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VITAMIN D

GENERAL INTRODUCTION

Also known as the ‘sunshine’ vitamin or ‘anti-ricketic factor’ and calciferol, Vitamin D is a fat-soluble
and non-essential vitamin, that is, the body can synthesize it. It was first identified in Cod Liver and
designated as Vitamin D following Vitamin A, B and C, which had been discovered earlier. Vitamin D
is unique because it can be made in the skin from exposure to sunlight. On exposure to sunlight, it can
be synthesized from a precursor that the body makes from cholestrol. Vitamin D exists in two forms,
Vitamin D2 and Vitamin D3.

The two forms are similar and both need to be activated before they can fully function. Vitamin D2, also
known as ergocalciferol, derives primarily from plant food (for example, found naturally in sun-exposed
mushrooms). Human beings do not make vitamin D2. The natural form of vitamin D in all animals and
the form synthesized in human skin on exposure to sunlight is vitamin D3 also known as cholecalciferol.
Since, humans synthesize vitamin D3, it is said to be the most “natural” form.

Vitamin D that comes from the skin or diet is biologically inert and requires conversion to biologically
active form which stimulates intestinal calcium absorption. This occurs in the liver and kidneys. Any
abnormalities in the functions of kidneys or liver can interfere with the activation of vitamin D. Vitamin
D plays certain important roles in the body. Its deficiency or toxicity, both result in serious
complications.

ROLES OF VITAMIN D:

The activate form of vitamin D is basically a hormone, that is, manufactured in one part of the body it
travels through blood to its target site where it causes a response ( most notably the kidneys, intestines
and bones).

 BONE GROWTH
Vitamin D’s special role is to assist the absorption of calcium and phosphorus. Without vitamin
D, only 10–15% of dietary calcium and about 60% of phosphorus are absorbed. Vitamin D
sufficiency enhances calcium and phosphorus absorption by 30–40% and 80%, respectively
while maintaining blood concentrations of these minerals. Vitamin D raises blood concentration

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 levels of these minerals in three ways. When the diet is sufficient the vitamin D enhances
mineral absorption from the GI tract. When the diet is insufficient, vitamin D provides the
needed minerals from other sources, either by reabsorption by the kidneys or by mobilization
from the bones into the blood. In these circumstances it works in combination with parathyroid
hormone.

 MUSCLE FUNCTION
Vitamin D in muscle cells encourages growth in children and preserves strength in adults.
 IMMUNE SYSTEM
Vitamin D receptors are present in activated T and B lymphocytes and in activated macrophages.
The most common autoimmune diseases, including type 1 diabetes, rheumatoid arthritis, and
multiple sclerosis can be successfully prevented early in life if adequate vitamin D levels are
maintained.
 DISEASE CONTROL AND PREVENTION:
 CARDIOASCULAR FUNCTION

The heart is basically a large muscle, and like skeletal muscle, it has receptors for vitamin D.
Deficiency of vitamin D doubles the risk of heart attack. It also increases risk of heart failure,
sudden cardiac death, stroke and other cardiovascular diseases, and cardiovascular death.
Vitamin D plays a role in controlling blood pressure and preventing artery damage. Vitamin
D works against arteriolosclerosis in different ways, by inhibition of vascular smooth muscle
proliferation, suppression of vascular calcification, depression of parathyroid hormone and
lowering insulin resistance.

 HYPERTENSION

Recent studies suggest that vitamin D has an important association with blood pressure.
Adequate levels of vitamin D can prevent hypertension.

 DIABETES

Vitamin D could be a contributing factor in the development of type 2 diabetes. This may
also mean, adequate intake of vitamin D can prevent diabetes type 2. The higher the vitamin

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 D level, the lower the blood glucose. Supplementation with vitamin D has been shown to
restore insulin secretion in animals.

 CANCER

Sunlight exposure may lower the risk of cancer. vitamin D might slow or prevent the
development of cancer, including promoting cellular differentiation, decreasing cancer cell
growth, stimulating cell death (apoptosis), and reducing tumor blood vessel formation
(angiogenesis).

 PARKINSON’S DISEASE

In the brain and nerve cells, vitamin D protects against cognitive decline and slows the
progression of Parkinson’s disease.

ABSORPTION

Vitamin D that is ingested is incorporated into chylomicrons, which are absorbed into the lymphatic
system and enter the venous blood.

