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
boneleading 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 lowalways
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
heartbeatuse calcium gluconate IV to treat
hyperkalemia (EKGpeaked 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

contd
***-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
contd
-hypoparathyroidism
-***hypomagnesemia
-sepsis
-pseudohypoparathyroidism
-calcitonin secretion with medullary
carcinoma of the thyroid

Causes of hypocalcemia
contd
-***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
contd
***Neoplastic Disease
-tumors producing PTH-related proteins
(ovary, kidney, lung)
-***mets to bone
-lymphoproliferative disease including
multiple myeloma
-secretion of prostaglandins and
osteolytic factors

10

Causes of hypercalcemia
contd
-***thiazide diuretic
-sarcoidosis
-pagets 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

11

RDA
-see

handout

sources

12

Deficiency
1)***boneto be discussed in osteoporosis
lecture
2) tetanydecreased serum levels increase
the irritability of nerve fibers resulting in
muscle spasms, fatal laryngospasm

***-Chvosteks sign: contraction of the facial m.

after tapping the facial n.
***-Trousseaus sign: carpal spasm after
occlusion of the brachial a. with blood pressure
cuff for 3 min

3) HTNcontroversial
4) prolonged QT--arrythmias

Toxicity
-***polyuria,

constipation, bone pain,

azotemia, coma
-stones, bones(bone pain), groans,
psychiatric overtones

13

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

14

absorption
-best occurs when calcium and phos are
ingested in equal amts (milk)
-vit D also increases absorption

RDA
-see

table (and for all RDAs)

15

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

16

Renal Disease

Causes of hypophosphatemia
-starvation
-TPN with inadequate phos content
-malabsorption, small bowel bypass
-vit D deficient and vit D resistant
osteomalacia

17

Causes of hypophosphatemia
contd
-phosphaturic drugs: theophylline, diuretics,
bronchodilators, corticosteroids
-hyperparathyoidism (primary or secondary)
-hyperthyroidism
-renal tubular defects
-hypokalemic nephropathy
-inadequately controlled DM
-***alcoholism

Causes of hypophosphatemia
contd
Intracellular shift of phosphorus
-administration of glucose
-anabolic steroids, estrogen, OCP
-respiratory alkalosis
-salicylate poisoning
Electrolyte abnormalities
-hypercalcemia
-hypomagnesemia
-metabolic alkalosis

18

Causes of hypophosphatemia
contd
Abnormal losses followed by inadequate
repletion
-***DM with acidosiswith aggressive therapy
-***recovery from starvation or prolonged catabolic
staterefeeding 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

19

Causes of hyperphosphatemia
contd
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

20

Toxicity
-symptoms

of the primary disorder

Magnesium

21

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

22

sources

Sources
-seeds,

nuts, legumes, unmilled cereal

grains, dark greens
-fish, meat, milk, fruits
-lost during refining of flour, rice, vinegar

23

Causes of hypomagnesemia
-malabsorption, chronic diarrhea,
laxative abuse
-prolonged GI suction
-small bowel bypass
-malnutrition
-***alcoholism
-refeeding

-TPN with inadequate Mg

24

Causes of hypomagnesemia
contd
-DKA
-diuretics
-hyperaldosteronism, Barrters syndrome
-hypercalcuria
-renal Mg wasting
-hyperparathyroidism
-postparathyroidectomy
-vit D therapy
-aminoglycosides, ***cisplatin, ampho B

Causes of hypermagnesemia
Decreased renal fxn
***Increased intakeabuse of Mg
containing antacids (MOM) and
laxatives in renal insufficiency

25

Deficiency
-anorexia,

growth failure, cardiac and

neuromuscular changesweakness,
irritability, mental derangement
-tetany, muscle cramps

Toxicity
-respiratorydepression,

apnea
-CVhypotension, cardiac arrest, EKG
(prolonged QRS and QT, heart block,
peaked T waves)
-GIN/V
-neuromuscularparesthesias,
somnolence, confusion, coma,
hyporeflexia, paralysis, apnea

26

Iron

Function
-respiratory

transport of O2 and CO2

-immune system
-cognitive performance
-found in Hgb (in RBCs) and myoglobin
(in muscles)
-cytochrome p450 system

27

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 cows milk, cheese, eggs,
dont
-gastric acidity enhances absorption (antacids
interfere)
-pregnancy, increased growth, Fe defic all
increase deficiency

28

 -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

29

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

30

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

31

absorption
Impaired

absorption in Crohns 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

32

Enhancing Factors
-glucose,

lactose, and soy protein

-red

wine
-human milk

Excretion
-fecesalmost

entirely
-***in urine with starvation, nephrosis,
DM, alcoholism, hepatic cirrhosis (zinc
supplementation in encephalopathy),
porphyria

33

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

34

 -immunologic

deficitslymphopenia,
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

35

***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

36

Acrodermatitis
Enteropathica

Toxicity
->100-300

mg/d

-rare
-interferes

with copper absorption

-decrease in HDL
-GI irritation, vomiting

37

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.

38

Mottled teeth in fluorosis

Maganese
-found

in many enzymes
-connective and bony tissue formation
-growth and reproduction
-CHO and lipid metabolism

39

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

40

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

41