IMPORTANT SEQS OF VITAMINS
NUTRITION AND MINERALS WITH
ANSWER KEY FOR 1ST YEAR MBBS
Educational Blog | October 27, 2014 | 1st Year MBBS | Comments (9)
All SEQs are not mentioned here. At the end of the Post You will find the Download Link of SEQs in
PDF format. In PDF file you will be able to see all the SEQs with Answer Key of Each as per
standard of UHS and all other Universities.
Q 1:Construct a balanced diet chart for a 70 kg man to fulfill 2700 Caloric requirement
keeping in mind the middle socioeconomic status of your client?
b:What do you understand by negative nitrogen balance?
Q:
12 year old boy presents to medical OPD of Hospital Lahore. His behavior is psychiatrically
abnormal and his conjunctiva of eyes shows jaundice. The Descemet’s membrane of cornea
shows a brown ring at the periphery. The serum level of a mineral is raised.
What is your most probable diagnosis? And which mineral metabolism is disturbed in this
case.
Give the sources of this mineral.
Q: In which respects the nutrients needed by a pregnant and lactating mother are different
from those needed by a young female? Give reasons
WHAT ARE THE SOURCES & METABOLIC ROLE OF VITAMIN B1
Whole grains, legumes are the richest sources
Natural sources are found mainly in combination with starch that is husk of grain.
Biochemical role:
Thiamine pyrophosphate (TPP) is the biologically active form of the vitamin, formed by the transfer
of a pyrophosphate group from ATP to thiamine. Thiamine pyrophosphate serves as a coenzyme in
the formation or degradation of α-ketols by transketolase, and in the oxidative decarboxylation of α-
keto acids.
How vitamin B12 is absorbed? Write the clinical conditions associated with vitamin B12.
Vitamin B12 deficiency is rarely a result of an absence of the vitamin in the diet. It is much more
common to find deficiencies in patients who fail to absorb the vitamin from the intestine, resulting in
pernicious anemia. The disease is most commonly a result of an autoimmune destruction of the
gastric parietal cells that are responsible for the synthesis of a glycoprotein called intrinsic
factor. Normally, vitamin B12 obtained from the diet binds to intrinsic factor in the intestine. The
cobalamin intrinsic factor complex travels through the gut and eventually binds to specific receptors
on the surface of mucosal cells of the ileum. The bound cobalamin is transported into the mucosal
cell and, subsequently, into the general circulation, where it is carried by B12-binding proteins. Lack
of intrinsic factor prevents the absorption of vitamin B12 resulting in pernicious anemia. Patients with
cobalamin deficiency is usually anemic, but later in the development of the disease they show
neuropsychiatric symptoms. However, central nervous system (CNS) symptoms may occur in the
absence of anemia. The CNS effects are irreversible and occur by
READ IT & MAKE CONCEPTS
Q- Which vitamin deficiency is associated with sub acute combined degeneration of spinal
cord?
Answer- Vitamin B12 deficiency is associated with sub acute combined degeneration of spinal cord.
Peripheral nerves are usually affected first, and patients complain initially of paresthesias. The
posterior columns next become impaired, and patients complain of difficulty with balance. In more
advanced cases, cerebral function may be altered as well. An accumulation of Methylmalonyl-CoA in
serum, has been suggested as a possible cause of neurologic defects seen in cobalamin deficiency
by decreasing lipid synthesis.
Impaired biosynthesis of phosphatidyl choline due to decreased levels of methionine and S-
adenosylmethionine (SAM) may also play a role in the neurologic symptoms of cobalamin deficiency
by compromising the repair of demyelination.
Q.- Which vitamin participates in the absorption of calcium from gut?
Answer- Vitamin D has an active role in the absorption of calcium from gut. Vitamin D promotes the
synthesis of calbindin protein that promotes the absorption of calcium from gut. This action is
brought about through nuclear receptors. it acts like a steroid hormone, binding to nuclear receptors
and enhancing gene expression, although it also has rapid effects on calcium transporters in the
intestinal mucosa
Q- A 2-year- old child presents with chronic cough, bronchitis, growth failure, chronic
diarrhea and growth failure. A deficiency of which vitamin should be considered?
Answer- The child is probably suffering from Vitamin A deficiency.
