Home/Essays Examples/Health/Epidemiology of Diabetes Mellitus Type-2

Epidemiology of Diabetes Mellitus Type-2


The classification of diabetes has changed to increase the accuracy of nomenclature; formerly categorized as insulin-dependent and non-insulin-dependent based on the need of insulin for long term management, the categories have changed to types 1 and two. This is based on the etiological process leading to the condition; as such, the former involves the destruction of cells in the islets of Langhanns; and the latter on dysfunctions of insulin production and/or functions (Shaw et al, 2000). As such, type2 diabetes was also formerly referred to as adult-onset diabetes since traditionally, it tended to affect adults.

The condition is characterized by hyperglycemia and relative (rather that absolute) deficiency of insulin (Robbins & Cotran, pp.1194-1195). Typical to both types of diabetes, the effects of the condition tend to spread from system to system, especially affecting the cardiovascular system; cause significant morbidity and mortality. Despite this, the etiological pathways of the two types are quite different and distinct; additionally, the type2 variant can be prevented and managed through changes in lifestyle without necessarily resulting to medical therapy.

Epidemiology of Diabetes Mellitus Type 2

This condition has a large number of patients’ world wide, and affects people from a diverse range of ethnic and racial origin. The world estimate for the prevalence of the condition stands at 120 million (Amos et al, 1997); and this is expected to increase to about 220 million by the year 2010 (Shaw et al, 2000). The mortality attributed to the condition and its co-morbidities is estimated as among the top five leading causes of death in most countries; however, the mortality and morbidity, is thought to be grossly as the true rate is not accurately reported upon demise of the patent (Fitch & Zimmet, 1988; Songer & Zimmet, 1995).

As a consequence of this, the true magnitude of the diabetes problem is not often appreciated by public health policy makers in many countries; and intervention measures have not been adequately developed. Meanwhile, the society and the economy continue to loose from the mortality and morbidity caused by diabetes (Fitch & Zimmet, 1988).

Among the issues that have not received proper attention in regards to the epidemiology of type2 diabetes is the conditions potential to develop into an epidemic; this may have stemmed from the fact that it is a chronic and non-infectious disease. This however, has been challenged by the documentation of high prevalence’s among the Pima Indians (Knowler et al, 1978); the Micronesian Nauruans of the Pacific (Dowse et al, 1991); and the Pacific and Asian islands inhabitants (Dowse et al, 1994; Zimmet et al, 1983; Dowse et al; 1990).

Indeed, the condition has developed to near epidemic levels in the developed countries (Zimmet, 1992); here, the minority groups have borne the brunt of the ever-increasing prevalence of the condition. A good example is among the Torres Straight Islanders and Australian Aboriginals (Zimmet et al,, 1990) other examples of disproportionate distribution of prevalence can be seen among African-Americans, Mexican Americans and Native-Americans in the United States (Bennett et al,, 1992); and Asian Indians who have migrated to the US [8saw].

The prevalence of diabetes mellitus type2 is projected to increase over the next few years (Amos et al, 1997); and is projected to pose a major threat to the health and the lives of entire nations if its march goes unchecked. Of particular concern is the projected cost of giving long term care to huge sections of the population, and the ability of some countries to afford this (Zimmet & Lefebvre, 1996; Shaw et al,, 2000).

The United States in particular is grappling with the problem of diabetes and its co-morbidities; and concerns have particularly been raised vis-à-vis the ability of the healthcare system to handle a steady increase of the prevalence if no interventions to check this increase are taken. Is has been estimated that about 23.6 million Americans have one form or the other of diabetes mellitus; this translates to about 7.8% of the population. Again, the problem of under-diagnosis again comes up even in a healthcare system that is as comprehensive as that of the US; such has been demonstrated by the disparity between the estimated figure and the confirmed figure of 17.9million [ADA, 2008]; however, the rate under-diagnosis is only 24%; this is an improvement from the 30% of 2005; and 50% of a decade ago. Out of these cases, diabetes mellitus type1 accounts for about 10% (Izzuchi, p199-219).

Already, the disease has been categorized as an epidemic in US by the Center for Disease Control (Gerberding, 2007); this was prompted by the doubling of the prevalence of the condition between 1990 and 2005; additionally, the prevalence increased by 13.5% between 2005 and 2007. A particular concern is the increased diagnoses of diabetes mellitus type2 among children; traditionally considered a disease of adults, the age of diagnosis is ever decreasing. This trend has been attributed to the steady increase in the prevalence of obesity among children in the United States [5wiki].

