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Questions on diet, energy and how to read a health claim
Energy balance, basal metabolic rate and what sets it; the energy value of carbohydrate, protein, fat and alcohol; what a balanced diet must supply, including essential amino acids, essential fatty acids, vitamins, minerals and fibre; BMI and its limits; cohort, case-control and randomised designs and what each can show; confounding, reverse causation and measurement error in dietary studies; relative and absolute risk; how to check a health headline against the study behind it; and how to weigh two studies whose results conflict.
20 original questions · 73 marks · the diet, energy and how to read a health claim notes · Nutrition, digestion and health evidence
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The table gives the results of a randomised controlled trial of a dietary supplement, constructed for this question rather than measured. Discuss what this trial does establish about the supplement, and what it does not.
Group Number of participants Number with a cardiovascular event in five years Percentage with an event Given the supplement 5000 200 4.0 Given a placebo 5000 250 5.0 Mark scheme
- B1 the participants were allocated by chance, so the two groups tend to be balanced on every variable including the ones nobody thought to measure, and the difference between them can be attributed to the supplement rather than to the kind of person who chooses to take one
- B1 the comparison group took a placebo, so participants and investigators can be blinded and the difference cannot be put down to expectation or to the treated group changing other habits once they knew
- B1 the effect is 200 events in 5000 against 250 in 5000, a relative risk of 4.0 ÷ 5.0 = 0.80, so a fifth fewer events in the treated group
- B1 in absolute terms that is a fall of 1.0 percentage point, so about 100 people would have to take the supplement for five years for one event to be avoided
- B1 it does not establish that the result applies to everyone: the participants volunteered and are not a random sample of the population, and five years is short against a disease that takes decades to develop, so the trial cannot say whether the benefit persists, grows or fades over a lifetime
- B1 it does not establish a net benefit, because the table records one outcome only: adverse effects and death from any cause are not shown, and a supplement that lowers one disease while raising another has not been shown to help
The table describes two studies of daily salt intake and stroke, constructed for this question rather than measured. A website quotes Study P as evidence that salt does not raise the risk of stroke. Evaluate the two studies and the website's claim.
Feature Study P Study Q Design Cross-sectional survey Cohort study Participants 800 volunteers recruited at a gym 24,000 adults from general practice lists How salt intake was measured Questionnaire on one occasion Sodium in 24-hour urine samples, twice Adjusted for Age and sex Age, sex, smoking, body mass index and alcohol Funded by A manufacturer of salted snacks A national research council Result No association between salt intake and stroke Relative risk of stroke 1.3 in the highest salt group against the lowest Mark scheme
- B1 Study P is cross-sectional, measuring salt and stroke at one moment, so it cannot show which came first; Study Q measured intake before strokes occurred
- B1 Study P is small and its gym volunteers are not representative: they are likely to be fitter and healthier, with few strokes, so a real effect could be missed; Study Q's larger sample from practice lists represents the population better and gives a more precise estimate
- B1 salt intake recalled once by questionnaire is measured with much more error than sodium in repeated 24-hour urine samples, and error in the exposure tends to hide an association
- B1 Study Q adjusted for more confounders, so its association is harder to explain by smoking, body mass or alcohol, although residual confounding remains possible in any observational study
- B1 Study P was funded by a company with an interest in the result, which does not make it wrong but is a reason to check its design and analysis closely
- B1 judgement: the website's claim is not supported. Study Q carries more weight and suggests that higher salt intake is associated with a higher risk of stroke; a finding of no association in a small, unrepresentative study does not show that there is no effect
A cross-sectional survey of 40 000 adults reports that those taking a vitamin supplement have a 12 per cent lower rate of heart disease than those who do not. A newspaper concludes that the supplement protects the heart. Evaluate that conclusion.
