Minerals

Mineral Physiology and Nutrition
General properties and bioavailability
• Minerals are inorganic elements and cannot be destroyed by cooking or storage, though minerals can be lost into cooking water if that water is discarded.
• Bioavailability is the portion of an ingested nutrient that is available for absorption and use. A mineral can be present in food but unavailable if it binds to other compounds.
• Phytates, found in legumes, seeds, nuts, and grains, bind divalent cations and reduce absorption. Affected minerals include iron, calcium, magnesium, and zinc.
• Oxalates, found in foods such as spinach, rhubarb greens, and sweet potatoes, can also bind minerals, especially calcium.
• Soaking foods may reduce phytate content; yeast can break down phytates during leavening. Cooking in water can reduce mineral content when minerals leach into the water.
• Interactions also affect mineral balance:
• High sodium intake and high protein intake can increase calcium excretion.
• High phosphorus intake can reduce magnesium absorption.
• High iron or calcium intake can inhibit manganese absorption.
• Vitamin C enhances absorption of non-heme iron but can reduce copper absorption.
• Trace-mineral content in plants depends partly on the soil and water where they are grown. Supplement use can raise intake above safe upper limits because trace minerals are needed only in small amounts.
Sodium (Na⁺)
• Function: Principal extracellular cation; important for action potentials, nerve communication, muscle contraction, and regulation of blood volume through its effect on osmolarity.
• Sodium is readily absorbed in the small intestine. The kidneys regulate blood sodium largely by adjusting reabsorption.
• The recommendation is based on chronic disease risk reduction, not an RDA or AI:
• 2.3 g sodium per day, equivalent to about 5.8 g salt.
• An ideal limit noted in the course materials is 1.5 g per day.
• Average U.S. intake was cited as about 3,400 mg per day, above the recommendation.
• Excess sodium can increase blood osmolarity and blood volume, contributing to elevated blood pressure and cardiovascular risk.
• Deficiency is uncommon from inadequate intake; it may occur after excessive sodium loss from vomiting, sweating, or diarrhea.
• Hyponatremia is abnormally low sodium concentration in extracellular fluid. It can occur when excessive water intake dilutes sodium and may cause headache, confusion, and seizures.
Potassium (K⁺)
• Potassium is the major intracellular cation. The sodium-potassium pump maintains higher potassium inside cells and is important for resting membrane potential and electrical excitability.
• Most dietary potassium is absorbed.
• Average intake is below the recommended level. Potassium-rich diets can help reduce hypertension risk by increasing sodium excretion and promoting blood-vessel dilation.
• Potassium deficiency can contribute to high blood pressure, irregular heartbeat, muscle weakness, glucose intolerance, kidney stones, and increased bone turnover.
• Aldosterone increases kidney sodium reabsorption and potassium secretion.
Calcium (Ca²⁺)
Functions and balance
• About 99% of the body’s calcium is stored in bones and teeth. Blood calcium is tightly regulated and usually changes little, even when intake is inadequate.
• Calcium contributes to muscle contraction, including regulation of heart contraction; intracellular signaling involving calmodulin and troponin; and blood clotting.
• Low blood calcium: Parathyroid hormone (PTH) release increases. PTH:
• Increases kidney calcium reabsorption, reducing calcium loss in urine.
• Stimulates kidney activation of vitamin D to calcitriol, which increases calcium absorption in the small intestine.
• Promotes calcium release from bone through osteoclast activity.
• High blood calcium: Calcitonin release increases. It promotes calcium excretion by reducing kidney reabsorption and may support calcium deposition in bone.
• Because blood calcium is maintained, inadequate calcium intake may be more evident in PTH or vitamin D measures than in blood calcium itself.
Intake, absorption, and health
• Calcium absorption is limited and affected by food composition, phytates, and oxalates. The lecture cited an absorption range of 5–30%; the reference sheet gives 30–50%, so the materials provide different estimates.
• Only about half of the U.S. population was described as meeting calcium recommendations. Recommendations are particularly important during adolescence, when peak bone mass is developing, and in older adults.
• Low calcium availability during adolescence and young adulthood can limit bone growth and peak bone mass, increasing the risk of osteoporosis later in life.
