Minerals

Dr Reed Berger

Nutrition Course Director

Visiting Clinical Professor

GI/Nutrition

General Lecture Format

� -test questions will come from clinical correlations--these will be relevant in clinical training and practice

� -items with *** and those with photos are important!!

Minerals

� A naturally occurring , homogeneous,

inorganic substance required by humans in

amts of 100 mg/day or more

� -functions

� -high and low serum levels

� -absorption

� -excretion

� -deficiency

� -toxicity

calcium

Calcium

-most abundant mineral in the body

-99% of calcium is in the bones and teeth

-the remaining 1% is in the blood and ECF in

cells and soft tissues

Skeletal Calcium

-if there is no reserve, calcium is drawn from bone—leading to deficiency

�Serum levels: 8.8 to 10.8 mg/dl

� **when albumin is low (malnutrition,

liver dz), calcium is decreased

�Ratio: for each gram albumin is

decreased below 4, add 0.8 to calcium

� -ionized calcium is increased in acidosis and decreased in alkalosis (increased bicarb binds calcium)

� ***-example: in resp alkalosis, total serum calcium is normal, but ionized is low—always check ionized level with acid/base disorders

Functions

� -building and maintaining bones and teeth

� -transport fxn of cell membranes and membrane stabilizer

� ***-nerve transmission and regulation of heartbeat—use calcium gluconate IV to treat hyperkalemia (EKG—peaked T waves)

� -ionized form initiates formation of the blood clot

� -cofactor in conversion of prothrombin to thrombin

Absorption

� -***absorbed mainly in the acidic part of the duodenum

� -absorption is decreased in the lower GI tract which is more alkaline

� 20-30% of digested calcium is absorbed

� Absorption is thru 1,25 (OH)2D3 (vit D derivative)--stimulates production of calcium binding protein and alk phos

� -unabsorbed form is excreted in feces

Factors that increase calcium

absorption

� -***more efficiently absorbed when the body is deficient

� -best absorbed in acidic environment (upper duodenum)

� -HCL in stomach allows better absorption in the proximal duodenum

� -taking calcium with food increases abs

� -fat increases intestinal transit time and increases absorption

Factors that decrease

absorption

� -***lack of vitamin D

� -oxalic acid forms insoluble complex which decreases absorption (rhubarb, spinach, chard, beet greens)

� -phytic acid found in outer husks of cereal grains also form insoluble complex

� -alkaline medium decreases abs.(lower GI tract)

� Aging decreases absorption

Maintenance of serum level

� -parathormone (PTH) by the parathyroid gland and thyrocalcitonin secreted by the thyroid gland maintain serum levels

� -***with decreased serum calcium levels, PTH increases and causes transfer of calcium from bone to blood to increase serum levels

� -decreased levels also cause kidney to reabsorb calcium more efficiently (might normally be excreted in the urine) and to increase intestinal absorption

� -when blood levels are increased, calcitonin acts by the opposite mechanisms as PTH to decrease serum levels

Maintenance of serum level

cont’d

� ***-always need to correct low Mg level

before treating a low calcium level

� -hypomagnesemia decreases tissue

responsiveness to PTH

Causes of hypocalcemia

-***malabsorption

-small bowel bypass, short bowel

-vit D deficiency

-alcoholism

-***chronic renal insufficiency

-***diuretic therapy

Causes of hypocalcemia

cont’d

-hypoparathyroidism

-***hypomagnesemia

-sepsis

-pseudohypoparathyroidism

-calcitonin secretion with medullary

carcinoma of the thyroid

Causes of hypocalcemia

cont’d

-***associated with low serum albumin

(ionized calcium will be wnl)

-decreased end organ response to vit D

-hyperphosphatemia

-***aminoglycosides, plicamycin, loop

diuretics, foscarnet

Causes of hypercalcemia

-milk-alkali syndrome

-vit D or vit A excess

-primary hyperparathyroidism

-secondary hyperparathyroidism (renal insuff, malabsorption)

-acromegaly

-adrenal insufficiency

Causes of hypercalcemia

cont’d

***Neoplastic Disease

-tumors producing PTH-related proteins (ovary, kidney, lung)

-***mets to bone

-lymphoproliferative disease including multiple myeloma

-secretion of prostaglandins and osteolytic factors

Causes of hypercalcemia

cont’d

-***thiazide diuretic

-sarcoidosis

-paget’s disease of bone

-***immobilization

-familial hypocalciuric hypercalcemia

-complications of renal transplant

-iatrogenic

Excretion

� -normal is 65-70% of ingested calcium

to be excreted in the feces and urine

� -strenuous exercise increases loss (in

sweat)

� -***immobility with bed rest and space

travel increase calcium loss because of

lack of bone tension

RDA

� -see handout

sources

Deficiency

� 1)***bone—to be discussed in osteoporosis lecture

� 2) tetany—decreased serum levels increase the irritability of nerve fibers resulting in muscle spasms, fatal laryngospasm� ***-Chvostek’s sign: contraction of the facial m. after tapping the facial n.