The child has chronic cough, bronchitis, growth failure and passage of light-colored, foul-smelling
stools. All these symptoms are due to increased susceptibility to infections as a result of the
keratinization of mucous membranes in the respiratory, GI, and urinary tracts. The thickened
mucosa cracks easily and the risk for bacterial infections increases. During infection the synthesis of
retinol binding protein is reduced in response to infection since it is a negative ‘Acute phase protein’,
that results in decreased circulatory concentration of the vitamin with further deterioration of the
immune system.
Q.- A 2-year- old child has been brought to Pediatric O.P.D with the complaint of painful and
difficult walking. General examination reveals bow legs and prominent costochondral
junctions. Which vitamin supplementation should be given as a part of the treatment?
Answer- Vitamin D supplementation is needed as a part of treatment since the child seems to be
suffering from Rickets. In young infants, rickets causes softening of the entire skull (Craniotabes). In
older infants with rickets, sitting and crawling are delayed, as is Fontenelle closure; there isbossing
of the skull and costochondral thickening. Costochondral thickening can look like bead like
prominences along the lateral chest wall(rachitic rosary). In children 1 to 4 yr, epiphyseal cartilage at
the lower ends of the radius, ulna, tibia, and fibula enlarge; Kyphoscoliosis develops, and walking is
delayed. In older children and adolescents, walking is painful; in extreme cases, deformities such
as bowlegs and knock-kneesdevelop.
Q.- Which vitamin deficiency is associated with Neural tube defects?
Answer- Neural tube defects are observed are due to maternal folic acid deficiency. Neural Tube
Defects (NTDs) are birth defects of the brain and the spinal cord (malformations of the brain and
spinal cord, causing anencephaly, spina bifida or encephalocele).It has been demonstrated that
periconceptional (before and during the first 28 days after conception) supplementation of women
with folic acid can decrease the risk of neural tube defects. Therefore, a daily intake of 400 µg folic
acid in addition to a healthy diet 8 weeks prior to and during the first 12 weeks after conception is
recommended. There is evidence that adequate folate status may also prevent the incidence of
other birth defects, including cleft lip and palate, certain heart defects and limb malformations. To
reduce the risk of neural tube defects, cereal grains are fortified with folate in some countries.
Q.- Which vitamin deficiency is associated with egg white injury?
Answer- Raw egg whites contain Avidin, a glycoprotein that strongly binds to biotin and prevents its
absorption. Thus, the ingestion of large quantities of raw egg white over a long period can result in a
biotin deficiency.
Q.- Name the coenzyme for the reaction for the conversion of Pyruvate to alanine.
Answer- Pyruvate to Alanine conversion is catalyzed by Transaminase (SGPT- Alanine transferase),
that requires vitamin B6-P as a coenzyme.
Q.- The bone marrow smear of a strict vegetarian female patient, presenting with weakness,
fissured tongue and paralysis reveals megaloblastic anemia. Which vitamin deficiency is
expected?
Answer- The patient is suffering from megaloblastic anemia. The cause seems to be B12 deficiency.
Although it is synthesized exclusively by microorganisms, for practical purposes vitamin B 12 is found
only in foods of animal origin, there being no plant sources of this vitamin. This means thatstrict
vegetarians (Vegans) are at risk of developing B12 deficiency.
Q.- A 56 – year-old male on Isoniazid therapy for tuberculosis has developed rashes on the
exposed parts of the body. What is the probable cause for these rashes?
Answer- The patient has developed pellagra. Prolonged treatment with the anti-tuberculosis drug,
Isoniazid, can cause niacin deficiency. Isoniazid may induce a state of pyridoxine deficiency by
combining with pyridoxine and generating inactive isoniazid-pyridoxal hydrazones, thus depleting the
supply of pyridoxine. Pyridoxine is needed in the endogenous pathway of niacin synthesis. Thus
diminished synthesis of niacin ultimately produces pellagra.
Q.- Why is it said that babies undergoing phototherapy for physiological jaundice are prone
to develop riboflavin deficiency?
Answer- Riboflavin is stable when heated and is not easily destroyed in the ordinary processes of
cooking but it is light-sensitive so it is degraded easily by light, that is why infants undergoing
phototherapy for jaundice get prone to this deficiency. Loss of riboflavin is also seen if foods are left
out in sunlight or in UV light. Because of this light sensitivity, riboflavin rapidly disappears from milk
kept in glass bottles exposed to the sun or bright daylight (85% within 2 hours).
Q.- A child from a very poor socio economic background has reported with loss of
vision.Make a probable diagnosis. What is the underlying cause for blindness?