• Calcium deficiency in children can impair growth. Excess calcium, particularly from supplements, may increase kidney-stone risk. The reference sheet lists the upper limit as twice the RDA.
Magnesium (Mg²⁺)
• Magnesium is a cofactor in many enzymatic reactions and is involved in ATP production, membrane transport, and synthesis of proteins, fats, and nucleic acids.
• It participates in muscle contraction and clotting, generally opposing some calcium effects.
• Average intake is below recommendations. Low intake may be associated with cardiovascular disease, stroke, hypertension, and diabetes; magnesium deficiency can also impair central nervous system activity and contribute to vessel constriction.
• The reference sheet describes the safety margin for supplemental magnesium as narrow: the upper limit applies to non-food sources and is at or below the RDA. The lecture advised favoring dietary sources over supplements.
Phosphorus and sulfate
• Phosphorus: Functions in pH buffering and is part of DNA, ATP, phospholipids, and phosphoproteins. Deficiency is unlikely because phosphorus is present in many foods. Excess can disrupt kidney function and bone metabolism; the reference sheet lists an upper limit of three times the RDA.
• Sulfate: Sulfur-containing amino acids, especially cysteine and methionine, provide much of the dietary sulfur. Sulfur contributes to protein structure; more rigid proteins such as hair and skin have high sulfur content. Deficiency is unlikely when protein intake is adequate.
Trace Minerals
General considerations
• Trace minerals are needed in small quantities, making excessive intake from supplements a concern.
• Multiple trace minerals affect insulin synthesis, storage, release, or action. Mineral imbalances can also alter the function of other minerals.
• Manganese excess can aggravate iron deficiency. Selenium deficiency can interfere with activation of thyroid hormone. Iron deficiency increases vulnerability to lead poisoning.
• Local factors—including soil composition, water sources, and lead pipes or paint—can affect mineral and contaminant exposure.
Iron (Fe)
Forms, absorption, and transport
• Iron functions in oxidation-reduction reactions, electron transport, and enzymes involved in making amino acids, collagen, hormones, and neurotransmitters.
• Heme iron comes from animal foods and is associated with hemoglobin. It is absorbed efficiently; the lecture stated that about 40% of absorbed iron can come from heme, while the reference sheet says heme accounts for about 10% of dietary iron.
• Non-heme iron is found in plant and animal foods. It is commonly ingested in ferric form (Fe³⁺) and must be reduced to ferrous iron (Fe²⁺) for absorption.
• Vitamin C enhances non-heme iron absorption by converting ferric to ferrous iron when consumed at the same time. Phytates reduce absorption by binding divalent cations.
• Meat contains an unidentified “meat factor” that enhances non-heme iron absorption; its mechanism has not been established.
• Vegetarians may need to consume about 1.8 times the recommended amount of iron to account for lower non-heme absorption. The reference sheet notes that women’s iron recommendations are roughly double men’s, and that women have difficulty meeting the RDA.
• Iron absorption responds to iron stores: low stores increase absorption. The liver stores iron bound to ferritin; excess iron can be stored as hemosiderin and released more slowly.
• Hepcidin regulates iron entry into and release from cells. Low iron reduces hepcidin, permitting greater iron availability.
• Iron is transported in the blood by transferrin. In iron deficiency, unbound transferrin increases. Iron is recycled from hemoglobin and transported, including from the liver to bone marrow, bound to transferrin.
Deficiency and toxicity
• Iron deficiency is the most common nutrient deficiency worldwide. Risk factors include menstruation, chronic bleeding, growth in children, and overweight or obesity.
• Deficiency can progress to microcytic, hypochromic anemia, with fatigue, weakness, and headaches.
• Indicators can change in stages:
1. Iron stores decline, reflected by lower serum ferritin.
2. Transported iron declines, with increased transferrin and less iron bound to transferrin.
3. Hemoglobin and hematocrit decline.
• Iron overload can cause hemochromatosis. Causes include repeated transfusions and excessive supplementation; treatment may include regular blood removal.
• Iron in an unbound state can promote free-radical reactions. Excess vitamin C can release iron from ferritin and may worsen iron overload; iron status should be evaluated before treating suspected deficiency.
