OBESITY

6. WHO (2003), Tech. Rep. Ser., N 916. TABLE 1

7. WHO (2002), Health Situation In the South-East Asia Region 1998-
2000, New Delhi. Adult weights and heights corresponding to recommended
8. Govt. of India (2011), National Health Profile 2011, Ministryof Health cut-off values for body mass index
and Family Welfare, New Delhi.
9. Drury, M.l. (1979). Diabetes Mellitus, Blackwell, Oxford.
10. Tuomilento J. et al. Prevention of type 2 diabetes Mellitus by changes
in lifestyle among subjects with impaired glucose tolerance, New
England Journal of Medicine 2002, 344: 1343-1350.
11. Know!er WC et al. Reduction in the incidence of type 2 diabetes with
lifestyleintervention of metformin,New England Journal of Medicine,
2002, 346: 393-403.
12. Keen, H. (1985). In: Oxford Textbook of Public Health, Vol.4, p.268. ..
142 32.3 34.3 37.3 40.3 44.4 50.4 60.5 80.7
13. Vessby B. eta!. Substituting dietary saturated for monounsaturated fat '
144 33.2 35.3 . 38A 41.5 45.6 51.8 62.2 82.9
impairs insuline sensitivity in healthy men and women : the KANWU
study. Diabetologia 2001, 44: 312-319. 146 34.i 36.2 39.4 42.6 46.9 53.3 63.9 85.3
14. Marshal JA et al., Dietary fat predicts conversion from impaired 148 35.0 37.2 40.5 43.8 48.2 54.8 65.7 87.6
glucose tolerance to NIDDM,The San Luis. Valley Diabetes Study, 150 . 36.0 38.2 41.6 45.0 49.5 56.3 67.5 90.0
Diabetes Care, 1994, 17 : 50-56. 152 37.0 39.3 42.7 46.2 50.8 57.8 69.3 92.4
15. Arky, R.A. (1983). Nutrition Reviews, 41(6)165.
154 37.9 40.3 43.9 47.4 52.2 59.3 71.1 94.9
16. WHO (2012), Prevention and Control of Non-communicable
Diseases: Guidelines for Primary health care in low-resource settings. 156 38.9 41.4 45.0 48.7 53.5 60.8 73.0 97.3
17. Melins,J.M. (1974). Lancet, 2: 1367. 158 39.9 42.4 46.2 49.9 54.9 62.4 74.9 99.9
18. Redhead, I.H. (1975). In: Screening in General Practice, C.R. Hart 160 41.0 43.5 47.4 51.2 56,3 64.0 . 76.8 102.4
(ed), ChurchillLivingstone. · 162 42.0 44.6 48.3 52.5 57.7 65.6 78.7 105.0
19. Anonymous (1978). Glycosylated Haemoglobin and diabetic control, 164 43,0 45,7 49.8 53.8 59.2 67.2 80.7 107.6
Brit, Med. J., 1: 1373-4.
166 44.1 46.8 51.0 55.1 .60.6 68.9 82.7 110.2
20. Sonksen, P.H. et al (1978). Home monitoring of blood glucose. Lancet,
1: 729-32. 168 45.2 48.0 52.2 56.4 62.1 70.6 84.7 112.9
21. DiabeticClinicstoday and tomorrow : Brit. Med. J. ( 1973) 2 : 534 and 170 46.2 49.1 53:5 57.8 63.6 72.3 86,7 115.6
Brit. Med. J. (1971) 4: 161. 172 47.3 50.3 . 54.7 59.2 65.1 74.0 88.8 118.3
174 48.4 51.5 56.0 60.6 66.6 75.7 90.8 121.1
··.·
1··. ·.·
.
