Living organisms appear to selectively concentrate certain elements from the environment while rejecting others. The adult human body contains approximately thirty-five elements. Four of these (hydrogen, oxygen, carbon, and nitrogen) constitute 99 percent of the atoms in the body. As a comparison, the most abundant elements in the Earth's crust are oxygen (67 percent), silicon (28 percent), and aluminum (8 percent). The remaining 1 percent of the elements in the human body (with the exception of sulfur) are the inorganic or mineral constituents of the body and thus form the ash when the body is "burned." Seven of the remaining elements, sodium, potassium, calcium, magnesium, phosphorus, sulfur, and chloride, together represent about 0.9 percent of the body's weight. The seventeen others make up the remaining 0.1 percent, some of which, but not all, are considered nutritionally essential. These elements appear in the body at measurable concentrations but may not perform an essential biological function. Cadmium is one such example. The newborn infant is virtually free of this element, but gradually accumulates cadmium by ingestion and inhalation, such that over a lifetime an average person living in an industrial society accumulates milligrams of this element. Not only does cadmium appear to serve no essential function in the body, it is also likely to be undesirable and potentially detrimental.
Most experts agree that thirteen mineral elements are nutritionally essential. These are minerals that when deficient consistently result in an impairment of a function that is prevented or cured by supplementation. There still is some question about seven others (Table 1).
The functions of mineral elements are structural, osmotic, catalytic, and signaling. Calcium plays the most obvious role as structural component of bone but also participates in many examples of cell signaling. Sodium, chloride, and potassium constitute the majority of minerals whose function is to maintain osmotic and water balance and membrane electrical potentials. The micro-mineral elements listed in Table 1 have historically been classified as "trace" elements primarily because they occurred at levels below past methods for detection. In general, these minerals function as biocatalysts. Iron is the most prominent example because a deficiency of iron is probably the most common nutritional deficiency on earth (anemia afflicts more than 15 percent of the world's population). Copper and zinc are the prototypical biocatalysts because virtually all of their known functions involve either catalytic or structural roles in many different enzymes. Copper is unique in that all of the known deficiency symptoms in experimental animal models can be explained on the basis of failure of known enzymes. Zinc deficiency, on the other hand, presents symptoms that are not directly attributable to any of the fifty or more enzymes in which it is found. Selenium, manganese, and molybdenum are also constituents of enzymes. Deficiency symptoms for selenium and manganese have been well characterized but a nutritional deficiency of molybdenum has not been satisfactorily demonstrated. The most compelling reason to include molybdenum among the thirteen nutritionally essential elements is because of its presence (and thus function) in several important enzymes. Some microminerals serve a very narrow range of biological functions. Iodine and cobalt are exclusively constituents of thyroid hormones and vitamin B12, respectively. No other role has been identified for these elements. The remaining mineral elements are those that occur in significant concentrations in the human body and most probably serve an important biological function. However, consistent findings regarding deficiency symptoms and specific biochemical functions have not been reported. Fluorine is a unique example of a mineral that currently has no definitive biological function but because it appears beneficial to dental health, it is a recommended nutrient.
Table 1
| Known nutritionally essential minerals |
| Element | Amount in 70-kgHuman (g) | Function |
| Macrominerals |
| Calcium | 1,200 | Component of bones; signal transduction in hormonal action, muscle contraction, blood clotting; and structural role in proteins |
| Phosphorus | 700 | Component of bone Necessary for activation of high energy intermediates |
| Potassium | 240 | Osmotic, electrolyte, and water balance |
| Chloride | 120 | Osmotic, electrolyte, and water balance |
| Sodium | 120 | Osmotic, electrolyte, and water balance |
| Magnesium | 35 | Activation of ATPases, kinases, and other enzymes |
| Microminerals |
| Iron | 4.0 | Catalytic redox reactions, oxygenation, and O2-carrying proteins |
| Zinc | 2.0 | Catalytic as a Lewis acid and structural function for some metalloenzymes |
| Copper | 0.1 | Catalytic in redox reactions some involving iron |
| Selenium | 0.020 | Structural and catalytic component of peroxidases, especially glutathione peroxidase. Provides antioxidant protection |
| Iodine | 0.015 | Component of thyroid hormones |
| Molybdenuma | 0.012 | Structural component of enzymes, especially xanthine oxidase and sulfite oxidase |
| Manganese | 0.015 | Catalytic role in enzymes involved in cartilage formation |
| Cob | 0.001 | Structural component of vitamin B12 |
Abbreviations: ATPase, adenosine triphosphatase.