Mark scheme
- B1 in support: the sample is large, so random error is small and the association is unlikely to have arisen by chance alone
- B1 in support: an association of this kind is a reasonable hypothesis to generate, and it can be tested directly by a design that settles the question
- B1 against: the design is cross-sectional, measuring a population at one moment, so it cannot say which came first. People already diagnosed may have started or stopped taking supplements because of the diagnosis
- B1 against: nobody allocated the supplement, so the two groups differ in many ways at once; people who take supplements tend to smoke less, exercise more and earn more, and a prevalence ratio of 0.88 is close enough to 1 to be produced by residual confounding alone
- B1 judgement: the conclusion is not supported by this study, which reports an association as though it were a cause; what would settle it is a randomised controlled trial of the supplement against a placebo, since randomisation balances the confounders nobody measured
In a population, 4 people in every 100 develop a particular cancer during their lifetime. A cohort study reports a relative risk of 1.25 for that cancer in people with a high intake of one food. Calculate the absolute lifetime risk for those people, calculate the increase in absolute risk in percentage points, and calculate how many people would have to eat that way for one extra case to arise.
Mark scheme
- M1 the absolute risk in the exposed group is the baseline absolute risk multiplied by the relative risk
- A1 4.0 × 1.25 = 5.0 per cent, so about 5 people in every 100 rather than 4
- M1 the increase in absolute risk is 5.0 − 4.0 = 1.0 percentage point, and the number needed for one extra case is one divided by that increase
- A1 1 ÷ 0.010 = 100 people
Compare a cohort study with a case-control study, referring to who is recruited, what measure each produces, and the main weakness of each.
Mark scheme
- B1 a cohort recruits people who are free of the disease and follows them forward in time, whereas a case-control starts with people who already have the disease and compares them with matched people who do not
- B1 a cohort records exposure before the disease appears, so the time order is right by construction, whereas a case-control asks both groups about past exposure and cannot establish which came first
- B1 a cohort gives incidence and a relative risk, whereas a case-control gives an odds ratio, because the investigator chose how many cases and controls to recruit and so cannot know the risk in either group
- B1 a cohort needs very large numbers and many years and is still open to confounding, whereas a case-control is quick and efficient for a rare disease but is open to recall bias and to unfair choice of controls
A cohort study finds that adults who reported eating the least fruit were later diagnosed with cancer more often than those who reported eating the most. Suggest two explanations for this association other than a protective effect of fruit, and suggest for each what the investigators could do to test it.
Mark scheme
- B1 confounding: people who eat more fruit also tend to smoke less, exercise more and be wealthier, and each of those affects cancer risk independently
- B1 that could be tested by adjusting for cigarettes smoked per day rather than for smoking as a yes-or-no variable, and by repeating the analysis in people who have never smoked
- B1 reverse causation: undiagnosed disease changes appetite and diet years before a diagnosis, so people who were already ill may have eaten less fruit because of the illness rather than the other way round
- B1 that could be tested by discarding the first few years of follow-up and re-running the analysis; if the association survives, reverse causation is a weaker explanation
A woman has a basal metabolic rate of 6.8 MJ per day and a physical activity level of 1.5, so her total daily energy expenditure is her basal metabolic rate multiplied by that figure. She takes in 2800 kcal per day. Taking 1 kcal as 4.184 kJ and adipose tissue as storing 29 MJ per kilogram, calculate her daily energy surplus and calculate the mass she would gain over 30 days if nothing else changed.
Mark scheme
- M1 total energy expenditure = basal metabolic rate × physical activity level = 6.8 × 1.5 = 10.2 MJ per day
- M1 energy taken in = 2800 × 4.184 = 11 715 kJ per day, which is 11.7 MJ per day
- A1 surplus = 11.7 − 10.2 = 1.5 MJ per day
- A1 over 30 days that is 45 MJ, and 45 ÷ 29 = 1.6 kg gained; the real gain would be smaller, because expenditure rises as mass rises
The table gives what one adult's food supplied in a day against the reference intake for that person, constructed for this question rather than measured. Identify the components that fall short, give a named consequence of each shortfall, and identify one reason this person could be called malnourished although the diet supplies enough energy.
