DEFICIENCY

DISEASES

DEFICIENCY
DISEASES
Vitamins and trace minerals are
required constituents of the human diet
since they are either inadequately
synthesized or not synthesized in the
human body.
Only small amounts of these substances
are needed for carrying out essential
biochemical reactions

Overt vitamin or trace mineral

deficiencies are rare in Western
countries due to a plentiful, varied, and
inexpensive food supply
multiple nutrient deficiencies may appear
together in persons who are chronically ill
or alcoholic.
subclinical vitamin and trace mineral
deficiencies, are quite common in the
normal populationgeriatric age group.

 Vitamin B12 and vitamin A stores are large,

and an adult may not become deficient for
1 or more years after being on a depleted
diet.
Folate and thiamine may become depleted
within weeks when eating a deficient diet.
Therapeutic modalities can deplete
essential nutrients from the body; e.g.,
hemodialysis

Roles for vitamins

and trace minerals
in diseases:
Deficiencies of vitamins and minerals may
be caused by disease states such as
malabsorption;
Both deficiency and excess of vitamins and
minerals can cause disease in and of
themselves (e.g., vitamin A intoxication and
liver disease);
Vitamins and minerals in high doses may be
used as drugs (e.g., niacin for
hypercholesterolemia).

Thiamine
(Vitamin B1)
First B vitamin to be identified vitamin B1
Functions:
Source of energy generation
decarboxylation of -ketoacids, such as pyruvate ketoglutarate, and branched-chain amino acids

Thiamine pyrophosphate acts as a coenzyme

for a transketolase reaction that mediates the
conversion of hexose and pentose phosphates
Thiamine plays a role in peripheral nerve
conduction

Dietary Sources:
yeast, organ meat, pork, legumes, beef,
whole grains, nuts.
Milled rice or grains contain little thiamine, if
any.

Thiamine deficiency is more common in cultures that

rely heavily on a rice-based diet.

Tea, Coffee, Raw fish, Shellfish

contain thiaminases, which can destroy the vitamin.

Drinking large amounts of tea or coffee can
theoretically lower thiamine body stores.

DEFICIENCY:
Poor dietary intake
At risk populations:

Alcoholism and chronic illness, such as cancer - Western

countries

Alcohol interferes directly with the absorption of thiamine and

with the synthesis of thiamine pyrophosphate

Women with prolonged hyperemesis gravidarum and

anorexia
Patients with an overall poor nutritional status on
parenteral glucose
Patients on chronic diuretic therapy due to increased
urinary thiamine losses
Motor vehicle accidents associated with head injury

Maternal thiamine deficiency infantile beriberi

in breast-fed children

Thiamine
deficiency causes:
1.

Early stage:

Anorexia
Nonspecific symptoms (e.g., irritability, decrease in shortterm memory)

2. Prolonged: beriberi
Wet beriberi

presents primarily with cardiovascular symptoms, due to impaired

myocardial energy metabolism and dysautonomia
can occur after 3 months of a thiamine-deficient diet
presents with an enlarged heart, tachycardia, high-output
congestive heart failure, peripheral edema, and peripheral neuritis

Dry beriberi

presents with a symmetric peripheral neuropathy of the motor and

sensory systems with diminished reflexes
neuropathy affects the legs most markedly, and patients have
difficulty rising from a squatting position

3. Wernicke's encephalopathy
Alcoholic patients with chronic thiamine
deficiency
horizontal nystagmus, ophthalmoplegia (due to
weakness of one or more extraocular muscles),
cerebellar ataxia, and mental impairment
When there is an additional loss of memory and
a confabulatory psychosis, the syndrome is
known as Wernicke-Korsakoff syndrome

Laboratory
Diagnosis:
Functional enzymatic assay of
transketolase activity measured before
and after the addition of thiamine
pyrophosphate

Abnormal: >25% stimulation by the addition

of
thiamine pyrophosphate (an activity
coefficient of 1.25)

High-performance liquid
chromatography (HPLC)

Treatment:
100 mg/d of thiamine should be given
parenterally for 7 days, followed by 10
mg/d orally until there is complete
recovery

Riboflavin
(Vitamin B2)
It is important for the metabolism of
fat, carbohydrate, and protein,
reflecting its role as a respiratory
coenzyme and an electron donor.
It also plays a role in drug and steroid
metabolism, including detoxification
reactions.

