Information, International Agency for Research on Cancer, Lyon, of aetiologies, environmental and genetic, acting jointly ( 1 ) .
The underlying cause of diabetes is the defective production
7. WHO ( 1 9 9 9 ) . Health Situation in the South-East Asia Region 1994-
or action of insulin, a hormone that controls glucose, fat and
1997, Regional office for SEAR, New Delhi.
amino acid metabolism. Characteristically, diabetes is a
8. WHO ( 1 9 8 3 ) . Techn. Rep. Ser., No. 695.
long-term disease with variable clinical manifestations and
9. Kabat, G . C . et al ( 1 9 8 6 ) . Int. J. Epi., 1 5 (4) 494-501.
progression. Chronic hyperglycaemia, from whatever cause,
10. Rothman, K.J. ( 1 9 8 0 ) . Preventive Medicine, 9 : 1 7 4 – 1 7 9 .
leads to a number of complications – cardiovascular, renal,
11. Doll, R a n d R. Peto ( 1 9 8 1 ) . J. Natl. Cancer Inst., 61 : 1 1 9 1 – 1 3 0 8 .
12. Broder, S . et al ( 1 9 8 4 ) . Ann. Int. Med., 1 0 0 : 543.
neurological, ocular and others such as intercurrent
13. Reddy, D.J. (1968). Cancer, Customs, Habits, Usages and infections.
Environment, Current Technical Literature, Mumbai.
14. W H O ( 1 9 8 5 ) . World Health Forum, 6 (2) 160-164. Classification
15. WHO ( 1 9 8 6 ) . Techn. Rep. Ser., No. 7 3 1 .
The classification adopted by WHO (2) is given in Table 1 .
16. WHO (1976). WHO handbook for standardized cancer registers
(hospital based). WHO Offset Pub! No. 25.
17. WHO ( 1 9 7 9 ) . Techn. Rep. Ser., No. 632.
Clinical classification of diabetes mellitus
18. WHO ( 1 9 8 6 ) . Cancer pain relief, WHO, Geneva.
19. Ken, Stanley ( 1 9 8 1 ) . World Health, Sept-Oct, pp 2 1 – 2 3 . 1. Dia b etes m ellitus ( O M)
20. Govt. of India, WHO (2006), Guidelines for Cervical Cancer i) Type 1 or Ins u lin-dependent diabetes mellitus
Screening Programme, Department of Cytology and Gynaecological
ii) Ty pe 2 or N o n – ins u lin dep e nden t diabetes m ellitus
Pathology, Postgraduate Institute of Medical Education and Research,
Chandigarh, India. iii) Malnutrition – related diabetes m ellitus (M R DM)
21. Editorial ( 1 9 8 5 ) . Lancet, 1 : 8 5 1 . iv) Other typ es (secondar y to p ancreat i c, hor m onal,
22. Tucker, A . K . ( 1 9 8 5 ) . Practitioner, 229-217. dru g- in du c e d, ge netic and o ther a b n o r m alities)
23. WHO ( 1 9 8 4 ) . Bull WHO, 62 (6) 8 1 7 – 8 3 0 . 2. Impaired glucose tolerance ( ]G T)
24. Mehta, F.S. et al ( 1 9 8 2 ) , Bull WHO, 60 (3) 4 4 1 – 446.
3. Ges t ati o nal diabetes m elli tu s ( GDM)
25. Gupta, P.C. etal ( 1 9 8 0 ) , Community Dentistry and Oral Epidemiology,
8 : 287 – 3 3 3 . Source (2)