• The reference sheet lists the iron upper limit as 2.5 times the women’s RDA and notes that food fortification can make excessive intake harder for people with lower iron requirements to avoid.
Zinc (Zn²⁺)
• Zinc supports enzymes involved in metabolism and digestion, transcription factors that regulate gene expression, insulin synthesis and release, thyroid-hormone action, immune function, clotting, retinal metabolism, and growth and development.
• About 5–50% of zinc in food may be absorbed; fractional absorption falls as zinc intake rises. Phytates reduce absorption, so zinc from high-phytate plant diets may be less available.
• Intestinal mucosal cells store zinc bound to metallothionein. Zinc is transported in the body by albumin.
• Zinc secreted by the exocrine pancreas into the intestine can be reabsorbed, forming an enteropancreatic circulation.
• Zinc deficiency can cause broad effects, including reduced appetite and metabolic rate, impaired growth, and changes in insulin or thyroid function. The lecture emphasized that deficiency may resemble other metabolic disorders and requires consideration of other causes.
• The reference sheet notes that U.S. average intake is generally above the RDA, but deficiency risk may be higher with vegetarian or high-phytate diets.
Iodine (I⁻)
• Iodine is a component of thyroid hormones, which regulate metabolic rate, growth, and reproduction.
• Reduced iodine absorption or intake lowers thyroid-hormone production and can increase thyroid-stimulating hormone (TSH), leading to goiter.
• Both iodine deficiency and excess can cause goiter, through different effects on thyroid activity.
• Goitrogens—including soy, cassava, millet, and cruciferous vegetables—can inhibit iodine absorption.
• Severe deficiency during pregnancy can impair physical and mental development; even mild deficiency in children can affect cognition. Iodized salt can improve intake, but processed foods may not use iodized salt.
• The reference sheet lists the iodine upper limit as seven times the RDA.
Selenium (Se)
• Selenium is part of glutathione peroxidase, an antioxidant enzyme, and contributes to thyroid-hormone metabolism.
• Deficiency can impair thyroid-hormone activation and is associated with Keshan disease (cardiomyopathy). Risk can be elevated in regions where soil is selenium-poor.
• Toxicity can cause hair loss and brittle nails. The reference sheet lists the upper limit as seven times the RDA.
Copper (Cu)
• Copper is a component of enzymes involved in oxygen-related reactions, collagen synthesis, histamine inactivation, and serotonin degradation.
• It is involved in converting ferrous iron to ferric iron so iron can bind to transferrin.
• Deficiency is rare with a typical U.S. diet. Toxicity is uncommon except with supplements or certain genetic disorders; excess copper can damage the liver. The reference sheet lists the upper limit as 11 times the RDA.
• Vitamin C can reduce copper absorption.
Manganese (Mn)
• Manganese is a cofactor for enzymes involved in carbohydrate, lipid, and amino-acid metabolism and bone formation. It is also involved in conversion of pyruvate to a citric-acid-cycle intermediate.
• Deficiency is rare. Phytates and high iron or calcium intake can reduce manganese absorption.
• Excess manganese can aggravate iron-deficiency symptoms. The reference sheet lists the upper limit as six times the AI.
Body Fluids and Water Balance
Fluid compartments and osmosis
• About two-thirds of body fluid is intracellular, where potassium is the predominant cation. About one-third is extracellular, where sodium is predominant.
• Extracellular fluid includes intravascular fluid (blood plasma) and interstitial fluid between cells.
• Selectively permeable membranes separate compartments; water movement also depends on aquaporin expression.
• Water moves toward the compartment with higher solute concentration (higher osmolarity).
• Because sweat is hypo-osmotic relative to extracellular fluid, sweating removes proportionally more water than solute. This raises blood and extracellular-fluid osmolarity and draws water out of cells, reducing cell volume and contributing to dehydration symptoms.
Sweating and blood-pressure regulation
• Sweat is a filtrate of blood. Sweat glands reabsorb some sodium and other ions as fluid passes through their ducts, making sweat less concentrated than extracellular fluid.
