Lecture #14

MINERALS
 LEARNING OBJECTIVES:

• Determine the different minerals and their classification

• Identify the functions and food sources of each mineral.
• Determine the individual requirements and PDRI of minerals
• Explain the health effects of deficiency and excess of each mineral.
• Explain how these minerals are digested and absorbed.
• Discuss the functions of water in body metabolism.
• Explain the forces influencing water distribution in the body.
• Determine the role of electrolytes in the body
• Describe how water and electrolytes balance can be maintained.
 MINERALS
DEFINITION
• An inorganic element that remains as ash when food is burned.
 CLASSIFICATION
• Macronutrient minerals- essential for human nutrition; present in amounts greater
than 5g; these include calcium (Ca), sodium (Na), phosphorous (P), potassium
(K), sulphur (S), chloride (Cl) and magnesium (Mg).

• Micronutrient minerals- essential for human nutrition; present in amounts less than
5g; these include iron (Fe), iodine (I), zinc (Zn), selenium (Se), manganese (Mn),
copper (Cu), molybdenum (Mo), cobalt (Co), and chromium (Cr).

• Minerals for which essentiality has not yet been established although there is
evidence of their participation in certain biologic reactions; these include silicon
(Si), vanadium (V), tin (Sn), barium (Ba), nickel (Ni), arsenic (As), boron (Bo),
fluoride (F), bromine (Br), strontium (Sr) and cadmium (Cd).

• Minerals found in the body that have not been assigned a metabolic role yet; these
include gold (Au) silver (Ag) aluminium (Al), mercury (Hg), bismuth (Bi),
gallium (Ga), lead (Pb), antimony (Sb), lithium (Li) and 20 others.
 GENERAL FUNCTIONS
1. Components of essential body compounds
• Ca and P in bones and teeth
• Cl hydrochloric acid
• I in the hormone thyroxine
• Co in Vitamin B12
• Zn in insulin
• S in methionine
• Fe in hemoglobin
2. Cofactors in biologic reactions
a. Some minerals act as cofactors binding to specific enzymes to
catalyse chemical reactions. Iron, zinc and copper form
complexes with enzymes called metalloenzymes.
b. Some ions act as cofactors for proteins that are not enzymes,
while others covalently bond to proteins to influence their
activities.
c. Proteins are activated by phosphorylation where a phosphate
ion (PO43-) attaches to a specific part of the protein.
d. The protein Hb incorporates iron that binds to oxygen.
e. Facilitation of absorption, digestion and transport.
i.Sodium facilitates the absorption of carbohydrates.
ii. Calcium facilitates the absorption of Vitamin B12.
f. Maintenance of acid-base balance.
- Acid-forming minerals: chloride, sulfur and phosphorus can
combine with H.
-Alkali-forming minerals: sodium, potassium, magnesium and
calcium can combine with OH.

g. Maintenance of water balance

-Electrolytes (Na, K, Cl) greatly influence the movement of water among
the fluid compartments.

h. Transmission of nerve impulses

-The exchange of Na and K across the cell membrane is responsible for
the transmission of a nerve impulse. The release of acetylcholine is
regulated by calcium

i. Regulation of muscle contraction

-Ca stimulates muscle contraction, and Na, K and Mg exert a relaxing
effect.
MACROMINERALS
1. Calcium

a. Description

• Most abundant mineral in the body

• Calcium makes up 1.5-2% of body weight
• About 99% of the mineral is present in bones, teeth and hard
tissues
• Most of it is in the form of a complex salt called hydroxyapatite
Ca10(PO4)6(OH2), with smaller amounts being associated with
carbonate and citrate
• Remaining 1% (about 1/3 of which is bound to protein) not
contained bones and teeth is present in the blood, extracellular
fluids and within the cells of soft tissues where it regulates many
important metabolic functions
• It must be maintained within the narrow range of 9-11 mg/dL for
the proper functioning of the cells.
Functions of Calcium

A. Physiological Functions:

1) Bone formation. The development of bone, which contains Ca and

other minerals, start in fetal life and is continuously being reshaped
and remolded throughout life according to body needs and stresses.
This bone remodeling takes place in 2 types of cells, namely:
a) osteoblasts – which continually form new bone matrix
b) osteoclasts – which balance this activity by absorbing bone
tissue

Adequate calcium is needed to permit optimal gains in bone mass and

density in the prepubertal and adolescent years.

