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DIABETES AND BLINDNESS IN KENYA: A chronic disease of

nutrition in transition

By Dr George Omolo Rombo (BSc, MSc, Post Grad Dip Ed, PhD),

Lecturer in Food Biochemistry, Processing and Safety,

Department of Foods, Nutrition and Dietetics,

Kenyatta University,

P. O. Box 43844, Nairobi.

Mobile 0723 161 865, E-mail gomolor@yahoo.com

and

Margaret Muoki, (BEd, MSc)

Research Assistant, Department of Foods, Nutrition and Dietetics,

Kenyatta University, P. O. Box 43844,

Nairobi.

ABSTRACT

Objective: To determine the extent of diabetes as a chronic disease in Kenya and relate it

to incidences of blindness in the country.

Data source: Literature review from archives, hospital records, newspapers, peer

reviewed journals and books.

Data selection: What do the experts say as reported in the journals and newspapers?

Data extraction: Journals, Archives, Ministry of Health, Hospitals, Newspaper reports.

Discussion: Healthy lifestyles and diet can help reduce diabetes. People with high risk of

developing Type 2 diabetes can reduce their chances of getting the disease by up to 50

per cent if they loose as few as 4 kg through exercise, for example.

Conclusion: Diabetes is characterized by increased blood glucose concentrations. These

are regulated by a loop comprising two components, the insulin- secreting β- cells of the

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pancreas and the insulin sensitive tissues such as the liver, muscles and adipose tissue

which respond to insulin.

WHAT IS DIABETES?

A person with diabetes has a condition in which quantities of glucose in the blood is too

high (hyperglycaemia). This is because the body does not produce enough insulin,

produces no insulin, or has cells that do not respond properly to the insulin produced by

the pancreas (Ngetich, 2010). The long term effects of diabetes can be devastating—

nerve damage, blindness, kidney failure and cardiovascular disease (Underwood, 2003).

Diabetes is a general term for diseases characterised by excessive thirst and urination.

Why is it called a chronic disease? Diabetes is a chronic disease because it is non-

communicable unlike diarrhoea, malaria, polio etc. Usually refers to diabetes mellitus. It

is characterised by elevated sugar levels in the blood and in urine. A fasting glucose

level of 7.0-µmol/L is considered normal while higher suggests diabetes. The normal

sugar level in the blood is regulated by the hormone insulin which is produced in the

islets of Langerhans in the pancreas (Atkinson and Maclaren, 1990: Arredondo, Jorquerra,

Carrasco, Elbala and Hertrampf, 2007). Diabetes is the fifth largest killer disease in the

world and with the modern lifestyles, it is likely to take more casualties with it (Lati,

2007; Ngirachu, 2008).

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Figure 1. The different types of cells of normal and diabetic patients

Source: Nash, 1990.

DIABETES IS A DISEASE OF AFFLUENCE

The prevalence of diabetes rises dramatically with industrialisation and concomitant rise

in obesity and sedentary (lifestyle with minimal physical activity ) lifestyles in

developing countries (Wylie-Rosett and Vinicor, 2001). In Kenya, for example, the rapid

rise in type 2 diabetes since independence has been attributed to change from high fibre

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traditional foods such as cassava, sorghum, millet, vegetables and etc to more refined

Western diets such as sifted maize meal, polished rice, white bread etc (Thorburn, Brand

and Truswell, 1987; Maina, 2007). Over 90 per cent of diabetes patients suffer from type

2 diabetes which is more common in people 30 years of age or more (Ngetich, 2010).

The consumption of foods with low glycemic index (GI), or high in soluble fibre like

legumes, improves blood glucose and lipids in people with type 2 diabetes (Brand,

Colagiuri, Crossman, Allen, Roberts, and Truswell, 1991; Frost, Wilding and Beecham,

1994).

