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Diabetes (Type I
B cell destruction, absolute deficiency.
A. Autoimmune…
Diabetes
Definition
- Characterised by raised blood glucose concentration as a result of deficient or diminished effectiveness of insulin (stimulates glucose receptors and transporters)
Type I
B cell destruction, absolute deficiency.
A. Autoimmune disorder
B Idiopathic
- Largely used to target younger people, can be prolonged onset
- Often occurs with other autoimmune diseases
- Antibodies expressed against insulin
Absolute deficiency = extreme symptoms presented as a result of metabolic breakdown.
- Can't survive without exogenous insulin.
Symptoms
- Polydipsia
- Polyuria
- Weightloss (breakdown of tissue)
- Fatigue
- Repeated infections
- Blurred vision (accumulation of glucose → water → blurs lens
Diabetic Ketoacidosis
- Production of high levels of ketones (toxic acids in blood)
- Insufficient insulin = tissues starved = breakdown of fat for fuel for ketones.
Symptoms
- Headache, sleepiness, confusion, coma, seizures, diarrhoea, shortness of breath, arrhythmia, nausea, vomiting
- Insulin treatment = rapid response
Incidence
- Prominent in European
- Increasing over time
Genetic Susceptibility
- 1 parent = 2%
- Both parents = 30%
- Sibling = 8%
- HLA = 16%
- HLA Non-identical = 1%
- ICA = 75% antibodies, most likely to cause Type I.
Environmental Component
- Some environmental factors
- Children follow patterns of development similar to country of residence not country of origin
Risk
- Genetic susceptibility necessary but not sufficient
- Viruses may trigger autoimmunity
- Lack of exposure to viruses
- Altered gut microbiota
- Seasonality
- Vit D deficiency
- Accelerated early growth
Early life diet:
- Early exposure to cows milk protein
- Breast-feeding = protective
- Early intro of solids
- Overfeeding: accelerated weight gain may lead to B cell overload and failure
-
Type II
A. Predominantly insulin resistant, relative insulin deficiency.
B. Predominantly secretory deficient, variable insulin resistance
- Phenotype rather than genotype, not a single disease.
- More complex
- Beta cells never completely shut down like in Type I, explains clinical differences
Types:
- Gestational
- Genetic defects of B cell or insulin
- Diseases of exocrine pancreas
- Drugs, chemicals
- Infections
- Endocrinopathies
Early stages: adequate insulin, tissues insensitive
- Pancreas responds by secreting more insulin
- Beta cells eventually become tired
Later stages: may have impaired insulin secretion
- End stage = so exhausted, end up NEEDING insulin
Major Predisposing Factors:
- Familial predisposition
- Excess central adiposity
- Lack of physical activity
- Poor dietary patterns
Study Findings
Folsom et al
- Central adiposity = more increased risk than peripheral (more metabolically active)
Fibre
- Protective against
- Most important protective factor from a nutritional perspective
Lifestyle Factors
- Weight loss, physical activity + fibre = convincing
Insulin Deficiency:
- Decreased glucose uptake by cell, glycogenesis
- Increased glycogenolysis, gluconeogenesis, lipolysis, free fatty acids, hepatic glucose production
Criteria for Diagnosis
- Random plasma glucose > 11.ommol/L
- Fasting glucose > 7mmol/L
- Oral glucose tolerance test
- HbA1c > 50mmol/L (prediabetes =40-49)
Prediabetes
- 25% of NZ adults
- Increasing Type II
Complications
- Blindness
- Renal failure
- Myocardial infarction
- Cerebral thrombosis
- Loss of sensation, amputation
- Very COMMON causes of all these serious complications
- Metabolic syndrome: shut down of metabolism as result
Prevention
Finnish Study
- Adults had IGT (prediabetes)
- Simple lifestyle dietary changes = dramatic reduction in development of diabetes
- More compliant with changes = larger effect
Knowler et al
- Drug developed to increase insulin sensitivity
- Did reduce prevalence compared to placebo, not as much as lifestyle changes though.
- Method of treatment = much the same as prevention
Treatment
- BMI 18.5-25kg/m2
- Diet and exercise - no change if not reduction
Weight Loss Reasoning:
- Improved blood glucose
- Improved insulin secretion
- Lower blood pressure + improved lipid profile
Glycaemic Load
- Reduces glucose in 2 studies
- Glycated proteins = 7.4% reduced on low GI diet.
High Carb vs Low Carb:
- Low carb = reduced plasma glucose concentration
- As % TE from CHO increases so do glycated protein levels
- If intake at higher end of scale, emphasis on high fibre and low GI forms of CHOs
-Ideally 40g/day fibre
Fats
- High fat, low CHO = no outstanding benefits, less risky methods of treating diabetes are known.