Nutrition and malnutrition
Balanced Diet, Energy Metabolism, Malnutrition (Marasmus, Kwashiorkor) and Obesity
Energy values of food, BMR, balanced diet, essential fatty acids, fibre, marasmus versus kwashiorkor, WHO care of severe malnutrition, and obesity. It also covers BMI cut-offs for South Asians, appetite control and how to tell Cushing syndrome from simple obesity.
Energy from food
| Nutrient | Energy |
|---|---|
| Carbohydrate | 4 kcal/g (17 kJ) |
| Protein | 4 kcal/g (17 kJ) |
| Fat | 9 kcal/g (37 kJ) |
| Alcohol | 7 kcal/g (29 kJ) |
- Fat yields more than twice as much energy per gram because its carbons are more reduced (less oxygen) than those of carbohydrate. Complete oxidation of one palmitate (C16) gives about 106 ATP (129 by older counting), against about 30–32 ATP from one glucose.
- Total energy expenditure = basal metabolic rate (60–70%) + physical activity (most variable) + thermic effect of food (about 10%; highest for protein).
- Typical adult needs: man about 2,500 kcal/day, woman about 2,000; pregnancy adds about 300 kcal/day in later trimesters and lactation about 500.
Basal metabolic rate
- BMR is the energy used at complete rest, awake, fasting and at comfortable temperature, mainly by liver, brain, heart, kidney and muscle. It is set chiefly by thyroid hormone, which increases Na⁺/K⁺-ATPase activity and mitochondrial oxygen use.
| Increases BMR | Decreases BMR |
|---|---|
| Hyperthyroidism (most marked) | Hypothyroidism, hypopituitarism |
| Fever (about 10–13% per °C) | Starvation and malnutrition |
| Catecholamines, sympathetic activity | Old age |
| Growth (children), pregnancy | Sleep |
| Male sex, larger lean body mass | Female sex, higher fat proportion |
| Cold exposure, burns, sepsis | Anaesthesia |
Remember Thyroid hormone is the main long-term setter of BMR; fever and catecholamines raise it acutely.
A balanced diet
| Nutrient | Share of energy |
|---|---|
| Carbohydrate | About 50–60%, mainly complex; free sugars under 10% (ideally under 5%) |
| Fat | About 20–35% (WHO advises under 30%); saturated under 10%; trans fat minimal |
| Protein | About 10–15%; about 0.8 g/kg/day for adults, more in children, pregnancy and illness |
- Salt under 5 g/day; at least five portions (400 g) of fruit and vegetables a day.
- Essential amino acids (cannot be made): phenylalanine, valine, threonine, tryptophan, isoleucine, methionine, histidine, leucine, lysine; arginine is semi-essential in children. Tyrosine becomes essential in PKU.
- Protein quality: egg protein is the reference (biological value about 100). Cereals lack lysine and pulses lack methionine, so eating them together (complementation) gives complete protein.
- Glycaemic index compares the blood glucose rise from a food with that from pure glucose.
Essential fatty acids
- Humans cannot insert double bonds beyond carbon 9, so linoleic acid (omega-6) and α-linolenic acid (omega-3) must come from the diet. Arachidonic acid becomes essential only if linoleic acid is lacking.
- Linoleic acid leads to arachidonic acid (prostaglandins, leukotrienes); α-linolenic acid leads to EPA and DHA (brain and retina).
- Rich sources: vegetable seed oils (sunflower, corn, soybean) for omega-6; fish oils and flaxseed for omega-3. Coconut oil is mostly saturated and contains the least essential fatty acid.
- Deficiency (long fat-free TPN): scaly dermatitis, hair loss, poor wound healing, growth failure.
Dietary fibre
- Non-starch polysaccharides that human enzymes cannot digest; aim for about 25–30 g/day.
| Type | Sources | Main benefit |
|---|---|---|
| Soluble (pectin, gums, β-glucan) | Oats, pulses, fruit | Forms a gel: slows glucose absorption and lowers LDL by binding bile acids |
| Insoluble (cellulose, lignin) | Wheat bran, whole grains, vegetables | Adds bulk, speeds transit, prevents constipation and diverticular disease |
- Colonic bacteria ferment fibre to short-chain fatty acids (butyrate feeds colonocytes). Excess bran adds phytate, which reduces mineral absorption.
Protein-energy malnutrition
| Feature | Marasmus | Kwashiorkor |
|---|---|---|
| Main deficit | Energy (and protein) | Protein, with infection and oxidative stress |
| Typical age | Under 1 year | 1–3 years, after weaning |
| Oedema | Absent | Present (hallmark; low albumin) |
| Weight | Severe wasting, under 60% expected | 60–80% (masked by oedema) |
| Look | Wizened old-man face, alert, hungry | Moon face, apathetic, irritable, anorexic |
| Skin and hair | Thin, loose skin | Flaky-paint dermatosis, sparse depigmented hair (flag sign) |
| Liver | Normal | Enlarged fatty liver (apolipoprotein synthesis fails) |
- Marasmic kwashiorkor combines both.
