Introduction
According to the World Health Organisation (WHO, 1999), diabetes mellitus is a condition of metabolic disorder which occurs as a result of defects in insulin, secretion action, or both. It is characterised by chronic hyperglycaemia resulting into long term damage dysfunction and failure of various organs. It was originally considered to be a disease characterised by wasting and the passage of large amount of sweat and urine leading to death over the course of few weeks or months. It is a deadly metabolic disorder which results from insufficient insulin production by the pancreas with subsequent impairment of glucose metabolism (Alade, 2000).
The usual age of onset is between forty and sixty but it has been reported in babies. Arnold (2009) reported that the disease is a hereditary ailment and so is more likely to be present if another member of the family has the same condition, or for example, if both parents have diabetes, it is likely that their children will develop it sooner or later. But if only one of the parents has diabetes, there is only one in five chance of the child developing the ailment.
According to diabetes Association of Nigeria (DAN) (2006), the good news is that diabetes did not mean patient will not live a healthy life. Diabetes is a common disease which affects 1 to 1.2 millions of people in Nigeria, of all ages, races, both men and women from all walks of life.
Anne (2004) buttressed that the disease is occurs as a result of high blood sugar due to inability to produce or inability to metabolise, sufficient quantities of the hormone insulin. It is characterised by excessive thirst and excretion of large amount of severely diluted urine. Diabetes mellitus is a prevalent, costly condition that causes significant morbidity and mortality. It is a heterogeneous group of disorder characterised by persistent hyperglycaemia. Diabetes is mainly caused by a combination of genetic and environmental risk factors (Arnolds, 2008). He connotes that other factor that imposed rare cause/forms of diabetes are directly inherited, such as mutation in mitochondrial DNA.
However, Abel (2010) opined that the disease is associated with reproductive complications causing problems for both mothers and their children. Although improved glycaemic control may decrease the risk of developing this complication, diabetes remains a very significant cause of social, psychological and financial burden in population worldwide.
Overview of diabetes mellitus
In recent times, the translation of many developing countries including Nigeria towards economical development, socialization, industrialization and urbanization has led to increasing manifestation of some chronic diseases in the society. Some common phenomenon associated with this occurrence are malnutrition, competition, pollution and global warming. In Nigeria, this trend is becoming prevalence in both urban and rural communities leading to a high incidence of chronic diseases such as cancer, diabetes, cardiovascular disease, etc (Rufus, 2008).
Nutrition is now recognised as a major modifiable determination in the development of some chronic diseases such as diabetes. Several evidence had empirically pinpointed that the consumption of food that are high in dietary fibre is effective to the prevention and management of diabetes mellitus, which is one of the non-communicable disease that have emerged with industrialization, globalization and adoption of western dietary pattern. Diabetes is facilitated by the current practices of advertising that has lead to the consumption of unhealthy foods and lack of physical activities and it is termed “nutrition transition” (Onyechi and Obeanu, 2010). They buttressed that these foods metabolism has some consequential effects on the insulin profile in healthy and non-insulin dependent diabetic patient.
However, diabetes mellitus is a disorder caused by various predispositions and precipitating factors which could be defined as a chronic disease characterised by disorder in carbohydrate and associated fat and protein metabolism. This is due to an absolute or relative deficiency in the action of insulin and possibly abnormally high amount of hormones, which oppose the effect of insulin, glycogen, epinephrine, growth hormones – carticosteriods and sympathomimetic amines and glucocorticiods (Matain and Escott-Stump, 2000; Koda-Kimble and Rotblatt, 1988). They connotes that patients with diabetes have inherited or acquired deficiency in the production of insulin by the pancreas, which results in an increased concentration of sugar in the blood. The disease is characterised by intolerance of glucose as well as changes in lipid and protein metabolism.
Lucas (2006) sees it as a complex illness that affects a lot of organs. He defines it as a medical condition which makes the patient produce a lot of urine and feel very thirsty frequently. Diabetes mellitus is a disease in which the pancreas produce insufficient amount of insulin or in which the body cell fails to respond appropriately to insulin. Insulin is a hormone that helps the body cell to absorb glucose (sugar) that can be used as a source of energy (Brunner and Surddath, 2009).
Classification and prevalence of diabetes mellitus
According to Famakinwa (2005), diabetes are classified into two main categories based on the etiology recognised.