Answer- As the child is from a family with poor socio economic background, perhaps he is suffering
from vitamin A deficiency.The earliest symptom of vitamin A deficiency is impaired dark adaptation,
or night blindness. Severe deficiency causes xerophthalmia, ultimately resulting in corneal ulcers,
scarring and blindness.
Q.- What is the possible link between intake of polished rice and sudden cardiac failure?
Answer- The link between intake of polished rice and sudden cardiac failure is thiamine deficiency
(wet beriberi).Polished rice or highly refined carbohydrates are poor sources of thiamine.
Thiamine deficiency is most commonly observed in chronic alcoholics or people subsisting on
polished rice or high carbohydrate refined diets.
Q.- What are folate antagonists? Enlist a few clinically important Folate antagonists.
Answer- – Folate antagonists were originally developed as antileukemic agents, but are now being
used and/or investigated in the treatment of a wide range of cancerous and non-cancerous
diseases. Sulfanilamide and Trimethoprim are antibiotics, Pyrimethamine is antimalarial while
Methotrexate is an anticancer drug.
Q.- Cancer patients on Methotrexate therapy, develop Glossitis and oral ulcers, what is the
possible reason?
Answer- Methotrexate, an analog of 10-methyl-tetrahydrofolate, inhibits dihydrofolate reductase and
has been exploited as an anti-cancer drug. Methotrexate blocks the cell’s ability to regenerate THF,
leading to inhibition of these biosynthetic pathways. The lack of nucleotides prevents DNA synthesis,
and these cancer cells cannot divide without DNA synthesis.
Unfortunately, the effects of Methotrexate are nonspecific and other rapidly dividing cells such as
epithelial cells in the oral cavity, intestine, skin, and blood cells are also inhibited. This leads to the
side effects associated with methotrexate (and other cancer chemotherapy drugs) such as mouth
sores, low white blood cell counts, stomach upset, hair loss, skin rashes, and itching.
Q.- Name the vitamin that acts as a coenzyme for the post translational modifications of
prothrombin.
Answer- The post translational modifications of prothrombin are carried out by gamma carboxylation
of its glutamic acid residues. The reaction is catalyzed by carboxylase enzyme which requires
vitamin K as a coenzyme. CO 2 and O2 are also required for this carboxylation process.The ability to
bind calcium ions (Ca2+) is required for the activation of the seven vitamin K-dependent clotting
factors, or proteins, in the coagulation cascade. Vitamin K-dependent gamma-carboxylation of
specific glutamic acid residues in those proteins makes it possible for them to bind calcium.
Q.- Treatment of pregnant women with warfarin can lead to fetal bone abnormalities (fetal
warfarin syndrome), what is the cause for this disorder?
Answer- Warfarin is a vitamin K antagonist; its mechanism of action involves inhibition of vitamin K
cycle producing vitamin K deficiency.The fetus gets the supply of vitamin K from maternal circulation
as there are no other sources, so the maternal vitamin K deficiency results in fetal deficiency. There
is gross impairment of gamma carboxylation of fetal vitamin K dependent proteins. Under
carboxylation adversely affects the capacity to bind the bone mineral that is the reason for the
malformed bones.
Q.- Vitamin B6 deficiency leads to niacin deficiency also, suggest the reason for it.
Answer- vitamin B6 is required as a coenzyme for the enzyme kynureninase, which is an enzyme of
the pathway of biosynthesis of niacin from tryptophan. In B6 deficiency, niacin is inappropriately
synthesized,B6 being unavailable at the Kynureninase step, hence niacin deficiency also sets in and
clinical manifestations of deficiencies of both vitamins are observed..
Q.- Name a water-soluble vitamin that is required for the synthesis of collagen.
Answer- Vitamin C is required for the synthesis of collagen. The enzymes Prolyl and lysyl
hydroxylases require vitamin C for their actions to form hydroxy proline and hydroxy lysine from
proline and lysine respectively. These post translational modifications are required for the formation
of triple helical structure of collagen. Deficiency of vitamin C leads to impaired hydroxylation
reactions with the resultant formation of a weak collagen.
Q.- What is the cause of hyperkeratinization in vitamin A deficiency?