METABOLISM

 SYNTHESIS:
Vitamin D is formed when 7-dehydrocholesterol, the cholesterol precursor in the skin is exposed
to solar ultraviolet B radiations and is converted to previtamin D3. In a heat-dependent process,
previtamin D3 is immediately converted to vitamin D. This heat need is fulfilled from the body’s
heat. Excess UVB rays transform previtamin D3 into biologically inactive metabolites,
tachysterol and lumisterol.
 ACTIVATION
Vitamin D that comes from the skin or diet is biologically inert and requires activation. Its first
hydroxylation occurs in the liver by the enzyme 25-hydroxylase to form calcidiol. The second
hydroxylation occurs in the kidneys by the enzyme 1-alpha-hydroxylase to form calcitriol, the
biologically active form of vitamin D.

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  REGULATION:

 The activity of 1-alpha-hydroxylase in the kidney is tightly regulated and serves as the major control
point in production of the active hormone. The major inducer of 1-alpha-hydroxylase is parathyroid
hormone, which is induced by low blood levels of phosphate.

RDAs:

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The new Recommended Dietary
Allowances (RDAs)
range between 600 and 800 IU/day
The new Recommended Dietary
Allowances (RDAs)
range between 600 and 800 IU/day
The new Recommended Dietary
Allowances (RDAs)
range between 600 and 800 IU/day
The Recommended Dietary Allowances of vitamin D range between 600 to 800 IU/day.

 Infants 0-12 months - 400 IU/day (10 mcg).

 Children 1-18 years - 600 IU/day (15 mcg).

 Adults-70 years - 600IU/day (15mcg)
 70 years - 800IU/day (20mcg)
DEFICIENCY:

Intake lower than 13 mcg is imposes serious threats.

 POSSIBLE REASONS
In vitamin D deficiency the production of calbindin slows, a protein that binds calcium in the
intestinal cells. Following may lead to vitamin D deficiency:
AGE

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 The skin's ability to make vitamin D lessens with age. This is because they have
decreased presence of skin’s precursor for UVB mediated synthesis of vitamin D. Moreover,
reduced mobility, decreased sun exposure and low fortified foods intake also contribute.
DARK SKIN
Dark-colored skin is less able to make vitamin D than fair-colored skin because people
with dark skin have great amounts of melanin in their epidermis. Melanin competes with 7-
dehydrocholesterol for absorption of UVB photons. Therefore, they need more exposure to light
than fair-colored people to produce the same amounts of vitamin D.
SUNSCREEN USERS
Sunscreens can efficiently absorb UVB radiation. This dramatically prevents the
interaction of UVB with vitamin D precursor and thus, the process of previtamin D3 generation.
It has been shown that a sunscreen with a sun protection factor of 8 reduces the production of
previtamin D3 by 95 percent. Increasing the sun protection factor to 15 reduces production of
previtamin D3 by 99 percent.
FAT MALABSORPTION
As a fat-soluble vitamin, vitamin D requires the presence of dietary fat in the gut for
absorption. Certain pathological conditions, such as cystic fibrosis (CF) are associated with fat
malabsorption and thus may lead to vitamin D deficiency.

ANTICONVULSANT DRUGS USAGE

Anticonvulsants, also called antiepileptic drugs, used to treat epileptic seizures and
bipolar disorder. It is well recognized that long-term use of some antiepileptic drugs can result in
osteomalacia. The induction of the catabolism of vitamin D by these drugs is thought to
contribute to their deleterious side effects.
CHRONIC KIDNEY DISEASES
Since kidney is involved in hydroxylation of vitamin D precursor to form activated form
of Vitamin D, chronic kidney diseases such as patients requiring dialysis, leads to an inability to
make sufficient biologically active vitamin D.
HUMAN BREAST MILK
A woman's breast milk only contains a small amount of vitamin D. Therefore breastfed infants
are at a risk for not receiving enough vitamin D.

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DISEASES

Vitamin D deficiency is common and may contribute to rickets, osteopenia, and osteoporosis and falls
risk in the elderly. Screening for vitamin D deficiency is important in high-risk patients, especially for
patients who suffered minimal trauma fractures.

 RICKETS
In rickets bones fail to calcify normally, causing growth retardation and skeletal abnormalities.
The bones become so weak that they bend when they have to support weight, called bowed legs.
Another sign is the beaded ribs due to weak attachment of the bones to the cartilage.