aBiochemical evidence only that it is essential.
bEssential only as a component of vitamin B12. |
Calcium and Phosphorus
Approximately 99 and 85 percent of the total calcium and phosphorus, respectively, in the human body are found in bone. Both ions leave the bone and are deposited back each day representing normal metabolic activity or "turnover" of bone. The remaining 1 percent of calcium is found in both extracellular and intracellular pools and is absolutely critical for normal body function such as muscle contraction and nerve activity. Although very rare, a sudden drop in extracellular concentrations of calcium (<50 percent) can lead to an emergency situation such as tetany or convulsions. Nerve cells bathed in hypocalcemic fluid spontaneously "fire," leading to uncontrolled nerve activation and muscle spasm. The majority of the extracellular calcium is in chemical equilibrium with bone. Approximately 30 percent is under hormonal control by several hormones, parathyroid hormone, vitamin D, and thyrocalcitonin. As a result, the concentration of extracellular calcium is remarkably constant. Blood levels of phosphorus fluctuate much more and appear to be determined in large part by urinary excretion.
The absorption of calcium from the diet is dependent on a number of dietary and physiological factors. Vitamin D is synthesized in skin when exposed to ultra-violet irradiation [290 to 315 nanometers of ultraviolet (UV) light]. Sunscreen lotions [Sun Protection Factor (SPF) 8] can reduce this synthesis as much as 90 percent. Inadequate sunlight exposure was most likely the cause of calcium deficiency rickets observed at the turn of the century in countries at northern latitudes. A change in dietary calcium absorption in humans appears to take several weeks to accomplish but accounts for the ability of humans to tolerate diets that provide relatively little calcium (200 to 400 mg/day). This activation process becomes less potent with age and may account in part for the increased calcium requirements with age.
Dietary factors affecting the absorption of calcium are well known. They include chelating organic acids such as oxalic and phytic acid. The former is the most potent and is responsible for the markedly diminished "availability" of calcium found in spinach.The amount of calcium contained by a food is only an approximation of the amount of calcium that is ultimately "available." Estimated fractional absorption (percent of intake absorbed into the body) of calcium from these foods ranges from 5 percent for spinach to 61 percent for broccoli. Vegetables of the Brassica family such as broccoli and cabbage appear to contain little oxalate and thus contain calcium that exhibits higher bioavailability than dairy products. Milk and dairy products have relatively high calcium content as well as relatively high fractional absorption (30 percent), resulting in the highest amount of calcium per serving. Lactose in milk enhances the absorption of calcium in infants but its effect in adults is less clear. Other dietary factors affect the retention of dietary calcium but have little impact on its absorption. For example, high intakes of either sodium or protein are thought to result in increased urinary losses of calcium. Protein increases renal calcium loss by increasing acid load while sodium increases losses via shared renal transporters. Both of these conditions may affect calcium balance and ultimately the requirements for this nutrient. The bone loss associated with chronic calcium losses or negative calcium balance may ultimately lead to weakened bones or osteoporosis. Calcium supplements may adversely affect the bioavailability of iron.