The GI of commercially available breakfast cereals varies over a 2 fold range, from 120-

130 for low fiber corn and rice cereals to almost 65 for psyllium-enriched, high fiber

cereals (Foster-Powell, Brand-Miller, 1995; Wolever, Vuksan and Eshuis, 1991).

Removal of fibre during modern processing of cereal foods could also be a major cause

of diabetes type 2 in developing countries (Tsihlias, Gibbs, McBurney and Wolever,

2000).

Rapid urbanisation of indigenous populations may also lead to rapid increase in

incidences of diabetes. Between 10 and 35 per cent of urbanised Australian Aborigines

and Pacific Island populations develop diabetes compared to only 3 per cent among

native white populations (American Diebetes Association, 2000; Sboros, 2001). Similar

effects were displayed by Falashas (or Black Jews) airlifted from Ethiopia to Israel

during the great hunger of early 1980s. These migrants had a rapid diet change from high

fibre injera and vegetables in Ethiopia to highly refined low fiber diet foods in Israel and

over fifty per cent developed type 2 diabetes (NIDDM) within a year or so (Hales, 1994).

Diabetes Mellitus. A chronic disorder of carbohydrate metabolism, characterized by

hyperglycemia (high sugar concentration in the blood) and glycosuria (high sugar

concentration in urine) and resulting from inadequate production or utilisation of insulin

(Taber‘s Cyclopedic Medical Dictionary, 1993). Persons fulfilling these conditions are

not a homogeneous group. Diabetes mellitus is classified according to two syndromes:

Type I, or insulin-dependent diabetes mellitus (IDDM) and Type II, or non-insulin-

dependent diabetes mellitus (NIDDM) see figure 1 above.

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In Type I, the patients secrete little or no insulin. Delivery of an insulin encoding gene

into diabetic rats and mice has helped them regulate their blood glucose levels (Olefsky,

2000; Lee, Kim, Kim, Shin and Yoon, 2000). In the past, this form of diabetes was

called juvenile-onset, ketotic, or brittle diabetes (Pearce et al, 2008).

In Type II, insulin is produced, but exogenous insulin is needed to control hyperglycemia.

Older terms for this form of diabetes were maturity-onset, non-ketotic, or stable diabetes.

Type II diabetes occurs much more frequently than Type I.

SYMPTOMS:

Principal symptoms are elevated blood sugar (hyperglycemia), sugar in urine (glycosuria),

excessive urine production (poyyuria), excessive thirst (polyphagia); itching, frequently

about the genitals. Urine specific gravity 1.020 to 1.040; sugar excessive; urine contains

diacetic acid, beta-hydroxybutyric acid, acetone when disease process is in advanced

stage. More common in women and after the age of 40 (see figure 2 below). Fasting

blood sugar raised above normal range of 5 to 8 µmol/L of blood; boils and carbuncles;

vascular changes may be present. Loss of weight; emaciation; weakness; and debility

(general weakness). When severe diabetes is allowed to progress without proper

treatment, coma ensues with weakness and sweet (acetone) odour of breath; nausea,

headache, vomiting, dyspnoea, sense of intoxication, delirium, and deep coma resulting

in death.

AETIOLOGY:

Basic cause is still unknown but the pathological defect is failure of β-cells of the

pancreas to secrete an adequate amount of insulin. In most instances diabetes mellitus is

the result of genetic disorder, but it may also result from a deficiency of beta cells caused

by inflammation, malignant invasion of the pancreas, or surgery. In the absence of

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insulin, glycogenesis (production of glucose from proteins and/or fats) and glycolysis

(conversion of glucose into energy) are adversely affected. After insulin is secreted by

the beta cells of the pancreas, it is transported to the cells of the body where it binds to

specific insulin receptors. The insulin then acts to promote glucose metabolism in the

cell and to inhibit glucose production by the liver.

COMPLICATIONS:

Diabetic acidosis due to excessive production of ketone bodies; low resistance to

infections, esp. those involving extremities; ulceration of lower extremities; increase in

incidence of toxaemia in pregnancy; cardiovascular and renal disorders; disturbances in

electrolyte balance.