- WHO severe acute malnutrition (6–59 months): weight-for-height below −3 Z, MUAC under 115 mm, or bilateral pitting oedema.
- Stunting (low height-for-age) means chronic malnutrition; wasting (low weight-for-height) means acute; underweight (low weight-for-age) mixes both.
- Nutritional assessment uses anthropometry, growth charts, clinical signs, dietary recall and proteins: albumin (half-life about 20 days) reflects long-term status, prealbumin (transthyretin) about 2 days reflects acute change.
Exam trap Oedema separates kwashiorkor from marasmus; weight alone can mislead because fluid hides the wasting.
Managing severe acute malnutrition
- The child's physiology is reductive: low metabolic rate, weak heart, sodium-loaded cells, depleted potassium, and infection without fever. Overloading with fluid, sodium, protein or iron is dangerous.
- Stabilisation phase (days 1–7): treat or prevent hypoglycaemia, hypothermia and dehydration (oral ReSoMal, low in sodium, high in potassium; IV only for shock), correct electrolytes (potassium, magnesium), give broad-spectrum antibiotics to all, correct micronutrients but withhold iron, and start cautious feeding with F-75 (75 kcal/100 mL, low protein) in small frequent feeds, every 2–3 hours day and night.
- Rehabilitation phase: switch to F-100 or ready-to-use therapeutic food for catch-up growth; start iron now; sensory stimulation and follow-up.
- Refeeding syndrome: when feeding restarts, insulin drives phosphate, potassium and magnesium into cells, causing hypophosphataemia, arrhythmia, heart failure and Wernicke encephalopathy. Start slowly and give thiamine first.
Obesity
- BMI = weight (kg) ÷ height² (m²). WHO: underweight under 18.5; normal 18.5–24.9; overweight 25–29.9; obese 30 or more; class III 40 or more. Asian cut-offs are lower because cardiometabolic risk rises at lower BMI: the Asia-Pacific classification used in South Asian guidelines calls 23–24.9 overweight and 25 or more obese (WHO public-health action points are 23 and 27.5).
- Worked example: 81 kg and 1.80 m gives 81 ÷ 3.24 = BMI 25: overweight by the international scale but obese by Asian cut-offs.
- Central obesity predicts risk better than BMI: waist over about 90 cm (men) or 80 cm (women) in South Asians; waist-to-hip ratio.
- Appetite control: the lateral hypothalamus is the feeding centre and the ventromedial nucleus the satiety centre; a ventromedial lesion causes overeating and obesity. Leptin from fat cells reduces appetite (obese people are leptin resistant); ghrelin from the stomach increases it.
- Complications: type 2 diabetes, hypertension, dyslipidaemia, coronary disease, stroke, obstructive sleep apnoea, osteoarthritis, fatty liver, gallstones, PCOS, varicose veins, cancers (endometrial, breast, colon, kidney, oesophageal adenocarcinoma), depression.
- Secondary causes: hypothyroidism, Cushing syndrome, drugs (antipsychotics, insulin, sulphonylureas, steroids, valproate), hypothalamic lesions, Prader–Willi syndrome.
- Cushing syndrome versus simple obesity: features favouring Cushing are wide purple striae, proximal muscle weakness, easy bruising, thin skin and osteoporosis; central fat and plain striae occur in both. Screen with the overnight dexamethasone suppression test or 24-hour urinary free cortisol.
- Management: diet and activity; drugs (orlistat, a lipase inhibitor; GLP-1 receptor agonists such as semaglutide; tirzepatide); bariatric surgery for BMI 40 or more, or 35 or more with comorbidity (lower thresholds for Asians).
How FCPS asks about this
- Energy per gram: fat 9 kcal, alcohol 7 kcal, carbohydrate and protein 4 kcal; palmitate yields about 106 ATP.
- Factor that increases BMR: hyperthyroidism (thyroid hormone is the main regulator); fever and pregnancy also raise it.
- Essential fatty acids: linoleic and α-linolenic acid; coconut oil has the least.
- Benefit of soluble fibre in oats and pulses: lowers LDL and slows glucose absorption.
- Feature separating kwashiorkor from marasmus: oedema (also fatty liver, flaky-paint skin).
- Feed in the stabilisation phase of complicated SAM: F-75 in small frequent feeds; iron withheld until rehabilitation.
- Feature suggesting Cushing syndrome rather than simple obesity: purple striae, proximal myopathy, easy bruising.
Test yourself on this topic
5 of the 21 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A severely malnourished patient starts nasogastric feeding at full calories. On day 2 he becomes confused and breathless with heart failure. Which electrolyte abnormality is most characteristic?
Answer: Hypophosphataemia
Refeeding syndrome: after starvation, carbohydrate intake triggers insulin release, driving phosphate, potassium and magnesium into cells for glycogen and protein synthesis and ATP production. Serum phosphate falls sharply (the hallmark), with hypokalaemia, hypomagnesaemia, thiamine deficiency (Wernicke) and fluid retention. Results: weakness, respiratory failure, arrhythmias, heart failure, confusion. Prevention: identify at-risk patients, start feeding slowly (about 10 kcal/kg/day), give thiamine before feeding, and monitor and replace electrolytes.