2) Teeth formation. Ameoblasts, specialized tooth forming cells in

the gums, deposit Ca and other constituents to form teeth
Functions of Calcium
B. Metabolic Functions:
1) Blood coagulation. Ionized Ca stimulates release of
thromboplastin from the blood platelet which catalyzes the
conversion of prothrombin to thrombin. In turn, thrombin
catalyzes conversion of fibrinogen in blood plasma to fibrin or
blood clot (blood coagulum)
2) Transmission of nerve impulses
3) Regulation of contraction-relaxation of the heart muscle
(heartbeat)
4) Regulation of cell membrane permeability by controlling the
passage of fluid through the cell walls
5) Activation of enzymes such as ATP, lipase and some protein-
splitting enzymes
6) Maintenance of acid-base and electrolyte balance
7) Immunity
8) Facilitates absorption of Vit. B12
9) Protection against carcinogens, e.g. radiostrontium
10) Protection against lead poisoning
Factors Influencing Calcium Absorption
1. Better absorption during increased needs (growth, pregnancy, lactation)
2. Vitamin D enhances- increasing permeability of intestinal membrane to
calcium and activating system
3. Low gastric PH (acidic) favors absorption
4. Hypochlorhydrin (alkaline) precipitates calcium
5. Increase meat intake increases calcium excretion
6. If increase ratio of lactose to calcium- forming of a soluble complex-
transport to intestinal wall
7. Ratio of calcium: P
8. Oxalates (alagaw, alugbati, spinach) decrease calcium absorb by
forming insoluble salts
9. Phytates (cereals, wheat, oats)
10. Excess fats- insoluble soaps (in fatty stools) with calcium
11. Laxatives food increase bulk- decrease calcium absorption
12. Lack of exercise- loss of bone calcium and ability to replace it
13. Mental stress/emotional instability
14. Alcohol intake decrease calcium
15. Caffeine decreases urinary calcium excretion
d. Calcium in Bones
i. in bone formation- calcium salts form crystals
“hydroxyapatite” on a matrix of protein collagen
ii. in bone mineralizing- crystals become denser, gives strength
and rigidity to bones
iii. in remodelling- bones gain and lose minerals, example:
withdrawal, deposits, osteoporosis
iv. in teeth formation- slower rate than bone formation and
fluoride hardens and stabilizes the crystal of teeth

Calcium in Body Fluids

i.1% but vital in different functions
ii. activates calmodulin (inactive protein)- relays messages from
cell surface to inside of the cell and maintains blood pressure
Calcium in Disease Prevention
-Lowers blood pressure if adequate
calcium intake since calcium supersedes
effects on high sodium intake

Calcium Balance (intestines, bones,

kidneys)
Osteoblasts- builds
Osteoclasts- breaks

If increase blood calcium- thyroid gland

secretes calcitonin.
Calcitonin inhibits vitamin D activation,
prevents calcium reabsorption in kidneys
and inhibits osteoclasts from breaking
down bones.

If decrease in blood calcium- parathyroid

glands secrete parathormone.
Parathormone stimulates vitamin D
activation, stimulates calcium
reabsorption in kidneys and stimulates
osteoclasts
e. Recommended intake
-Refer to PDRI 2015
-These allowances take into account the need to protect children in whom skeletal
needs are much more important determinants of calcium requirement than are urinary
losses and in whim calcium supplementation has been found to have a beneficial
effect in children accustomed to low calcium intakes

f. Conditions with increased risk for Ca deficiency

i. Vitamin D deficiency
ii. long term dietary inadequacy
iii. High protein diets
iv. High fiber diets
v. Fat malabsorption/steatorrhea
vi. Achlorhydria
vii. Immobilization/sedentary lifestyle
viii. Decreased gastrointestinal (GI) transit time
ix. Stress
x. Long-term use of thiazide diuretics
g. Populations with increased risk for Ca deficiency
i. Teenagers
ii. Older women
iii. Pregnancy and lactation