26. Wahi, P.N. ( 1 9 6 8 ) , Bull WHO, 3 8 : 495.
27. WHO ( 1 9 8 5 ) . WklyEpi,Rec., 60 ( 1 7 ) . 125-129. Type 1 diabetes (Insulin-dependent diabetes mellitus) is
28. Reddy, C . R . R . M . et al ( 1 9 7 6 ) . lnd.J.Cancer, 1 3 : 1 6 1 . the most severe form of the disease. Its onset is typically
29. WHO ( 1 9 8 4 ) . Bull WHO, 62 (6) 861-869. abrupt and is usually seen in individuals less than 30 years of
30. Warnakulasuriya, K.A.A.S. et al ( 1 9 8 4 ) . Bull WHO, 62 (2) 243-250. age. It is lethal unless promptly diagnosed and treated. This
31. Miller, D . L . and R.T.D. Farmer, eds ( 1 9 8 2 ) . Epidemiology of Diseases, form of diabetes is immune-mediated in over 90 per cent of
cases and idiopathic in less than 10 per cent cases. The rate
32. Zaninetti, P. et al ( 1 9 8 6 ) . Int.J.Epi. 15 (4) 477.
of destruction of pancreatic � cell is quite variable. Rapid in
33. Brinton, L.A. et al ( 1 9 8 6 ) . lnt.J.Cancer, 3 8 : 339.
some individuals and slow in others. Type 1 diabetes is
34. The WHO Collaborative Study of Neoplasis and Steroid
usually associated with ketosis in its untreated state. It occurs
Contraceptives ( 1 9 85 ) . Brit.Med.J., 2 9 0 : 961-965.
mostly in children, the incidence is highest among 10-14
35. Parkin, D . M . et al ( 1 9 8 4 ) . Bull WHO, 62 ( 2 ) 163-182.
year old group, but occasionally occur in adults. It is
36. GLOBOCAN 2 0 1 2 , Fact Sheet ( 2 0 1 2 ) , Breast Cancer Incidence and
Mortality Worldwide 2012 Summary.
catabolic disorder in which circulating insulin is virtually
37. Clemmesen, J. (1979). In: Measurement of Levels of Health, WHO absent, plasma glucagon is elevated, and the pancreatic
Reg.Publ.EUROSer.No.7 , p. 199. � cells fail to respond to all insulinogenic stimuli. Exogenous
38. H u ghe s L E. and Courtney, S . P. (1985). B rit.Med. J . 290 : 1229 insulin is therefore required to reverse the catabolic state,
(editor i a l) . ·
prevent ketosis, reduce the hyperglucagonaemia, and reduce
39. Hislop , T.G. et al ( 1 9 8 6 ) . lnt.J.Epi., 15 (4) 469.
blood glucose (3).
40. MacMahon, B. et al ( 1 9 7 0 ) . Bull WHO, 4 3 : 209-217.
Type 2 diabetes is much more common than type 1
41. Miller, A . B . and Bulbrook, R . D . ( 1 9 8 0 ) . N.Eng.J.Med., 3 0 3 : 1246-
1248. diabetes. It is often discovered by chance. It is typically
42. M arks, M. ( 1 9 8 5 ) . Practitioner, 2 2 9 : 225. gradual in onset and occurs mainly in the middle-aged and
43. Pi k e, M . C . and R. K . Ross ( 1 9 84 ) . Br.Med.Bull., 40 (4) 351-354. elderly, frequently mild, slow to ketosis and is compatible
44. Pike, M . C . etal ( 1 9 8 3 ) . Lancet, 2 : 926-929. with long survival if given adequate treatment. Its clinical
45. Frisch, R.E. e t a l (1981). J A M A , 2 4 6 : 1559-1563. picture is usually complicated by the presence of other
46. Muir, C . S . ( 1 9 8 1 ) . World Health, Sept-Oct , pp 8 – 1 1 . disease processes.
47. WHO ( 1 9 8 5 ) . WHO Chronicle, 3 9 (3) 1 0 9 – 1 1 1 .
Impaired glucose tolerance (!GT) describes a state
48. GLOBOCAN 2 0 1 2 , Fact Sheet ( 2 0 1 2 ) , Lung Cancer I ncidence and
Mortality Worldwide 2012, Summary.