Component Supplied in the day's food Reference intake Energy 9.6 MJ 9.5 MJ Protein 58 g 52 g Iron 5 mg 15 mg Vitamin C 8 mg 40 mg Calcium 760 mg 700 mg Fibre 12 g 30 g Mark scheme
- B1 iron, at 5 mg against a reference intake of 15 mg: iron is needed for the haem group of haemoglobin, so a shortfall causes anaemia and less oxygen is carried
- B1 vitamin C, at 8 mg against 40 mg: vitamin C is needed to hydroxylate proline in collagen, and unhydroxylated collagen cannot form a stable triple helix, which is scurvy
- B1 fibre, at 12 g against 30 g: fibre is the bulk the large intestine works on, so a shortfall causes constipation and is associated with a higher risk of bowel disease
- B1 malnutrition means any mismatch between what a diet supplies and what the body needs, in either direction, so a person taking in enough energy and protein while short of three other components is malnourished
A woman has a mass of 68 kg and a height of 1.65 m. Calculate her body mass index to three significant figures, and calculate how many kilograms she would need to lose to bring her body mass index down to exactly 24.0 kg m⁻², assuming her height stays the same.
Mark scheme
- M1 BMI = mass ÷ height², so height² = 1.65² = 2.7225 m²
- A1 BMI = 68 ÷ 2.7225 = 25.0 kg m⁻², to three significant figures
- M1 mass at BMI 24.0 = 24.0 × 2.7225 = 65.34 kg
- A1 mass to lose = 68 − 65.34 = 2.7 kg, to two significant figures
Using a reference intake of 0.75 g of protein per kilogram of body mass per day, calculate the daily protein requirement of a 58 kg adult, and calculate what percentage of a diet supplying 1900 kcal per day that protein requirement represents, taking the energy value of protein as 17 kJ per gram and 1 kcal as 4.184 kJ.
Mark scheme
- B1 protein requirement = 0.75 × 58 = 43.5 g per day
- M1 energy from that protein = 43.5 × 17 = 739.5 kJ per day; total diet energy = 1900 × 4.184 = 7949.6 kJ per day
- M1 percentage = 739.5 ÷ 7949.6 × 100
- A1 9.3 per cent, to two significant figures
Explain what is meant by the 'healthy-user effect', and explain why it makes a small relative risk from an observational dietary study hard to interpret.
Mark scheme
- B1 people who choose to adopt one healthy behaviour, such as eating more wholegrain food, also tend to smoke less, exercise more, be wealthier and see a doctor sooner, and this whole bundle of associated behaviours is the healthy-user effect
- B1 because all of these differences travel together, a study comparing people who do and do not eat wholegrain food is really comparing two different kinds of people in many ways at once, not just in their wholegrain intake
- B1 adjusting statistically for one or two of these factors, such as smoking status, cannot remove the effect of all the others, especially ones that were never measured at all
- B1 a relative risk close to 1, such as 1.1 or 1.2, is small enough that this leftover, unmeasured confounding could produce it on its own, so such a finding cannot safely be read as evidence that the food itself is protective
An essential amino acid is one the body cannot make, so it must be supplied in the diet. The protein in maize contains very little of the essential amino acids lysine and tryptophan. Explain why a person whose only source of protein is maize may be unable to make enough of some of their own proteins, even when they eat plenty of maize.
Mark scheme
- B1 each protein has a fixed primary structure coded by its gene, so it can be made only if every amino acid in its sequence is available, including lysine and tryptophan
- B1 the body cannot make lysine or tryptophan, so when the small dietary supply runs out, synthesis of any protein containing them stops at that point
- B1 the amount of these proteins made is therefore limited by the essential amino acid in shortest supply, however much of the other amino acids is eaten
An essential amino acid is one the body cannot make, so it must be supplied in the diet; a non-essential amino acid can be made in the body from other molecules. Explain why calling an amino acid 'essential' does not mean that it matters more to the body than a 'non-essential' one.