: . .: ... OIJESITY c 176 49.6 52.7 57.3 62.0 68.1 77.4 92.9 123.9
178 50.7 53.9 58.6 63.4 69.7 79.2 95.0 126.7
Obesity may be defined as an abnormal growth of the 180 51.9 .55.1 59.9 64.8 71.3. 81.0 97.2 129.6
adipose tissue due to an enlargement of fat cell size 182 53.0 56.3 61.3 66.2 72.9 82.8 99.4 132.5
(hypertrophic obesity) or an increase in fat cell number 184 54.2 57.6 62.6 67.7 74.5 84.6 101.6 135.4
(hyperplastic obesity) or a combination of both (1). Obesity 186 55.5 58.8 64.0 . 69.2 76.1 . 86.5 103.8 138.4
is often expressed in terms of body mass index (BMI) 188 56.6 60.1 65.4 70.7 77.8 88.4 106,0 141.4
(see Table 1). Overweight is usually due to obesity but can 190 57.8 61.4 66.8. 72.2 79.4 90.3 108;3 144.4
arise from other causes such as abnormal muscle For easy reference and calculation of BM! values corresponding to
development or fluid retention (2). recommended cut-offs, first find the height of the individual in the
However, obese individuals differ not only in the amount left hand column. The weights given in the row for that height
correspond to various recommended cut-off values for adult BM!.
of excess fat that they store, but also in the regional Weight for two normal BM! values are also included.
distribution of the fat within the body. The distribution of fat
induced by the weight gain affects the risk associated with Source: (6)
obesity, and the kind of disease that results. It is useful
therefore, to be able to distinguish between those at Overweight and obesity are the fifth leading risk of global
increased risk as a result of "abdominal fat distribution" or deaths. Worldwide, obesity has more than doubled since
"android obesity" from those with the less serious "gynoid" 1980. In 2008, more than 1.4 billion adults, 20 years and
fat distribution, in which fat is more evenly and peripherally older, were overweight. Of these over 200 million men and
distributed around the body. nearly 300 million women were obese (3).
In 2012, more than 40 million children under 5 years of
Prevalence age were overweight. Once considered a high-income
Obesity is perhaps the most prevalent form of country problem, overweight and obesity are now rising in
malnutrition. As a chronic disease, prevalent in both low-and middle-income countries, particularly in urban
developed and developing countries, and affecting children settings. Close to 30 million overweight children are living in
as well as adults, it is now so common that it is replacing the developing and 10 million in developed countries (3).
more traditional public health concerns including Childhood obesity is associated with a higher chance of
i.mdernutrition. It is one of the most significant contributors obesity, premature death and disability in adulthood. In
to ill health. For industrialized countries, it has been addition, it is associated with future risk of increased
suggested that such increase in body weight have been breathing difficulties, increased risk of fractures,
caused primarily by reduced levels of physical activity, hypertension, early markers of cardiovascular disease,
rather than by changes in food intake or by other factors. It insulin resistance and psychological effects.
is extremely difficult to assess the size of the problem and At least 3.4 million adults die each year as a result of
compare the prevalence rates in different countries as no being overweight or obese. In addition, 44 per cent of the
exact figures are available and also because the definitions diabetes burden, 23 per cent of ischaemic heart disease
of obesity are not standardized. burden and between 7 to 41 per cent of certain cancer
 NON-COMMUNICABLE DISEASES
burdens are attributable to overweight and obesity (3).
Overweight and obesity are linked to more deaths
worldwide than underweight.
In India, the non-communicable risk factor survey phase 2
was carried out in the year 2007-2008, in the states of
Andhra Pradesh, Kerala, Madhya Pradesh, Maharashtra,
Tamil Nadu, Uttarakhand and Mizoram. The survey shows
high prevalence of overweight in all age groups except in
15-24 years group. Overweight prevalence was higher
among females than males and in urban areas than in rural
areas. Low prevalence was recorded among lower level of
education (ill-literate and primary level), and in people
whose occupation was connected with agriculture or manual
work (4).
In India, 1.3 per cent males and 2.5 per cent females
aged more than 20 years were obese in the year 2008 (5).
As obesity is a key risk factor in natural history of other
chronic and non-communicable diseases, the typical time
sequence of emergence of chronic diseases following the
increased prevalence of obesity is important in public health
planning. The first adverse effects of obesity to emerge in
population in transition are hypertension, hyperlipidaemia
and glucose intolerence, while coronary heart disease and
the long-term complications of diabetes, such as renal failure
begin to emerge several years (or decades) later (7). It is
matter of time before same mortality rates for such diseases
will be seen in developing countries as those prevailing
30 years ago in industrialized countries (8).