Deficiency:
lesions of the mucocutaneous surfaces of
the mouth and skin
corneal vascularization,
Anemia
personality changes have been described
with riboflavin deficiency

Riboflavin is extremely sensitive to

light, and milk should be stored in
containers that protect against
photodegradation.

Laboratory
Diagnosis:
measurement of red blood cell or
urinary riboflavin concentrations or by
measurement of erythrocyte
glutathione reductase activity, with and
without added FAD

Dietary sources:
Milk, other dairy products, and
enriched breads and cereals
lean meat, fish, eggs, broccoli, and
legumes

Niacin (Vitamin B3)

The term niacin refers to nicotinic acid and
nicotinamide and their biologically active
derivatives.
Nicotinic acid and nicotinamide are absorbed
well from the stomach and small intestine.
Niacin bioavailability is high from beans, milk,
meat, and eggs; bioavailability from cereal
grains is lower.
Since flour is enriched with the "free" niacin
(i.e., non-coenzyme form), bioavailability is
excellent.

Deficiency:
causes pellagra, which is mostly found
among people eating corn-based diets in
parts of China, Africa, and India.
in North America, it is found mainly
among alcoholics
in patients with congenital defects of
intestinal and kidney absorption of
tryptophan (Hartnup disease). - in
patients with carcinoid syndrome.

Early symptoms:
loss of appetite, generalized weakness and
irritability, abdominal pain, and vomiting.
Bright red glossitis then ensues, followed by a
characteristic skin rash that is pigmented and
scaling, particularly in skin areas exposed to
sunlight
Vaginitis and esophagitis may also occur.
Diarrhea, depression, seizures, and dementia
are also part of the pellagra syndromethe
four Ds: dermatitis, diarrhea, and dementia
leading to death.

Treatment:
Oral supplementation of 100200 mg of
nicotinamide or nicotinic acid three
times daily for 5 days.
High doses of nicotinic acid (2 g/d in a
time-release form) are used for the
treatment of elevated cholesterol and
triglyceride levels and/or low highdensity lipoprotein (HDL) cholesterol
level.

Toxicity:
Flushing always starts in the face and may be
accompanied by skin dryness, itching, paresthesia, and
headache. Premedication with aspirin may alleviate
these symptoms. Flushing is subject to tachyphylaxis
and often improves with time.
Nausea, vomiting, and abdominal pain also occur at
similar doses of niacin.
Hepatic toxicity is the most serious toxic reaction
due to niacin and may present as jaundice with
elevated aspartate aminotransferase (AST) and
alanine aminotransferase (ALT) levels.

Pyridoxine
(Vitamin B6)
It refers to a family of compounds
including pyridoxine, pyridoxal,
pyridoxamine, and their 5'-phosphate
derivatives.
It is also involved in heme and
neurotransmitter synthesis and in the
metabolism of glycogen, lipids, steroids,
sphingoid bases, and several vitamins,
including the conversion of tryptophan to
niacin.

Dietary Sources:
Plants contain vitamin B6 in the form of
pyridoxine, whereas animal tissues
contain PLP and pyridoxamine phosphate.
The vitamin B6 contained in plants is
less bioavailable than that from animal
tissues.
Rich food sources of vitamin B6 include
legumes, nuts, wheat bran, and meat,
although it is present in all food groups.

Deficiency:
Includes epithelial changes, as seen frequently with
other B vitamin deficiencies.
Severe deficiency can lead to peripheral neuropathy,
abnormal electroencephalograms, and personality
changes including depression and confusion.
In infants: diarrhea, seizures, and anemia
Microcytic, hypochromic anemia; platelet dysfunction
Hyperhomocysteinemia and increased risk of
cardiovascular disease, and also associated with
inflammation and elevated C-reactive protein levels.
Certain medications such as isoniazid, L-dopa,
penicillamine, and cycloserine interact with PLP due to
a reaction with carbonyl groups. Pyridoxine should be
given concurrently with isoniazid to avoid neuropathy.

 Increased ratio of AST (or SGOT) to ALT (or SGPT)

seen in alcoholic liver disease reflects the relative
vitamin B6 dependence of ALT.
Vitamin B6 dependency syndromes that require
pharmacologic doses of vitamin B6:
cystathionine -synthase deficiency
pyridoxine-responsive (primarily sideroblastic)
anemias
gyrate atrophy with chorioretinal degeneration
100200 mg/d of oral vitamin B6 is required for
treatment.
Safe upper limit for vitamin B6 :100 mg/d
When toxicity occurs, it causes a severe sensory
neuropathy, leaving patients unable to walk. Some
cases of photosensitivity and dermatitis have also
been reported.