Answer- Vitamin A (Retinoic acid) regulates the synthesis of keratin by regulating its gene
expression. In vitamin A deficiency keratin is excessively synthesized resulting in hyperkeratinization
of mucus membranes which can easily crack to allow bacterial invasion with the resultant increased
frequency of infections in vitamin A deficiency. Since vitamin A decreases the expression of keratin
gene, vitamin A is given therapeutically for the treatment of acne.
Q.- What is the absorbable form of Thiamine?
Answer- Thiamine occurs in the human body as free thiamine and in various phosphorylated forms:
thiamine monophosphate (TMP), thiamine triphosphate (TTP), and thiamine pyrophosphate (TPP),
which is also known as thiamine diphosphate. Thiamine pyro phosphate is the active form of
Thiamine. It is rapidly converted to its active form, in the brain and liver by a specific enzyme, TPP
synthetase. The synthesis of TPP from free thiamine also requires the presence of magnesium and
adenosine triphosphate (ATP).
Q.- Name the active form/forms of Riboflavin.
Answer- Riboflavin (B2) exists in two active forms FMN (flavin mono nucleotide) and FAD (flavin
adenine dinucleotide). In the body, riboflavin occurs primarily as an integral component of the
enzymes. These coenzymes participate in a large majority of the reactions in the body.
Q.- Which forms of Cobalamine is required for the methylation of Homocysteine to
Methionine ?
Answer- Methyl Cobalamine form is required for the methylation of homocysteine to Methionine.
1. Which vitamin deficiency is associated with lactic acidosis?
Answer- Lactate, a product of anaerobic glucose metabolism, is generated from pyruvate with
lactate dehydrogenase as a catalyst. Pyruvate is normally aerobically metabolized to CO 2 and H2O in
the mitochondrion. Initially pyruvate is converted to Acetyl co A with pyruvate dehydrogenase
complex acting as a catalyst requiring thiamine, niacin, riboflavin, pantothenic acid and lipoic acid as
coenzymes. Acetyl co A is completely oxidized in the Krebs cycle.
Normally, pyruvate is in a state of equilibrium with lactate and under condition like thiamine
deficiency, when PDH complex becomes less active, the equilibrium is shifted towards production of
lactate. Lactate is cleared from blood, primarily by the liver, with the kidneys (10-20%) and skeletal
muscles to a lesser degree. Lactic acidosis results from an increase in blood lactate levels when
lactate production exceeds consumption and body buffer systems become overburdened.
Q.- Which vitamin supplementation is given to treat morning sickness of pregnancy?
Answer- B6 is given to treat morning sickness of pregnancy. It is also given to treat radiation
sickness, muscular dystrophies and epileptiform convulsions.
Q.- What are the clinical manifestations of B12 deficiency?
Answer- The hallmark of symptomatic vitamin B12 deficiency is megaloblastic anemia. The
megaloblastic state also produces changes in mucosal cells, leading to glossitis, as well as other
vague gastrointestinal disturbances such as anorexia and diarrhea. Cobalamine deficiency also can
present with numerous neurologic manifestations including: numbness, paresthesias, weakness,
ataxia, abnormal reflexes and diminished vibratory sensation.
Q.- For which defect in the body, Schilling test is carried out?
Answer- Scilling test is carried out for the diagnosis of pernicious anemia. The Schilling test can
determine if the deficiency is due to absence of intrinsic factor, or some malabsorption disorder. The
Schilling test measures Cbl (cobalamine)absorption by increasing urine radioactivity after an oral
dose of radioactive Cbl.
Q- Which type of Transcobalamine is required for the transportation of vitamin B12?
Answer- Three plasma transport proteins have been identified. Transcobalamine I and III (differing
only in carbohydrate structure) are secreted by white blood cells. Although approximately 90% of
plasma vitamin B12 circulates bind to these proteins, only Transcobalamine II is capable of
transporting vitamin B12 into cells.
.
Q.-What is the basis of using B6-P as a drug for treating infantile convulsions?
Answer- B6-P is required for the decarboxylation of amino acids. Glutamic acid undergoes
decarboxylation under the activity of decarboxylase enzyme in the presence of B6-P to form GABA
(gamma amino butyric acid) which is an inhibitory neurotransmitter. Thus there is relief of
convulsions which is a state of hyper excitation, by B6P through promoting the synthesis of GABA.
Q.-Which vitamin is required for the absorption of amino acids from the gut?
Answer- Vitamin B6 is required for the active absorption of amino acids from the gut.
Q.- Name the synthetic form of vitamin K.