Epidemiological determinants
The aetiology of obesity is complex, and is one of
multiple causation:
(a) AGE : Obesity can occur at any age, and generally
increases with age. Infants with excessive weight gain have
an increased incidence of obesity in later life (9). About
one-third of obese adults have been so since childhood (1).
It has been well established that most adipose cells are
formed early in life and the obese infant lays down more of
these cells (hyperplastic obesity) than the normal infant.
Hyperplastic obesity in adults is extremely difficult to treat
with conventional methods.
(b) SEX : Women generally have higher rate of obesity
than men, although men may have higher rates of
overweight. In the Framingham, USA study, men were found
to gain most weight between the ages of 29 and 35 years,
while women gain most between 45 and 49 years of age
(10), i.e. at menopausal age. It has been claimed that
woman's BM! increases with successive pregnancies. The
recent evidence suggested that this increase is likely to be,
on an average, about 1 kg per pregnancy. On the other hand
in many developing countries, consecutive pregnancies at
short intervals are often associated with weight loss rather
than weight gain (8).
(c) GENETIC FACTORS : There is a genetic component
in the aetiology of obesity. Twin studies have shown a close
correlation between the weights of identical twins even
when they are reared in dissimilar environments (11). The
profile of fat distribution is also characterized by a significant
heritability level of the order of about 50 per cent of the total
human variation. Recent studies have shown that the
amount of abdominal fat was influenced by a genetic
component accounting for 50-60 per cent of the individual
differences (8).
(d) PHYSICAL INACTIVITY There is convincing
evidence that regular physical activity is protective against
unhealthy weight gain. Where as sedentary lifestyle
particularly sedentary occupation and inactive recreation
such as watching television promote it, physical activity and
physical fitness are important modifiers of mortality and
morbildity related to overweight and obesity (12). In some
individuals a major reduction in activity without the
compensatory decrease in habitual energy intake may be
the major cause of increased obesity, e.g. in athletes when
they retire and in young people who sustain injuries etc.
Physical inactivity may cause obesity, which in turn restricts
activity. This is a vicious circle. It is the reduced energy
output that is probably more important in the aetiology of
obesity than used to be thought (11).
(e) SOCIO-ECONOMIC STATUS : The relationship of
obesity to social class has been studied in some detail. There
is a clear inverse relationship between socio-economic status
and obesity. Within some affluent countries, however,
obesity has been found to be more prevalent in the lower
socio-economic groups.
(f} EATING HABITS : Eating habits (e.g., eating in
between meals, preference to sweets, refined foods and fats)
are established very early in life. The composition of the
diet, the periodicity with which it is eaten and the amount of
energy derived from it are all relevant to the aetiology of
obesity. A diet containing more energy than needed may
lead to prolonged post-prandial hyperlipidaemia and to
deposition of triglycerides in the adipose tissue resulting in
obesity (13). Nowadays television and print media is playing
an important role in producing obesity by heavy
advertisement of fast food outlets of energy-dense,
micronutrient poor food and beverages (usually classified
under the "eat least" category in diet guidelines) of
multinational corporations, which influence the daily eating
habits. The consumer demand by itself may be influenced by
advertising, marketing, culture, fashion and convenience
(8). It has been calculated that a child whose energy
requirement is 2000 kcal/day and who consumes
100 kcal/day extra will gain about 5 kg a year (10). The
accumulation of one kilo of fat corresponds to 7, 700 kcal of
energy (14).
(g) PSYCHOSOCIAL FACTORS : Psychosocial factors
(e.g., emotional disturbances) are deeply involved in the
aetiology of obesity. Overeating may be a symptom of
depression, anxiety, frustration and loneliness in childhood
as it is in adult life. Excessively obese individuals are usually
withdrawn, self-conscious, lonely and secret eaters. An
insight into the circumstances in which the obesity has
developed is essential for planning the most suitable
management.
(h) FAMILIAL TENDENCY: Obesity frequently runs in
families (obese parents frequently having obese children), but
this is not necessarily explained solely by the influence of
genes.