Ascorbic Acid
(Vitamin C)

Antioxidant activity, promotion of nonheme iron

absorption, carnitine biosynthesis, the conversion of
dopamine to norepinephrine, and the synthesis of
many peptide hormones.
It is also important for connective tissue metabolism
and cross-linking (proline hydroxylation), and it is a
component of many drug-metabolizing enzyme
systems, particularly the mixed-function oxidase
systems.
Almost complete absorption of vitamin C occurs if
<100 mg is administered in a single dose; however, only
50% or less is absorbed at doses >1 g.
Enhanced degradation and fecal and urinary
excretion of vitamin C occur at higher intake levels.

Dietary sources:
citrus fruits, green vegetables
(especially broccoli), tomatoes, and
potatoes.
Consumption of five servings of fruits
and vegetables a day provides vitamin C
in excess of the RDA, 90 mg/d for
males and 75 mg/d for females.
Smoking, hemodialysis, pregnancy, and
stress (e.g., infection, trauma) appear to
increase vitamin C requirements.

Deficiency:
causes scurvy.
This is seen primarily among the poor and elderly,
in alcoholics who consume <10 mg/d of vitamin C,
and also in individuals consuming macrobiotic diets.
In addition to generalized fatigue, symptoms of
scurvy primarily reflect impaired formation of
mature connective tissue and include bleeding into
skin; inflamed and bleeding gums; and
manifestations of bleeding into joints, the
peritoneal cavity, pericardium, and the adrenal
glands.
In children, vitamin C deficiency may cause
impaired bone growth.

Laboratory
diagnosis:
Vitamin C deficiency is made on the basis
of low plasma or leukocyte levels.

Administration of vitamin C (200 mg/d)

improves the symptoms of scurvy within a
matter of several days.
High-dose vitamin C supplementation (e.g., 12
g/d) might slightly decrease the symptoms and
duration of upper respiratory tract infections.
Vitamin C supplementation has also been
reported to be useful in Chdiak-Higashi
syndrome and osteogenesis imperfecta.

Toxicity:
Taking >2 g of vitamin C in a single dose may
result in abdominal pain, diarrhea, and nausea.
Advise patients with a past history of kidney
stones to not take large doses of vitamin C
High doses of vitamin C can induce hemolysis in
patients with glucose-6-phosphate
dehydrogenase deficiency, and doses >1 g/d can
cause false-negative guaiac reactions as well as
interfere with tests for urinary glucose.

Biotin
a water-soluble vitamin that plays a role
in gene expression, gluconeogenesis, and
fatty acid synthesis and serves as a CO2
carrier on the surface of both cytosolic
and mitochondrial carboxylase enzymes.
also functions in the catabolism of
specific amino acids (e.g., leucine).

Dietary Sources:
Excellent food sources of biotin include
organ meat such as liver or kidney, soy,
beans, yeast, and egg yolks; however,
egg white contains the protein avidin,
which strongly binds the vitamin and
reduces its bioavailability.

Deficiency:
Adult: biotin deficiency results in mental
changes, paresthesia, anorexia, and nausea.
A scaling, seborrheic, and erythematous
rash may occur around the eyes, nose, and
mouth as well as on the extremities.
Infants: presents as hypotonia, lethargy,
and apathy. In addition, the infant may
develop alopecia and a characteristic rash
that includes the ears.

Laboratory
diagnosis:
biotin deficiency can be established
based on a decreased urinary
concentration or an increased urinary
excretion of 3-hydroxyisovaleric acid
after a leucine challenge.

Treatment:
requires pharmacologic doses of biotin,
using up to 10 mg/d. No toxicity is
known.

Pantothenic Acid
(Vitamin B5)
is a component of coenzyme A and
phosphopantetheine, which are involved in
fatty acid metabolism and the synthesis of
cholesterol, steroid hormones, and all
compounds formed from isoprenoid units.
is involved in the acetylation of proteins.
The vitamin is excreted in the urine, and
the laboratory diagnosis of deficiency is
made on the basis of low urinary vitamin
levels.

 Liver, yeast, egg yolks, whole grains, and

vegetables are particularly good sources of Vit.
B12
The symptoms of pantothenic acid deficiency
are nonspecific and include gastrointestinal
disturbance, depression, muscle cramps,
paresthesia, ataxia, and hypoglycemia.
Pantothenic acid deficiency is believed to have
caused the burning feet syndrome seen in
prisoners of war during World War II.
No toxicity of this vitamin has been reported.