h. Food sources
Dilis (dried and fresh), alamang (dried and fresh), dried fish; shellfish and crustaceans,
milk, cheese, ice cream, soybeans, mongo and other dried beans, leafy vegetables

i. Effects of deficiency
i. Stunted growth and retarded calcification of bones and teeth
ii. Rickets (due to lack of Ca or P, lack of vitamin D, or an imbalance in Ca : P ratio)
iii. Osteoporosis (condition in which absolute amount of bone in the skeleton has been
diminished but which in the remaining bone mass is of normal composition)
iv. Osteomalacia (decalcification of bone where there is a reduction in the mineral
content of the bone but not in the total amount of bone)
v. Tetany- reduction in circulating ionized Ca resulting in increased excitability of the
nerve and spasmodic and uncontrolled contractions of muscle tissues
vi. High blood pressure
Vii. Colon Cancer
j. Effects of toxicity
i. Hypercalcemia (a condition characterized
by an excess of Ca in the blood and soft
tissues); occurs in infants with high intake
of vitamin D
ii. Calcium rigor (a state of tonic muscle
contraction that results when Ca level rise
above normal due to abnormality in
parathyroid functioning)
iii. Hypercalcuria/renal calculi

k. Interrelationship with other nutrients

i. Vitamin D, phosphorous, sodium, protein
and fiber affect Ca absorption and
metabolism.
ii. Magnesium (another divalent cation)
competes with Ca for absorption and is
needed for the secretion of PTH.
iii. Malabsorption of fat can interfere with
Ca absorption due to the formation of soaps.
2. Phosphorous
a. Description
i. Phosphorous is second to calcium in abundance in the human body.
ii. Constitutes about 1% of total body weight, largely in the form of phosphate
(PO4)
iii. 85% of the mineral is found in the bones, 14% in cells in soft tissues and 1% in extracellular
fluid.

b. Function
i. Calcification of bones and teeth
ii. Metabolism of energy by all cells
iii. Important in the absorption and transport of nutrients
iv. An essential component of nucleic acid (DNA and RNA), adenosine triphosphate (ATP),
adenosine diphosphate, coenzymes and some vitamins
v. A major component of cell membranes and intracellular organelles
vi. Regulation of acid-base balance

c. Absorption and metabolism

i. Released by the action of intestinal enzymes phosphatases
ii. Absorbed into the blood with the help of Vitamin D. Blood phosphorous level is regulated by
the parathyroid gland that interacts with Vitamin D to control the absorption of the mineral.
iii. Factors affecting Ca absorption and metabolism are the same with phosphorous.
d. Recommended intake
i. For the recommended intake, please refer to the PDRI
ii. Ability of the body to synthesize the vitamin makes it difficult to estimate
minimal dietary requirements. Daily intake of 100 IU is adequate to protect
against rickets and promote normal bone growth, provided that the diet is
also sufficient in Ca and P.
iii. The quantities of calcium and phosphorous are more important than their
ratios.

e. Conditions and populations with increased risk for phosphorous

deficiency
Those with celiac disease, sprue, hyperthyroidism, insulin injections, the
alcoholics and premature infants.

f. Food sources
Meat, fish, poultry, glandular organs, egg yolk, milk, cheese, beans, nuts
and seeds, whole grain cereals
g. Deficiency
i. Rare but may cause tetany and hypertension.
ii. Develops in alcohol abuse, alcoholism, kidney
disorders, prolonged vomiting or diarrhea.

h. Interrelationship with other nutrients

i. Sodium is essential to ensure optimum phosphorous
absorption.
ii. An increase in Mg consumption decreases
phosphorous absorption.
3. Magnesium
a. Description
i. Half of the body’s magnesium is
in the bones.
ii. 1% is in the extracellular fluid.