• Sweating reduces blood volume and venous return, which lowers stroke volume. During prolonged exercise, heart rate rises to help maintain blood delivery.
• Reduced blood pressure and stretch at the kidney’s afferent arteriole, together with increased sympathetic activity, stimulate renal granular cells to release renin.
• The renin–angiotensin–aldosterone system (RAAS) proceeds as follows:
1. Renin converts liver-produced angiotensinogen to angiotensin I.
2. Angiotensin-converting enzyme (ACE), including ACE in the lungs, converts angiotensin I to angiotensin II.
3. Angiotensin II constricts arterioles, stimulates thirst, and promotes aldosterone release from the adrenal cortex.
4. Aldosterone increases kidney sodium reabsorption and potassium secretion. Retained sodium supports water retention and helps restore blood volume and pressure.
• Increased extracellular-fluid osmolarity stimulates antidiuretic hormone (ADH) release from the posterior pituitary. ADH increases kidney water reabsorption and stimulates thirst.
• Together, sodium and water retention help restore blood volume and pressure; water intake helps reduce elevated osmolarity and restore cell volume.
Water input and output
• Water input comes from drinking, foods, and metabolism. Fruits and vegetables contain substantial water; dry foods such as crackers contain little.
• Metabolism produces a small amount of water—about 200 mL per day in an average human—not enough to meet daily needs.
• Water output includes:
• Obligatory kidney loss: The kidneys can concentrate urine only to about 1,200 mOsm, so some water loss is unavoidable.
• Sweating: Variable with activity, temperature, humidity, and individual sweat rate.
• Respiratory loss: Dry air must be humidified in the airways. Loss is greater in cold or arid environments; nasal breathing allows more humidification than mouth breathing.
• Fecal loss: Some water remains in feces rather than being reabsorbed.
• Diarrhea, vomiting, burns, and diabetes-related polyuria can increase water loss.
• Caffeine and alcohol can have diuretic effects. Water is generally preferable for hydration; needs may rise substantially with heat, dry conditions, or prolonged activity.
• The general water-intake guidance discussed was about 2–3 liters per day (8–12 cups), with more needed when losses are elevated. Hard water contains more calcium and magnesium than soft water and may reduce lead leaching from pipes.
Dehydration and hyperhydration
• Dehydration results when water output exceeds water input. Symptoms are related to percentage of body-weight loss:
• 1–2%: fatigue, discomfort, loss of appetite.
• 3–4%: impaired performance, reduced urine, impatience.
• 5–6%: headache, impaired temperature regulation, increased respiration.
• 7–10%: dizziness, muscle spasms, delirium.
• A 10-pound loss in a 200-pound person is 5% of body weight.
• Impaired temperature regulation and cessation of sweating in a hot environment are warning signs requiring intervention.
• Depending on severity and cause, rehydration may require oral rehydration therapy or medical treatment such as IV saline.
• Hyperhydration is excessive water gain relative to loss. Excessive water intake can dilute extracellular sodium and cause hyponatremia, with headache, confusion, and seizures; severe cases can be fatal.
Mineral Review Concepts
• Sodium ingestion raises blood osmolarity, which stimulates ADH release; ADH increases water reabsorption and helps counter the osmolarity increase.
• Minerals are highly water-soluble, so cooking in water can reduce mineral content if the cooking water is discarded.
• Absorbed iron is primarily in ferrous form. Vitamin C increases non-heme iron absorption, while meat contains an unidentified factor that also enhances absorption.
• Iron deficiency can increase unbound transferrin; serum ferritin reflects iron stores.
• Potassium deficiency can increase blood pressure partly by reducing sodium excretion and by reducing potassium-related vasodilation.
• Low blood calcium stimulates PTH, which increases calcitriol synthesis and calcium retention; high blood calcium stimulates calcitonin.
• Cold, dry air increases respiratory water loss. Rising plasma osmolarity draws water out of cells, reducing cell volume.
• Low blood volume stimulates renin, then angiotensin II and aldosterone; aldosterone primarily increases sodium reabsorption.
• Phytates reduce absorption of divalent cations by binding them.
• Iron-deficiency anemia is typically microcytic and hypochromic.