Calcium deficiency occurs primarily as rickets or osteomalacia in young children. Bones are deformed (bowed legs) and weak due to inadequate calcification of the protein matrix of bone. This deficiency can arise as a result of too little dietary calcium (relatively rare) or inadequate vitamin D synthesis. Historically, the latter has been the major cause brought about primarily because of reduced exposure to sunlight. It is conceivable, however, that dietary factors such as oxalates and cultural customs (clothing) may interact to play a role in the development of rickets especially since recent cases have been reported in areas of the world near the equator where sunlight should not be limiting. Calcium deficiency does not appear to be a primary cause of osteoporosis. This condition is characterized not by inadequate bone mineralization but by a loss of total bone both protein matrix and mineral. Bones weaken and become susceptible to fracture.
Sodium and Chloride
Total body sodium is approximately one-tenth of that of calcium. One-third of body sodium is found in bone but its metabolic significance is unknown. Sodium and chloride constitute the major cation and anion, respectively, in the extracellular fluid of humans. Sodium is the primary determinant of the osmotic pressure of the extracellular fluid and as such is the main determinant of extracellular fluid volume. The sodium ion concentration changes less than 3 percent day in and day out despite dramatic fluctuations in sodium intake. This is a reflection of a very tightly controlled and highly regulated system to maintain constant osmotic pressure. Through most of human evolution, the availability of dietary salt has been very highly restricted. Much of dietary sodium (and chloride) were derived from sources such as meat and vegetables, which contain very low levels. Consequently, humans and other mammals have evolved physiological mechanisms that permit sodium conservation under extreme conditions. This physiological conservation system comprised of pressure receptors, renal renin, lung angiotensinogen, adrenal aldosterone, and vassopression all makes dietary requirements extremely difficult to assess. For example, the Yanomamo Indians in Northern Brazil have been found to excrete as little as 1 mEq/day of sodium (Na) per day. This reflects a dietary consumption of approximately 60 mg salt per day (over 100 times less than that which is normally consumed in Western populations). At the other extreme are the northern Japanese, who consume nearly 26 grams of salt each day. These regions of Japan have unusually high incidences of cerebral hemorrhage, most likely related to the high incidence of hypertension. Other areas of the world such as Northern Europe and the United States consume approximately 10 g/day or less of salt. The sodium and potassium contents of some selected foods are shown in Figure 1. It is apparent that many "unprocessed" foods contain very little sodium. Estimates of sodium intake suggest that over 85 percent of the sodium consumed in Western diets is sodium added during processing. This is clearly illustrated by the progressively higher sodium content of peas (fresh, frozen, and canned) and perhaps more important, the dramatic reduction in potassium content. The net result is a reversal of the naturally low sodium to potassium ratio found in all fresh plants.
A deficiency of sodium normally does not occur even in areas where salt is scarce. The abnormal loss of sodium and other electrolytes, however, could occur under conditions of extreme sweat loss, chronic diarrhea and vomiting, or renal disease, all of which produce an inability to retain sodium. Acute episodes of diarrhea or vomiting resulting in a loss of 5 percent of body weight could lead to shock. The most important therapy under these circumstances is to restore sodium and water or circulatory volume. Chloride deficiency has been reported in infants consuming low-sodium chloride formulas. They show signs of metabolic alkalosis, dehydration, anorexia, and growth failure. Potassium depletion most notably affects cardiac function where either elevations or reductions in serum potassium can cause arrythmias.
Magnesium
Magnesium is an important intracellular ion involved in many enzymatic reactions of food oxidation and cell constituent synthesis. Approximately 60 percent of total body magnesium is found in bone, where approximately half can be released during bone resorption. Magnesium food sources are widely distributed in plant and animal products with the highest content found in whole grains and green (high chlorophyll) leafy vegetables. Refining wheat with the removal of the germ and outer layers may remove nearly 80 percent of the magnesium from wheat. Meats and most fruits and vegetables are poor sources of magnesium. The absorption of magnesium appears to be unrelated to the absorption of calcium (that is, is independent of vitamin D) and is relatively unaffected by food constituents. Phytate and phosphates, however, may adversely affect magnesium availability by forming insoluble products although their practical significance is unclear. Experimental magnesium deficiency has been produced in humans. Urinary magnesium drops virtually to zero while plasma levels are relatively well preserved. The change in urinary excretion reflects a "urinary threshold" for magnesium. After continued deficiency, however, neuromuscular activity is affected, ultimately leading to tremors and convulsions. Serum and urinary calcium levels are profoundly reduced and not restored by parathyroid hormone administration. It was concluded that magnesium is essential for the mobilization of calcium from bone. A deficiency of magnesium under normal conditions is unlikely but may occur with the presence of other illnesses such as alcoholism or renal disease.