b. Functions
i. Involved in bone mineralization
ii. ATP metabolism
iii. Synthesis of proteins, fats and
glucose and cells transport system
iv. Muscle contraction
v. Clotting
vi. Immune function
vii. Prevents dental caries
viii. Nerve transmission of
impulses
c. Absorption and metabolism
i. Absorption of Mg from food ranges from 20% to 70%
ii. Transported by specific carrier and vitamin D sensitive transport
system
iii. Rate of absorption is decreased by the same factors that affect Ca.
iv. Absorption is influenced by PTH.

d. Recommended intake
For the recommended intake, please refer to the PDRI.
Recommended intake is based on a requirement of 4mg/kg body
weight/day for adults to achieve a positive magnesium balance.

e. Food sources
Nuts, legumes, whole grains, dark green leafy vegetables, seafood,
chocolate, cocoa
f. Deficiency disease: Low Magnesium Tetany
i. Symptoms associated with low plasma Mg levels: irritability, nervousness and
convulsions due to overstimulated nerves and increased muscular contraction.
ii. Mg deficiency rarely occurs because of the efficiency in which the kidneys reabsorb
the mineral.

g. Conditions and populations with increased risk for Mg deficiency

Vomiting, diarrhea, alcoholism, protein malnutrition, diuretic use, malabsorption, renal
disease, diabetes, parathyroid disease, stress and postsurgical patients.

h. Toxicity
Overconsumption of the mineral is not likely to cause toxicity except in persons with
renal insufficiency.
i. Interrelationship with other nutrients
i. Mg is antagonistic to Ca.
ii. Mg can influence the balance between extracellular and intracellular K. the
mechanism of action is still not clear.
4. Sulfur
a. Description
i. Present in every cell in the body, particularly in cartilage and keratin of
skin, nails and hair.
ii. Occurs in a number of forms in the body: as sulfur within organic
compounds such as amino acids, sulfur within ions, sulphate ion (SO 42-),
and the sulphite ion (SO32-).
iii. Any excess sulfur is excreted in the urine.

b. Functions
i. A constituent of the sulfur-containing amino acids (methionine,
cysteine and cystine)
ii. A constituent of the vitamins thiamine, pantothenic acid and biotin,
vitamin-like lipoic acid, insulin, heparin, glutathione, coenzyme A
iii. Participates in detoxification reactions
iv. A constituent of structural tissues mucopolysaccharides and sulfate in
lipids
v. Needed in energy metabolism and enzyme activation
c. Recommended intake
There is no recommended intake for the mineral. Since allprotein
food provides sulfur, the need for the mineral is met when protein
intake is adequate.

d. Food sources
All protein-containing foods

e. Deficiency
A deficiency in sulfur occurs only when there is severe protein
deficiency.

f. Toxicity
Toxicity occurs only if sulfur-containing amino acids are taken in
excessive amounts.
5. Sodium
a. Description
About 50% of the total body sodium is found in the extracellular fluids, 40% in the
skeleton and 10% inside the cells.

b. Functions
i. Maintenance of normal extracellular fluid balance
ii. Maintenance of normal pH value of extracellular fluids
iii. Needed in the absorption of glucose and in the transport of other nutrients
iv. Aids in nerve impulse transmission and muscular contraction

c. Absorption and metabolism

i. Absorbed in the small intestine and is transported by the blood throughout the
body
ii. Blood passes the kidneys; it is filtered out and then partially reabsorbed into the
blood to maintain the normal blood sodium levels.
iii. Concentration of sodium in the extracellular fluid is determined by renin-
angiotensin-aldosterone system and sympathetic nervous activity.
iv. Aside from urinary losses, sodium is also lost via the skin.
d. Recommended intake
For the recommended intake, please refer
PDRI.

e. Food sources
Salt, soy sauce, processed foods

f. Deficiency
Muscle cramps, mental apathy, loss of
appetite, persistent vomiting or diarrhea,
heavy sweating, or diuretic therapy can
deplete body sodium resulting in
hyponatremia (low sodium blood levels).

