Lecture 34

Question 1

minerals

Answer 1

• macrominerals: Ca, P, Mg, Na, K, Cl, S
• microminerals: Fe, Zn, Cu, Se, Cr, I, Mn, Mo, F
• ultra trace minerals: As, B, Ni, Si, V, Co
• non-nutrient: Pb

pg 839

Question 2

mineral overview

Answer 2

• mineral balance tightly regulated -> GI tract does absorption from food based on needs, kidneys excrete excess or reabsorbs
• not destroyed by heat, acid, oxygen, or UV
• can leach into cooking water
• fluid/electrolyte and acid/base balance -> extracellular/intracellular
• bone and teeth formation
• cofactors in: antioxidant systems, energy production, muscle contraction, nerve transmission
• mineral deficiency and toxicity is rare

pg 842

Question 3

sodium and chloride

Answer 3

maintains water balance, osmotic equilibrium, acid-base balance and membrane potential (electrical gradient)

• primary extracellular electrolytes
• absorption of glucose, galactose and free AAs by Na+-linked transporters
• Cl- for HCl in stomach
• hypertension: where sodium goes, water follows; stimulates ADH (vasopressin) by pituitary -> increases water retention, blood volume, and vasoconstriction
• hyper- and hyponatremia: excess water loss (hyper) or decreased aability to excrete water (hypo)

pg 844

Question 4

sodium

Answer 4

• high sodium intake correlates with HTN, heart disease, and stroke
• DASH eating pattern aims to reduce sodium and increase potassium intakes
• higher Na intake is associated with higher Ca excretion
• sodium deficiency: muscle cramps, mental apathy, loss of appetite; hyponatremia during ultra-endurance athletic activities
• sodium - excessive intakes: edema and acute HTN, prolonged high intake associated with HTN
• processed foods and added table salts are primary sources

pg 844

Question 5

potassium

Answer 5

• nutrient of public health concern -> especially for people on dialysis
• major intracellular cation (intracellular electrolyte)
• concentration differential maintained by Na+/K+ ATPase
• narrow range of normal serum K+ (hyper- or hypokalemia can result in cardiac arrythmias and skeletal muscle weakness)
• thiazide and loop diuretics cause K loss
• K helps lower HTN -> causes kidneys to excrete excess Na
• helps buffer blood and preserve Ca and P in the bones
• increased risk of HTN, kidney stones, and loss of bone mass with moderately low dietary intake
• deficiency/excess: muscle weakness, lethargy, paralysis, cardiac arrhythmias
• rich sources: meat, milk, fruits, veggies, grains, legumes

pg 846

Question 6

calcium

Answer 6

• nutrient of public health concern
• ~98% of bone as hydroxyapaptite
• involved in: signaling, muscle contraction, blood clotting
• binds to and alters enzyme activity: calmodulin, phospholipase A2 and protein kinase C
• sources: dairy products, fortified foods (juices, cereals, some mineral waters), beet greens, bok choy, broccoli, kale

pg 848

Question 7

phosphorus

Answer 7

• important for people on dialysis
• ~85% in bone as hydroxyapatite (crystal form)
• intracellular organic compounds: phospholipids, nucleic acids, ATP, and creatine phosphate
• as ATP, transferred to kinase and as Pi to phosphorylase -> removal or addition of phosphorus regulate the enzyme activity
• sources: animal foods, protein, peas, phosphate additives

pg 848

Question 8

calcium regulation

Answer 8

• dietary deficiency does not change blood calcium -> it reduces bone calcium
• allows for homeostasis of serum levels

pg 849

Question 9

hypercalcemia

Answer 9

• over production of PTH (hyperparathyroidism)
• malignancy
• causes constipation and kidney stones
• treatment: limit calcium intake

pg 850

Question 10

hypocalcemia

Answer 10

• deficiency of PTH (hypoparathyroidism)
• hypocalcemic tetany
• vitamin D deficiency
• chronic low intake of calcium
• treatment: vit D and Ca supplements or foods high in both

pg 850

Question 11

hyperphosphatemia

Answer 11

• decreased PTH levels
• renal failure
• excess free phosphorus can combine with Ca2+ and form crystals -> deposit in soft tissue
• problem for dialysis patients
• treatment: limit P intake, P binders