intermediate- “at-risk” group – between diabetes mellitus
49. WHO ( 1 9 8 2 ) . Bull WHO, 60 (6) 809-819. and normality. It can only be defined by the oral glucose
50. Notani, P. N . e t a l ( 1 9 7 7 ) . lnt.J.Cancer, 1 4 : 115. tolerance test (see Table 3 ) .
51. J ussawalla, D . J . and Jain, D . K . ( 1979). Br it. J .Cancer 4 0 : 437.
52. WHO ( 1 9 7 9 ) . Techn.Rep.Ser., No. 636. I n s u l i n resistance syndrome (Syndrome X)
53. Doll , R. and Peto, R. ( 1 9 7 6 ) . Brit.Med.J., 2 : 1525.
In obese patients with type 2 diabetes, the association of
54. GLOBOCAN 2 0 1 2 , Fact Sheet ( 2 0 1 2 ) , Stomach Cancer, Incidence
hyperglycaemia, hyperinsulinaemia, dyslipidaemia and
and Mortality Worldwide 2012, Summary.
hypertension, which leads to coronary artery disease and
stroke, may result from a genetic defect producing insulin
DIABETES MELLITUS resistance, with the latter being exaggerated by obesity. It
has been proposed that insulin resistance predisposes to
Once regarded as a single disease entity, diabetes is now hyperglycaemia, which results in hyperinsulinaemia (which
seen as a heterogeneous group of diseases, characterized by may or may not be of sufficient magnitude to correct the
a state of chronic hyperglycemia, resulting from a diversity hyperglycaemia) and this excessive insulin level then
contributes to high levels of triglycerides and increased Unfortunately, there is still inadequate awareness about
sodium retention by renal tubules, thus inducing the real dimension of the problem among the general public.
hypertension. High levels of insulin can stimulate There is also a lack of awareness about the existing
endothelial proliferation to initiate atherosclerosis (3). interventions for preventing diabetes and the management of
complications. Inadequacies in primary health care systems,
Problem statement which are not designed to cope with the additional challenges
posed by the chronic non-communicable diseases, result in
poor detection of cases, suboptimal treatment and
Diabetes is an “iceberg” disease. Although increase in insufficient follow-up leading to unnecessary disabilities and
both the prevalence and incidence of type 2 diabetes have severe complications, often resulting in early death.
occurred gloablly, they have been especially dramatic in
The age-adjusted mortality rates among the people with
societies in economic transition, in newly industrialized
diabetes are 1.5 to 2.5 times higher than in the general
countries and in developing countries. Currently the number
population (6). In Caucassian population, much of the
of cases of diabetes worlwide is estimated to be around
excess mortality is attributable to cardiovascular disease,
347 million, of these more than 90 per cent are type 2
especially coronary heart disease; amongst Asian and
diabetes. In 2008, an estimated 1 . 2 million people died from
American Indian population, renal disease is a major
consequences of high blood sugar (4). More than 80 per
contributor (6); whereas in some developing societies,
cent diabetes deaths occur in low and middle income
infections are an important cause of death. It is conceivable
that the decline in mortality due to coronary heart disease
The apparent prevalence of hyperglycaemia depends on which has occurred in many affluent countries may be halted
the diagnostic criteria used in epidemiological surveys. The or even reversed if rates of type 2 diabetes continue to rise.
global prevalence of diabetes in 2008 was estimated to be This may occur if the coronary risk factors associated with
1 0 % in adults aged 2 5 + years. The prevalence of diabetes diabetes increase to the extent that the risk they mediate
was highest in the Eastern Mediterranean Region and the outweighs the benefit accrued from improvements in
Region of the Americas ( 1 1 % for both sexes) and lowest in conventional cardiovascular risk factors, and the improved
the WHO European and Western Pacific Regions (9% for care of patients with established cardiovascular disease (6).
both sexes). The magnitude of diabetes and other In addition to non-insulin dependent diabetes, which is
abnormalities of glucose tolerance are considerably higher rather silent, chronic, often unidentified killer mostly among
than the above estimates if the categories of ‘impaired the adult population, the insulin dependent form of the
fasting’ and ‘impaired glucose tolerance’ are also included. disease (type 1 ) makes an even more dramatic appearance
The estimated prevalence of diabetes was relatively in affected children. They develop symptoms of ketoacidosis
consistent across the income groupings of countries. Low and often die, since the majority do not have access to
income countries showed the lowest prevalence (8% for adequate medical care, and since insulin is not available or
both sexes), and the upper-middle-income countries showed too expensive. It is estimated that the prevalence of type 1
the highest ( 1 0 % for both sexes) (5). diabetes in Asia is relatively low, accounting for about
Unfavourable modification of lifestyle and dietary habits 9. 7 per cent of all diabetes mellitus cases in the Region. The
that are associated with urbanization are believed to be the insulin dependent diabetes registry at Chennai (India)
most important factors for the development of diabetes. The reported an incidence of 1 0 . 5 per 1 0 0 , 0 0 0 children in the
prevalence of diabetes is approximately twice in urban areas age group of 1 0 – 1 2 years ( 7 ) .
