Investigate the causes and effects of named nutritional and environmental diseases, including diabetes (type 2), cardiovascular disease and mesothelioma

What this dot point is asking

NESA wants you to describe the causes, mechanisms and effects of named nutritional and environmental diseases. Type 2 diabetes, cardiovascular disease and mesothelioma cover the three main categories: metabolic-nutritional, lifestyle-related and toxic environmental exposure.

The answer

Type 2 diabetes mellitus

Burden. Approximately 1.3 million Australians have type 2 diabetes (T2DM); around 5 percent of adults. The number is rising with obesity rates.

Causes.

• Genetic. Family history doubles risk. Susceptibility variants in TCF7L2, KCNQ1 and others.
• Lifestyle. Obesity (BMI over 30), sedentary behaviour, energy-dense diets high in refined carbohydrates and saturated fats.
• Demographic. Age over 45, certain ancestries (Indigenous Australian, South Asian, Pacific Islander).
• Gestational diabetes. History increases lifetime risk.

Mechanism. Insulin normally binds receptors on muscle, liver and fat cells, triggering glucose uptake via GLUT4 transporters. In T2DM, intracellular fat metabolites and inflammatory signalling impair insulin receptor signalling, producing insulin resistance. Beta cells compensate by hypersecreting insulin; over years they exhaust, glucose rises, and diabetes appears.

Effects. Chronic hyperglycaemia non-enzymatically glycates proteins, damaging blood vessel walls.

• Microvascular. Retinopathy, nephropathy, peripheral neuropathy.
• Macrovascular. Heart attack, stroke, peripheral vascular disease.
• Other. Foot ulcers and amputation, recurrent infection, NAFLD, dementia risk.

Cardiovascular disease

Burden. Cardiovascular disease (CVD) is the leading cause of death in Australia, killing approximately 42 000 people each year. It includes coronary heart disease, stroke, heart failure and peripheral vascular disease.

Causes (risk factors).

• Modifiable. Smoking, hypertension, dyslipidaemia (high LDL, low HDL), diabetes, obesity, sedentary behaviour, poor diet, excess alcohol, chronic stress.
• Non-modifiable. Age, male sex, family history, certain ancestries.

Mechanism: atherosclerosis.

1. Endothelial injury. LDL cholesterol, hypertension, smoking and high glucose damage the arterial endothelium.
2. LDL infiltration. LDL enters the intima and is oxidised.
3. Foam cell formation. Macrophages engulf oxidised LDL, becoming foam cells.
4. Plaque growth. Smooth muscle cells migrate and proliferate. A fibrous cap forms over a lipid-rich necrotic core.
5. Stenosis or rupture. Plaques narrow the artery, reducing blood flow (angina). Rupture exposes the necrotic core to blood, triggering thrombosis. A coronary thrombus causes myocardial infarction (heart attack); a cerebral thrombus causes ischaemic stroke.

Effects.

• Angina pectoris. Chest pain on exertion due to coronary artery narrowing.
• Myocardial infarction. Death of cardiac muscle from sustained ischaemia.
• Heart failure. Loss of cardiac output capacity after infarction.
• Stroke. Loss of brain function from cerebral artery occlusion.

Management.

• Lifestyle. Smoking cessation, dietary change (Mediterranean, DASH), exercise, weight loss.
• Pharmaceutical. Statins (lower LDL), antihypertensives (ACE inhibitors, beta blockers), antiplatelets (aspirin, clopidogrel), anticoagulants in selected cases.
• Procedural. Coronary angioplasty with stenting, coronary artery bypass grafting (CABG), valve replacement.

Mesothelioma

Burden. Australia has one of the highest mesothelioma incidence rates in the world (around 700 to 800 cases per year), driven by extensive historical asbestos use in construction and at the Wittenoom blue asbestos mine in Western Australia (operational until 1966).

Cause. Inhalation or ingestion of asbestos fibres (chrysotile, crocidolite, amosite). Less common: erionite (a similar fibrous mineral) and high-dose radiation.

Mechanism. Detailed in the past-question answer above. Fibres lodge in the pleura, generate chronic inflammation and reactive oxygen species, and mutate tumour suppressor genes (BAP1, NF2, CDKN2A). Latency is 20 to 50 years.

Effects. Malignant pleural mesothelioma presents with chest pain, breathlessness from pleural effusion, weight loss and fatigue. The cancer is largely confined to the pleural cavity but is invasive, encasing the lung and resisting surgical removal. Peritoneal mesothelioma is less common and affects the abdominal cavity.

Management. Largely palliative. Pleurectomy and extrapleural pneumonectomy in selected patients. Chemotherapy with pemetrexed plus cisplatin. Immunotherapy (nivolumab plus ipilimumab) extends median survival modestly. Median survival from diagnosis remains under 12 months.

Prevention. Asbestos was progressively banned in Australia from 1989; total ban in 2003. Home renovators remain at risk; pre-1990 buildings should be tested before renovation.

Other nutritional and environmental diseases (worth knowing)

Iodine deficiency. Causes goitre and congenital cretinism. Reduced markedly in Australia by iodised salt and iodised baker's flour.

Folate deficiency. Causes neural tube defects in fetuses. Reduced by mandatory folate fortification of bread flour (Australia, 2009).

Vitamin D deficiency. Causes rickets in children and osteomalacia in adults. Reappearing in heavily veiled or housebound populations.

Lead poisoning. Causes neurological damage in children. Reduced by removal of lead from petrol (1986 to 2002) and house paint.

Air pollution. PM2.5 from traffic and bushfires causes COPD and ischaemic heart disease. Black Summer (2019 to 2020) bushfire smoke caused approximately 400 excess deaths in eastern Australia.

Worked example

A 55-year-old former carpenter develops chest pain and breathlessness. Chest CT shows pleural thickening and effusion. Biopsy confirms epithelioid mesothelioma. He recalls cutting asbestos cement sheeting in the 1980s without respiratory protection.

Causal analysis.

• Exposure: occupational inhalation of asbestos fibres approximately 35 years ago.
• Mechanism: fibres lodged in pleura, chronic inflammation, ROS-mediated DNA damage, tumour suppressor mutation, malignant transformation.
• Latency: consistent with the 20 to 50 year window.

Management. Pleural drainage for symptom relief, chemotherapy with pemetrexed plus cisplatin, palliative care, compensation through the Dust Diseases Tribunal.

Common traps

Saying type 2 diabetes is "caused by eating too much sugar." It is more accurately driven by chronic excess of total energy intake leading to obesity and insulin resistance. Refined carbohydrates contribute but are not the sole cause.

Confusing atherosclerosis and arteriosclerosis. Atherosclerosis is lipid plaque formation. Arteriosclerosis is general hardening of arteries.

Forgetting mesothelioma's latency. Diagnosis 30 to 50 years after a brief but high-dose exposure is typical.

Generic "lifestyle" risk factors. Markers want specific mechanisms: smoking causes endothelial damage and oxidative stress; LDL promotes foam cell formation; hypertension shears the endothelium.

In one sentence

Type 2 diabetes is a multifactorial metabolic disease driven by genetic susceptibility plus obesity and inactivity, cardiovascular disease is driven by atherosclerosis from modifiable lifestyle risk factors and dyslipidaemia, and mesothelioma is an environmentally caused cancer from inhaled asbestos fibres with decades of latency before malignant transformation.