g. Toxicity
Edema, acute hypertension, osteoporosis
6. Potassium
a. Description
Concentrated in the intracellular fluids, about 250g

b. Functions
i. Cell integrity
ii. Participates in many biochemical reactions inside the cell, particularly those
involved in the release of energy from food and the synthesis of protein and glycogen
iii. Maintains normal fluid balance
iv. Maintains acid-base balance
v. Aids in nerve impulse transmission and muscular contractions
vi. Acts along with Mg as a muscle relaxant opposing the muscle-contracting
stimulus of Ca
vii. Important in the release of insulin by the pancreas
viii. For regulation of heart rhythm

c. Absorption
i. Distributed in the blood from the intestine mainly by diffusion
ii. Enters the cell against a concentration gradients and therefore requires an active
transport mechanism
iii. Potassium is excreted into urine.
d. Recommended intake
For the recommended intake, please refer to the PDRI.

e. Food sources
Fresh foods, particularly fruits, vegetables and legumes

f. Deficiency - Hypokalemia
i. Muscular weakness, paralysis, confusion
ii. Prolonged vomiting or diarrhea, regular use of certain drugs (diuretics, steroids and
laxatives), severe protein-energy malnutrition, and surgery could result in potassium
deficiency.

g. Toxicity
Muscular weakness, vomiting, cardiac arrest, hyperkalemia
7. Chloride
a. Description
i. Comprises about 0.15% of adult weight
ii. Widely distributed
iii. Concentration is high in cerebrospinal fluids, GI
secretions and gastric juices

b. Functions
i. Maintains normal fluid and electrolyte balance
ii. A constituent of hydrochloric acid
iii. Helps maintain acid-base balance in body fluids

c. Absorption
i. Readily absorbed in the GI tract
ii. Excreted in the urine and sweat.

d. Food sources
Salt, soy sauce, meat, seafood, milk, eggs,
processed foods

e. Deficiency
A diet deficient in chloride does not normally occur.

f. Toxicity symptoms
Vomiting causing dehydration
Summary of associated disorders resulting from deficiency or
excessive intake of macrominerals
Macromineral Deficiency Toxicity
Calcium  Stunted growth and  Hypercalcemia
retarded  Renal calculi
 Rickets  Depressing effect on
 Osteomalacia utilization of fat,
 Osteoporosis phosphorous, iodine,
 Tetany iron, magnesium and
zinc.
Phosphorous  Same as in Calcium  Hyperphosphatemia
Potassium  Hypokalemia  Hyperkalemia
 Muscle irritability,
weakness and
paralysis
 Heart may develop a
gallop rhythm and
cardiac arrest
 Poor intestinal tone
 Nausea and lack of
appetite
Sodium  Muscle cramps  Hypertension
 Disturbed acid-base
balance resulting
from diarrhea,
vomiting and profuse
sweating
Magnesium  Hypomagnesemic  Hypermagnesemia
tetany results to hypertension
and may cause
decreased tendon
reflexes
Chloride  Endocrine disorders 
such as hyperactivity
of the adrenal cortex
resulting in
hypochloremic
alkosis
MICROMINERALS
1. Iron
a. Description
i. An adult male contains 40-50 mg of iron per kilogram body weight, while the adult
female contains 35-50 mg.
ii. More than two thirds of the body is in the form of functional iron (perform specific
role), which is bound within the Hb molecule or within the myoglobin in muscle tissues.
iii. Non functional iron (storage form) is found in the liver, spleen and bone marrow.

b. Functions
i. As part of the protein Hb and myoglobin, iron binds to oxygen molecules and transport
O2 through the blood (in Hb) or stores O2 within muscles in myoglobin.
ii. As part of Hb, it is involved in the formation of red blood cells (RBCs).
iii. A cofactor of non-heme enzymes and other proteins

c. Absorption and Metabolism

i. Available to the body either in the heme form (present only in animal products) or
nonheme form (iron in plant foods)
ii. Absorption occurs primarily in the duodenum and jejunum.
iii. A variety of factors influence iron absorption.
1) Size of dose: the higher the intake of iron, the lower the percentage of iron
absorb.
2) Body needs: those deficient in iron absorb more the mineral.
3) Form of iron: ferrous form Fe2+ is better absorb than ferric form Fe3+.

iv. Factors enhancing the absorption of non heme iron:

1) Increase acidity
2) Animal tissue protein

v. Factors inhibiting the absorption of non heme iron:

1) Low gastric acidity
2) High dietary calcium and phosphorous intake
3) High manganese intake
4) Dietary fiber
5) Certain proteins
6) Phytates and oxalates
7) Polyphenols

vi. After absorption, iron is carried to the blood bound to the protein transferrin.
vii. Iron is stored in the liver in the form of ferritin and hemosiderin.
viii. 90% of iron is released in the breakdown of cells.
d. Recommended intake
i. For the recommended intake, please refer to the PDRI (2015). The recommended
intake for Filipinos is based on the amount of dietary iron needed to meet absorbed iron
requirements. This would correspond to the amount needed to cover basal losses plus
growth for children and menstrual losses for women of reproductive age adjusted for bio
availability of iron in typical complete meals consumed by Filipinos (Appendix A).
ii. For infants, it is assumed that the iron provided by breast milk is adequate to meet the
iron needs of infants exclusively fed human milk from birth to six months.
iii. The consumption of iron rich foods and iron fortified foods is recommended for women
from adolescence onwards.
iv. Iron supplementation is recommended to meet the needs of pregnant and lactating
women.
v. The estimated iron requirement during the first trimester of pregnancy and the first six
months of lactation are actually higher than the requirements for menstruating non-
pregnant and non-lactating to allow for build-up of iron stores during these periods.

e. Interrelationship with other nutrients

Vitamin C enhances iron absorption by acting as a reducing agent and forms a chelate with
non heme ferric iron at an acid pH. The chelate remain soluble in the small intestine, thus
improving intestinal absorption of non heme iron.
f. Food sources
Liver and glandular organs, fish, egg yolk, shell fishes, leafy vergatables, except
amplaya leaves, soy beans.

g. Deficiency
Microcytic, hypochromic anemia results in low Hb stores, fatigue, weakness,
pallor, poor resistance to cold temperature, apathy.

h. Toxicity
Caused by poor quality sources cookery; excessive excretiondue to blood loss;
inadequate form due to lack of B12 caused by lack of IF.
i. Hemosiderosis or siderosis is a condition with large deposits of iron deposit,
hemosiderin in the liver (use of supplement failure to regulate iron absorption)
ii. Hemochromatosis is a genetic disorder that enhances absorption.

i. Issues
i. Iron and cancer- iron may be involved in causing cancer by damaging DNA
through its free radical activity.
ii. Heart disease- the attack of free radicals on ferritin activates the oxidative role
of iron against LDL.
2. Zinc
a. Description
i. Commonly found as the divalent ion
ii. Amount of mineral in an adult ranges from 1.5-3g
iii. Occurs in all cells,tissues, organs, fluids and secretion but is mainly concentrated (about
90% of the body zinc in muscle bone)
iv. Over 95% is bound within various metalloenzymes of cells and cell membranes.
v. Most of the zinc in the blood is in the RBCs, which contain the zinc containing enzyme
carbonic anhydrase needed to convert carbon dioxide to bicarbonate ions (HCO3).

b. Functions
i. A component of more than 200 enzymes, participating in a wide variety of metabolic
processes such as synthesis and degradation of carbohydrates, lipids, proteins and nucleic
acids.
ii. Interacts with insulin facilitating the uptake of glucose by the cells of adipose tissue
iii. Needed for the normal development and maintenance of the body’s immune system.
iv. Important in stabilizing membranes structure and in guarding it against peroxidative
damage.
v. Important in night vision
vi. Important in mobilizing Vitamin A from liver stores
vii. Facilitates wound healing and blood clotting
c. Absorption and metabolism
i. Absorbed in the small intestine and is carried into the blood and goes to the pancreas where
it is used in the formation of some digestive enzyme
ii. The absorbed zinc binds to metallothionein, a sulfur-rich protein that binds with metals
such as zinc.
iii. Binds with another protein (cysteine-rich intestinal protein) to transport the mineral to the
blood
iv. Zinc that is carried within blood plasma is bound with different carrier proteins, such as
albumin and transferrin.
v. The liver takes up some 30-40% of absorbed zinc, while the rest is distributed throughout
the different organs and tissues.
vi. Zinc loss from the body is via body surface, kidney and the GI tract. Most of the zinc is
excreted in the feces.