(i) ENDOCRINE FACTORS : These may be involved in
occasional cases, e.g., Cushing's syndrome, growth
hormone deficiency. ·
(j) ALCOHOL : A recent review of studies concluded that
the relationship between alcohol consumption and adiposity
was generally positive for men and negative for women (6).
(k} EDUCATION : In most affluent societies, there is an
inverse relationship between educational level and
prevalence of overweight (6).
(/} SMOKING : Reports that the use of tobacco lowers

body weight began to appear more than 100 years ago, but
detailed studies have been reported only during the past
10 years or so. In most populations, smokers weigh
somewhat less than ex-smokers; individuals who have never
smoked fall somewhat between the two.
(m) ETHNICITY : Ethnic groups in many industrialized
countries appear to be especially susceptible to the
development of obesity and its complications. Evidence
suggests that this may be due to a genetic predisposition to
obesity that only become apparent when such groups are
exposed to a more affluent lifestyle (8).
(n) DRUGS : Use of certain drugs, e.g., cortico-steroids,
contraceptives, insulin, ~-adrenergic blockers, etc. can
promote weight gain (8).
Use of BMIto classify obesity
Body mass index (BMI) is a simple index of weight-for-
height that is commonly used to classify underweight,
overweight and obesity in adults. It is defined as the weight in
kilograms divided by the square of the height in metres (kg/m2).
For example, an adult who weighs 70 kg and whose
height is 1.75 m will have a BMI of 22.9:
BMI = 70 (kg)/1. 752 (m2) = 22.9
The classification of overweight and obesity, according
to BMI, is shown in Table 2. Obesity is classified as a
BMI : .: : 30.0. The classification shown is in agreement with
that recommended by WHO (12), but includes an additional
subdivision at BMI 35.0-39.9 in recognition of the fact that
management options for dealing with obesity differ above a
BMI of 35. The WHO classification is based primarily on the
association between BMI and mortality.
TABLE 2
Classification of adults according to BMI
' -, .... .~
·. . . . ' ' -_ _- - - ·. '
·. BM! · B.isJ<9fcomorbidities·· ··
.Classlflcation
Underweight < 18.50
Normal range ·
18.50-24.99
Overweight : ~ 25.00
Pre-obese 25.00-29.99
Obese classI 30.00-34.99
Obese class II 35.00"39.99
Obese class III ~40.00
Source : (12)
These BMI values are age-independent and the same for
both sexes. The table shows a simplistic relationship
between BMI and the risk of comorbidity, which can be
affected by a range of factors, including the nature of the
diet, ethnic group and activity level. The risks associated
with increasing BMI are continuous and graded and begin at
a BMI above 25.
Although it can generally be assumed that individuals
with a BMI of 30 or above have an excess fat mass in their
body, BMI does not distinguish between weight associated
with muscle and weight associated with fat. As a result, the
relationship between BMI and body fat content varies
according to body build and proportion, and it has been
shown repeatedly that a given BMI may. not correspond to
the same degree of fatness across populations. Polynesians,
for example, tend to have a lower fat percentage than
OBESITY
Caucasian Australians at an identical BMI. In addition, the
percentage of body fat mass increases with age up to 60-65
years in both sexes, and is higher in women than in men of
equivalent BMI. In cross-sectional comparisons, therefore,
BM! values should be interpreted with caution if estimates of
body fat are required.
INTRA-ABDOMINAL (CENTRAL) FAT
ACCUMULATION AND INCREASED RISK
Compared with subcutaneous adipose tissue, intra-
abdominal adipose tissue has more cells per unit mass,
higher blood flow, more glucocorticoid (cortisol) receptors,
probably more androgen (testosterone) receptors, and
greater catecholamine-induced lipolysis. These differences
make intra-abdominal adipose tissue more susceptible to
both normal stimulation and changes in lipid accumulation
and metabolism. Furthermore, intra-abdominal adipocytes
are located upstream from liver in the portal circulation. This
means that there is a marked increase in the flux of
nonesterified fatty acid to the liver via the portal blood in
patients with abdominal obesity.