� ***-Trousseau’s sign: carpal spasm after occlusion of the brachial a. with blood pressure cuff for 3 min

� 3) HTN—controversial

� 4) prolonged QT--arrythmias

Toxicity

� -***polyuria, constipation, bone pain,

azotemia, coma

� -”stones, bones(bone pain), groans,

psychiatric overtones”

Phosphorus

�Levels maintained by parathyroid gland

Functions

� -structure of teeth and bones

� -essential component in cell

membranes, nucleic acids,

phospholipids

� -phosphorylation of glucose

� -buffer system in ICF and kidney

absorption

-best occurs when calcium and phos are

ingested in equal amts (milk)

-vit D also increases absorption

RDA

� -see table (and for all RDA’s)

sources

Sources

***dietary sources should be restricted in renal disease (usually see increased phos, decreased Ca)

� -protein sources

� -meat, poultry, fish, eggs, legumes, nuts, milk, cereals, grains

Renal Disease

Causes of hypophosphatemia

-starvation

-TPN with inadequate phos content

-malabsorption, small bowel bypass

-vit D deficient and vit D resistant

osteomalacia

Causes of hypophosphatemia

cont’d

-phosphaturic drugs: theophylline, diuretics, bronchodilators, corticosteroids

-hyperparathyoidism (primary or secondary)

-hyperthyroidism

-renal tubular defects

-hypokalemic nephropathy

-inadequately controlled DM

-***alcoholism

Causes of hypophosphatemia

cont’d

Intracellular shift of phosphorus

-administration of glucose

-anabolic steroids, estrogen, OCP

-respiratory alkalosis

-salicylate poisoning

Electrolyte abnormalities

-hypercalcemia

-hypomagnesemia

-metabolic alkalosis

Causes of hypophosphatemia

cont’d

Abnormal losses followed by inadequate

repletion

-***DM with acidosis—with aggressive therapy

-***recovery from starvation or prolonged catabolic

state—refeeding syndrome

-***chronic alcoholism, especially with nutritional

repletion, assoc with hypomagnesemia—”

-recovery from severe burns

Causes of hyperphosphatemia

-excessive growth hormone

(acromegaly)

-hypoparathyroidism assoc with low Ca

-pseudohypoparathyroidism assoc with

low Ca

-***chronic renal insufficiency

-acute renal failure

Causes of hyperphosphatemia

cont’d

Catabolic states, tissue destruction

-stress or injury, rhabdomyolysis (esp with

renal insufficiency)

-chemotherapy of malignant disease,

particularly lymphoproliferative disease

Excessive intake or absorption

-laxatives or enemas containing phosphate

-hypervitaminosis D

Deficiency

� -fatal

� -usually rare with food intake

� -***respiratory muscle collapse

� -heart failure

� -muscle aches, bone pain, and fracture

Toxicity

� -symptoms of the primary disorder

Magnesium

Function

-bone, muscle contractility, nerve

excitability

-antagonistic to calcium

--in a muscle contraction, Mg relaxes, and

calcium contracts

--low Mg can cause pregnancy induced

HTN

Absorption / Excretion

� -absorption varies

� -similar to calcium (low pH, upper GI), however, no Vit D required-kidney conserves Mg when intake of Mg is low

� -large losses with vomiting because of high levels of gastic juice

sources

Sources

� -seeds, nuts, legumes, unmilled cereal

grains, dark greens

� -fish, meat, milk, fruits

� -lost during refining of flour, rice, vinegar

Causes of hypomagnesemia

-malabsorption, chronic diarrhea, laxative abuse

-prolonged GI suction

-small bowel bypass

-malnutrition

-***alcoholism

-refeeding

-TPN with inadequate Mg

Causes of hypomagnesemia

cont’d-DKA

-diuretics

-hyperaldosteronism, Barrter’s syndrome

-hypercalcuria

-renal Mg wasting

-hyperparathyroidism

-postparathyroidectomy

-vit D therapy

-aminoglycosides, ***cisplatin, ampho B

Causes of hypermagnesemia

Decreased renal fxn

***Increased intake—abuse of Mg

containing antacids (MOM) and

laxatives in renal insufficiency

Deficiency

� -anorexia, growth failure, cardiac and

neuromuscular changes—weakness,

irritability, mental derangement

� -tetany, muscle cramps

Toxicity

� -respiratory—depression, apnea

� -CV—hypotension, cardiac arrest, EKG (prolonged QRS and QT, heart block, peaked T waves)

� -GI—N/V

� -neuromuscular—paresthesias, somnolence, confusion, coma, hyporeflexia, paralysis, apnea

Iron

Function

� -respiratory transport of O2 and CO2

� -immune system

� -cognitive performance

� -found in Hgb (in RBC’s) and myoglobin

(in muscles)

� -cytochrome p450 system

Absorption and transport

� -dietary iron exists in heme (Hgb and myoglobin) and non-heme

� -***heme Fe is absorbed better

� -non-heme Fe has to be present in the duodenum or upper jejunum in soluble form if it is to be absorbed

� -in Fe deficiency, 50% can be absorbed

� -***2-10% of Fe from veggies is absorbed and 10-30% is absorbed from animal protein

