seeds, are also high in the mineral. While abundant in foods, dietary copper intake has been decreasing since the 1930s. Approximately one in four Canadians are well below the RDA for copper (Klevay, 2011). Since copper is needed for iron absorption, people who get enough iron but are lacking in copper may experience iron-deficiency anemia. Other symptoms of deficiency include tremors, tingling sensations, awkward walking patterns, numbness and fatigue. Digestive conditions, such as celiac dis- ease as well as bariatric surgery, may increase risk for deficiency. Copper toxicity is rare from food but can occur due to over-supplementation or due to certain genetic con- ditions. Though rare, copper toxicity can also occur due to a tainted water supply (National Research Council, 2000). Milder cases can result in vomiting, diarrhea, yellowing of skin and muscle pain. More serious cases can result in liver damage, heart failure, kidney failure and even death. Copper toxicity is also the main complication of Wilson’s disease, a condition in which the liver in unable to remove excess copper, leading to its accumulation in the brain, liver and eyes. Iodine is an essential component of the two thyroid hormones: thyroxine (T4) and triiodothyronine (T3) (Figure 9.24). These two hormones, secreted by the thyroid gland, have metabolic effects all over the body. They are involved in the regulation of fuel use, protein synthesis, heartbeat, body temperature regulation, muscle contraction and cell turn- over. Figure 9.24: Iodine is required for the synthesis of the thyroid hormones T4 and T3. Figure 9.25: Sources of iodine. All table salt in Canada is iodized – that is, fortified with iodine. This is the main source of iodine in the Cana- dian diet and has been since 1949 when the iodization of table salt became mandatory. It is also found naturally in fish, dairy products and eggs, as well as plant products such as seaweed, nuts and enriched bread (Figure 9.25). Iodine deficiency affects approximately two billion people worldwide (Lazarus, 2015). A quarter of these individ- uals exhibit clinical symptoms of deficiency. Iodine deficiency compromises the thyroid gland’s ability to make thyroid hormones. It is common in areas where food is scarcer and salt is not iodized. In adults, iodine deficiency can lead to hypothyroidism, which typically manifests as a goiter (Figure 9.26). A goiter is an enlargement of the thyroid gland, which is located at the base of the neck. Iodine is needed to make thyroid hormones, but if iodine is insufficient, the thyroid gland enlarges as it tries harder to make these hormones. This condi- tion is mostly reversible with iodine supplementation. However, if a goiter has been present for a long time, it may only shrink subtly after iodine supplementation. The goiter is a physical sign of iodine deficiency, but other health concerns can arise. When left untreated, deficiency can also promote heart disease, peripheral neuropathy, infertility and mental health issues such as depression. Figure 9.26: Goiters are enlargements of the thyroid gland due to iodine deficiency. Congenital iodine deficiency syndrome, previously known as cretinism, occurs when iodine is deficient in the prenatal or postnatal nutrition of a child. Pregnant women have a higher need for iodine; if it is lacking, several neurolog- ical issues can arise in the child. Mental deficiencies, deaf mutism, difficulties with muscular control and slowed growth can result due to congenital iodine deficiency (Zimmermann, 2009). Accordingly, prenatal vitamins containing iodine are recommended to promote the healthy development of the fetus. Iodine poisoning, which typically results from excessive supplementation, can promote diarrhea, nausea and vomiting. In more severe cases it can lead to the swelling of airways, limiting breathing, a lowered heartrate and even coma. Iodine excess can also lead to iodine-induced hyperthyroidism, which can promote an accelerated heartrate, mus- cle weakness and unexplained weight loss. Interestingly, iodine excess can also cause goiters as the thyroid gland swells in an attempt to produce more thyroid hormones. Though iodine toxicity is rare in North America from dietary intake, it has been evidenced in Japanese populations who consume excess iodine, mostly from seaweed (Zava & Zava, 2011). Selenium has roles in reproduction, the production and metabolism of the thyroid hormones, as well as in the synthesis of DNA. Its most known role, however, is as an essential component of the antioxidant glutathione peroxidase (Figure 9.16). Selenium has been studied for its potential to reduce the risk of CVD. A systematic