People in the middle and towards the end of their lifespan still remain the major high-risk group for the development of diabetes mellitus type2. As such, in the United States, about 20% of the people aged above the age of 65 have developed the condition; and likely some of its co-morbidities.

Another high risk group is determined by the presence of obesity in the individual; the link between obesity and diabetes mellitus type2 has been established; and the prevalence of the condition among children and adolescent has been shown to be parallel to that of obesity [NIH, 2007]; and the increase in the incidence of obesity in this age group has been followed by the development of the condition. Additionally, obesity has been linked with diabetes among the other age groups; as such, approximately 55% of the patients who have been diagnosed with type2 diabetes mellitus in the United States have also been diagnosed with obesity (Eberhart, 2004).

Patho-Physiology of Diabetes Mellitus Type-2

Diabetes mellitus type2 develops in the situation where the body does not respond to intrinsic insulin; as such the body may be producing adequate amount of insulin but the blood sugar levels remain high despite of this; the dysfunction of blood glucose metabolism in type-2 diabetes is therefore ‘post-receptor’ and is primarily due to insulin resistance. This is contrary to the situation in diabetes mellitus type-1 where there is an absolute deficiency of insulin due to a failure in the mechanisms of production. Consequently, while the latter can be treated with administration of exogenous insulin, the treatment of the former is not as straight forward.

The onset of diabetes type-2 is insidious; and may go unnoticed for many years since the production of insulin my go on during this period despite the resistance. This has probably the reason why the condition is more under-diagnosed than its type-1 contemporary. Due to its insidious onset, the condition is also relatively milder; and the development of severe signs such as coma does not occur as frequently as in type1. The condition should, however, be taken with outermost seriousness since wrong or poor management might lead to serious future complications such as blindness and heart disease.

As a condition, the etiology of the condition has not been established; development of the condition has been linked to other risk factors such as obesity. Diabetes can also develop secondary to other conditions or situations such as defects in the genotype, surgery, trauma and adverse effects of medication for example some steroidal based drugs; such is usually referred to as secondary diabetes.

Genetic conformation of an individual has been blamed for increasing the risk of developing diabetes mellitus type-2; suspicions were raised by the observation that relatives, especially members of a nuclear family, tended to develop the condition in a more-or-less predictable manner. The condition has also been linked with mutations of genes especially the Isle Amyloid Polypeptide gene which precipitates development of a severe form of the condition with an early onset (Sakagashira et al, 1996; Cho et al, 2003).

The link between the condition and obesity has been attributed to the deposits of adipose tissue characteristic to excess weight; those especially in the abdominal cavity and around viscera have been shown to be a source of chemicals such as cytokines resulting in adverse effects to other organs precipitating diabetes. On the other hand, studies have linked diabetes with obesity with the former causing the latter rather than vise versa; as such, insulin resistance, characteristic of type-2 diabetes causes a derangement of cellular metabolism resulting in the storage of calories in form of fat, and thus to obesity (Camastra et al,, 1999).

Diabetes and co-morbidities

The proclivity of diabetes to cause other diseases has been recognized for a long time. This can be attributed to the fact that diabetes, as a dysfunction of glucose metabolism, affects the heart or functions of many body cells and thus systems; and that it would be virtually impossible for the condition to occur in isolation.

Among the functions of the body affected include the ability to mount an effective immune resistance; this, combined with the elevated levels of sugar in blood results to an increased susceptibility of the patient to infections. Other functions that are affected are those that require a high energy balance in the metabolism; such include wound healing; patients with diabetes show very poor healing of wounds, including surgical ones; and small wound may develop into large, septic lesions which may warrant amputation of the affected limb.

The high concentration of glucose in blood leads to damage to the renal and cardiovascular system. In the former, the system is overworked by the extra burden of eliminating the glucose from the blood, resulting in glycosuria. Cardiovascular disease is commonly seen as arterial disease, coronary heart disease and hypertension.

Trends in Diagnosis

The way diabetes is diagnosed has been subject to a number of far-reaching changes over the years. The World Health Organization (WHO), in 1985, set the threshold for positive diagnosis that was based on the 75g glucose tolerance test (OGTT); this went ahead to become the gold standard for the years thereafter [WHO, 1985]. The thresholds were based on, among other things, the development of retinopathy and the levels of glucose at which the output of endogenous insulin begins to reduce (Shaw et al, 2000). The WHO definition of diabetes is that of a single result showing an elevation of blood glucose accompanied by clinical signs of the condition; alternatively, diabetes can also be defined from two separate readings showing a fasting plasma glucose (FPG) greater or equal 126 mg/dl (7.0 mmol/l); or a plasma glucose greater or equal to 11.1 mmol/l two hours after administration of an oral dose, that is as after carrying out a glucose tolerance test [WHO, 2007].

