WHO defines it as tissue concentrations of vitamin A low
enough to have adverse health consequences even if there
is no evidence of clinical xerophthalmia .
In addition to the specific signs and symptoms of
xerophthalmia and the risk of irreversible blindness, nonspecific symptoms include increased morbidity and
mortality, poor reproductive health, increased risk of
anaemia, and contributions to slowed growth and
In 1987, WHO estimated that vitamin A deficiency was endemic in 39
countries based on the ocular manifestations of xerophthalmia or
deficient serum (plasma) retinol concentrations (<0.35 µmol/l).
Globally, night blindness is estimated to affect 5.2 million preschoolage children and 9.8 million pregnant women which corresponds to
0.9% and 7.8% of the population at risk of VAD, respectively.
Low serum retinol concentration (<0.70 µmol/l) affects an estimated
190 million preschool-age children and 19.1 million pregnant women
globally. This corresponds to 33.3% of the preschool-age population
and 15.3% of pregnant women in populations at risk of VAD, globally.
Xeropthalmia reportedly affects 5 million Asian
children and causes a total and partial blindness
among 1,60,000 to 1,85,000 Indian children .
Over one million children die by vitamin A
deficiency and about 3,50,000 others go
blind, every year worldwide.
The WHO Regions of Africa and South-East Asia were
found to be the most affected by vitamin A deficiency for
both population groups.
Despite a marked increase in submitted data, there are
still numerous countries lacking national prevalence data.
There is a need to inform and motivate governments and
agencies to collect, and report to WHO, national data on
the prevalence of deficiency and, whenever possible,
vitamin A programme coverage conditions prevailing at
the time that population assessment data were collected.
Vitamin A deficiency can have two different
•The first cause of vitamin A deficiency is
called a primary deficiency which is when
not enough vitamin A is consumed by the
•A secondary deficiency in vitamin A is when
the individual consumes enough vitamin
A, but the vitamin A is either not absorbed
correctly or utilized correctly.
PRIMARY CAUSE OF VITAMIN A DEFICIENCY
•The primary source of vitamin A deficiency is not enough
vitamin A or beta carotene in the diet. Vitamin A rich foods
can be both from animal and plant sources.
•Liver, eggs, cheese are all animal sources of vitamin A while
carrots, broccoli and leafy vegetables such as spinach
provide large amounts of beta carotene, which is converted
by the body into vitamin A.
• A lack of proper daily intake of vitamin A will result in
symptoms of vitamin A deficiency.
SECONDARY CAUSE OF VITAMIN A
A secondary cause of vitamin A deficiency and its symptoms is when
the ingested vitamin A is not absorbed by the small intestines or
when it is not released by the liver when needed. Because vitamin A
is fat soluble, it can be stored by the liver, but certain
diseases, especially damage to the liver from alcoholism can reduce
the ability of the liver to release vitamin A properly.
There are a large number of conditions that can cause vitamin A to
not be absorbed from food sources in the small intestines.
Infection with the nematode roundworm
parasite Ascaris lumbricoides lowers serum
Zinc is needed by the small intestines to absorb
vitamin A, therefore a deficiency in zinc will
often lead to a deficiency in vitamin A.
Because vitamin A is transported into the body
along with fats, any condition that impairs fat
absorption can lead to vitamin A deficiency.
The most common of these is liver disease that
results in poor bile quality.
Vitamin A functions at two levels in the body.
The first is in the visual cycle in the retina of
the second is in all body tissues systemically
to maintain growth and the soundness of
In the visual system, carrier-bound retinol is transported to
ocular tissue and to the retina by intracellular binding and
Rhodopsin, the visual pigment critical to dim-light vision, is
formed in rod cells after conversion of all-trans retinol to
retinaldehyde, isomerization to the 11-cis-form, and binding
Alteration of rhodopsin through a cascade of
photochemical reactions results in ability to see objects in
dim light .
The speed at which rhodopsin is regenerated relates to the
availability of retinol.
Night blindness is usually an indicator of inadequate
available retinol, but it can also be due to a deficit of other
nutrients, which are critical to the regeneration of
rhodopsin, such as protein and zinc.
The growth and differentiation of epithelial cells throughout the body are
especially affected by vitamin A deficiency (VAD). Goblet cell numbers
are reduced in epithelial tissues.
The consequence is that mucous secretions with their antimicrobial
Cells lining protective tissue surfaces fail to regenerate and
differentiate, hence flatten and accumulate keratin.
Both factors - the decline in mucous secretions and loss of cellular
integrity - diminish resistance to invasion by potentially pathogenic
organisms. The immune system is also compromised by direct
interference with production of some types of protective secretions and
Classical symptoms of xerosis (drying or non wetability) and
desquamation of dead surface cells as seen in ocular tissue
(i.e., xerophthalmia) are the external evidence of the changes also
occurring to various degrees in internal epithelial tissues.