These are:
- Primary diabetes mellitus
- Secondary diabetes mellitus
Primary diabetes mellitus
This is mainly chronic diabetes that is associated with the insulin organs of the body. It is further divided into four groups viz;
- Insulin dependent diabetes mellitus (IDDM) or juvenile onset, also known as type I diabetes mellitus.
- Non-insulin dependent diabetes mellitus (NIDDM) or adult onset also known as type II diabetes mellitus.
- Gestational diabetes mellitus (GDM) which is recognised during or after pregnancy (WHO, 1985).
- Impaired glucose tolerance (IGT) which may occur in liver disease e.g. hepatitis and liver cirrhosis (Rein, 2005).
Secondary diabetes mellitus
This type 2 diabetes mellitus is associated with specific genetic syndrome. These include malnutrition-related diabetes mellitus (MRDM), surgery, induced drugs or chemicals, infections, pancreatic diseases, other endocrine diseases and abnormalities of insulin or receptors. They are associated with recognisable pathological process (Onyechi and Ibeanu, 2010)
However, malnutrition-related diabetes mellitus is further divided into two categories namely;
- Fibro-Calculous pancreatic diseases (FCPD): This is seen in young diabetics below age 30 years. The key seaburn is a widespread formation of calculi (stones) in the main pancreatic dust and its branches without any calcification in the pancreas itself. The abdominal pain begins at age of 10 years and become complications at the age of 30 years. It occurs as a result of excessive consumption of cassava and protein malnutrition at early childhood (Bajaj, 1988).
- Protein Deficiency diabetes mellitus (PDDM): This is initiated by protein malnutrition at an early childhood that results to functional impairment of pancreatic beta-cells. A continuing low level of protein intake may make this process progressive and irreversible, resulting in the clinical onset of diabetes mellitus at a young age (Bajaj, 1988).
Prevalence/incidence of diabetes mellitus
Diabetes mellitus is one of the chronic non-communicable diseases that have emerged in recent times and has become a global problem, a major epidemic of the millennium and one which shows no sign of abating (Ismail, 2006).
The prevalence of diabetes in the African region ranges from 2 – 3 % and progressively doubles annually. And 80% of the diabetic patients are undiagnosed and death due to diabetes are expected to double over the next decade (IDF, 2006).
A national study of non-communicable disease in Nigeria shows that 2.8% of the population had diabetes (MOHSS, 1997). The prevalence was shown to be higher in females and those with increasing age (Onyechi and Okenwa, 2010; SCN, 2006).
Etiology of diabetes mellitus
Etiology entails the scientific study of the causes of a disease. According to Onyechi and Ibeanu (2010), the pancreas is the organ responsible for the production of the two hormones involved in diabetes. These two hormones are insuline and glucagons. Insulin lowers blood glucose. In diabetes, insulin is absent, deficient or ineffective. Insufficient insulin results in decreased removal of glucose from the blood. Glucagons raise blood glucose. In diabetes, glucagon is present in excessive amount and may account partially for hyperglycaemia in diabetes. Insulin and glucagons exist in a delicate balance. High concentration of insulin should stimulate glucagons release which low concentration should suppress glucagons release. In diabetes, the co-ordination of insulin and glucagons secretion is lacking and glucagons levels become high in relationship with insulin. A high level of glucagons causes the release of excess glucose in the bloodstream. Any interference in the production and balance of insulin and glucagons predisposes an individual to show clinical manifestation of diabetes mellitus (Onyechi and Ibeanu, 2010).
However, Johnson (2010) emphasized that the main factor that causes interference between the insulin and glucagons is characterised by disorder in carbohydrate and associated fat and protein metabolism. Insulin is the key to efficient glucose utilization. It promote the uptake of glucose, fatty acids and amino acids and their conversion to storage forms in most tissues. While in muscles, insulin promotes the uptake of glucose and its storage as glucagons in response to food ingestion (via enteroinsular mechanisms) (Onyechi and Ibeanu, 2010).
Long-term complication of diabetes mellitus
Long term complication of diabetes mellitus occurs as a result of prolonged hyperglycaemia caused by inadequate metabolic control (Raskin and Rosenstock, 1986) substantial evidence has identified two major types of long term complication of diabetes mellitus.
- Microvascular complication of diabetes mellitus
- Macrovascular complication of diabetes mellitus
Microvascular complication diabetes mellitus
These are complications that affect the small blood vessels. There are three organs affected by these complications – the eye (retinopathy), the kidney (nephropathy) and nerve (neuropathy). These processes occurs because the walls of the capillaries that supply these tissue with blood and nutrient (Franz, 2000).