Various subsequent studies have, however, resulted in digression from this standard, and modification of the same to make it more accurate. Of particular note is the recommendations of the American Diabetes Association recommendation that the fasting plasma glucose (FPG) rather than the OGTT should be adopted as the standard test for both clinical diagnoses and epidemiological studies; since the former has better reproducibility and is relatively easier to perform than the latter (Shaw et al,, 2000). Additionally, there has been a consensus by both ADA and WHO that in a patient who shows an abnormal test for glucose should have the test repeated on a different day for confirmation of the same.

Treatment of Diabetes Mellitus Type-2

Diabetes has no cure; the key in treatment of the condition is the management of blood sugar. As such, the condition is chronic and requiring long term care often involving the more that one branch of the medical profession in case the effects of hyperglycemia; such include ophthalmologists, surgeon and cardiologists. In the past, these consequences were more-or-less inevitable; and the patient usually was progressive and terminal.

Treatment regimes have however been developed and two main goals formulated; prevention of progression of the condition from the point at diagnosis and prevention of development of co-morbidities; and maintaining the quality of life that is usually threatened by such a debilitating condition.

These goals are usually pursued through various interventions ranging from pharmaceutical, dietary, social, psychological and physical (exercise); as such, effective treatment of diabetes requires a multidisciplinary approach ranging from medical to lay practitioners. Treatment also has an important aspect of self-care; that involves self-monitoring, self-medication and lifestyle adjustments.

The major challenge in the management of diabetes and its co-morbidities on a population level is the less that ideal state of coordination among the various branches of the healthcare sector; as such, the transition from one level of the system to another, for example from a general practitioner to a specialist is not smooth, and may result in the loss of crucial information and/or time. This among other things has raised the concern vis-à-vis the ability of such a disjointed system to handle diabetes on an epidemic level.


Of particular importance in the subject of prevention is being able to detect early signs of the condition before the development of overt disease. As mentioned before, high risk epidemiological groups have been identified depending on age, weight and familial predisposition. People in these groups can be screened for glucose metabolism abnormalities and interventions put in place to prevent occurrence of diabetes; such onset has been shown to be delayed through dietary changes and increased physical activity (Raina & Kenealy, 2008). Such can also be combined with prophylactic pharmaceutical therapy involving drugs such as metformin, xenical and acarbose (Santaguida et al, 2005; Torgerson et al, 2004).


On the level of an individual, the outcome for treatment and the prospect of prevention are favorable. Everyday, new information regarding treatment is generated so as to enable medical professionals to accurately diagnose and effectively treat the condition.

The worrisome part of the disease, however, is when viewed on a population level. The ever-increasing prevalence of the condition is not a good sign; this is particularly due to the fact that the condition is progressive and chronic. In the future, healthcare systems and indeed governments may be burdened with a large number of completely incapacitated people which the economy may not be able to support both in health expenses and social support.