Diabetic neuropathy is estimated to occur in 40 per cent of patients in whom diabetes has

been present for about or over 25 years. A single peripheral nerve may be involved, the

autonomic nervous system may be involved, or cranial nerves may be affected.

Age in Years

Figure 2. Number of diabetic patients in United States

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where age-distribution data exists for the years 1990 and 1998.

Note that there were general increases in percentages

over the eight years.

Source: Center for Disease Control cited in Adler and Kalb, 2000

However, in Kenya, despite rapid increase in diabetes

type I among children, over 90 per cent of reported cases

of diabetes are of the type II which is mainly caused

by sedentary lifestyles copied from the West.

(The Star, 2001; AFP, 2010; Mwaniki, 2010).

Diabetics are prone to develop retinopathy, glaucoma, and various type of neuropathy.

Eye involvement is common, and 0.2 per cent of diabetics become blind each year. This

complication is much less frequent in the insulin-dependent type than the non-insulin-

dependent type. The retinal changes may be of the non-proliferative type withy retinal

ischemia and areas of infarction. In the proliferative type, new vessels are formed in the

retina and these may lead to retinal detachment. These new vessels are destroyed by use

of photocoagulation; this helps to prevent further deterioration of vision.

Cardiovascular disease is the major cause of death in diabetics. In addition, peripheral

vascular disease may lead to ischemia and gangrene of the lower limbs. Amputation(s)

may be required. Press reports add that one in twenty people living in rural areas has

diabetes and in urban areas the number could be as high as one in ten especially among

the urban poor (Kiage, 2010) . One of the most serious complications complications

from diabetes is blindness. The eye can be affected by diabetes in several ways,

including:

Diabetic retinopathy

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High sugar in the blood can cause walls of the vessels in the retina to weaken. Blood

may then leak into the eye cavity. This could lead to blindness.

Cataracts

Clouding of the eye lenses can develop in early age and cause blindness. This may be

corrected by simple cataract surgery or insertion of an intraocular lens will most ties lead

to visual restoration.

Transient refractive disorders

When blood sugar is either too high or too low one can develop sudden long or short

sightedness. Fortunately the situation comes back to normal one the sugar is controlled.

CONTROL OF BLOOD SUGAR LEVELS

Cardiovascular disease is the major cause of death in diabetics. In addition, peripheral

vascular disease may lead to ischemia and gangrene of the lower limbs. Amputation(s)

may be required if the levels of sugar in the blood is not controlled (Adler and Kalb,

2000) .

Glaucoma

This is a condition resulting from progressive damage of the optic nerve often associated

with high pressure inside the eye. This eventually leads to irreversible loss of vision.

People with diabetes are nearly twice as likely to get glaucoma as other adults. There are

no early symptoms until profound visual lose has occurred. Regular eye check-up can

detect stages and treatment given to avert blindness.

The commonest and perhaps the most serious of these complications is diabetic

retinopathy. It is the leading cause of blindness in the US and is on the rise in Kenya.

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People with long duration of diabetes and whose blood sugar is not well controlled are at

a higher risk of getting diabetic retinopathy. Other conditions like hypertension,

pregnancy, obesity and smoking puts one at a higher risk of diabetic retinopathy.

There are usually no symptoms of diabetic retinopathy until there is sudden loss of vision.

Sometimes there is blurring of vision and floaters, but these are non-specific. It is

therefore necessary for diabetic patients to have a complete eye examination by a

qualified eye specialist [ophthalmologist] at least once a year.

LEASER SURGERY

If diabetic retinopathy is detected the eye doctor can perform simple laser procedure in

the eye to prevent progression of the problem. This procedure is usually done in the

clinic and takes no more than 10 to 15 minutes.

When done properly and at the right time, it is effective in preventing one from getting

blind. Follow up in the clinic after the laser is necessary and in some cases the doctor

may repeat the procedure after certain interval.