There is good evidence that abdominal obesity is
important in the development of insulin resistance, and in
the metabolic syndrome (hyperinsulinaemia, dyslipidaemia,
glucose intolerance, and hypertension) that link obesity with
CHO (8). Premenopausal women have quantitatively more
lipoprotein lipase (LPL) and higher LPL activity in the
gluteal and femoral subcutaneous regions, which contain fat
cells larger than those in men, but these differences
disappear after menopause (8).
Assessment of obesity
Before we consider assessment of obesity, it will be useful
to first look at body composition as under;
a. the active mass (muscle, liver, heart etc.)
b. the fatty mass (fat)
c. the extracellular fluid (blood, lymph, etc.)
Low (but risk of other d. the connective tissue (skin, bones, connective tissue)
clinical problems increased)
Structurally speaking, the state of obesity is characterized
Average
by an increase in the fatty mass at the expense of the other
parts of the body. The water content of the body is never
Increased increased in case of obesity.
Moderate Although obesity can easily be identified at first sight, a
Severe precise assessment requires measurements and reference
Very severe standards. The most widely used criteria are :
1. BODY WEIGHT
Body weight, though not an accurate measure of excess
fat, is a widely used index. In epidemiological studies it is
conventional to accept + 2 SD (standard deviations) from
the median weight for height as a cut-off point for obesity.
For adults, some people calculate various other indicators
such as (10) :
(1) Body mass index (Quetelet's index)
Weight (kg)
=
Height2(m)
(2) Pondera/ index
Height (cm)
=
Cube root of body weight (kg)
 NON-COMMUNICABLE DISEASES
(3) Brocca index
= Height (cm) minus 100
For example, if a person's height is 160 cm,
his ideal weight is ( 160-100) = 60 kg
(4) Lorentz's formula
Ht (cm) -150
= Ht (cm) - 100
2 (women) or 4 (men)
(5) Corpulence index
Actual weight
= 3 shows the relative risk of health problems associated with
Desirable weight
This should not exceed 1.2
The body mass index (BM!) and the Brocca index are
widely used. A FAO//WHO/UNU Report gives the much
needed reference tables for body mass index (see Table 1)
which can be used internationally as reference standards for
assessing the prevalence of obesity in a community.
2. SKINFOLD THICKNESS
A large proportion of total body fat is located just under
the skin. Since it is most accessible, the method most used is
the measurement of skinfold thickness. It is a rapid and
"non-invasive" method for assessing body fat. Several
varieties of callipers (e.g., Harpenden skin callipers) are
available for the purpose. The measurement may be taken
at all the four sites - mid-triceps, biceps, subscapular and
suprailiac regions. The sum of the measurements should be
less than 40 mm in boys and 50 mm in girls (15).
Unfortunately standards for subcutaneous fat do not exist
for comparison. Further, in extreme obesity, measurements
may be impossible. The main drawback of skinfold
measurements is their poor repeatability.
3. WAIST CIRCUMFERENCE AND WAIST:
HIP RATIO (WHR)
Waist circumference is measured at the mid point
between the lower border of the rib cage and the iliac crest.
It is a convenient and simple measurement that is unrelated
to height, correlates closely with BM! and WHR and is an
approximate index of intra-abdominal fat mass and total
body fat. Changes in waist circumference reflect changes in
risk factors for cardiovascular disease and other forms of
chronic diseases. There is an increased risk of metabolic
complications for men with a waist circumference ~ 102 cm,
and women with a waist circumference > 88 cm (12).
Over the past 10 years or so, it has become accepted that
a high WHR ( > 1.0 in men and > 0.85 in women) indicates
abdominal fat accumulation.
4. OTHERS
In addition to the above, three well-established and more
accurate measurements are used for the estimation of body
fat. They are measurement of total body water, of total body
potassium and of body density. The techniques involved are
relatively complex and cannot be used for routine clinical
purposes or for epidemiological studies (8). The introduction
of measuring fat cells has opened up a new field in obesity
research.