than in rural population.
A bulk of evidence from studies on migrants indicates
The population in India has an increased susceptibility to
that the ethnic, presumably genetic, vulnerability of Asians
diabetes mellitus. This propensity was demonstrated by
manifests into diabetes when subjected to unfavourable life
multiple surveys of migrant Indians residing in Fiji,
styles. Population-based surveys completed recently in
Singapore, South Africa, U.K. and USA. The rates of
Bangladesh, India and Indonesia have shown considerable
diabetes in migrants from the Indian subcontinent have
increase in the prevalence rate of the disease in both urban
consistently shown to exceed those of the local population.
and rural dwellers when compared to results obtained
earlier. The results of prevalence studies of diabetes mellitus in
India were systematically reviewed with emphasis on those
Diabetic patients, if undiagnosed or inadequately treated,
utilizing the standard WHO criteria for diabetes diagnosis.
develop multiple chronic complications leading to
During the year 2004, there were an estimated 3 7 . 7 million
irreversible disability and death. Coronary heart disease and
cases of diabetes in the country, of these 2 1 . 4 million were
stroke are more common in diabetics than in the general
in urban areas and 1 6 . 3 million in rural areas. The estimated
population. Microvascular complications like diabetic renal
total mortality due to diabetes was 1 . 0 9 lac; 62.5 thousand
disease and diabetic retinopathy and neuropathy are serious
in urban areas and 4 6 . 6 thousand in rural areas. Same year
health problems resulting in deterioration of the quality of
2 . 2 million DALYs were lost due to the disease (8).
life and premature death. In fact, diabetes is listed among
the five most important determinants of the cardiovascular
disease epidemic in Asia. Lower limb amputation are at least
10 times more common in diabetic than in non-diabetic E p i d e m i o l o g i c a l determinants
individuals in developed countries, more than half of all
1 . AGENT
non-traumatic lower limb amputations are due to
diabetes (5). Metabolic disorders in pregnant diabetic The underlying cause of diabetes is insulin deficiency
women as well as those caused by gestational diabetes which is absolute in type 1 diabetes and partial in type 2
(diabetes diagnosed for the first time during pregnancy) diabetes. This may be due to a wide variety of mechanisms:
pose a high health risk, to both the mother and foetus. (a) pancreatic disorders – inflammatory , neoplastic an d
other disorders such as cystic fibrosis, (b} defects in the those born before. Maternal diabetes associated with
formation of insulin, e.g., synthesis of an abnormal, intrauterine growth retardation and low birth weight, when
biologically less active insulin molecule; (c} destruction of associated with rapid growth catch-up later on, appears to
beta cells, e.g., viral infections and chemical agents, increase the risk of subsequent diabetes in the child ( 6 ) .
(d} decreased insulin sensitivity, due to decreased numbers
of adipocyte and monocyte insulin receptors. (e} genetic 3 . ENVIRONMENTAL RISK FACTORS
defects, e.g., mutation of insulin gene; and (f} auto Susceptibility to diabetes appears to be unmasked by a
immunity. Evidence is accumulating that the insulin number of environmental factors acting on genetically
response to glucose is genetically controlled. The overall susceptible individuals. They include : (a) SEDENTARY
effect of these mechanisms is reduced utilization of glucose LIFESTYLE : Sedentary life style appears to be an
which leads to hyperglycaemia accompanied by glycosuria. important risk factor for the development of type 2 diabetes.