Answer- Three compounds have the biological activity of vitamin K phylloquinone, the normal dietary
source, found in green vegetables;menaquinones, synthesized by intestinal bacteria, with differing
lengths of side chain; and menadione and menadiol diacetate, synthetic compounds that can be
metabolized to phylloquinone.
Q.- Name the inhibitors of vitamin K that act as anticoagulants.
Answer- Although vitamin K is a fat-soluble vitamin, the body stores very little of it, and its stores are
rapidly depleted without regular dietary intake . The oral anticoagulants, such as Dicumarol and
warfarin, inhibit coagulation through antagonism of the action of vitamin K.
Q.-The synthesis of which vitamin is inhibited by Sulphonamides?
Answer- The synthesis of folic acid is inhibited by sulphonamides (sulphanilamides). Because its
shape is similar to that of p-aminobenzoic acid, sulfanilamide inhibits the growth of bacteria by
interfering with their ability to use p-aminobenzoic acid to synthesize folic acid. Sulfa drugs were the
first antimetabolites to be used in the treatment of infectious disease. Because humans don’t make
folic acid, sulfanilamide is not toxic to humans in the doses that inhibit bacteria. This ability to inhibit
bacteria while sparing humans made them useful in preventing or treating various infections.
Q.- Which form of vitamin A -11 cis Retinal or 11-cis Retinol is required for vision?
Answer- Vitamin A, in the strictest sense, refers to retinol. However, the oxidized metabolites,
retinaldehyde and retinoic acid, are also biologically active compounds. The term retinoids includes
all molecules (including synthetic molecules) that are chemically related to retinol. Retinaldehyde
(11-cis) is the essential form of vitamin A that is required for normal vision, whereas retinoic acid is
necessary for normal morphogenesis, growth, and cell differentiation.
Q.- Why is it said that Niacin and vitamin D are not true vitamins?
Answer- The distinguishing feature of the vitamins is that they generally cannot be synthesized by
mammalian cells and, therefore, must be supplied in the diet.Vitamin D, which is formed in the skin
after exposure to sunlight, and niacin, which can be formed from the essential amino acid
tryptophan, do not strictly comply with this definition. However, the ability to utilize tryptophan for
niacin synthesis is inefficient (60 mg of tryptophan are required to synthesize 1 mg of niacin).
Q.- What is the cause of bleeding tendencies in obstructive jaundice?
Answer- In obstructive jaundice there is obstruction to the outflow of bile. Bile salts are needed for
the absorption of fat soluble vitamins. Vitamin K, a fat soluble vitamin has an active role in
coagulation of blood. In conditions of malabsorption or obstructive jaundice, Vitamin K deficiency
sets in with the resultant impaired coagulation of blood and bleeding tendencies.
– What is the cause for neurological manifestations in B6P deficiency?
Answer- It is required for the synthesis of neurotransmitters like Serotonin, GABA (Gamma amino
butyric acid) and also Dopamine, norepinephrine and epinephrine . These are produced by
decarboxylation reactions .B6-P is also required for the synthesis of sphingomyelins and other
sphingolipids that are required for the formation of myelin sheath. Therefore deficiency of B6-P
results in impairment of such reactions and hence neurological deficit.
4- What are the different forms in which the disease Beriberi can be manifested ?
Answer- Beriberi is the outcome of vitamin B1(thiamine) deficiency. It is manifested as dry, wet,
infantile, cerebral (Wernicke’s Korsakoff syndrome) or shoshin beriberi.
8- What is the cause of reduced RBC Transketolase activity in Thiamine deficiency?
Answer- Transketolase enzyme is the enzyme of HMP pathway, a pathway of glucose utilization.
Thiamine as TPP (active form- Thiamine pyrophosphate form) is required as a coenzyme for the
functioning of this enzyme. In thiamine deficiency, the activity of this enzyme goes down and that is
estimated in red blood cells to diagnose the underlying deficiency.
9- Why are alcoholics more prone to Thiamine deficiency?
Answer- Reduced dietary intake and impaired absorption are the important causes of thiamine
deficiency in chronic alcoholics.
3- Why are premature infants given vitamin K injections immediately after birth?
Answer- Newborn infants, in general, have low vitamin K status for the following reasons:
1. a) Vitamin K is not easily transported across the placental barrier;
2. b) The newborn’s intestines are not yet colonized with bacteria that synthesize
menaquinones; and
3. c) The vitamin K cycle may not be fully functional in newborns, especially premature infants.