Refeeding syndrome
- Insulin drives phosphate, K⁺, Mg²⁺ into cells
- Hallmark: hypophosphataemia
- Also thiamine deficiency, fluid retention
- Start slow, thiamine first, monitor
Remember Feed slowly, the phosphate falls quickly.
Why the other options are wrong
- Hypernatraemia Sodium and fluid retention occur, but phosphate is the hallmark.
- Hypercalcaemia Not typical.
- Hyperkalaemia Potassium falls.
- Hypermagnesaemia Magnesium falls.
A 2-year-old weaned onto a starchy diet has pitting oedema, a distended abdomen with an enlarged fatty liver, flaky skin and sparse pale hair. What is the diagnosis?
Answer: Kwashiorkor
Kwashiorkor is protein deficiency with relatively adequate calories: low albumin causes oedema; apoprotein deficiency stops fat leaving the liver, causing fatty enlargement; skin shows 'flaky paint' dermatosis and hair becomes sparse and discoloured (flag sign); children are apathetic. Marasmus is overall energy deficiency: severe wasting of muscle and fat, 'old man' face, no oedema, albumin near normal. Both may coexist (marasmic kwashiorkor).
Kwashiorkor vs marasmus
- Kwashiorkor: protein lack → oedema, fatty liver, flaky skin, flag sign
- Marasmus: calorie lack → wasting, no oedema
- Mixed: marasmic kwashiorkor
Remember Kwashiorkor is puffy; marasmus is skinny.
Why the other options are wrong
- Marasmus Severe wasting without oedema.
- Rickets Vitamin D deficiency.
- Coeliac disease Gluten enteropathy; no flaky-paint skin.
- Nephrotic syndrome Oedema from protein loss in urine, no skin and hair changes.
A child with hyperphagia, obesity, hypotonia and hypogonadism has a deletion on the paternal chromosome 15q11–13. What is the diagnosis?
Answer: Prader–Willi syndrome
Genomic imprinting: the same 15q11–13 region gives different syndromes depending on which parent's copy is lost. Prader–Willi: paternal deletion or maternal uniparental disomy (hyperphagia, obesity, hypotonia, hypogonadism, learning disability). Angelman: maternal deletion or paternal disomy (happy puppet, seizures, ataxia, inappropriate laughter).
Imprinting
- Prader–Willi: Paternal deletion (P–P)
- Angelman: Maternal deletion (M–A)
- Also uniparental disomy of the other parent
Remember Prader–Willi = Paternal; Angelman = Mum.
Why the other options are wrong
- Angelman syndrome Maternal deletion; laughter, seizures.
- Fragile X syndrome CGG repeat, macro-orchidism.
- Turner syndrome 45,XO female.
- Klinefelter syndrome 47,XXY male.
Complete oxidation of one molecule of palmitate (C16) yields approximately how many ATP?
Answer: About 106 ATP
Palmitate: 7 cycles of β-oxidation give 7 FADH₂ and 7 NADH, and 8 acetyl-CoA (each about 10 ATP via the TCA cycle). Total about 108 ATP, minus 2 ATP for activation (palmitoyl-CoA) = about 106. This explains why fat yields about 9 kcal/g versus 4 kcal/g for carbohydrate.
Palmitate yield
- 7 β-oxidation cycles, 8 acetyl-CoA
- ≈ 106 ATP (after 2 for activation)
- Fat 9 kcal/g vs carbohydrate 4 kcal/g
Remember Palmitate pays over a hundred.
Why the other options are wrong
- About 32 ATP Glucose.
- About 2 ATP Anaerobic glycolysis.
- About 38 ATP Older glucose figure.
- About 12 ATP One acetyl-CoA plus a little.
Which dietary fat most raises plasma LDL cholesterol?
Answer: Saturated and trans fats
Saturated fats (animal fat, ghee, palm and coconut oil) and trans fats (partially hydrogenated vanaspati) raise LDL; trans fats also lower HDL. Replacing them with monounsaturated (olive, canola) and polyunsaturated fats lowers LDL. Omega-3 fats (fish oil) lower triglycerides.
Dietary fats
- ↑LDL: saturated, trans (ghee, vanaspati)
- Trans also ↓HDL
- Omega-3: ↓triglycerides
Remember Ghee and vanaspati raise LDL.
Why the other options are wrong
- Monounsaturated fats Lower LDL.
- Polyunsaturated omega-3 fats Lower triglycerides.
- Polyunsaturated omega-6 fats Lower LDL.
- Medium-chain triglycerides only Not the main LDL raiser.
Where this sits in the CPSP syllabus
- Paper 1: Nutrition, vitamins and minerals, Balanced diet, energy, protein-energy malnutrition and obesity
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