Lack of exercise may alter the interaction .between insulin
2 . HOST FACTORS
and its receptors and subsequently lead to type 2 diabetes
(a) AGE : Although diabetes may occur at any age, (2). (b) DIET : A high saturated fat intake has been
surveys indicate that prevalence rises steeply with age. Type associated with a higher risk of impaired glucose tolerance,
2 diabetes usually comes to light in the middle years of life and higher fasting glucose and insulin levels (6). Higher
and thereafter begins to rise in frequency. Malnutrition proportions of saturated fatty acids in serum lipid or muscle
related diabetes affects large number of young people. The phospholipid have been associated with higher fasting
prognosis is worse in younger diabetics who tend to develop insulin, lower insulin sensitivity and a higher risk of type 2
complications earlier than older diabetics. (b) S E X : In some diabetes. Higher unsaturated fatty acids from vegetable
countries (e.g., UK} the overall male-female ratio is about sources and polyunsaturated fatty acids have been
equal (9). In south-east Asia, an excess of male diabetics has associated with reduced risk of type 2 diabetes and lower
been observed ( 1 ) , but this is open to question. (c) GENETIC fasting and 2-hour glucose concentrations. Higher
FACTORS: The genetic nature of diabetes is undisputed. proportions of long-chain polyunsaturated fatty acids in
Twin studies showed that in identical twins who developed skeletal muscle phospholipids have been associated with
type 2 diabetes, concordance was approximately 90 per cent increased insulin sensitivity (6). In human intervention
(2); thus demonstrating a strong genetic component. In studies, replacement of saturated by unsaturated fatty acids
type 1 diabetes, the concordance was only about 50 per cent leads to improved glucose tolerence and enhanced insulin
indicating that type 1 diabetes is not totally a genetic entity. sensitivity. However, long chain polyunsaturated fatty acids
(d) GENETIC MARKERS :Type 1 diabetes is associated with do not appear to confer additional benefit over
HLA-88 and 8 1 5 , and more powerfully with HLA-DR3 and monounsaturated fatty acids. When total fat intake is high
DR4. The highest risk of type 1 diabetes is carried by (greater than 37 per cent of total energy}, altering the quality
individuals with both DR3 and DR4. On the other hand of dietary fat appears to have little effect ( 1 3 ) . (c) DIETARY
type 2 diabetes is not HLA-associated (2). (e) IMMUNE FIBRE : In many controlled experimental studies, high
MECHANISMS : There is some evidence of both cell intakes of dietary fibre have been shown to result in reduced
mediated and of humoral activity against islet cells. Some blood glucose and insulin levels in people with type 2
people appear to have defective immunological diabetes and impaired glucose tolerance ( 1 4 ) . Moreover an
mechanisms, and under the influence of some environmental increased intake of wholegrain cereals, vegetables and fruits
“trigger”, attack their own insulin producing cells. (all rich in NSP} was a feature of diets in randomized
(!) OBESITY: Obesity particularly central adiposity has long controlled trials. Thus the evidence for a potential protective
been accepted as a risk factor for type 2 diabetes and the risk effect of dietary fibre appears strong. A minimum daily
is related to both the duration and degree of obesity. The intake of 20 grams of dietary fibre is recommended (6).
association has been repeatedly demonstrated in Table 2 shows a summary of lifestyle and dietary factors
longitudinal studies in different populations, with a striking associated with diabetes.(d) MALNUTRITION: Malnutrition
gradient of risk apparent with increasing level of 8MI, adult (PEM} in early infancy and childhood may result in partial
weight g a i n , waist circumference or waist to hip ratio. Indeed failure of �-cell function. Damage to beta cells may well
waist circumference or waist to hip ratio (reflecting explain the associated impaired carbohydrate tolerance in
abdominal or visceral adiposity} are more powerful kwashiorkor (2). (e) A L C O H O L : Excessive intake of alcohol
determinants of subsequent risk of type 2 diabetes than 8MI can increase the risk of diabetes by damaging the pancreas
(6). Central obesity is also an important determinant of and liver and by promoting obesity (2). (!) VIRAL
insulin resistance, the underlying abnormality in most cases INFECTIONS: Among the viruses that have been implicated
of type 2 diabetes. In some instances obesity reduces the are rubella, mumps, and human coxsackie virus 84. Viral
number of insulin receptors on target cells. Voluntary weight infections may trigger in immunogenetically susceptible
loss improves insulin sensitivity and in several randomized people a sequence of events resulting in �-cell destruction.