– Name the antioxidant vitamins.
Answer-An antioxidant is a substance that significantly decreases the harmful effects of “reactive
species”, such as reactive oxygen and nitrogen molecules that disrupt normal physiological function
on a cellular level in humans. Examples include the antioxidant vitamin C, vitamin E, and the
carotenoids (vitamin A). Selenium is also an antioxidant. A multitude of other nutrients, including
minerals such as copper, manganese, and zinc, flavonoids, and coenzyme Q10, also possess
antioxidant properties.
– What are the clinical findings in a case of Rickets?
Answer- Rickets is caused by a failure of osteoid to calcify in growing children. It occurs due to
vitamin D deficiency. The clinical manifestations include-frontal bossing,bow legs, knock-
knees, rachitic rosary along the costochondral junctions, Harrison groove and in more severe
instances in children older than 2 years, vertebral softening leading toKyphoscoliosis. In the long
bones, laying down of uncalcified osteoid at the metaphysis leads to spreading of those areas,
producing knobby deformity.
– Which water soluble vitamin is stored in liver ?
Answer- Vitamin B12 is the only water soluble vitamin that is stored in the body (in the liver). The
liver contains 2000–5000 mcg of stored vitamin B12. Since daily losses are 3–5 mcg/d, the body
usually has sufficient stores of vitamin B12 so that vitamin B12 deficiency develops more than 3 years
after vitamin B12 absorption ceases.
– Why is vitamin D considered a hormone?
Answer- Vitamin D is actually a hormone since its mechanism of action resembles that of hormones.
Like hormones it is required only in small amount. Most if not all actions of vitamin D are mediated
through a nuclear transcription factor known as the vitamin D receptor (VDR) similar to hormones.
4.- Name a confirmatory test to diagnose underlying Thiamine deficiency.
Answer- R.B.C Transketolase activity and 24-h urinary thiamine excretion may be measured to
diagnose underlying thiamine deficiency.
synthesis, and these cancer cells cannot divide without DNA synthesis.
9-Which vitamin is known to participate in the hydroxylation reactions?
Answer- Vitamin C, also known as ascorbic acid participates in the hydroxylation reactions. Vitamin
C is the coenzyme for two groups ofhydroxylases. These are copper-containing hydroxylases and
the α -ketoglutarate-linked iron-containing hydroxylases.
– Which vitamin deficiency is known to cause bleeding gums?
Answer- Vitamin C deficiency causes bleeding gums. Gums may become swollen, purple, spongy,
and friable; they bleed easily in severe deficiency.
15- Name a vitamin which is used therapeutically as a lipid lowering drug
Answer- Niacin reduces plasma triglyceride and LDLc levels and raises the plasma concentration of
HDLc. Niacin is also the only currently available lipid-lowering drug that significantly reduces plasma
levels of Lp (a). If properly prescribed and monitored, niacin is a safe and effective lipid-lowering
agent.
Q- Discuss the steps of activation of vitamin D, and explain the reason for the fact that
Vitamin D is toxic in excess, but excessive exposure to sunlight does not lead to vitamin D
toxicity.
Answer- Vitamin D3 (cholecalciferol) can be synthesized by humans in the skin upon exposure to
ultraviolet-B (UVB) radiation from sunlight, or it can be obtained from the diet. When exposure to
UVB radiation is insufficient for the synthesis of adequate amounts of vitamin D 3 in the skin,
adequate intake of vitamin D from the diet is essential for health. Plants synthesize ergosterol, which
is converted to vitamin D2 (Ergocalciferol) by ultraviolet light.
In response to ultraviolet radiation of the skin, a photochemical cleavage results in the formation of
vitamin D from 7-dehydrocholesterol. Cutaneous production of vitamin D is decreased by melanin
and high solar protection factor sunblocks, which effectively impair skin penetration of ultraviolet
light. The increased use of sunblocks in North America and Western Europe and a reduction in the
magnitude of solar exposure of the general population over the past several decades has led to an
increased reliance on dietary sources of vitamin D. In the United States and Canada, these sources
largely consist of fortified cereals and dairy products, in addition to fish oils and egg yolks. Vitamin D
from plant sources is in the form of vitamin D2, whereas that from animal sources is vitamin D3.
These two forms have equivalent biologic activity and are activated equally well by the vitamin D
hydroxylases in humans