Iron
Over 65 percent of body iron is found in hemoglobin, the respiratory pigment used to transport oxygen within and between tissues. One-third of body iron is a "storage" form that can be mobilized during times of need. The amount of "storage" iron may vary greatly with age and gender. Food sources of iron are complicated by numerous factors that affect the bioavailability of dietary iron. Non-heme sources of iron are found in plant and vegetable products and the absorption from these sources (versus heme found in meat products) is generally lower and influenced to a greater extent by total diet composition. Vitamin C is probably the most signficant enhancer of non-heme iron absorption, while plant phenolics such as tannins found in teas and phytates found in cereals are some of the most potent inhibitors. None of these factors, however, affect the absorption of heme iron found in meats. Iron status can markedly affect the amount of iron absorbed from a meal—low status increases iron absorption. The effect is most pronounced for non-heme iron, changing over fourfold compared to 50 percent for heme iron. Although iron status can influence absorption, the most important determinant of iron availability is the composition of the diet. It is clear that non-heme iron absorption is markedly affected by the characteristics of the food with which it is eaten and that there are clear differences in the nature of absorption of heme and non-heme iron. Iron deficiency is seldom related to iron intake per se. Major causes of anemia (too little hemoglobin) include blood loss and/or diets containing either no enhancers (such as meat or ascorbic acid) or high levels of inhibitors. Infection can also change iron metabolism significantly such that much of the anemia in the world is due to chronic infection. The losses for iron for both men and women are known precisely but the amount of dietary iron requirement depends on the overall diet.
Zinc
Zinc is present in all tissues and performs both structural and catalytic functions in many different enzymes. Unfortunately, changes in the activities of these enzymes are not sufficient to explain the pathological effects of experimental zinc deficiency. Experimental animals refuse to eat experimental diets that are very low in zinc. Human zinc deficiency was demonstrated nearly two decades ago in the United States. Young children from 6 months to 5 years of age showed low amounts of zinc in the hair relative to other groups. Hair zinc and taste acuity were restored after three to five months of zinc supplementation. Earlier studies also revealed zinc deficiency in regions of Iran and Egypt. It is very difficult to assess zinc status in humans. Serum zinc is not adequate to assess nutritional status. In experimental situations, serum zinc falls remarkably (<50 percent) following a low zinc intake without immediate (or apparent) ill effects. In 1974, a Recommended Dietary Allowance (RDA) of 15 mg/day was established for zinc. (It was not until 1974 that we had enough information to estimate an RDA for zinc, at which time the value was established at 15 mg. The RDA presented in 1989 gives 15 mg per day for adults. The 2001 Institute of Medicine value is 11 mg per day.) Approximately 70 percent of zinc consumed by most people is derived from animal products. Cereals contain appreciable zinc but the availability varies considerably. Several plant compounds interfere with the absorption of zinc. The most prominent of these is phytates (inositol hexa-and pentaphosphate). These inhibitors most likely contribute to the natural incidence of dietary zinc deficiency observed in humans.