review of 25 observation- al studies found that those whose selenium blood levels were 50% higher than others had a 24% reduced risk of CVD (Flores-Mateo et al., 2006). However, a review of randomized control trials found that supplementation had no effect on cardiovascular events (Rees et al., 2013). There is currently no strong evidence base to support the use of selenium supplementations in the prevention or management of CVD, but attaining adequate amounts through the diet is recom- mended. The potential cancer-reducing effects of selenium have also been researched. A systematic review of 69 studies including more than 300,000 people found that individuals with higher levels of selenium were at lower risk for breast, lung, colon and prostate cancers (Cai et al., 2016). This affect was established due to selenium obtained from foods. However, the potential cancer-protective effects of selenium supplementation have not been established with well-de- signed randomized control trials (Lippman et al., 2009). Selenium is found in both plant and animal products (Figure 9.27). Fish, shellfish, eggs and chicken are high in selenium, as are plants such as brazil nuts, sunflower seeds and shitake mushrooms. However, the concentration of selenium in plant foods depends on the quality of the soil in which they were grown. For instance, one study found that depending on where they were grown, the selenium con- tent of brazil nuts varied from almost 300% of the RDA to as low as 11% (Silva Junior et al., 2017). Figure 9.27: Sources of selenium. While rare in the Canada, more that a billion people worldwide may be affected by selenium deficiency (Fordyce, 2013). Selenium deficiency increases the risk of male infertility, muscle weakness, fatigue, hair loss and a weakened immune system. Individuals who are selenium deficient and experience a secondary stress such as a viral infection, have a higher risk for Keshan disease. Keshan disease is a potentially fatal disease of the heart muscle. It was first evidenced in the Keshan province of China, but has been found all over the country, as well as in other areas of the world where selenium content in the soil is low. Since the Chinese government mandated the application of a selenium mixture to crops, disease incidence has dropped dramatically (Liu et al., 2002). The incidence of selenium deficiency may increase worldwide, however, as climate change is predicted to decrease the selenium content of soil by more than 50% (Jones et al., 2017). Selenium excess can increase the risk of hair loss, nail discoloration, muscle and joint pain, headache and gastro- intestinal symptoms. Early symptoms may include a metallic taste in the mouth and breath that smells like garlic. Seleni- um supplements that are ingested in dosages far above the upper limit can lead to selenium poisoning. This can promote neurological symptoms, breathing problems, kidney failure, heart attack and, though rare, even death. In 2008, there was an outbreak of selenium toxicity in the USA due to a dietary supplement that claimed that it could maintain energy and sustain health. The selenium content in the product was 200 times higher than that stated on the label, leading to a toxic intake of selenium and symptoms such as diarrhea, fatigue, hair loss and joint pain (MacFarquhar et al., 2010). Molybdenum is a cofactor in certain enzymatic reactions. Molybdenum enzymes help break down sul- fites (Figure 9.28), which can promote allergic reactions, diarrhea, and breathing difficulties if they build up in the blood. Figure 9.29: Sources of molybdenum Figure 9.28: Molybdenum is a cofactor in the breakdown of sulfites. The molybdenum content of plants varies depending on soil quality. Legumes are the best sources of molybdenum, while lentils are also rich in the mineral (Figure 9.29). Organ meats, such as liver and kidney, as well as dairy products are good ani- mal sources of molybdenum. Since molybdenum is abundant in a lot of foods and we only need a trace amount, deficiency is rare. Molybdenum toxicity is rare and is typically due to over-supplementation. Excessive intake may affect growth, promote kidney failure or promote the development of seizures and brain damage. However, since deficiency is rare, not enough data has been collected to know the true symptoms of toxicity. Fluoride is an ion of the naturally occurring mineral fluorine. It is not typically deemed essential because it is not required for growth or to sustain life. However, it does have health-promoting effects through its well-established ability to strengthen bones and teeth. With calcium and phosphorus, fluoride forms a crystal structure called