Approximately 70.0% of the world's
malnourished children live in
Asia, resulting in the region having the
highest concentration of childhood
About half of the preschool children are
malnourished ranging from 16.0% in the
People's Republic of China to 64.0% in
Prevalence of stunting and underweight
are high especially in South Asia where
one in every two preschool children is
The World Bank estimates that India is ranked 2nd in
the world of the number of children suffering
from malnutrition, after Bangladesh (in 1998), where
47% of the children exhibit a degree of malnutrition.
The prevalence of underweight children in India is
among the highest in the world, and is nearly double
that of Sub-Saharan Africa with dire consequences
for morbidity, mortality, productivity and economic
The UN estimates that 2.1 million Indian children die
before reaching the age of 5 every year – four every
minute – mostly from preventable illnesses such as
diarrhoea, typhoid, malaria, measles and pneumonia.
The causes of PEM can either
be direct or indirect.
The direct factors, which are commonly referred to as
immediate factors include:
(i) Inadequate food intake
(i) Inadequate food intake
Inadequate food intake is the result of limited access
to food in terms of quality and quantity.
Diseases notably malaria and measles lead to loss of
appetite, increased rate of metabolism due to fevers
thereby increasing the body’s nutrient demands.
Diarrhoea reduces the absorption of food
nutrients, whereas vomiting decreases food intake.
Intestinal parasites compete for nutrients with the body
e.g. hookworm competes for iron.
Indirect causes of PEM include:
(i) Food insecurity and limited access to foodstuffs
• Families cannot acquire or produce enough food to cater
for energy needs.
• Lack of or limited access to land or agriculture
inputs, marketing and distribution of foods.
• Poor farming practices often due to lack of
knowledge, money, time or equipment.
• Poor weather conditions like failure of rains, floods etc.
• Lack of time to gather food, prepare it properly and
provide special dishes for young children. Among the time
consuming and energy expending activities of the rural
African housewife are the fetching of water from long
• Urbanization and rapid migration to the larger towns
resulting in unemployment and low incomes.
(ii) Poor water / sanitation and inadequate health services.
• Health services may be of low quality, expensive, non-existent or
• Lack of pre-natal and child health care.
• Inadequate management of sick children.
• Inadequate water and sanitation facilities.
(iii) Inadequate maternal and childcare practice.
• Families do not give adequate time and resources for women and
children’s health, dietary and emotional needs.
• Poor caring practices, including the inappropriate care of sick children.
• Not utilizing health care facilities for special needs of pregnant mothers
or adolescent girls.
• Not supporting mothers to breastfeed adequately.
• Inadequate diets for women including food taboos during and after
Various body systems adapt as much as
possible to the decreased nutrient
• Insulin levels low
– Leads to hormonal changes that ultimately
affect thyroxin and lowers thermogenesis
and oxygen consumption (lowers basal
• Non-vital hormonal secretion decrease
– i.e. sex hormones
•Red blood cell production decreases due to
decreased oxygen demands due to lowered amount
of lean body mass.
• Cardiac muscle atrophies in parallel with
loss of lean body mass
Cardiovascular reflexes are altered
– can lead to postural hypotension and decreased
– In severe PEM can get peripheral circulation
failure comparable to hypovolemic shock
RESPIRATORY ADJUSTMENTS IN
Lowered basal metabolic rates
•decreased ventilatory response to
hypoxia and increased carbon
• Deterioration of function and
emphysema like changes have been
CARDIAC AND RENAL FUNCTION
Decreased renal plasma flow and
glomerular filtration rate are due to
decreased cardiac output
Water clearance and ability to concentrate
and acidify urine are not impaired
PEM – IMMUNE SYSTEM CHANGES
Marked depletion of lymphocytes from
the thymus and atrophy of the thymus
• Cells from the t-lymphocyte regions of
the spleen and lymph nodes are
PEM - ELECTROLYTES
• Total body potassium is reduced in
– Due to decreased muscle proteins
and loss of intracellular potassium
• Decreased amounts of ATP, due to
decreased energy substrates ,alters
cellular exchange of sodium and
Na-K-ATP pump actively pumps
potassium into and sodium out of cells
– when this is not working, results in
potassium loss and increased
– Water goes with sodium, so there may
be intracellular overhydration.
PEM – GASTROINTESTINAL FUNCTION
• Severe protein deficiency results in
– impaired intestinal absorption of lipids and
– a decreased rate of glucose absorption
• The greater the protein deficit, the great
the functional impairment
•Also a decrease in gastric, pancreatic and
bile production with normal to low enzyme
and conjugated bile acid concentration
– Diarrhoea when fed due to these alterations
and perhaps also irregular GI motility and
GI bacterial overgrowth.
• Hypoproteinemia leads to intestinal edema
which decreases luminal absorption which
lead to diarrhoea
• Diarrhea aggrevates the malabsorption
and can further decrease nutritional status
• Diarrhea disappears with nutritional
PEM – CENTRAL AND PERIPHERAL
NERVOUS SYSTEM ADJUSTMENTS
• Early life PEM leads to decreased
brain growth (cell number and size)
Velocity of nervous conduction