Nutritional Disease: When Nutrient Balance Affects Body Function

Multiple choice

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Short Answer Model Answers

SA1 (4 marks): Normal role: iodine is an essential structural component of thyroid hormones T3 and T4, synthesised by the thyroid by incorporating iodine into thyroglobulin [1]. When iodine is deficient: insufficient iodine → thyroid cannot synthesise adequate T3/T4 → blood thyroid hormone falls → the anterior pituitary detects this via negative feedback (T3/T4 normally suppresses TSH) → releases increased TSH [1]. Why TSH causes goitre: elevated TSH stimulates thyroid follicular cell proliferation (more cells) and hypertrophy (larger cells) → the gland enlarges → visible goitre [1]. Why it cannot restore T3/T4: hormone synthesis requires iodine as a substrate; if dietary iodine remains insufficient, the enlarged thyroid still cannot produce adequate T3/T4 regardless of size or TSH stimulation, the substrate limitation cannot be overcome by increased cellular activity [1].

SA2 (5 marks): Step 1, dietary: chronic excess saturated fat is transported to the liver, stimulating increased synthesis and secretion of LDL → raised blood LDL [1]. Step 2, infiltration: elevated LDL infiltrates the sub-endothelial intima, particularly at sites of endothelial injury, where it is oxidised by reactive oxygen species [1]. Step 3, inflammatory plaque: oxidised LDL triggers recruitment of monocytes that become macrophages and engulf oxidised LDL via scavenger receptors → lipid-laden foam cells accumulate as a fatty streak → fibrous atherosclerotic plaque [1]. Step 4, obstruction: over years the plaque narrows the arterial lumen → reduced coronary blood flow → angina under increased demand [1]. Step 5, acute event: the fibrous cap ruptures, exposing the lipid core → platelets aggregate and the coagulation cascade activates → thrombus forms → complete coronary occlusion → downstream myocardium is deprived of oxygen and dies → myocardial infarction [1].

SA3 (6 marks): (a) Deficiency diseases result from absence of an essential biochemical component, the nutrient performs an irreplaceable function (collagen cofactor, oxygen carrier, hormone precursor) and its removal directly prevents that function. Excess diseases result from chronic metabolic overload, pathways that work normally at physiological levels are overwhelmed by sustained excess, producing cumulative damage (insulin resistance from chronic hyperinsulinaemia; vascular damage from elevated LDL/glucose) [1.5]. (b) Micronutrient stores are limited, vitamin C stores deplete within 2–3 months, after which collagen synthesis fails body-wide; excess diseases require years to decades of cumulative damage before symptoms appear (atherosclerosis begins in early adulthood but heart attacks occur at 50–70). The body has no way to 'store excess' safely; damage accumulates silently [1.5]. (c) Epidemiological transition: vaccines, antibiotics, sanitation and the end of famine controlled deficiency disease, while the industrialised food supply made calorie-dense, nutrient-poor, processed food cheap and ubiquitous, and sedentary lifestyles replaced active ones [1.5]. (d) Deficiency diseases are highly amenable to individual prevention, supplementation, dietary change or fortification (iodised salt) reliably prevents them by supplying the missing nutrient. Excess diseases are harder, they require sustained behavioural change across decades, involve genetic predispositions beyond individual control, and are powerfully shaped by the food environment and socioeconomic factors; population-level structural interventions (labelling, sugar taxes, urban design) are needed alongside individual change [1.5].