fluorapatite, which hardens tooth enamel. Fluoride therefore contributes to tooth integrity and health. Accordingly, several munici- palities in Canada add fluoride to tap water to reduce the risk of dental caries in the population (Box 9.3). Box 9.3: Water fluoridation. In 2000, the Centers for Disease Control and Prevention stated that water fluorination is one of the 10 greatest public health achievements of the 20th century, due to its ability to reduce tooth decay (Centers for Disease Control, 2000). Indeed, a systematic review of 155 prospective epidemiological studies found that water fluorination was effective at reducing tooth decay by 35% (Iheozor-Ejiofor et al., 2015). However, many people oppose water fluorination and it is the topic of debate and contention. This has led to signifi- cant differences in water fluorination rates across Canada. Fluoridation rates vary from 0% in Nunavut and Yukon, to 75% in Ontario, with a national average of 45% (Rabb-Waytowich, 2009). One of the main argu- ments against water fluorination is the cost, estimated to range from 60 cents to one dollar per person per year. This could amount to a cost of more than $30 million per year if the entire country fluorinated their water. Individuals against water fluoridation also propose that the increased risk of fluorosis is a reason to not fluoridate the water. However, levels of fluoride in the water are limited to prevent fluorosis. Another argument against fluoridation of water is the fact that fluoride can now be attained through toothpaste and dental fluoride treatments, so the need for water treatment may be unnecessary. High intakes of fluoride intake can lead to fluorosis, which is most common in children under eight. Fluorosis negatively affects tooth enamel, promoting tooth discolor- ation. In rare cases it can lead to tooth damage. The charac- teristic sign of fluorosis is the appearance of white spots on the teeth, which increase in size with the degree of fluorosis (Neville et al., 2015). Individuals with mild fluorosis tend to be more resistant to dental caries. However, at more severe ranges, teeth can develop a brown discoloration (Figure 9.30). Accordingly, the fluoride concentration of fluoridated water is maintained at levels that both reduce the risk of caries and dental fluorosis. Figure 9.30: Severe fluorosis of the teeth. In this chapter, we have covered the essential minerals, as well as fluoride. Other minerals, including boron, arsenic, nickel, bromine, lithium, strontium and silicon, also have known roles in the body. However, they are either not currently deemed essential or debate exists about whether they are required to sustain life. More research is needed before they are established or ruled out as essential. Minerals are inorganic elements that play a wide range of structural and functional roles in the body. Many mineral effects are exerted through their actions as mineral cofactors, promoting various enzymatic activities. Consuming adequate amounts of minerals through a diet including a wide range of animal and plant products can reduce the risk for deficiency. In general, minerals are less bioavailable from plants, but a well-planned plant-based diet can meet needs. Minerals are inorganic elements that are essential from the diet. Minerals promote body structure and can facilitate body processes. Minerals can act as cofactors, promoting the activity of enzymes that catalyze various body process- es. Major minerals are needed in larger amounts, while trace minerals are needed in smaller amounts from the diet. They are both important to body structure and function. Soil quality can affect the bioavailability of minerals from plants. In addition, oxalates, phytates and tannins in plants can impair the absorption of certain minerals like iron. Animal products are typically higher in minerals. The mineral content of animal products depends on what they ate and their relative size. Getting adequate amounts of the minerals can prevent deficiency symptoms. Consuming minerals beyond their recommended amounts does not typically provide further health benefits. Mineral toxicity from food is extremely rare. Toxicity symptoms are typically evidenced when indi- viduals consume excessive amounts of minerals from supplements. Consume adequate amounts of minerals to reduce the risk of deficiency. Avoid over-supplementation of minerals to avoid toxicity. Certain conditions increase the risk for mineral deficiency and toxicity. Healthcare practitioners can be consulted to avoid this risk. Abrahamsen, B., Brask-Lindemann, D., Rubin, K. H., & Schwarz, P. (2014). 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