Factors affecting absorption

� -***ascorbic acid is the most potent enhancer

� -animal proteins (beef, pork, veal, lamb, liver, fish, chicken) enhance

� -but, proteins from cow’s milk, cheese, eggs, don’t

� -gastric acidity enhances absorption (antacids interfere)

� -pregnancy, increased growth, Fe defic all increase deficiency

� -phytate and tannins decrease abs

� -Fe used for enrichment are less

absorbed than elemental Fe

� -increased intestinal motility decreases

absorption because it decreases

contact time for absorption

Storage

� -stored as ferritin and hemosiderin

� -long term high Fe ingestion or frequent blood transfusions can lead to accumulation of Fe in the liver

� -***hemosiderosis develops in individuals who consume a lot of Fe or have a genetic defect resulting in increased Fe absorption

� -in associated with tissue damage, it is called hemochromatosis

Excretion

� -lost thru bleeding, feces, sweat,

exfoliation of hair and skin

� -none in urine

Sources and Intakes

� -best source is liver

� -oysters, shellfish, kidney, lean meat, poultry, fish

� -dried beans, veggies, dark molasses

� -egg yolks, dried fruit, enriched breads,

� -requirements are highest in infancy and adolescence

� -females stay high because of menstruation

� -decrease with menopause and increased with pregnancy

Deficiency

� -most common deficiency

� -most at risk: <2 yrs old, teens, pregnancy, elderly

� -***anemia (hypochromic, microcytic)

� -tx: diets high in absorbable Fe and/or Fe supplements (ferrous sulfate, ferrous gluconate)

� -can be caused by injury, hemorrhage, illness, poor diet

Zinc

� -involved in synthesis or degradation of CHO, proteins, lipids, nucleic acids

� -stabilizes RNA and DNA

� involved in transcription and replication

� -needed for bone enzymes and osteoblastic activity

absorption

� Impaired absorption in Crohn’s or

pancreatic insufficiency

� -plasma zinc levels act as acute phase

reactants and fall by 50% with injury

(like platelets)

Inhibiting Factors

� -fiber, phytate

� -high doses of copper

� -Fe competes with zinc for absorption

Enhancing Factors

� -glucose, lactose, and soy protein

� -red wine

� -human milk

Excretion

� -feces—almost entirely

� -***in urine with starvation, nephrosis,

DM, alcoholism, hepatic cirrhosis (zinc

supplementation in encephalopathy),

porphyria

Sources and Intakes

� -meat, fish, poultry, milk

� -oysters, shellfish, meat, liver, cheese,

whole grains, dry beans, nuts

Deficiency

� -short stature, hypogonadism, anemia

� -with diets high in unrefined cereal and

unleavened bread

� -delayed wound healing, alopecia

� ***-acrodermatitis enteropathica=AR dz with

zinc malabsorption

� -eczematoid skin lesions, alopecia, diarrhea,

bacterial and yeast infections, death

� -immunologic deficits—lymphopenia,

thymic atrophy

***Causes of

deficiency�Anorexia Nervosa

� TPN without zinc (diarrhea, small bowel fistulas)

�High intake of phytate, tannins, binding drugs (EDTA), oxalate

�High iron intake

�Malabsorption syndromes

�Acrodermatitis enteropathica

�Diarrhea

�Pancreatico-cutaneous fistula

�Proximal entero-cutaneous fistulas

�Hemolytic anemias (sickle cell anemia)

�Renal failure patients on dialysis

***Zinc Deficiency

42 yo female with chronic uremia on dialysis. Recently started

on iron supplement for anemia. Presents with rash,

hypogeusia, hyposmia and poor dark adaptation.

Acrodermatitis

Enteropathica

�Autosomal recessive disease

associated with a defect causing a

reduction in zinc absorption

�Can be treated by pharmacologic

doses of oral zinc

Acrodermatitis

Enteropathica

Toxicity

� ->100-300 mg/d

� -rare

� -interferes with copper absorption

� -decrease in HDL

� -GI irritation, vomiting

Fluoride

� -tooth enamel

� -resistance to dental caries

� -fluoridation of h20 has decreased

caries by half

� -found in drinking h20, teflon pots and

pans (cooked in these)

� -toxicity at doses >0.1 mg/kg/d

Prevention of dental caries

� ***Incidence of dental fluorosis (mottled

teeth) occurs with increased intake

above 1-2 ppm.

Mottled teeth in fluorosisMottled teeth in fluorosis

Maganese

� -found in many enzymes

� -connective and bony tissue formation

� -growth and reproduction

� -CHO and lipid metabolism

Absorption and Excretion

� -after absorption, it appears rapidly in

the bile and is excreted in the feces

� -concentrated in liver and increases with

liver disease

Sources and Intakes

� -whole grains, legumes, nuts, teas, fruit,

veggies, instant coffee, and tea

Deficiency

� -wt loss, ataxia, dermatitis, N/V,

decreased hair growth, impaired

reproductive activity, decreased

pancreatic function and CHO

metabolism

Toxicity

� -accumulates in liver and CNS—

parkinsonian sx