Macrovascular complication diabetes mellitus
These are complications that affect large blood vessels. This is due to atherosclerosis of blood vessel which results in reduced blood flow to tissue. The insulin resistance induce numerous metabolic changes. This is known as the metabolic syndrome or insulin resistance syndrome. It is associated with abnormal lipid levels (dyslipidemia), hypertension, genetic, smoking, sedentary lifestyle, high fat diet, renal failure and microalbuminuria (Mahan and Escott-Stumo, 2000). Diabetic patients are more susceptible to coronary heart disease, stroke and peripheral vascular diseases (Koda-Kimble and Rotblatt, 1988).
However, Rotimi et al. (2001) highlighted some factors associated with diabetes mellitus as;
- Genetic factors
- Viral factors
- Obesity
- Stress
Non-compliance
Behavioural scientists have studied the problem of non-compliance (non-adherence) extensively. More than 95% of diabetes care is done by the diabetes and health professional have very little control over how patients manage their illness. Several researchers finding clearly indicate that diet and excessive exercise can delay onset of symptoms of diabetes for years and are useful in preventing diabetes than melfirmin (Funnel, 2002).
However, Ada (2008), categorised non-compliance into the following stages, viz;
- Primary non-compliance: Occurs when the patient fails to have the medication dispensed.
- Secondary non-compliance: Occurs when patients take prescribed diet but not in a correct proportion.
- Intentional non-compliance; Occurs when doctor’s diagnosis is rejected by the patient.
- Unintentional non-compliance: Can be related to social, demographic, psychological and chemical variable.
According to Dawson and Newell (2002), some reasons for non compliance to diabetic diet are as follows;
- Poor doctors/patient relationship and communication.
- Wilful decisions of the patients to be non-compliance to physicians instructions.
- Financial burden
- Low social economic factors such as drinking, smoking, etc.
- Depression
- Paranoid disorders
- Hypertension
- Psychological factors, etc.
Effect of non-compliance to diet
- Inability to control blood sugar (hyper and hypoglycaemia): This will lead to complication like retinopathy.
- Amputation: Due to the disease condition, bacteria will thrive in kidney to necrosis impairing blood supply to lower extremities. The leg gangrenous then amputation sets in.
- Frequent hospital visit and increase in the length of hospital stay because non compliance brings about degeneration of wound and wound breakdown (Ada, 2010).
- Infertility: This problem is associated with either physical/or psychological root and depression which is common with diabetes. Diabetes damages the nerves that control sexual acts and high glucose level can damage the nerves that control the blood glucose level.
- Loss of job.
- Family dysfunction process due to the traumatic condition.
- Reduction in income of the diabetics.
- Death due to prolonged complications.
- Loss of vision, kidney failure and multiple neurological symptoms.
- Intra-urine growth retardation.
Measures to improve compliance
Gonzalez et al (2005) highlighted the following measure to improve compliance among diabetic patient via;
- Health education: Health education helps to improve compliance and reduce complications due to unawareness of disease condition.
- Counselling: This will help to win the patient’s mind towards accepting health education.
- Follow up: This could be in form of visitation at home, phone calls to encourage patient’s compliance (Ministry of Health, 2004).
References
Anderson, J.W. (1986). Dietary Fibre in Nutrition Management of Diabetes. In: Dietary Fibre Basic and Clinical Aspects pp 343-360 (GV Vahouny & D Kritchevsky, editoes). New York: Pleneum Press.
Anderson, J.W., Deakins, D.A. & Bridges, S.R. (1990). Soluble Fibre Hypocholesterolemic Effects and Proposed Mechanism. In: Dietary Fibre, Chemistry, Physiology and Health Effects pp 339-363. (D Kritchevsky, C Bonfield and JW Anderson editors) London: Plenum Press.
Brennan, C.S., Roberts, F.G., Low, A.G. & Ellis, P.R. (1993). The Use of Microscopy in the Evaluation of the Effects of the Galatomannon Deposits of Guar Endosperm on Starch in Guar Wheat Bread. Subsequent Physiological Implication in the Pig. Proc. Nutr. Soc 53:286A
Crapo, P.A., Reaven, G. and Olefsky, J. (1971). Post-Prandial Plasma Glucose and Insulin Responses to Different Complex Carbohydrates. Diabetes 26:117-183.
Coulston, A., Greenfield, M. Krammer, F., Tokey, T and Reaven, G. (1980). Effect of Sources of Dietary Carbohydrate on Plasma Glucose and Insulin Responses to Test Meals in Normal Subjects. Am. J. Clin Nutr. 33:1282-1297.