Copper
Although the importance of copper deficiency in animals has been recognized since the 1930s, it is still not possible to establish an RDA for copper in humans because of the uncertainty regarding the quantitative requirements. There is no doubt that copper is an essential nutrient for humans. Current estimates of the minimum copper requirement are between 0.4 and 0.8 mg/day. Copper is critical for the function of several enzymes, especially blood ceruloplasmin. The activity of this enzyme in blood falls dramatically in experimental animals soon after giving copper-deficient diets and is thought to be a good indicator of copper depletion even in humans. Ceruloplasmin is essential for iron absorption (it catylizes the oxidation of Fe2× to Fe3× required for binding of iron to the blood transport protein, transferrin) and explains the anemia observed in copper deficiency. In contrast to zinc, all of the symptoms of a copper defeciency under experimental conditions can be explained by changes in various enzymes that require copper. Two inherited diseases associated with abnormal copper metabolism have been observed—one (Menkes' disease) is associated with copper deficiency, while the other (Wilson's disease) is a disease of excessive copper accumulation. Excessive intake of zinc can precipitate a copper deficiency. An example of zinc-induced copper deficiency has been reported in humans and is attributed to a reduction in the absorption of copper. Excessive zinc may induce intestinal proteins that bind copper and thereby prevent its transfer from the intestine into the body.
Iodine
Approximately 80 percent of total body iodine (20 milligrams) is found in the thyroid gland. All of the iodine that leaves this gland does so as a component of the thyroid hormones—thyroxine and triiodothyronine. In fact, all of the functional significance of iodine is as a component of these hormones. Iodine deficiency represents the most common cause of preventable mental deficits in the world's population. Since most of the world's iodine is found in the oceans, coastal areas are not deficient. However, mountainous areas such as the Himalayas, European Alps, and the mountains of China, as well as the flooded river valleys of Asia, areas where leaching of iodine from soils has occurred for eons, produce iodine-deficient crops and plants. Iodine deficiency during pregnancy causes cretinism, a diet-related birth defect that is characterized by permanent mental retardation and severe growth stunting. In young children and adults, iodine deficiency results in enlarged thyroid glands or goiter. Although various foods such as cassava, cabbage, and turnips contain goitrogens, substances that interfer with iodine metabolism, their practical signficance is not clear. Cassava, the dietary staple in regions of Africa and other areas, may be the exception, especially when not well cooked. The cyanide released by the ingestion of this plant is transformed and ulitmately leads to an inhibition of the uptake of iodine by the thyroid. Goiter was once common in areas of the United States near the Great Lakes and westward to Washington State, but the introduction of iodized salt almost competely eliminated goiter in these areas by the 1950s. The minimum requirement for iodine to prevent goiter is approximately 1 μg/kg/day whereas the recommended intake is nearly twice this amount.
Selenium
Although selenium was first recognized as a toxic trace element for livestock, it is now clear that selenium is an essential nutrient for all animals. During the 1930s, livestock grazing in parts of the Great Plains of North America were found to contract a disease characterized by hair loss, lameness, and death by starvation. The cause of this disease was excess selenium obtained from the plants grown in soils containing high selenium concentration. In fact, selenium, more than any other essential trace element, varies greatly in its concentration in soils throughout the world. Plants accumulate selenium from soils but are not thought to require selenium for growth. Although human toxicity was not observed in affected regions in the United States, endemic selenium poisoning has been observed in high-selenium regions of China where the symptoms included loss of hair and nails. China also possesses regions of very low selenium where, in fact, humans have been diagnosed with selenium deficiency—Keshan disease (cardiomyopathy) and Keshan–Beck disease (degenerative joint disease). Although other factors may be involved, selenium deficiency is clearly a predisposing factor. Selenium functions as part of several important enzymes. The most prominent is a soluble enzyme, glutathione peroxidase, whose function is to reduce hydrogen peroxide and organic (lipid) peroxides, thus preventing the oxidative destruction of cell membranes. Selenium is incorporated into the enzyme as the amino acid selenocysteine by reactions that are unique to selenium. Together with vitamin E, selenium, as a structural component of glutathione peroxidase, forms an antioxidant defense against oxidative stress. The requirement for selenium has been estimated by various methods. On the basis of intakes in regions of China with and without deficiency disease, approximately 20 μg/day is considered an adequate amount to prevent deficiency. The estimated safe and adequate selenium intake suggested by the U.S. National Research Council ranged from 50 to 200 μg/day in 1980. An amount to maintain the highest serum glutathione peroxidase activity appears to be 70 and 55 μg/day for an average man or woman, respectively, which became the Recommended Dietary Allowance (RDA) in 1989. In 1996, the World Health Organization recommended 40 and 30 μg/day for men and women, respectively. Intakes greater that 400 μg/day are considered to be the maximum safe level. Selenium is thus an example of a nutrient that possesses a relatively narrow range of intakes that are safe and that meet requirements.