 OSTEOMALACIA
Poor mineralization results in increasingly soft, flexible, brittle, and deformed bones. 
 OSTEOPOROSIS
Vitamin D deficiency sets the stage for loss of calcium from the bones, which can result in
fractures.

 MUSCLE WEAKNESS
Poor muscle strength and weakness may be associated with vitamin D deficiency, which leads to
an increased risk of falls (sarcopenia), gradual muscle atrophy and reduced physical
performance.
 RHEUMATOID ARTHRITIS
Vitamin D deficiency may lead to Rheumatoid Arthritis, an autoimmune disease with painful,
swollen joints and regular fever and fatigue.
 PAGET’S DISEASE
It is a chronic disorder of bone that typically results in enlarged and deformed bones in one or
more regions of the skeleton and excessive bone breakdown. Vitamin D deficiency is found to be
associated with Paget’s disease.
 DIABETES

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 Vitamin D deficiency could be a contributing factor in the development of both type 1 and type 2
diabetes. Evidence indicates that vitamin D treatment improves glucose tolerance and insulin
resistance. Vitamin D deficiency leads to reduced insulin secretion.
 DEPRESSION
Mood changes with season, a common phenomenon is that anxiety and depression increase
during winter months. An extreme case of this seasonality is a clinical syndrome called seasonal
affective disorder (SAD), also known as winter depression. One explanation is the changing
level of vitamin D3 during winter. 

TOXICITY

The Tolerable Upper Intake Level for vitamin D is 4000 IU/day (100 mcg).

DIAGNOSIS:

Diagnosis of vitamin D toxicity is confirmed by high serum calcium and high serum vitamin D levels.
Vitamin D, particularly its active hormonal form, calcitriol, is a highly potent molecule, capable of
producing serious toxic effects, including death, at milligram intake levels. Following are some
complications associated:

 HYPERCALCEMIA
Excess vitamin D raises the concentration of calcium in blood. High levels of blood calcium can
cause confusion, disorientation, and problems with heart rhythm.
 KIDNEY STONES
Precipitation of excess vitamin D in kidneys, from where it excreted may form stones in them.
 HYPERPHOSPHATEMIA
It is an electrolyte imbalance with elevated levels of phosphate in blood. The kidneys naturally
control levels of phosphates. However, if the kidneys are not working efficiently, they may not
be able to remove enough phosphate, leading to high levels in the body.
 POLYURIA AND POLYDIPSIA

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 Vitamin D deficiency may lead to excessive urination volume or polyuria. It occurs when urine
volume exceeds 2.5 liters per day. This, in turn, leads to polydipsia which is characterized by
excessive thirst.
 ECTOPIC CALCIFICATION
Ectopic calcification is defined as inappropriate biomineralization occurring in soft tissues. 
Ectopic calcifications are typically composed of calcium phosphate salts.
 HYPERVITMINOSIS D
Taking too much vitamin D can cause unpleasant side effects, such as nausea,
vomiting, constipation, and appetite loss.
 OBESITY
Vitamin D may regulate the cells of the adipose tissue in ways that might influence the
development of obesity.

TREATMENT

Treatment consists of decrease in vitamin D intake and avoiding all calcium containing food in diet such as milk,
curd, etc.

SOURCES

 RICH SOURCES

Milk and dairy products, eggs, salmon, , mackerel cod liver oil, sundried mushrooms, egg yolk and
fortified milk (at least 2 cups a day), orange juice, are rich sources of vitamin D. Adequate sunlight
exposure (10 am to 2 pm with arms and leg exposed) is also an important source of vitamin D.

 FAIR SOURCES
Fatty fish such as tuna and sardines, margarine, are poor sources of vitamin D.
 POOR SOURCES
Egg yolk, beef liver and cheese
 SUPPLEMENTS

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 Taking vitamin D from supplements is beneficial. It can be found in multivitamin-mineral
supplements. However, high-dose single supplements of vitamin D3 are less expensive, more
commonly available and more effective.