Choline
a precursor for acetylcholine,
phospholipids, and betaine
necessary for the structural integrity
of cell membranes, cholinergic
neurotransmission, lipid and cholesterol
metabolism, methyl-group metabolism,
and transmembrane signaling

Dietary sources:
Choline is widely distributed in food
(e.g., egg yolk, wheat germ, organ meat,
milk) in the form of lecithin
(phosphatidylcholine).

Deficiency:
Deficiency has occurred in patients
receiving parenteral nutrition devoid of
choline, & results in fatty liver, elevated
transaminase levels, and skeletal muscle
damage with high creatine
phosphokinase values.

Laboratory
Diagnosis:
Diagnosis is currently made on the
basis of low plasma levels

Toxicity:
Toxicity results in hypotension,
cholinergic sweating, diarrhea,
salivation, and a fishy body odor.
The upper limit for choline has been set
at 3.5 g/d.

Flavonoids
constitute a large family of polyphenols that
contribute to the aroma, taste, and color of fruits
and vegetables.
major groups of dietary flavonoids include
anthocyanidins in berries; catechins in green tea and
chocolate; flavonols (e.g., quercitin) in broccoli, kale,
leeks, onion, and the skins of grapes and apples; and
isoflavones (e.g., genistein) in legumes.
have been shown to have antioxidant activity and to
affect cell signaling
have been postulated to play a role in the prevention
of several chronic diseases, including
neurodegenerative disease, diabetes, and
osteoporosis.

VITAMIN AND
TRACE MINERAL
DEFICIENCY
AND EXCESS

Vitamin A
refers to retinol, including retinaldehyde and
retinoic acid.
Retinoids

includes all molecules (including synthetic

molecules) that are chemically related to retinol.

Retinaldehyde

is the essential form of vitamin A that is required

for normal vision

Retinoic acid

is necessary for normal morphogenesis, growth,

and cell differentiation

Other Functions:

plays a role in iron utilization

humoral immunity
T cellmediated immunity
natural killer cell activity
Phagocytosis

Vitamin A is commercially available in

esterified forms since it is more stable
as an ester.

Metabolism:
Liver

contains approximately 90% of the vitamin A

reserves
secretes vitamin A in the form of retinol
interacts with a second protein, transthyretin
which prevents vitamin A from being filtered
by the kidney glomerulus protecting the body
against toxicity of retinol.

Retinoic acid is a ligand for certain nuclear

receptors that act as transcription
factors.

 Retinoid receptors regulate transcription

by binding as dimeric complexes to specific
DNA sites in target genes.
retinoid receptors play an important role in
controlling cell proliferation and
differentiation.
Retinoic acid is useful in the treatment of
promyelocytic leukemia and cystic acne
because it inhibits keratinization,
decreases sebum secretion, and possibly
alters the inflammatory reaction.

Dietary Sources:
Liver, fish, and eggs are excellent food
sources for preformed vitamin A
vegetable sources of provitamin A
carotenoids include dark green and
deeply colored fruits and vegetables.

retinol activity equivalent (RAE) is used to

express the vitamin A value of food.
1 RAE is defined as 1 g of retinol, 12 g of
carotene, and 24 g of other provitamin A
carotenoids.

Deficiency:
Vitamin A deficiency is endemic where diets are
chronically poor, especially in Southern Asia, Africa,
some areas of Latin America, and the Western
Pacific, including parts of China.
Vitamin A status is usually assessed by measuring
serum retinol or blood spot retinol or by tests of dark
adaptation.
normal range 1.053.50 mol/L (30100 ug/dL)
Xerophthalmia is a condition which includes milder
stages of night blindness and conjunctival xerosis
(dryness) with Bitot's spots, corneal ulceration and
necrosis.
Keratomalacia (softening of the cornea) leads to
corneal scarring and blindness.

Treatment:
A common approach to prevention is to supplement
young children living in high-risk areas with 60 mg
every 46 months, with a half-dose given to infants 6
11 months of age.
Xerophthalmia should be treated with 60 mg of Vit A
in oily solution.
extremely low-birth-weight infants,who is likely to be
vitamin Adeficient should be supplemented with
1500 g (or RAE) of vitamin A, three times a week for
4 weeks
Vitamin A deficiency in patients with malabsorptive
diseases who have symptoms of night blindness are
treated for 1 month with 15 mg/d of a water-miscible
preparation of vitamin A.