Edwards, C.A. and Read, N.W. (1990). Fibre and Small Intestinal Function. In Dietary Fibre Perspective 2. Pp 52-57 (A.R. Leeds, Editors). London: John Libey
Goddard, M.S., Young, G. and Marcus, R. (1984). The Effect of Amylase Content on Insulin and Glucose Responses to Ingested Rice. Am. J. Clin. Nutr. 39: 388-392
Holt, S., Heading, R.C., Carter, D. C. Prescott, L.F. and Tothill, P. (1979). Effects of Gel Fibre and Gastric Emptying and Absorption of Glicose and Paracetamol. Lancet i: 636-639
Jenkin, D.J.A., Leeds, A.R., Gassull, M.A., Wolever, T.M.S. Goff, D.V., Alberti, G.M.M. and Hockaday, T.D.R. (1976). Unabsorbable Carbohydrate and Diabetes: Decreased Post-Prandial Hyperglycaemia. Lancet ii: 172-174.
Jenkins, D.J.A., Leeds, A.R., Gassuli, M.A., Cochet, G. and Albert, G.M.M. (1977). Decrease in Post-Prandial Insulin and Glucose Concentration by Guar and Pectin. Am. Intern Med. 86:20-23.
Jenkins, D.J.S., Wolver, T.M.S., Leeds, A.R. Gassull, A.M., Haisman, P., Dilawari, J., Goff, D.V., Metz, G.L. & Alberti, K.G.(1978). Dietary Fibre, Anologues and Glucocose Tolerance: Importance of Viscosity. Br. Med. J. 279: 1392-1394
Jenkins, D.J.A., Wolever, T.M.S., Nineham, R., Taylor, R., Metz, G.L., Bacon, S. and Hockaday, T.D.R. (1978). Guar Crispbread in the Diabetes. Diet Br.Med J. 279: 1744-1746.
Jenkins, D.J.A. Wolever, T.M.S., Nineham, R. Bloom, S., Ahern,J., Albert, K.G. and Hockaday, T.B.R. (1980). Exceptionally Low Blood Glucose Response to Dried Beans; Comparism with other Carbohydrates Foods Br. Med. J. 2:578-580.
Jenkins, D.J.A., Thomas, D.M. Wolever, M.S. Taylor, R.I. Barker, H.M., Fielden, H., Baldwin, J.M., Bowling, A.C. Newman, H.C. Henkins, A.L. & Goff, D.V. (1981). Glycaemic Index of Food: A Physiological Basis for Carbohydrate Exchange. Am. J.Clin. Nutr. 34: 362-366.
Johnson, I.T. and Gee, J.M. (1981). The Effect of Gel Forming Gum on the Intestinal Unstirred Layer and Sugar Transport in Vitro: Gut 22:398-408
Mann, J.I. (1985). Diabetes Mellitus: Some Aspect of Aetiology and Management of Non-Insulin Dependent Diabetes. In Dietary Fibre, F bre Depleted Fods and Disease. Chapter 16 (H. Trowell, D. Burkitt and K. Heaton eds).London: Academic Press.
Maranda, P.M. and Hortwitz, D.L. (1978) High Fibre Diets in the treatment of Diabetes Mellitus. Am. Int. Med. 88: 482-486.
Mahann, K. and Escott-Stump, S. (2000) Food and Nutrition and Diet Therapy. Publishers Saunders Pennsylvennia, U.S.A.
Onyechi, U.A. (1995). Potential Role of Indiginous Nigeria Foods in the Treatment of Non-Insulin Dependent Diabetes Mellitus (NIDDM) PHD Thesis, Kings College, University of London.
Scheeman, B.O. (1982) Pancreatic and Digestive Functions In Dietary Fibre in Health and Disease pp 73-89 GV Vahonny & D. Kritchevsky. New York. Plenum Press.
Uchenna, A.O. & Vivianenne, N.J. (2010). Diabetes Mellitus, Potentials of Indigenous Plant Foods in the Prevention and Management. University of Nigeria Press. Enugu.
WHO (2005) Preventing Chronic Diseases: A vital Investment. WHO, Geneva.
WHO/FAO (2003). Nutrition and the Prevention of Chronic Disease. A Report at a Joint WHO/FAO Expert Consultation, Geneva 28, WHO Technical Report Series 916 WHO, Geneva.