When diabetic retinopathy is not detected early or proper laser treatment has not been

done, bleeding may occur inside the eye. When this happens one will need a more

complicated surgical procedure called vitriotectomy, which has lower chances of

restoring of normal vision.

To prevent diabetic eye problems one needs to: Have proper yearly eye check-up in a

reputable eye clinic or hospital, ensure that your doctor checks for signs of cataract and

glaucoma as well during each check-up if you are pregnant see the eye doctor during the

first three months and do not smoke (Kiage, 2010).

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SYMPTOMS

Blurred vision (due to the blood glucose build-up in the eye )

Pain in the leg muscles and feet (due to the lower oxygen level in the blood)

Heart problems (arising from the glucose and fatty acid build-up in the blood)

Thirst at regular intervals

Pain during urination

Headaches and confusion

Nausea and sweating

Weakness and hunger

Amputation

Slurred speech and trembling

Unconsciousness (possibly leading to coma)

Severe complications can lead to death

TYPES OF DIABETES

There are two types of diabetes: type 1, the easily-recognisable type which is treated

with insulin is usually genetic, and type 2, which has a slow onset and is often

undiagnosed and is caused by obesity and/or sedentary lifestyles in developing countries

(Wylie-Rosett and Vinicor, 2001; Knip and Akerblom, 2005). The trouble with type 1

diabetes is the immune system, which instead of attacking invasive bacteria and viruses,

it attacks the insulin producing β cells of the islets of Langerhans in the pancrease. This

leads to a decline in the production of insulin hence elevated glucose concentration in the

blood (Underwood, 2003). Between 50 and 65 per cent of type 2 diabetes patients

remain undiagnosed because of the lack of specific symptoms (Knip and Akerboom,

2005).

As a result, a number of diabetes patients are being admitted to public hospitals to have

their feet or legs amputated, cataracts removed, or to be treated for kidney failure and

stroke – due to late diagnoses of type 2 diabetes.

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TREATMENT:

Consists of diet, insulin, exercise, and hygienic measures. At first the patient should be

placed on a well-balanced diet adequate in all basic essential: carbohydrates, proteins,

fats, vitamins, minerals, and fluids. In many patients this may be all that is required.

Obese persons with this disease should be placed on a diet that will enable them to lose

weight. Control of diabetes is much more difficult in an obese person. Blood sugar

determinations should be made at frequent intervals. Glucose levels in the urine may be

monitored by the patient or family as often as necessary. In addition, the availability of

kits for use at home enables patients to monitor blood glucose level at home. Long-term

blood glucose regulation may be objectively assessed by determining the glycosylated

haemoglobin (haemoglobin A1c) in blood (Pearce, Noakes, Keogh and Klipton, 2008).

Dietary therapy was the only treatment available in the era before insulin therapy

(Gerhard, Ahmann, Meeuws, McMurry, Duell and Connor, 2004). As discussed by

Joslin, (1928) dietary carbohydrate had to be restricted in patients with type 1 diabetes

because of impaired carbohydrate metabolism. Such diets were ketogenic and consisted

of largely fats and proteins- the ―good foods of life,‖ eg. meat, cream, butter, cheese, and

eggs. These diets alone were major sources of death among diabetic patients (Joslin,

1928). The discovery of insulin in 1921 (Banting and Best, 1922), made it possible to

introduce carbohydrate containing foods in to the diabetic diet. However, type 2 diabetes

does not respond to insulin and may only be treated by exercise and diet therapy (Knip

and Akerblom, 2005).

HOW MANY KENYANS ARE DIABETIC?

At least 1.2 million Kenyans have diabetes (Weru, 2008) or is it 2 million according to

reports by Dr Acharya of Nairobi University? (Ngetich, 2010)?. Out of these cases, more

than 20,000 children suffer from the disease in Kenya. Diabetes is, actually also, the

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leading cause of heart diseases such as hypertension, heart attack and cancer among

young children in the country (Mwaniki, 2010).