Toxicity:
Acute toxicity is manifested by:
increased intracranial pressure
Vertigo
Diplopia
bulging fontanels in children
Seizures
exfoliative dermatitis
Death
13-cis-retinoic acid, has been associated with birth
defects.
contraception should be continued for a least 1 year,
and possibly longer, in women who have taken 13-cis
retinoic acid.

Vitamin D
1, 25 Dihydroxyvitamin D is the active
derivative.
Principal function is maintenance of blood
calcium and phosphorous levels and an
antiproliferative hormone.
Dietary level per day associated with overt
deficiency in adults less than 2.0 ug/d.
Contributing factors to deficiency
includes:
Aging, lack of sunlight exposure, fat
malabsorption, deeply pigmented skin.

Deficiency:
Clinical findings

Rickets: skeletal deformation, rachitic rosary,

bowed legs; osteomalacia

Rachitic rosary
prominent knobs of bone at
the costochondral
joints of rickets patients creating the
appearance of large beads under the skin
of the rib cage, hence the name by analogy
with the beads of a rosary.

Vitamin E
Vitamin E is a collective name for all
stereoisomers of tocopherols and tocotrienols.
only the 2R tocopherols meet human
requirements.
Functions:

acts as a chain-breaking antioxidant and is an

efficient pyroxyl radical scavenger, which protects
low-density lipoproteins (LDLs) and
polyunsaturated fats in membranes from oxidation.
also inhibits prostaglandin synthesis and the
activities of protein kinase C and phospholipase A2.

Metabolism:
vitamin E is taken up from chylomicrons
by the liver after absorption.
hepatic a-tocopherol transport protein
mediates intracellular vitamin E
transport and incorporated into very
low-density lipoprotein (VLDL).

Dietary Sources:
widely distributed in the food supply and is
particularly high in sunflower oil, safflower
oil, and wheat germ oil.
tocotrienols are notably present in soybean
and corn oils.
Vit E is also found in meats, nuts, and
cereal grains, and small amounts are
present in fruits and vegetables.
RDA for vitamin E is 15 mg/d (34.9 mol or
22.5 IU) for all adults.

Deficiency:
Vitamin E deficiency is seen in only
severe and prolonged malabsorptive
diseases, such as celiac disease, or
after small-intestinal resection.
laboratory diagnosis of vitamin E
deficiency is made on the basis of low
blood levels of tocopherol (<5 g/mL, or
<0.8 mg)

Treatment:
Symptomatic vitamin E deficiency should
be treated with 8001200 mg of
tocopherol per day.
Patients with abetalipoproteinemia may
need as much as 50007000 mg/d.
Vitamin E has been suggested to increase
sexual performance, to treat intermittent
claudication, and to slow the aging process,
but evidence for these properties is
lacking.

Toxicity:
High doses of vitamin E (>800 mg/d)may
reduce platelet aggregation and
interfere with vitamin K metabolism and
are therefore contraindicated in
patients taking warfarin.
Nausea, flatulence, and diarrhea have
been reported at doses >1 g/d.

Vitamin K
Two natural forms of vitamin K

Vitamin K1, also known as phylloquinone, from

vegetable and animal sources.
Vitamin K2, or menaquinone, which is
synthesized by bacterial flora and found in
hepatic tissue.

Vitamin K is required for the carboxylation

of glutamic acid necessary for calcium
binding to carboxylated proteins such as:
prothrombin (factor II); factors VII, IX, and
X; protein C; protein S; and proteins found in
bone (osteocalcin) and vascular smooth muscle.

Dietary Sources:
Vitamin K is found in green leafy
vegetables such as kale and spinach;
also present in margarine and liver.
present in vegetable oils and is
particularly rich in olive, canola, and
soybean oils.
The average daily intake is estimated to
be approximately 100 g/d.

Deficiency:
symptoms of vitamin K deficiency are due
to hemorrhage
newborns are particularly susceptible
low fat stores, low breast milk levels of vitamin
K, sterility of the infantile intestinal tract,
liver immaturity, and poor placental transport.

Intracranial bleeding, as well as

gastrointestinal and skin bleeding, can
occur in vitamin Kdeficient infants.

