Diabetes

•Diabetes mellitus (DM) is a common syndrome and caused by lack or decreased effectiveness of endogenous insulin

•Insulin is needed to facilitate entrance of glucose from blood to cells to be used in different metabolic processes.

• In DM, insulin released from pancreas is reduced or body cells are resistant to the released insulin (due to e.g. obesity).

• In such cases, glucose remains in blood leading to hyperglycemia with consequence microangiopathy.

• The elevated level of glucose leads to increase in urinary output (polyurea) with subsequent dehydration and continuous thirst (polydepsia).

•On the other hand, deficient intracellular glucose leads to the use of other alternatives (protein and fat) to generate the required energy, with subsequent production of ketone bodies (Diabetic ketoacidosis)

•The protein and fat catabolism leads to suppressed immunity and rapid loss of weight respectively.

•Nervous cells in the hunger center in the brain will be deprived of glucose ( like all other cells in the body) which will result in continous feeling of being hungry (polyphagia)

•All these mechanisms contribute to produce the DM triad: polyurea, polyphagia and loss of weight.

•The chronic hyperglycemia of diabetes is associated microangiopathy with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels.

Classification of primary diabetes

•Type 1 (insulin-dependent (IDDM), juvenile onset):

•Only 5–10% of those with diabetes•May occur at any age but more common

in patients <30y.•results from a cellular-mediated

autoimmune destruction of the β-cells of the pancreas

•Some patients, particularly children and adolescents, may present with ketoacidosis as the first manifestation of the disease.

•These patients are also prone to other autoimmune disorders such as Hashimoto’s thyroiditis, vitiligo, autoimmune hepatitis and pernicious anemia.

Type 2 (non-insulin dependent (NIDDM), maturity onset):

•90–95% of those with diabetes• the cause is a combination of resistance to

insulin action and an inadequate compensatory insulin secretory response

•a degree of hyperglycemia sufficient to cause pathologic and functional changes in various target tissues, but without clinical symptoms, may be present for a long period of time before diabetes is detect

•Most patients with this form of diabetes are obese, obesity itself causes some degree of insulin resistance

•Insulin resistance may improve with weight reduction and/or pharmacological treatment of hyperglycemia but is seldom restored to normal

The risk of developing this form of diabetes increases with:

•age,• obesity, •and lack of physical activity.•In women with prior GDM•Individuals with hypertension or

dyslipidemia

Gestational diabetes mellitus (GDM)

•GDM is defined as any degree of glucose intolerance with onset or first recognition during pregnancy.

•GDM complicates 4% of all pregnancies in the U.S., resulting in 135,000 cases annually

Presentation of DM

•Acute: Ketoacidosis

•Sub-acute: Weight loss, polydipsia, polyuria, lethargy, irritability, infections (candidiasis, skin infection, recurrent infections slow to clear), genital itching, blurred vision, tingling in hands/feet.

•With complications: Presentation with skin changes, peripheral neuropathy with risk of foot ulcers, amputations, nephropathy, eye disease

•Asymptomatic: DM may be detected on routine screening during well man/woman checks .

Criteria for the diagnosis of diabetes mellitus•1. Symptoms of diabetes plus casual

plasma glucose concentration ≥200 mg/dl (11.1 mmol/l).

•Casual is defined as any time of day without regard to time since last meal.

•The classic symptoms of diabetes include polyuria, polydipsia, and unexplained weight loss.

or•2. FPG ≥126 mg/dl (7.0 mmol/l).•Fasting is defined as no caloric intake for at

least 8 h.

•Or•2-h postload glucose ≥200 mg/dl (11.1

mmol/l) during an OGTT. •The test should be performed as described

by WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.

Treatment

•In some individuals with diabetes, adequate glycemic control can be achieved with weight reduction, exercise, and/or oral glucoselowering agents.

•Individuals with extensive -cell destruction and therefore no residual insulin secretion require insulin for survival.

NutritionalManagementof D M•Diets rich in monounsaturated fat reduce

total and low-density lipoprotein cholesterol without adverse effects on high- density lipoprotein cholesterol or triglyceride levels

•a range of carbohydrate (45–60%) and fat (25–35%) intakes is compatible with good diabetes control provided that low glycaemic index carbohydrates and foods high in monounsaturated fat are promoted.

•monounsaturated fatty acids should provide between 10 and 20% total energy

Glycemic index of certain food items

•Low GI: Pasta, Basmati rice, wholegrain products, porridge, oat-based cereal bars, lentils and pulses including baked beans, and kidney beans

•High GI: Corn Flakes, Rice Krispies, sugared cereals, white bread, rice (other than Basmati), potatoes, fruit juice, bananas, honey sandwich

•for those people with Type 1 diabetes, especially

• in those with hypertension, intakes of protein should not exceed 10–20% total energy because of the increased risk of nephropathy

•It is recommended that a diet rich in foods which naturally contain significant quantities of antioxidants, especially fruit and vegetables, is followed

•The normal protein requirements are:• . 2 g/kg per day in early infancy•. 1 g/kg per day for a 10-year-old•. 0.8 g/kg in later adolescence towards

adulthood

Nutritional recommendations for childhood and adolescent Type 1 diabetes

•Total daily energy intake should be distributed as follows:

• (i) Carbohydrate >50%•mainly as complex higher fibre carbohydrate•moderate sucrose intake• (ii) Fat 30–35%•Mainly monounsaturated fat• (iii) Protein 10–15% (decreasing with age)•Fruit and vegetables (recommend five

portions per day)