pg 850

Question 12

hypophosphatemia

Answer 12

• hereditary (hereditary hypophosphatemia rickets -> early childhood)
• overuse of aluminum-containing antacids
• overuse of phosphate binders
• treatment: P supplements or foods high in P (processed foods), active vitamin D

pg 850

Question 13

calcium and phosphate

Answer 13

Ca²⁺/Pi ratio important for bone formation -> needs to be roughly 2/1

pg 850

Question 14

epidemiology - Rickets

Answer 14

• not a reportable disease in the USA (but still seen)
• nutritional rickets is the main type reported outside the US, followed by vitamin D-dependent, vitamin D-resistant, and renal rickets
• CDC says there are 5 cases per million children aged 6 mths to 5 yrs of age
• most affected children are African American

pg 851

Question 15

magnesium

Answer 15

• deficiencies are rare: weakness, confusion, convulsions, bizarre muscle movements of eye and face, hallucinations, difficulty swallowing, growth failure in children
• alcohol abuse, protein malnutrition, kidney disorders, prolonged vomiting and diarrhea
• insufficient Mg intake associated with T2D
• Mg protects against heart disease and HTN -> low magnesium restricts walls of arteries and capillaries
• Mg toxicity: symptoms from nonfood Mg are diarrhea, alkalosis, and dehydration
• sources: nuts, legumes, whole grains, dark green veggies, seafood, chocolate, cocoa
• too much magnesium from supplements can stop the heart (lead to cardiac arrest)

pg 853

Question 16

iron

Answer 16

• nutrient of public health concern
• hemoglobin, myoglobin
• component of catalytic (hydroxylase) and noncatalytic (ETC carrier proteins and heme prosthetic group) reactions
• free ion can be toxic because of ROS production
• iron is absorbed in Fe²⁺ form and stored (bound to ferritin) or transported (bound to transferrin) in Fe³⁺
• ferritin in healthy individuals is about 1/3 saturated
• ferroportin is regulated by hepatic peptide, hepcidin -> induces internalization and lysosomal degradation of ferroportin
• hepcidin expression is suppressed during Fe deficiency

pg 855

Question 17

iron absorption enhancers and inhibitors

Answer 17

Absorption-Enhancing Factors

• MFP factor enhances the absorption of non-heme iron
• when non-heme iron is consumed with vitamin C, absorption of iron increases
• citric acid and lactic acid from foods, HCl from the stomach, and sugars enhance non-heme iron absorption

Absorption-Inhibiting Factors

• phytates and fibers from legumes, grains, rice
• veggie proteins in soybeans, legumes, nuts
• calcium in milk
• tannic acid and other polyphenols in tea, coffee, grains, oregano, red wine

MFP factor unidentified component of meat, fish, and poultry that enhances the absorption of non-heme iron present in other foods eaten at the same time

pg 856

Question 18

sources of iron

Answer 18

• red meats, fish, poultry, shellfish
• eggs
• legumes
• enriched/fortified breads and cereals
• broccoli, parsley

pg 856

Question 19

iron deficiency and overload

Answer 19

• recycled iron meets 90% of body needs
• Fe deficiency: microcytic anemia -> decreased Hb synthesis, decreased RBC size
• Fe overload: hereditary hemochromatosis -> mutation of high iron (HFE) gene -> damage to the liver, pancreas and heart; hyperpigmentation with hyperglycemia (bronze diabetes); mutations to the proteins of Fe metabolism (lower levels of hepsidin)

pg 857

Question 20

iron deficiency anemia

Answer 20

• women, preterm infants, toddlers at higher risk -> children can develop irreversible intellectual impairment
• trauma (sudden large blood loss)
• symptoms: fatigue, pallor (pale), irritability, SOB, sore tongue, brittle nails, pica (craving non-food substances), frontal headache, blue tinge to whites of eyes, decreased appetite
• treatment: Fe supplements, take with orange juice or vitamin C source, avoid taking with milk or antacids

pg 858

Question 21

copper

Answer 21

• important for ferroxidases such as ceruloplasmin and hephaestin (several enzymes require copper)
• major food sources: legumes, whole grains, and seafood