Over 58 per cent of patients admitted at Kenyatta Hospital are diabetic. Unless safe

lifestyles are adopted, 4.5 per cent of Kenyans could be diabetic in the next ten years

according to Dr William Maina, Head of The Department of Non-Communicable

Diseases and Sanitation in the Ministry of Public Health. He adds that, between 5-10 per

cent of children in Kenya suffer from type I diabetes and insulin is needed to treat them.

Type two diabetes affects mainly adults and is estimated to affect over 3.3 per cent of

Kenyans (Weru, 2008). There are two types of glucometers used by diabetics to measure

the levels of sugar in the blood at home (Likimani, 2002). It has been predicted that by

the year 2010 one in six adults over the age of 40 will have Type 2 diabetes in Kenya

(Daily Nation, 2008).

HEALTHY LIFESTYLES MAY HELP REDUCE DIABETES

People with high risk of developing Type 2 diabetes can reduce their chances of getting

the disease by up to 50 per cent if they loose as few as 4 kg, exercise regularly and follow

a healthy diet. Initially type 2 diabetes was very common in adults but recent trends

show a sharp increase among obese children (The Star, 2001; Klein, Sheard, Pi-Sunyer,

Daly, Wylie-Rosett, Kulkarni and Clark, 2004 ). Regular exercise and aerobic fitness

also improve insulin sensitivity and glycemic control (National Institute of Health,

National Heart, Lung, and Blood Institute, and National Institute of Diabetes, Digestive

and Kidney Disorders, 1998: US Department of Health and Human Services, Centers for

Disease Control, 1996; Hu, Sigal and Rich-Edwards, 1999.) and may reduce the risk of

or development of diabetes (Wei, Gibbons, Mitchell, Kampert, Lee and Blair, 1999), and

even reduce the mortality rate among patients with type 2 diabetes (Church, Cheng and

Ernest, 2004).

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CONCLUSIONS

Diabetes is characterized by increased blood glucose concentrations. These are regulated

by a loop comprising two components, the insulin-secreting β-cells of the pancreas and

the insulin sensitive tissues such as the liver, muscles and adipose tissues which respond

to insulin. Loss of blood glucose control is due to a β-cell failure, resulting in insulin

deficiency, insulin resistance of the target tissues (liver, muscles and adipose tissues).

Type 1 is perceived to be a chronic immune-mediated disease with sub clinical prodrome

(a prodrome is a symptom indicative of an approaching disease) characterized by

selective loss of insulin producing β-cells in the pancreatic islets in genetically

susceptible people (Knip, 2002). The preclinical disease is asymptomatic and may last

from a few months to more than 10 years. Acute clinical onset, ketoacidosis and

dependency on exogenous insulin are characteristic features, and may lead to absolute

dependency on insulin injections or death (Pearce et al., 2008). Type 1 diabetes is

genetic and it afflicts mainly young children.

Type 2 diabetes is typically a metabolic disorder of obese middle aged or old people with

slow clinical onset and a non-insulin dependence (Wilkin, 2001). Type 2 diabetes is a

component of the metabolic syndrome characterized by obesity, insulin resistance, lipid

abnormalities, hypertension, cardiovascular disease and the rapidly urbanizing

populations of developing countries (Knip and Akerblom, 2005). Type 2 diabetes is

environmental and largely an adult disease.

References

1. Adler, J. and Kalb, C., 2000. Diabetes: A growing crisis especially among those

in their prime. Newsweek September 4th

, 2000, pp. 56-63.

2. AFP, 2010. Western diseases spread to Third World: Explosion a result

of importing lifestyles from developed nations of the West

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Daily Nation, October 14th

, 2010. pg. 22.

3. American Diabetes Association. American Diabetes Association Clinical

Practice Recommendations 2000, 23(Supplement1).

4. Arredondo, M., Jorquera, D., Carrrasco, E., Albala, C. and Hertrampf, E., 2007.

Microsatellite polymorphysm in the heme oxygenase-1 gene promoter is associated

with iron status in persons with type2 diabetes mellitus.