controlled trials has shown to reduce the risk of progression (g) CHEMICAL AGENTS: A number of chemical agents are
from impaired glucose tolerence to type 2 diabetes ( 1 0 , 11). known to be toxic to beta cells, e . g . , alloxan, streptozotocin,
However, many obese subjects are not diabetic. Thus obesity the rodenticide VALCOR, etc ( 1 5 ) . A high intake of cyanide
by itself is inadequate to account for all, or even most, cases producing foods ( e . g . , cassava and certain beans} may also
of type 2 diabetes; physical inactivity and/or deficiencies of have toxic effects on �-cells. (h) STRESS : Surgery, trauma,
specific nutrients may also be involved (2). Obesity appears and stress of situations, internal or external, may “bring out”
to play no role in type 1 diabetes pathogenesis (12). the disease. (i) OTHER FACTORS : High and low rates of
(g) MATERNAL DIABETES : Offsprings of diabetic diabetes have been linked to a number of social factors such
pregnancies including gestational diabetes are often large as occupation, marital status, religion, economic status,
and heavy at birth, tend to develop obesity in childhood and education, urbanization and changes in life style which are
are at high risk of developing type 2 diabetes at an early age. elements of what is broadly known as social class. One of
Those born to mothers after they have developed diabetes the most important epidemiological features of diabetes is
have a three-fold higher risk of developing diabetes than that it is now common in the lower social classes whereas
TABLE 2 diagnosis of diabetes. Mass screening programmes have used
glucose measurements of fasting, postprandial or random
Summary of strength of evidence on lifestyle factors
blood sample. The measurement of glucose levels in random
and risk of developing type 2 diabetes
.. ;,·:-: ..
· � . . .·
blood samples is considered unsatisfactory for
· · Decreased . . I� cr�iaJ�d . epidemiological use; at the most, it can give only a crude
estimate of the frequency of diabetes in a population (2). The
fasting value alone is considered less reliable since true
Convincing Voluntary weight loss Overweight and
in overweight and obesity · fasting cannot be assured and spurious diagnosis of diabetes
obese people Abdominal may more readily occur. Therefore, for epidemiological
obesity purposes, the 2-hour value after 75 g oral glucose may be
Physical activity Physical inactivity used either alone or with the fasting value (2). Automated
biochemistry has now made it possible to screen thousands of
Probable NSP Saturated fats · samples for glucose estimation. The criteria for the diagnosis
of diabetes, proposed by WHO, are given in Table 3 .
Possible 11-3 fatty acids Total fat intake TABLE 3
Low glycaeml.c Trans-fatty acids
The WHO recommendations for the diagnostic criteria for
. index foods
diabetes and intermediate hyperglycaemia
Insufficient Vitamin E Excess alcohol· Diabetes
Fasting plasma glucose 2: 7 .0 mmol/1 ( 126 mg/di).
2-h plasma glucose* > 11 . 1 rnmol/l (200 mg/di)
NSP. = non-starch polysaccharides.
a Includes gestational diabetes. Impaired Glucose Tolerance (!GT)
b As a global public health recommendation, infants should be
Fasting plasma glucose < 7:0 mmol/1 (126 mg/di)
exclusively breast-fed for the first six months of life to achieve
optimal growth, development and health. and
2-h plasma glucose* 2: 7.8 and« 11 . 1 mmol/l
(140 mg/di to 200 mg/di)
50 years ago, the gradient was the reverse. One reason
Impaired Fasting Glucose (IFG)
could be rapid changes in lifestyle in lower classes.