pg 860

Question 22

Menkes disease

Answer 22

• X-linked, ATP7A gene, kinky hair disease
• efflux of dietary copper from enterocytes into portal circulation by copper transporting ATPase (ATPaseA) is impaired -> systemic copper deficiency
• progressive neurological degeneration and CT disorders
• urinary and serum free and ceruloplasmin bound copper are low
• treatment: subQ injections of Cu solution, treatment w/in 28 days of birth, low body temp (hypothermia) in newborn period, prolonged yellowing of skin in newborn
• considered a lethal condition

pg 861

Question 23

Wilson disease

Answer 23

• ATP7B gene, have at birth
• efflux of excess copper from liver by ATPaseB is impaired -> accumulates in liver, leaks into blood, deposited into brain, eyes, kidney and skin, hepatic dysfunction
• free copper is high in serum and urine
• symptoms: failure to thrive, menstrual period irregularities, increased risk of miscarriage and infertility, anemia, easy bruising and prolonged bleeding, kidney stones, early-onset arthritis, osteoporosis, mental health symptoms
• also, Kaiser-Fleischer rings (corneal deposits of copper)
• treatment: diet low in Cu, Cu chelators

pg 862

Question 24

iodine

Answer 24

• for synthesis of thyroid hormones, triiodothyronine (T3) and thyroxine (T4)
• thyroperoxidase does three things -> oxidation, iodination, and coupling to synthesize T3 or T4
• 90% of the secreted thyroid hormone is T4
• sources: iodized salt, seafood, seaweed, bread and dairy products -> plants grown in iodine-rich soils, animals that feed on plants grown in iodine-rich soils
• function: in target tissue (liver and developing brain) -> T4 converted to T3 by Se-containing deiodinases -> T3 binds to nuclear receptor -> binds to the thyroid response element in DNA

pg 864

Question 25

hypothyroidism

Answer 25

• under ingestion of iodine -> excessive stimulation of TSH
• fatigue, weight gain, decreased thermogenesis, and decreased metabolic rate
• congenital hypothyroidism: irreversible intellectual disability, short stature
• Hashimoto’s Thyroiditis: autoimmune destruction of thyroid peroxidase
• low salt diets
• goitrogen (glucosinolates in cabbage) overconsumption

pg 865

Question 26

hyperthyroidism

Answer 26

• overproduction of thyroid hormone
• Graves Disease: an antibody mimicking effects of TSH -> dysregulation of thyroid hormone production
• treatment: radioiodine therapy, antithyroid drugs, prednisone for eyes

pg 865

Question 27

zinc

Answer 27

• sources: shellfish, meats, poultry, milk, cheese, whole grains, legumes
• deficiency: may occur in pregnant women, young children, the elderly; GROWTH retardation; delayed sexual maturation; impaired immune function; hair loss, eye and skin lesions; altered taste, loss of appetite, and delayed wound healing
• toxicity: loss of appetite, impaired immunity, low HDL, copper and iron deficiencies, vomiting and diarrhea, exhaustion, headaches

pg 867

Question 28

selenium

Answer 28

• sources: seafood, meat, whole grains, veggies (dependent on soil content)
• antioxidant -> glutathione peroxidase (selenocysteine) -> basis for RDA
• thyroid hormones (deiodinases)
• deficiency: TPN, associated with heart disease and some cancers; Keshan disease -> endemic cardiomyopathy with high fatality rates, congestive heart failure, acute heart failure, and cardiac arrhythmia
• toxicity: loss and brittleness of hair and nails; skin rash, fatigue, irritability, and nervous system disorders; garlic breath odor

pg 868

Question 29

lead is NOT a nutrient

Answer 29

• no known requirement for lead in diet
• may: damage fertility, damage unborn child, cause harm to breast-fed children (effects on or via lactation)
• very toxic to aquatic life with long lasting effects
• cut off for children: 5 μg/dL in blood (10 μg/dL for pregnant women) -> biological exposure index (BEI) is 30 μg/dL; typically asymptomatic
• 100 mg/m³ in air is immediately dangerous to life or health (IDLH)
• lead based paint, dust, contaminated soil, lead plumbing, folk remedies (pay-loo-ah to treat fevers)

pg 870