American Journal of Clinical Nutrition 86:1347-1353.

5. Atkinson, M. A. and Maclaren, N. K., 1990. What causes diabetes?

Scientific American July 1990, pp. 42-49.

6. Banting, F. G. and Best, C. M., 1922. The internal secretion of the pancreas.

Journal of Laboratory and Clinical Medicine 11(5): 465-480.

7. Brand, J. C., Colagiuri, S., Crossman, S., Allen, A.., Roberts, D. C. K. and

Truswell, A. S., 1991. Low glycemic index foods improve long term glycemic

control in NIDDM. Diabetes Care 14: 95-101.

8. Church, T. S., Cheng, Y. J. and Ernest, C. P., 2004. Exercise capacity and body

composition as predictors of mortality among men with diabetes.

Diabetes Care 27: 83-88.

9. Daily Nation 2008. Diabetes: Are You at risk? Daily Nation February 23rd

, 2008.

10. Foster-Powell, K. and Brand-Miller, J., 1995. International tables of glycemic index.

American Journal of Clinical Nutrition 62(suppl): 871S-893S.

11. Frost, G., Wilding, J. and Beecham, J., 1994. Dietary advice based on the glycemic

index improves dietary profile and metabolic control in type 2 diabetic patients.

15

Diabetes Medicine 11: 397-401.

12. Gerhard, G. T., Ahmann, A., Meeuws, K., McMurry, M. P., Duell, P. B., and

Connor, W. E., 2004. Effect of a low fat diet compared with those of

a high monosaturated fat diet on body weight, plasma lipids and lipoproteins,

and glycemic control in type 2 diabetes.

American Journal of Clinical Nutrition 80: 668-673.

13. Hales, C. N., 1994. Fatal nutrition and adult diabetes.

Scientific American 1(3): 54-62.

14. Hu, F. B., Sigal R. J., and Rich-Edwards, J. W., 1999. Walking compared with

rigorous physical activity and risk of type 2 diabetes in women: a prospective study.

Journal of American Medical Association 282: 1433-1439.

15. Joslin, E. P., 1928. The Treatment of Diabetes Mellitus 4th

, ed. Philadelphia,

Lea and Febiger.

16. Kiage, D., 2010. Avoid losing your vision from diabetes.

The Standard October 21st, 2010. pg 25.

17. Klein, S., Sheard, N. F., Pi-Sunyer, X., Daly, A., Wylie-Rosett, J., Kulkarni, K.

and Clark, N. G., 2004. Weight management through life cycle modification for the

prevention and management of type 2 diabetes: rationale and strategies. A statement

of the American Diabetes Association, the North American Association for the Study

of Obesity, and the North American Society for Clinical Nutrition.

American Journal of Clinical Nutrition 80: 257-263.

18. Knip, M., 2002. Natural cause of preclinical type 1 diabetes.

Hormonal Research 57(Supplement 1): 6-11.

19. Knip, M. and Akerblom, H. K., 2005. Early nutrition and later diabetes risk.

16

In: Early Nutrition and its Later Consequences: New Opportunities. Advances in

Experimental Medicine and Biology vol. 569. Berthold Koletzo, Peter Dodds,

Hans Akerblom and Margaret Ashwell, (eds). Springer Sciences, Berlin, pp. 142-150.

20. Lati, A., 2007. Grace Jalang‘o: Shedding light on diabetes.

The Standard February 10th

, 2007, pg 14.

21. Lee, H. C., Kim, S. J., Kim, K. S., Shin, H. C. and Yoon, J. W., 2000.

Remission in models of type 1 diabetes by gene therapy using a single chain

Insulin analogue. Nature 408: 483—487.

22. Likimani, L., 2002. The common problems. East African Standard

September 21st, 2002.