Mark scheme
- B1 a protein's primary structure is fixed by its gene, so to make it the cell needs every amino acid in the sequence, whichever kind it is
- B1 if any amino acid, essential or not, is unavailable when it is needed, the polypeptide cannot be completed, so a non-essential one is just as necessary to the proteins that contain it
- B1 the term therefore describes where the amino acid comes from, the diet or the body's own synthesis, and not how important it is
Dietary intake in large cohort studies is often recorded using a food frequency questionnaire, and adults are known to under-report their energy intake by roughly a fifth to a third compared with objective measurements, and the shortfall is larger in people with a higher body mass. Suggest why this kind of error is more damaging to a study's conclusions than random error of the same average size.
Mark scheme
- B1 the size of the under-reporting is related to a person's body mass, so it is not the same for everyone: it does not simply add noise that averages out across the study
- B1 this kind of error is a bias, meaning it pushes results in a particular direction rather than scattering them randomly around the true value
- B1 a study that adjusts for reported energy intake, or that compares groups by what they report eating, can therefore reach a systematically wrong conclusion in a specific direction, even with a very large sample size, since a bigger sample only reduces random error and does nothing to a bias present in every participant
In 2015 the International Agency for Research on Cancer placed processed meat in Group 1, 'carcinogenic to humans', the group that also holds tobacco smoking. Explain why this classification does not mean that eating processed meat is as dangerous as smoking.
Mark scheme
- B1 the classification is a statement about the strength of the evidence that a substance causes cancer in humans at all, not about the size of the risk it causes
- B1 both processed meat and tobacco smoke were judged to have sufficient evidence of causing cancer, which is why they share the same category
- B1 the size of the risk each carries differs enormously, by more than a factor of ten
Cohort studies found that people with more beta-carotene in their diet or blood developed lung cancer less often. Randomised trials that gave smokers beta-carotene supplements found more lung cancer in the supplemented groups than in the placebo groups. Explain why the trials are given more weight on the question of cause, and explain how both findings can be correct.
Mark scheme
- B1 the trials allocated the supplement at random, so the groups were balanced on confounders, including ones nobody measured, and confounding is very unlikely to explain their result
- B1 in the cohorts, people eating more vegetables also tend to smoke less, earn more and live more healthily, so beta-carotene may have been a marker of a healthier life rather than the cause of lower risk
- B1 the studies tested different exposures: a diet rich in vegetables can go with lower risk while high-dose supplements given to smokers do not protect them
In an investigation of the vitamin C content of apple juice, 1.0 cm³ of DCPIP solution was decolourised by a mean of 0.60 cm³ of a vitamin C standard containing 1.0 mg cm⁻³, and by a mean of 2.40 cm³ of apple juice; the results are invented for this question. Calculate the vitamin C content of the apple juice in mg per 100 cm³.
Mark scheme
- M1 mass of vitamin C that decolourises 1.0 cm³ of DCPIP = 0.60 × 1.0 = 0.60 mg
- M1 concentration in the juice = 0.60 ÷ 2.40 = 0.25 mg cm⁻³
- A1 25 mg per 100 cm³
State the conditions under which basal metabolic rate is measured, and state what a person's basal metabolic rate mostly depends on.
Mark scheme
- B1 at complete rest, awake, at a comfortable temperature and twelve hours or more after a meal
- B1 lean body mass: muscle, liver, kidney and brain are metabolically expensive tissues while adipose tissue is cheap
Explain why publication bias can make a dietary supplement appear more effective than it is.
Mark scheme
- B1 studies that find a positive or striking effect are more likely to be published than studies that find no effect
- B1 so the published studies, and any review or meta-analysis built only from them, overstate the average effect of the supplement
A student used DCPIP to measure the vitamin C content of a fruit juice. Suggest one reason why the value obtained might be higher than the true vitamin C content of the juice, and one reason why it might be lower.
Mark scheme
- B1 higher: other reducing substances in the juice also decolourise DCPIP, so less juice is needed to reach the end point
- B1 lower: vitamin C in the juice was oxidised by air, warmth or light before it was tested; or the colour of the juice hid the end point so too much juice was added
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