Hazards of obesity
Obesity is a health hazard and a detriment to well-being
which is reflected in the increased morbidity and mortality:
(a) INCREASED MORBIDITY : Obesity is a positive risk
factor in the development of hypertension, diabetes, gall
bladder disease and coronary heart disease and certain
types of cancers, especially the hormonally related and large
bowel cancers. There are in addition, several associated
diseases, which, although not usually fatal, cause a great
deal of morbidity in the community, e.g., varicose veins,
abdominal hernia, osteoarthritis of the knees, hips and
lumbar spine, flat feet and psychological stresses particularly
during adolescence. Obese persons are exposed to increased
risk from surgery. Obesity may lead to lowered fertility. Table
obesity. (b) INCREASED MORTALITY : The Framingham
Heart Study in United States showed a dramatic increase in
sudden death among men more than 20 per cent overweight
as compared with those with normal weight. The increased
mortality is brought about mainly by the increased incidence
of hypertension and coronary heart disease. There is also an
excess number of deaths from renal diseases. Obesity lowers
life expectancy. More information is needed about the
relationship between different degrees of obesity and
morbidity and mortality. Please see in chapter 10 under
heading "Nutritional factors in selected diseases" for dietary
factors of obesity.
TABLE 3
Relative risk of health problems associated with obesity•
~~~:~¥;d 'ti\: ; .:>~~~~;Jd!~:;;, ~'J'iJ1:'i~¥;t~~Jfe~if~~~;t~~{I;i!.t,11i~;,iif.,
Type 2 diabetes CHO Cancer (breast cancer in
postmenopausal women,
endometrial cancer,
. colon cancer)
Gallbladder Hypertensfon Reproductive hormone
disease abnormalities
Dyslipidaemia Osteoarthritis Polycystic ovary syndrome
(knees) r,
Insulin resistance Hyperuricaemia . Impaired fertility
and gout
Breathlessness Low back pain due to .
obesity
Sleepapnea Increased risk of anaesthesia
· .compllcations
· Fetal defects associated with
maternal obesity
aAll relative risk values are approximate.
Source: (8)
Prevention and control
Weight control is widely defined as approaches to
maintaining weight within the 'healthy' (i.e. 'normal' or
'acceptable') range of body mass index of 18.5 to 24. 9 kg/m2
throughout adulthood (WHO Expert Committee, 1995). It
should also include prevention of weight gain of more than 5
kg in all people. In those who are already over-weight, a
reduction of 5-10 per cent of body weight is recommended
as an initial goal (7).
Prevention of obesity should begin in early childhood.
Obesity is harder to treat in adults than it is in children. The
control of obesity centres around weight reduction. This can
be achieved by dietary changes, increased physical activity
and a combination of both. (a) DIETARY CHANGES: The
following dietary principles apply both to prevention and
treatment : the proportion of energy-dense foods such as
simple carbohydrates and fats should be reduced; the fibre
 VISUAL IMPAIRMENT AND BLINDNESS

content in the diet should be increased through the proposed a uniform criterion and defined blindness as
consumption of common un-refined foods; adequate levels "visual acuity of less than 3/60 (Snellen) or its equivalent"
of essential nutrients in the low energy diets (most (2). The current WHO International Classification of
conventional diets for weight reduction are based on 1000 Diseases (ICD-10) describes the levels of visual impairment
kcal daily model for an adult) should be ensured, and as shown in Table 1.
reducing diets should be as close as possible to existing The term "low vision" included in the previous revision
nutritional patterns (16). The most basic consideration is has been replaced by the categories 1 and 2 to avoid
that the food energy intake should not be greater than what confusion with those requiring low vision care.
is necessary for energy expenditure. It requires modification
of the patient's behaviour and strong motivation to lose TABLE 1
weight and maintain ideal weight. Unfortunately, most
attempts to reduce weight in obese persons by dietary Revision of categories of visual impairment
advice remain unsuccessful. (b) INCREASED PHYSICAL
ACTIVITY: This is an important part of weight reducing
··- £¢~~nfi~~f~I~!~#~~·tir~8~t~?-fit~·-~·;"Y~:' r .: d·.-;.·:;cx ..
programme. Regular physical exercise is the key to an ····frW:~i~~i~b·~~:i(;f}¢,:ii~~i:i#qF~-~~~hf!i~tj~J
increased energy expenditure. (c) OTHERS: Appetite 6/18
suppressing drugs have been tried in the control of obesity.