d. Recommended intake
For the recommended intake, please refer to the PDRI

e. Interrelationships with other nutrients

i. Zinc2+ absorption is impaired by the following divalent cations: Cd2+, Cu2+, Ca2+, and
Fe2+.
ii. The cations compete with one another for:
1) Facilitating binding ligands in the intestinal lumen
2) Receptor sites in the enterocytes; or
3) Intracellular binding ligands with mucosal cells.
f. Food sources
Zinc from animal foods is more readily absorbed than that in plant foods. Sources
include meat, poultry, fish, grains and vegetables.

g. Deficiency Symptoms
Deficiency manifestations are diverse: hair loss, dermatitis and skin changes,
growth retardation, impaired taste acuity, delayed wound healing, decrease dark
adaptation (night blindness), immunologic abnormalities, and delayed sexual
maturity.

h. Toxicity symptoms
The following are some adverse effects of a prolonged intake of dietary zinc
supplements:

i. Zinc-induced copper deficiency anemia

ii. Depressed levels of white blood cell
iii. Increased low-density lipoprotein and decreased high-density lipoprotein
cholesterol
iv. Decreased serum ferritin and haematocrit levels
3. Copper
a. Description
i. Occurs in the cuprous (Cu+) and cupric (Cu2+) states
ii. Involved in oxidation-reduction reactions
iii. Body’s copper content ranges form 50-120mg
iv. Highest concentration of the mineral is in the liver, with less amounts in the
heart, kidneys, spleen and brain
v. Copper in the blood and tissues is normally bound to proteins

b. Functions
Copper is essential as an activator of key enzymatic reactions. Some copper-containing
enzymes and the reactions they catalyse are:
i. Cytochrome c oxidase: catalyzes the oxidation of the cytochrome c, a, and a3
complex by oxygen in the respiratory chain
ii. Ceruloplasmin: (a) oxidizes ferrous ions; (b) transports copper to Tissue sites;
and (c) acts as a scavenger of free radicals and superoxide ions
iii. Superoxide dismutase: toxic oxygen removal
iv. Lysyl oxidase: collagen synthesis
v. Dopamine beta-hydroxylases: neurotransmitter synthesis
vi. Tyrosine oxidase: melanin synthesis
c. Absorption and metabolism
i. About 25-40% of dietary copper is absorbed from all parts of
the GI tract, including the stomach and large intestine.
ii. Binds with proteins such as metallothionein, which slows down
Cu absorption into the blood
iii. Removed from the plasma by the liver from where it is
excreted into the bile or used in the synthesis of ceruloplasmin,
the copper-containing enzyme
iv. Released from the liver under the control of the adrenal gland.
The body utilizes some of the plasma copper in the synthesis of
superoxide dismutase in the bone marrow.
v. Copper is excreted in both the feces and the urine.

d. Recommended intake
Recommended intake for the mineral has not been determined in the
Philippines. The US RDA (2001) for copper is 10mg/day or
900ug/day.
e. Interrelationship with other nutrients
i. High intake of iron or vitamin C decreases the
absorption of copper.
ii. Zinc decreases copper absorption.
iii. Calcium is antagonistic to copper.
iv. Copper from complexes with molybdenum and
sulfur, decreasing copper absorption.

g. Deficiency
i. Copper deficiency is seen among children with
protein-deficiency and iron-deficiency anemia.
Deficiency symptoms include decreased serum
copper and anemia, impaired glucose tolerance,
poor wound healing, immune defects and central
nervous system and cardiovascular disorders.
ii. Menke’s kinky hair syndrome is an inherited
condition characterized by low serum copper and
ceruplasmin levels. This disease prevents the
release of Cu into the general circulation.

h. Toxicity
Hereditary condition known as Wilson’s disease
that is associated with chronic copper toxicity due
to a failure to excrete copper in bile.
4. Iodine
a. Description
i. The body contains 20-30mg of iodine that is concentrated in the thyroid gland.
ii. Dietary iodine is mainly in the form of iodine.