IODINE
GENERAL INTRODUCTION
Iodine is an essential trace mineral. It commonly occurs in the body as anion of iodide or as
iodate salts. It forms a vital component of the thyroid hormones thyroxine (T4) and tri-
iodothyronine (T3), which are crucial regulators of the metabolic rate and physical and mental
development in humans. By controlling the rate at which the cell uses oxygen, these hormones
influence the amount of energy expended during metabolism. They regulate body temperature,
growth, blood cell production and nerve and muscle functions. Iodine is also important in the
health of mammary tissue.

ABSORPTION
Iodate is rapidly and efficiently absorbed in the proximal part of small intestine as iodide. Salt
foritificants and food additives are also readily broken down and reduced to iodide in the
intestinal lumen. In addition, some organic iodine complexes, such as thyroid hormones added to
animal feeds can be absorbed intact. Larger organic complexes are lost in the feces. Iodide is
absorbed by the intestinal sodium-iodide co-transporter. It is available for uptake by all tissues of
the body. Majority of iodide , about 80 percent, is absorbed by the thyroid gland. Significant
amounts are absorbed by the salivary glands and the lactating mammary glands. Mechanism of
uptake is stimulated by the Thyroid Stimulating Hormone (TSH) released by the pituitary gland.
Excess iodine is excreted from the body in the urine. The iodide content of foods can be
significantly affected by the way the foods are cooked. For example boiling the food reduces
their iodine content approximately by half, where as frying reduces it by approximately 20
percent.
RDAs
The Recommended Dietary Allowance for Iodine are
 Birth to 6 months - 110 mcg/day
 Infants 7–12 months - 130 mcg/day

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 Children 1–8 years - 90 mcg/day
 Children 9–13 years - 120 mcg/day
 Teens 14–18 years - 150 mcg/day
 Adults - 150 mcg/day.

DEFICIENCY
The thyroid gland needs at least 60 mcg/day of iodine. Levels lower than this cause deficiency.
Iodine deficiency diminishes the production of thyroid hormone. The body increases its
production of TSH in an attempt to escalate iodine uptake. Iodine deficiency can cause a wide
range of disorders, collectively known as iodine-deficiency disorders.
 FETAL DEFICIENCY
The fetal brain is particularly susceptible to iodine deficiency if the mother is iodine deficient.
The neurological damage is irreversible and devastating, resulting in mental retardation and
speech and hearing defects.
 CRETINISM
Cretinism is the mental and physical retardation of a person that is caused by iodine deficiency
during pregnancy. It is untreated congenital hypothyroidism. The fetus and the infant are
neurologically vulnerable due to the incomplete brain development in humans at birth. A
progressive intellectual deterioration occurs with each passing week in the absence of
appropriate thyroxine replacement. Cretins lack weight gain and have stunted growth, fatigue,
lethargy, and thickened facial features, cool, dry and pale skin.
Treatment in infancy can reverse the physical changes, but not the neurological damage.
 GOITER
If a deficiency persists, the TSH produced by pituitary stimulates the thyroid follicles of the
thyroid gland to enlarge and multiply to absorb as much iodine as possible. The gland enlarges to
form a visible lump in the neck, the characteristic goiter appearance. Very large goiters can block
the esophageal passage and cause damage to larynx.
Goiter causes symptoms of hypothyroidism- cold intolerance, weight gain, sluggishness and
decreased body temperature.

TOXICITY

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The Tolerable Upper Intake Level for Iodine is 1100 mcg/day.
High amounts of iodine inhibit synthesis of thyroid hormone and stimulate growth of thyroid
gland.
 INDUCED GOITER
A mother who had an excess intake of iodine during pregnancy, it is likely that her infant will
have induced goiter. The iodine induced goiter in the fetus can suffocate and potentially kill the
fetus. If the mother has hyperthyroidism during pregnancy, the fetus is at risk of many
complications such as growth retardation and a premature birth. 

 MYXEDEMA
Under activity of the thyroid gland is known as myxedema.
Every patient with myxedema has hypothyroidism, but not every hypothyroid patient has
myxedema. Characteristic symptoms are weakness, cold intolerance, mental and physical
slowness, dry skin, typical facial features and hoarse voice. 
 Primary treatment is administration of adequate doses of thyroid hormone either given
intravenously or given by nasogastric tube.

 HYPOTHYROIDISM
TSH is produced by the pituitary gland to stimulate the thyroid gland for the increased
production of thyroid hormone. Inhibition of synthesis of thyroid hormone by thyroid gland can
elevate the levels of TSH in blood.

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