  1. American Diabetes Association: Total Prevalence of Diabetes and Pre-diabetes.
  2. Amos AF, McCarty DJ, Zimmet P (1997): The rising global burden of diabetes and its complications: estimates and projections to the year 2010. Diabet Med 14 (Suppl. 5):S7–S85
  3. Bennett PH, Bogardus C, Zimmet P, Tuomilehto J (1992): The epidemiology of non-insulin dependent diabetes: non-obese and obese. In International Textbook of Diabetes Mellitus. Alberti KGMM, DeFronzo R, Keen H, Zimmet P, Eds. London, Wiley, p. 147–176
  4. Camastra S, Bonora E, Del Prato S, Rett K, Weck M, Ferrannini E (1999). Effect of obesity and insulin resistance on resting and glucose-induced thermogenesis in man. EGIR (European Group for the Study of Insulin Resistance). International Journal of Obesity and Related Metabolic Disorders 23 (12): 1307–13
  5. Cho YM, Kim M, Park KS, Kim SY, Lee HK (2003). S20G mutation of the amylin gene is associated with a lower body mass index in Korean type 2 diabetic patients. Diabetes Research and Clinical Practice 60 (2): 125–9
  6. Diabetes rates are increasing among youth NIH. Web.
  7. Dowse G, Zimmet P, Finch C, Collins V (1991): Decline in incidence of epidemic glucose intolerance in Nauruans: implications for the thrifty genotype. American Journal of Epidemiology 133:1093–1104
  8. Dowse G, Spark R, Mavo B, Hodge AM, Erasmus RT, Gwalimu M, Knight LT, Koki G, Zimmet PZ (1994): Extraordinary prevalence of non-insulin-dependent diabetes mellitus and bimodal plasma glucose distribution in the Wanigela people of Papua New Guinea. Medical Journal of Australia 160:767–774
  9. Dowse G, Gareeboo H, Zimmet P, Alberti KGMM, Tuomilehto J, Fareed D, Brissonnette LG, Finch CF (1990): High prevalence of NIDDM and impaired glucose tolerance in Indian, Creole and Chinese Mauritians. Diabetes 39:390–396
  10. Eberhart, M. S.; Ogden, C, Engelgau, M, Cadwell, B, Hedley, A. A., Saydah, S. H. (2004) Prevalence of Overweight and Obesity Among Adults with Diagnosed Diabetes — United States, 1988–1994 and 1999–2002. Morbidity and Mortality Weekly Report (Centers for Disease Control and Prevention) 53 (45): 1066–8. Web.
  11. Finch CF, Zimmet PZ (1988): Mortality from diabetes. In The Diabetes Annual/4. Alberti KGMM, Krall LP, Eds. Amsterdam, Elsevier, p. 1–16
  12. Gerberding, Julie Louise (2007), Diabetes, Atlanta: Centres for Disease Control.
  13. Inzucchi SE, Sherwin RS. The Prevention of Type 2 Diabetes Mellitus. Endocrinol Metab Clin N Am 34 (2205) 199-219.
  14. Knowler W, Bennett P, Hamman R, Miller M (1978): Diabetes incidence and prevalence in Pima Indians: a 19-fold greater incidence than in Rochester, Minnesota. American Journal of Epidemiology 108:497–504, 1978
  15. Raina Elley C, Kenealy T (2008). Lifestyle interventions reduced the long-term risk of diabetes in adults with impaired glucose tolerance. Evidence Based Medicine 13 (6): 173.
  16. Robbins and Cotran, Pathologic Basis of Disease, 7th Ed. pp 1194-1195
  17. Sakagashira S, Sanke T, Hanabusa T. (1996). Missense mutation of amylin gene (S20G) in Japanese NIDDM patients: Diabetes 45 (9): 1279–81.
  18. Santaguida PL, Balion C, Hunt D. (2005). Diagnosis, prognosis, and treatment of impaired glucose tolerance and impaired fasting glucose: Evid Rep Technol Assess (Summ) (128): 1–11
  19. Songer TJ, Zimmet PZ (1995): Epidemiology of type II diabetes: an international perspective. Pharmacoeconomics 8 (Suppl. 1):1–11
  20. Torgerson JS, Hauptman J, Boldrin MN, Sjöström L (2004). Xenical in the prevention of diabetes in obese subjects (XENDOS) study: a randomized study of orlistat as an adjunct to lifestyle changes for the prevention of type 2 diabetes in obese patients. Diabetes Care 27 (1): 155–61
  21. World Health Organization: Diabetes Mellitus: Report of a WHO Study Group. Geneva, World Health Org., 1985 (Tech. Rep. Ser., no. 727)
  22. World Health Organization. Definition, diagnosis and classification of diabetes mellitus and its complications: Report of a WHO Consultation. Part 1. Diagnosis and classification of diabetes mellitus.
  23. Zimmet P, Taylor R, Ram P, King H, Sloman G, Raper LR, Hunt D (1983): The prevalence of diabetes and impaired glucose tolerance in the biracial (Melanesian and Indian) population of Fiji: a rural-urban comparison. American Journal of Epidemiology 118:673–688
  24. Zimmet P: Kelly West Lecture (1991): Challenges in diabetes epidemiology: from West to the Rest. Diabetes Care 15:232–252, 1992
  25. Zimmet P, Dowse GK, Finch CF, Serjeantson S, King H (1990): The epidemiology and natural history of NIDDM: lessons from the South Pacific. Diabetes Metab Rev 6:91–124
  26. Zimmet P, Lefebvre P (1996): The global NIDDM epidemic: treating the disease and ignoring the symptom (Editorial). Diabetologia 39:1247–1248