Manganese
Normal body content of manganese is very low—approximately 15 milligrams or very similar to iodine. In contrast to iodine, manganese deficiency has not been observed in humans but has occurred naturally in chickens and experimentally in many other species. Manganese is required by several enzymes, which may or may not be inolved in the symptoms of a manganese deficiency. Symptoms include impaired growth, skeletal abnormalities, and defects in lipid and carbohydrate metabolism. The role of manganese in the synthesis of the mucopolysaccharide component of bone and cartilage is the most crucial whereas mineralization of bone appears to be independent of manganese. Excessive manganese will interfere with iron absorption. Under conditions of iron deficiency, manganese absorption is increased. Both iron and manganese appear to share a common site for absorption. The recommendations for manganese intake are based on estimates of normal dietary intakes of 2 to 5 mg/day. This amount is thought to be sufficient to replace the 50 percent of body manganese that is lost every 3 to 10 weeks.
Chromium
Chromium is one of the most intriguing and potentially important trace elements because it appears to influence the action of a critical hormone, insulin. Unfortunately, the definitive role of chromium in this regard awaits further study. Decreased sensitivity of peripheral tissues to insulin appears to be the primary biochemical lesion in experimental chromium deficiency. Impaired glucose tolerance has been attributed to chromium deficiency in several experimental models. Also, several patients receiving total parenteral nutrition have responded to chromium supplementation in the predicted manner, that is, improved glucose tolerance. These findings have established chromium as an essential nutrient for humans but the specific deficiency symptoms in those who receive enteral feeding have not emerged. Overt chromium deficiency is very unlikely under normal conditions due to the small amounts of chromium needed. Moreover, a marginal deficiency is very difficult to identify due to the lack of reliable markers for diagnoses concerning chromium. Currently, there is little or no evidence that chromium supplements are either warranted or effective. Even the recommended intakes for adults (50 to 200 μg/day) are uncertain due to the lack of reliable methods for assessment.
Fluoride
Fluoride is not generally considered to be an essential element for humans. It is, however, considered beneficial in that normal intakes appear to reduce the incidence of dental caries. The mechanism of this benefit is thought to be due to incorporation of fluoride into the mineral matrix of tooth enamel, thus producing a more resistant mineral apatite crystal. Over 99 percent of the fluoride found in the body is found in bones and teeth as a component of this mineral apatite crystal. An unusually high intake of fluoride causes permanently discolored or mottled teeth, a condition identified in children drinking water with 2 to 3 parts of fluoride per million. The level of fluoride commonly maintained in municipal water supplies is 1 part per million.
Silicon and Nickel
Silicon is the most abundant mineral in the Earth's crust. It is thus surprising that a need for silicon in biological systems has not been more prominent. Limited research conducted since 1974 has indicated a role for silicon in the development of mature bones in chickens and rats. A human requirement has not been established but estimates in the range of 10 to 20 mg/day have been suggested. Most likely intakes of this magnitude occur under normal conditions. Nickel deficiency has been experimentally produced in several species. Growth depression and changes in iron metabolism have been described. Nickel has been discovered in the enzyme urease from bacteria, fungi, yeasts, algae, plants, and invertebrates. Many other enzymes exist for which nickel is apparently a component. Thus, it is likely that nickel plays an essential functional role in higher organisms, including humans.