Fasting plasma glucose 6 . 1 to 6.9 mmol/l
( 1 1 0 mg/di to 125 mg/di)
SCREENING FOR DIABETES
and (if measured)
In the past, the commonest approach to diabetes 2-h plasma glucose*# < 7.8 mmol/1 (140 mg/di)
screening was a preliminary, semi-quantitative test for
glucose in a urine sample, followed by an oral glucose * Venous plasma glucose 2-h after ingestion of 75g oral glucose
tolerance test for those found to have glycosuria. The
# If 2-h plasma glucose is not measured, status is uncertain as
underlying assumption is that early detection and effective
diabetes or !GT cannot be excluded.
control of hyperglycaemia in asymptomatic diabetics
reduces morbidity. S o u r c e : (16)
1 . Urine e x a m i n a t i o n
Urine test for glucose, 2 hours after a meal, is commonly
used in medical practice for detecting cases of diabetes. All Screening of the whole population for diabetes is not
those with glycosuria are considered diabetic unless considered a rewarding exercise (17, 18). However,
otherwise proved by a standard oral glucose tolerance test. screening of “high-risk” groups is considered more
Most studies now confirm that although glucose is found in appropriate. These groups are: ( i ) those in the age group 40
urine in the most severe cases of diabetes, it is often absent and over ( i i ) those with a family history of diabetes ( i i i ) the
in milder forms of the disease, and such cases are likely to be obese (iv) women who have had a baby weighing more than
missed by urine test. This is known as lack of “sensitivity”. 4.5 kg (or 3.5 kg in constitutionally small populations)
(v) women who show excess weight gain during pregnancy,
To be more precise, the sensitivity of the test (i.e.,
proportion of people with disease who have a positive test) and (vi) patients with premature atherosclerosis.
varies between 10-50 per cent. The lack of sensitivity means
PREVENTION AND CARE
that many diabetics would have been missed if this had been
the only test. That is, the test yields too many “false
1 . Primary prevention
negatives”. Further, glycosuria may be found in perfectly
normal people; this gives rise to “false-positives”. Since the Two strategies for primary prevention have been
specificity of the test is over 90 per cent, the yield of false suggested: (a) population strategy, and (b) high-risk
positives is not very high. For these reasons, urine testing is strategy (2).
not considered an appropriate tool for case-finding or
a. POPULATION STRATEGY
epidemiological surveys of the population (2).
The scope for primary prevention of type 1 diabetes is
2 . B l o o d sugar testing limited on the basis of current knowledge and is probably
Because of the inadequacies of urine examination, not appropriate (2). However, the development of
“standard oral glucose test” remains the cornerstone of prevention programmes for type 2 diabetes based on
elimination of environmental risk factors is possible. There is check-ups, recognition of symptoms associated with
pressing need for primordial prevention – that is, glycosuria and hypoglycaemia, etc.
prevention of the emergence of risk factors in countries in
Table 4 shows some of the individual interventions in
which they have not yet appeared. The preventive measures
diabetes with evidence of efficacy.
comprise maintenance of normal body weight through
adoption of healthy nutritional habits and physical exercise. TABLE 4
The nutritional habits include an adequate protein intake, a Individual interventions in diabetes with evidence of efficacy
high intake of dietary fibre and avoidance of sweet foods.
Elimination of other less well defined factors such as protein
deficiency and food toxins may be considered in some
populations. These measures should be fully integrated into Lifestyle interventions for Reduction of35-58% in
preventing type 2 diabetes in incidence
other community-based programmes for the prevention of
people of high risk … .• .
non-communicable diseases ( e . g . , coronary heart disease).
Metformin for preventing type 2 Reduction of 25-31 % in
b. HIGH-RISK STRATEGY . diabetes for people �t high risk incidence
There is no special high-risk strategy for type 1 diabetes. Glycaemlc control in people R�ductii’.Ji:i df:30% in
At present, there is no practical justification for genetic with HbAlc greater than 9% microvascular disease per 1.
counselling as a method of prevention (2). percentdrop in HbAlc
:. �’. .· . . ‘ “- . – – .