23. Maina, W., 2007. Diabetes cases to rise from 3.5 per cent to 10 per cent.

Daily Nation September 3rd

, 2007

24. Mwaniki, M., 2010. Surge in diabetes cases ‗worrying.‘ Daily Nation

November 2nd

, 2010. pg. 10.

25. Nash, M., 1990. A slow savage killer: Scientists are battling high blood sugar,

the affliction that strikes millions. Time November 26th

, 1990., pp. 52-59.

26. National Institutes of Health, National Heat, Lung and Blood Institute, and National

Institute of Diabetes, Digestive and Kidney Diseases, 1998. Clinical Guidelines on

the Identification, Evaluation and Treatment of Overweight and Obesity

Among Adults. Bethesda, MD., NIH.

27. Ngetich, K. 2010. Two million Kenyans suffer from diabetes.

Kenya Times March 31st, 2010. pg. 18.

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28. Ngirachu, J., 2008. Worrying trend as children develop disease that is linked to

lifestyle:Diabetes was in the past thought to affect older and affluent people

in society. Daily Nation November 14th

, 2008, page 14.

29. Olefsky, J., M., 2000. Gene therapy for rats and mice suffering from type 1 diabetes.

Nature 408: 420—421.

30. Pearce, K. L., Noakes, M, Keogh, J. and Clifton, P. M., 2008. Effect of carbohydrate

distribution on postprandial glucose peaks with the use of continuous glucose

monitoring in type 2 diabetes. Journal of American College of Nutrition 87: 638-644.

31. Sboros, M., 2001. Diabetics can still live the good life. The Star

November 14th

, 2001, pg 11.

32. Taber’s Cyclopedic Medical Dictionary 1993. Diabetes Mellitus. Taber’s Cyclopedic

Medical Dictionary (C. L. Thomas, ed.). F. A. Davis, Philadelphia, pp. 532-535.

33. The Star 2001. Healthy lifestyle helps beat diabetes. The Star May 9, 2001, pg 13.

34. Thorburn, A. W., Brand, J. C. and Truswell, A. S., 1987. Slowly digested and

absorbed carbohydrate in traditional bushfoods: a protective factor against diabetes.

American Journal of Clinical Nutrition 45:98-106.

35. Tsihlias, E. B., Gibbs, A. L., McBurney, M. I. and Wolever, T. M. S., 2000.

Comparison of high and low glycemic index breakfast cereals with

monosaturated fat in the long term dietary management of type 2 diabetes.

American Journal of Clinical Nutrition 72:439-449.

36. Underwood, A., 2003. Stopping Type ! diabetes: A radical new treatment could

offer hope for millions. Newsweek January 6th

, 2003. pg. 57.

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37. US Department of Health and Human Services, Centers for Disease Control. 1996.

Physical Activity and Health: A Report of The Surgeon General. Washington D. C.,

US Government Printing Office.

38. Wei, M., Gibbons, L. W., Mitchell, T. L., Kampert, J. B., Lee, C. D. and Blair, S. N.,

1999. The association between cardio respiratory fitness and impaired

fasting glucose and type 2 diabetes mellitus in men.

Annals of International Medicine 130: 89-96.

39. Weru, J., 2008. 1.2 million Kenyans have diabetes: The Government is in

the process of introducing comprehensive national policy on treatment of disease.

The Standard November 8th

, 2008.

40. Wilkin, T. J., 2001. The accelerator hypothesis: weight gain as the missing

link between Type1 and Type 2 diabetes. Diabetologia 44: 914-922.

41. Wolever, T. M. S., Vuksan, V. and Eshuis, H., 1991. Effect of method of

administration of psyllium on the glycemic response and carbohydrate digestibility.

Journal of American College of Nutrition 10: 364-371.

42. Wylie-Rosett, J. and Vinicor, F., 2001. Diabetes mellitus. In: Present Knowledge

in Nutrition. (B. Bowman and R. M. Russell, eds.), ILSI Press, Washington, D. C.,

pp. 552-563.