Molybdenum
Molybdenum is an essential component of at least three important enzymes found in animals and humans. A deficiency of one of these enzymes, sulfite oxidase, can have severe consequences—seizures and severe mental retardation in infancy. This deficiency has arisen in patients with genetic mutations in cofactor synthesis but not as a primary molybdenum deficiency. The dietary requirements of molybdenum cannot be given, or even approximated, for any animal species including humans. A deficiency of molybdenum has not been observed under natural conditions for any species. Despite this, the biochemical role of molybdenum as a component of several enzymes establishes it as an essential nutrient for humans.
Calcium and Osteoporosis
The relationship between dietary calcium and osteoporosis has been studied for many years. Early indications suggested that dietary calcium intake was not correlated with bone density (a indicator of bone strength) or the bone loss that naturally occurs with aging. The complexity of the issue is illustrated by observations that many people consume relatively low calcium diets and yet show little evidence of osteoporosis. The genetic contribution to bone density is well established. Studies of identical twins demonstrate that a considerable proportion of the variation in bone density is attributable to inheritance. Mothers with osteoporosis have daughters (thirty years of age) who possess bone density that is significantly less than agematched controls. Dietary intervention with calcium has been attempted in many different studies. Those in the past decade suggest that some changes may be effected by increased calcium intake but they are relatively minor and perhaps short-lived. For example, calcium supplements of 500 mg/day over three years were found to affect bone density of some bones significantly only in older women whose habitual calcium intakes were relatively low (>400 mg/day). Supplements had no effect in older women who had higher habitual calcium intakes. This study seemed to indicate that there might be a subset of elderly women who may benefit from increased calcium intake. Because vitamin D has such a critical role in the absorption of calcium, some workers have examined both vitamin D status and calcium supplementation. Overall, the results not surprisingly support the idea that vitamin D may be a limiting factor in the absorption of dietary calcium. Many other dietary variables may also be important in optimizing the effectiveness of dietary calcium. Dietary acidity, which is promoted by protein intake and ameliorated by the consumption of fruits and vegetables, may contribute. Alkaline diets rich in potassium appear to reduce the loss of body calcium and thus preserve bones. Elevated sodium intake also appears to increase urinary calcium losses. Therefore, the development of osteoporosis is unlikely to be a simple matter of too little dietary calcium consumption, especially in the later years of life, but more of an effect of total dietary conditions superimposed on a particular genetic background.
Sodium and Potassium
In the early 1950s, scientists found that experimental animals could be selected genetically to be susceptible to dietary salt-induced hypertension. Lewis K. Dahl and colleagues established a genetic strain of rat that was sensitive to high dietary salt. These rats showed remarkably elevated blood pressure when dietary salt was increased approximately ten times above normal. The rats' kidneys appeared to have a genetically programmed sensitivity to salt-induced hypertension. However, in the absence of high dietary salt, these animals were normal. Dietary potassium was also recognized as an important factor since high concentrations could ameliorate the effect of sodium chloride. Establishing a direct link between high dietary salt intake and hypertension in humans has been difficult to prove. The problem has been that not all individuals within a population are equally sensitive. Much evidence has come from studies of populations with widely differing salt intake. Populations whose sodium intake is low (less than 100 milligrams of salt) do not appear to develop elevated blood pressure with age. Those whose intake is relatively high do show increased blood pressure with age and evidence of increased incidence of essential hypertension. Recent studies with nonhuman primates have clearly shown that changes in salt intake alone are sufficient to induce changes in blood pressure. Many other studies suggest that lower potassium intake may also be important in the etiology of elevated blood pressure. Certain individuals may be more susceptible or sensitive to sodium-induced changes in blood pressure (similar to experimental animals). All of the known mutations resulting in a phenotype of hypertension involve some aspect of sodium renal excretion and/or retention. It is likely, then, that genetic sodium sensitivity will be a prerequisite to an environmentally induced development of hypertension.
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