Since NIDDM appears to be linked with sedentary life Blood pressure control in Reduction of 3,5% in
style, over-nutrition and obesity, correction of these may people whose pressure is macrovascular arid .
higher than 130/80 mmHg microvascular disease per
reduce the risk of diabetes and its complications. Since
. lQ.mrnHg drop in
alcohol can indirectly increase the risk of diabetes, it should
be avoided. Subjects at risk should avoid diabetogenic drugs
like oral contraceptives. It is wise to reduce factors that Reduction of 60 to 70% In . I
I �nnual eye examinations .. .. ,
serious vision loss •..
promote atherosclerosis, e . g . , smoking, high blood pressure,
elevated cholesterol and high triglyceride levels. These Foot care in people with high · Reduction of SO to 60% in . ,
programmes may most effectively be directed at target risk of ulcers · . serious foot disease ·
Angiotensin converting Reduction of 42% in
enzyme inhibitor use in nephropathy; 22% drop
2 . Secondary prevention
an people with diabetes . in. cardiovascular disease
When diabetes is detected, it must be adequately treated.
The aims of treatment are : (a) to maintain blood glucose
levels as close within the normal limits as is practicable (see Home blood glucose monitoring : Assessment of control
Table 3 ) , and (b) to maintain ideal body weight. Treatment is has been greatly aided by the recent facility of immediate,
based on (a) diet alone – small balanced meals more reasonably accurate, capillary blood glucose measurements
frequently, (b) diet and oral antidiabetic drugs, or (c) diet either by one of the many meters now available or the direct
and insulin. Good control of blood glucose protects against reading Haemoglukotest strips (20).
the development of complications. Please see in chapter 1 0
The patient should carry an identification card showing
“Nutrition and health” under title “Nutritional factors in
his name, address, telephone number (if any) and the details
selected diseases” for details.
of treatment he is receiving. In short, he must have a
Proper management of the diabetic is most important to working knowledge of diabetes. All these mean education of
prevent complications. Routine checking of blood sugar, of patients and their families to optimize the effectiveness of
urine for proteins and ketones, of blood pressure, visual primary health care services.
acuity and weight should be done periodically. The feet
should be examined for any defective blood circulation 3 . Tertiary prevention
(Doppler ultrasound probes are advised), loss of sensation
Diabetes is major cause of disability through its
and the health of the skin. Primary health care is of great
complications, e.g., blindness, kidney failure, coronary
importance to diabetic patients since most care is obtained
thrombosis, gangrene of the lower extremities, etc. The main
at this level.
objective at the tertiary level is to organize specialized clinics
Glycosylated haemoglobin : There should be an estimation (Diabetic clinics) and units capable of providing diagnostic
of glycated (glycosylated) haemoglobin at half-yearly and management skills of a high order. There is a great need
intervals. This test provides a long-term index of glucose to establish such clinics in large towns and cities ( 2 1 ) . The
control. This test is based on the following rationale: glucose tertiary level should also be involved in basic, clinical and
in the blood is complexed to a certain fraction of haemoglobin epidemiological research. It has also been recommended
to an extent proportional to the blood glucose concentration. that local and national registries for diabetics should be
The percentage of such glycosylated haemoglobin reflects the established (2).
mean blood glucose levels during the red cell life-time
( i . e . , about the previous 2-3 months) ( 1 9 ) . References
1. WHO ( 1 9 8 0 ) . Techn. Rep. Ser., No. 646.
Self-care : A crucial element in secondary prevention is
2. WHO ( 1 9 8 5 ) . Techn. Rep. Ser., No. 7 2 7 .
self care. That is, the diabetic should take a major
3. Lawrence M. Tierney, Jr. Stephen J. McPhee Maxine A. Papadakis
responsibility for his own care with medical guidance – e.g.,
( 2 0 0 2 ) , Current Medical Diagnosis and Treatment, 41st e d . , Lange
adherence to diet and drug regimens, examination of his
own urine and where possible blood glucose monitoring; self
4. WHO ( 2 0 1 2 ) , Diabetes Fact Sheet No. 3 1 2 , Sept. 2 0 1 2 .
administration of insulin, abstinence from alcohol,
5. WHO ( 2 0 1 1 ) , Global Status Report on Non-communicable Diseases,
maintenance of optimum weight, attending periodic 2010.