They are generally inadequate to produce massive weight
loss in severely obese patients. Surgical treatment (e.g., 6/18 6/60
gastric bypass, gastroplasty, jaw-wiring, to eliminate the
eating of solid food have all been tried with limited success
(17). In short, one should not expect quick or even tangible
results in all cases from obesity prevention programmes.
Health education has an important role to play in teaching
the people how to reduce overweight and prevent obesity.
A fruitful approach will be to identify those children who are Light perception
at risk of becoming obese and find way of preventing it.

References
1. Hager, A. (1981). Br. Med. Bull., 37 (3) 287. . Undetermined or unspecified.
2. Aykroyd, W.R. and J.Mayer (1968). Food and Nutrition Terminology. * Or counts fingers at 1 metre.
In: WHO Doc NUT/68.6, Geneva.
3. WHO (2014), Obesity and overweight, Fact sheet No. 311, May 2014. Source: (2)
4. Govt. of India (2011), National Health Profile2011, Ministryof Health
and Family Welfare, New Delhi. The problem
5. WHO (2014), World Health Statistics 2014.
6. WHO (1995). Tech. Rep. Ser. No. 854. WORLD
7. WHO (2002), International Agency for Research on Cancer, IARC
Handbooks of Cancer Prevention - Weight Control and Physical In 2010, an estimated 285 million people worldwide were
Acitivity, IARCPress, Lyon 2002. visually disabled, of whom nearly 39 million were blind and
8. WHO (2000). Tech. Rep. Ser. No. 894. 246 million were with low vision, about 90 per cent of them
9. Charney, E. et al (1976). N. Eng. J. Med., 295: 6. living in developing countries. About 80 per cent of
10. International Children's Centre, Paris (1984). Children in the Tropics, blindness is avoidable (treatable or potentially preventable).
No.151. However, a large proportion of those affected remain blind
11. Falkner, F.ed (1980). Prevention in Childhood of Health Problems in for want of access to affordable eye care. Blindness leads not
Adult Life, WHO, Geneva.
12. WHO (2003), Tech. Rep. Ser. No. 916. only to reduced economic and social status but may also
13. Oliver, M.F. (1981). Br. Med. Bull., 37 (1) 49. result in premature death. The major causes of blindness
14. Beaton, G.H. (1976). In: Nutrition in Preventive Medicine Annex 2, P. and their estimated prevalence are cataract (33 per cent);
482. Beaton, G.H. and J.M. Bengoa (eds). WHO, Geneva, Monograph glaucoma (2 per cent); and uncorrected refractive errors
Ser.No. 62. · (myopia, hyperopia or astigmatism (43 per cent) (3). The
15. James, W.P.T. (1982). Medicine International, 1 (15) 664. number of people visually impaired from infectious disesases
16. Tasher, T. (1986). Food and Nutrition Bull., 8 (3) 12. The United has greatly reduced in the last 20 years.
Nations University.
17. Garrow, J.S. (1981). In : Recent Advances in Medicine, Vol 18, About 82 per cent of all people who are visually impaired
Churchill Livingstone. are aged 50 years and older, while this age group comprises
about 20 per cent of the world's population. With an
1· ·. · ylSUALtMPAIRMENTAND BLINDNESS .. , increasing elderly population in many countries, more
people will be at risk of age-related visual impairment. An
estimated 19 million children are visually impaired. Of these,
A compilation published by WHO in 1966 (1) lists 12 million children are visually impaired due to refractory
65 definitions of blindness. As might be expected the errors, a condition that could be easily diagnosed and
definitions differed widely. Terms such as total blindness, corrected. 1.4 million are irreversibly blind for the rest of
economic blindness, and social blindness were in vogue.
their lives (3).
The 25th World Health Assembly in 1972 noted the
complexity of the problem and considered the need for a Overall, visual imairment worldwide has decreased since
generally. accepted definition of blindness and visual the early 1990s. This decrease is principally the result of a
impairment for national and international comparability. reduction of visual impairment from infectious diseases
Taking into consideration existing definitions, the WHO through public health action.