 Vit K (1 mg IM) is given prophylactically at

the time of delivery
in adults may be seen in patients with
chronic small-intestinal disease,
obstructed biliary tracts, or after smallbowel resection.
Broad-spectrum antibiotic treatment can
precipitate vitamin K deficiency by
reducing gut bacteria, which synthesize
menaquinones

Treatment:
Vitamin K deficiency is treated using a
parenteral dose of 10 mg.
For patients with chronic malabsorption
12 mg/d of vitamin K should be given
orally, or 12 mg/week can be taken
parenterally.

Toxicity:
Toxicity from dietary phylloquinones and
menaquinones has not been described.
High doses of vitamin K can impair the
actions of oral anticoagulants.

Zinc
an integral component of many
metalloenzymes in the body;
it is involved in the synthesis and
stabilization of proteins, DNA, and RNA
plays a structural role in ribosomes and
membranes.
absolutely required for normal
spermatogenesis, fetal growth, and
embryonic development.

Dietary Sources:
Meat, shellfish, nuts, and legumes are
good sources of bioavailable zinc.
absorption of zinc from the diet is
inhibited by
dietary phytate, fiber, oxalate, iron, and
copper, as well as by certain drugs including
penicillamine, sodium valproate, and
ethambutol.

Deficiency:
The diagnosis of zinc deficiency is usually made
by a serum zinc level of <12 mol/L (<70 g/dL).
described in many diseases, including diabetes
mellitus, HIV/AIDS, cirrhosis, alcoholism,
inflammatory bowel disease, malabsorption
syndromes, and sickle cell disease.
can cause stunted growth in children,
decreased taste sensation (hypogeusia), and
impaired immune function.
Severe chronic zinc deficiency has been
described as a cause of hypogonadism and
dwarfism

Toxicity:
Acute zinc toxicity after oral ingestion
causes
nausea, vomiting, fever, respiratory
distress, excessive salivation, sweating, and
headache.

Chronic large doses of zinc may depress

immune function and cause hypochromic
anemia.

Copper
is an integral part of numerous enzyme
systems including amine oxidases,
ferroxidase (ceruloplasmin),
cytochrome-c oxidase, superoxide
dismutase, and dopamine hydroxylase.
also a component of ferroprotein, a
transport protein involved in the
basolateral transfer of iron during
absorption from the enterocyte.

Copper plays a role in

iron metabolism
melanin synthesis
energy production
neurotransmitter synthesis, and CNS
function
the synthesis and cross-linking of elastin
and collagen;
scavenging of superoxide radicals.

Deficiency:
The diagnosis of copper deficiency is based on low
serum levels of copper (<65 g/dL) and low
ceruloplasmin levels (<20 mg/dL).
Copper-deficiency anemia has been reported in
patients with malabsorptive diseases and nephrotic
syndrome
patients treated for Wilson's disease.
chronic high doses of oral zinc, which can interfere with
copper absorption

Menkes kinky hair syndrome

is an X-linked metabolic disturbance of copper metabolism
characterized by mental retardation, hypocupremia, and
decreased circulating ceruloplasmin

Toxicity:
Copper toxicity is usually accidental.
In severe cases, kidney failure, liver
failure, and coma may ensue.
In Wilson's disease, mutations in the
copper-transporting ATP7B gene lead to
accumulation of copper in the liver and
brain.

Selenium
is a component of the enzyme
glutathione peroxidase, which serves to
protect proteins, cell membranes, lipids,
and nucleic acids from oxidant
molecules.

Dietary Sources:
seafood, muscle meat, and cereals.

Deficiency:
Keshan disease is an endemic
cardiomyopathy found in children and
young women residing in regions where
dietary intake of selenium is low (<20
ug/d).

Chromium
Chromium potentiates the action of
insulin in patients with impaired glucose
tolerance, by increasing insulin
receptormediated signaling.

Dietary Sources:
include yeast, meat, and grain products.

Chromium-6, a product of stainless steel

welding and is a known pulmonary
carcinogen, as well as a cause of liver,
kidney, and CNS damage.

Fluoride
it is useful for the maintenance of
structure in teeth and bone.

Deficiency:
Adult fluorosis results in mottled and
pitted defects in tooth enamel as well
as brittle bone (skeletal fluorosis).

Manganese and
Molybdenum
deficiencies have been reported in
patients with rare genetic
abnormalities.
patients receiving prolonged total
parenteral nutrition.

Deficiency:
bone demineralization, poor growth,
ataxia, disturbances in carbohydrate
and lipid metabolism, and convulsions.