b. Functions
i. As part of the thyroid hormones, it is essential in regulating body’s growth, development
and metabolic rate;
ii. Essential in the conversion of carotene to Vitamin A
iii. Protein synthesis
iv. Carbohydrate absorption
v. RBC production
vi. Nerve muscle function

c. Absorption and metabolism

i. Absorbed mainly in the small intestine, distributed in the extracellular fluids
ii. Reduced first to the absorbable iodide ions
iii. One third of the absorbed iodide in the blood plasma is taken up by the thyroid gland for
synthesis of the thyroid hormones thyroxine (T4) and triiodothyronine (T3).
iv. The rest of the iodide is excreted mainly in the urine, while some amounts are lost via the
skin and feces
d. Recommended intake
i. For the recommended intake, please refer to the PDRI (2015). The
recommended intake for adults corresponds to the intake necessary to maintain
plasma iodide level above the critical limit to be associated with the onset of
goiter.
ii. Pregnant and lactating mothers as well as adolescents are at risk of developing
a deficiency of iodine.

e. Interrelationship with other nutrients

i. Goitrogens (from cabbage, kale, cauliflower, broccoli, turnips, brussel sprouts
and mustard greens) are substances that interfere with iodine metabolism
inhibiting hormonogenesis.
ii. The following goitrogens may affect iodide uptake by the thyroid gland,
organification of the iodide or hormone release from the thyroid cells; halide ions
such as Bromide (Br), astatide (At), and thiocyanate (SCN). Cassava contains
cyanogen glucosides, with thiocyanates as metabolites.

f. Food source
Iodized salt, seafoods, seaweeds
g. Deficiency
i. Iodine deficiency disorders (IDD) include
goiter, hypothyroidism, impaired mental
function, spontaneous abortions, stillbirths,
congenital abnormalities and increased infant
mortality.
ii. Cretinism is the developmental defect in
infants characterized by mental retardation,
deaf-mutism, and neuromuscular defects.
iii. Myxedema is a form of cretinism, seen in
adults and characterized by dry thick skin,
puffy face and eyelids, enlarged tongue ,
husky voice, decreased reproductive ability
and mental deterioration.

h. Toxicity
Hyperthyroidism (also known as Grave’s
disease or exophthalmic goiter)
5. Selenium
a. Description
i. Found in minute amounts of the body, concentrated in other glandular
organs, blood, and muscles
ii. The two forms of Se mainly present in food are selenomethionine
(synthesized by plants) and selenocysteine (synthesized by animals).

b. Function
As part of the enzyme “glutathione peroxidase”, it calatlyzes the breakdown
of toxic hydroperoxides making the mineral an essential component of the
body’s antioxidant defense system.

c. Absorption and metabolism

i. Bound to proteins (globulins and lipoproteins)
ii. Taken up by the RBCs, liver, heart, spleen, nails and tooth enamel
iii. Major routes of Se excretion are urinary (50-60% of total amount excreted)
and fecal (40-50% of total excretory output).
d. Recommended intake
i. For the recommended intake, please refer to the PDRI
ii. FAO/WHO recommends 31 ug/day to provide adequate reserves based on satisfactory levels of plasma
selenium and glutathione peroxidase activity.

e. Interrelationship with other nutrients

i. Se is a vitamin E sparer.
ii. Se protects against the toxicity of Cd, Hg, and Ag.
iii. The potency of selenomethionine is reduced in methionine deficiency.

f. Food sources
Seafoods, liver, meats, whole grain and airy products are good sources

g. Deficiency
i. Clinical manifestations include muscle pain and weakness, cardiomyopathy, and a loss of pigmentation
(pseudo-albinism)
ii. Keshan disease is a selenium deficiency condition that causes heart enlargement

h. Toxicity
i. Loss of hair and nails, dental carries, dermatitis, peripheral neuropathy, irritability and fatigue and
lesions of the skin and nervous system
ii. Selenosis- selenium poisoning that can be caused by an excessive intake of Se usually provided in
supplements. Se is toxic at levels 20-30 times the requirements
 NEXT MEETING

• Continue discussion of microminerals

• Discuss water and electrolytes
• Refer to the PPT of RAAS mechanism