Chapter 26 — Self-Check Quiz

20 questions. Answers with explanations at the end. Aim for 16+.

Questions

1. Which of these is in §26.1's "highly responsive to food" tier?

• a) Lp(a)
• b) Liver fat
• c) Family history
• d) Coeliac genetics

2. Which does not meaningfully respond to diet?

• a) Triglycerides
• b) Blood pressure
• c) Lp(a)
• d) HbA1c

3. §26.1b's unifying frame is that liver fat, triglycerides, glycaemia, blood pressure and weight are:

• a) Five independent conditions
• b) Five readouts of one process — ectopic and visceral fat accumulation
• c) Unrelated to each other
• d) All genetically determined

4. In DiRECT, remission at 12 months among those who lost 15 kg or more was approximately:

• a) 20%
• b) 86%
• c) 50%
• d) 7%

5. In DiRECT, remission among those losing under 5 kg was approximately:

• a) 7%
• b) 40%
• c) 60%
• d) The same as those losing 15 kg

6. Remission is more likely when:

• a) Diabetes has been present for decades
• b) Diabetes is of shorter duration, when beta-cell function is more recoverable
• c) The person is older
• d) Duration makes no difference

7. The strongest evidence for LDL-C causality comes from:

• a) Observational cohorts alone
• b) Convergence of Mendelian randomization, multiple drug classes, familial hypercholesterolaemia, and mechanistic work
• c) A single large trial
• d) Animal studies

8. Typical LDL-C reduction from a full "portfolio" dietary approach, versus a moderate statin:

• a) 50% versus 10%
• b) 20–30% versus 30–50%
• c) They are identical
• d) Diet always outperforms

9. ApoB is a better risk marker than LDL-C when:

• a) They agree
• b) They are discordant — commonly in insulin resistance and raised triglycerides
• c) Cholesterol is very low
• d) Never

10. HDL-C is best understood as:

• a) A treatment target
• b) A marker of metabolic state — pharmacological raising has repeatedly failed to reduce events
• c) Directly protective
• d) Irrelevant

11. The DASH-Sodium trial showed that the effects of the DASH pattern and sodium reduction were:

• a) Mutually cancelling
• b) Additive
• c) Identical
• d) Absent

12. The SSaSS salt-substitute trial is unusual because it:

• a) Was observational
• b) Provided randomized evidence for hard outcomes — stroke, major cardiovascular events and death
• c) Measured only blood pressure
• d) Was conducted in athletes

13. Potassium-enriched salt substitutes are contraindicated in:

• a) Everyone over 60
• b) Advanced chronic kidney disease and with potassium-retaining medications
• c) Hypertension
• d) Diabetes

14. The chapter discounts the sodium J-curve cohorts partly because:

• a) They were industry funded
• b) Intake estimation from spot urine samples is a poor proxy, plus reverse causation
• c) They were too small
• d) They were never published

15. Weight loss of about 10% or more in fatty liver disease can:

• a) Only reduce steatosis
• b) Improve fibrosis — the outcome that matters most
• c) Do nothing
• d) Worsen the condition

16. Which is an established diet-related cancer risk factor?

• a) Sugar consumption specifically
• b) Alcohol — an IARC Group 1 carcinogen
• c) Non-organic produce
• d) Seed oils

17. During cancer treatment, nutritional goals:

• a) Are the same as for the general population
• b) Invert — maintain weight and lean mass, adequate protein, eat what can be tolerated
• c) Should focus on elimination diets
• d) Are irrelevant

18. In chronic kidney disease, which does not invert?

• a) Protein — often restricted
• b) Potassium — may need limiting
• c) Sodium reduction — still recommended
• d) Salt substitutes — contraindicated

19. Phosphate additives in processed food are:

• a) Less bioavailable than food phosphate
• b) Far MORE bioavailable than naturally occurring food phosphate
• c) Identical in bioavailability
• d) Not permitted

20. HbA1c reflects roughly three months of glycaemia, so it should not be rechecked before:

• a) One week
• b) 8–12 weeks
• c) Two years
• d) It can be rechecked daily

Answers

1. b) Liver fat. ⚠️ Along with triglycerides, HbA1c, blood pressure and weight — the metabolic numbers, which reflect a person's CURRENT state and therefore move fast. §26.1.

2. c) Lp(a). ⚠️ Genetically determined, an independent cardiovascular risk factor, and diet does essentially nothing to it. Measure it once in a lifetime — because a raised result changes how aggressively everything else should be managed, and because people spend years trying to diet away a number food cannot move. §26.1, §26.6.

3. b) Five readouts of one process. ⚠️ When intake persistently exceeds what subcutaneous tissue can comfortably store, fat accumulates in liver, pancreas, muscle and viscera — and that ectopic fat produces every tier 1 number. Which is why one intervention improves five conditions at once. (⚠️ Qualifications: not everyone with a given condition has this process, and where you store fat is substantially genetic — hence waist measurement adding what BMI misses.) §26.1b.

4. b) ~86%. §26.3.

5. a) ~7%. ⚠️ That gradient — roughly 86% at ≥15 kg, ~57% at 10–15 kg, ~34% at 5–10 kg, ~7% at <5 kg — is the most useful set of numbers in the chapter, because it converts "try to lose weight" into a quantified prediction. §26.3.

6. b) Shorter duration. ⚠️ Beta-cell function is more recoverable earlier in the disease course; DiRECT recruited people diagnosed within six years. §26.3.

7. b) Convergence across methods. ⚠️ Different genes, different drugs, different mechanisms, the same relationship between LDL-C lowering and event reduction. That is what a settled question looks like — and the contrast with almost everything in Part IV is the point. §26.5.

8. b) 20–30% versus 30–50%. ⚠️ Both halves matter: diet moves LDL-C meaningfully AND for someone at high risk, declining a statin in favour of diet is choosing the smaller intervention. They are additive, not alternative. §26.5.

9. b) When discordant. ⚠️ Every atherogenic particle carries exactly one ApoB, so ApoB counts particles while LDL-C measures the cholesterol inside them. Insulin resistance and raised triglycerides produce many small cholesterol-depleted LDL particles — LDL-C looks acceptable, particle number is high, and risk tracks the particle number. §26.6.

10. b) A marker of metabolic state. ⚠️ CETP inhibitor trials raised HDL-C and did not reduce events. Chapter 2's reverse causation in one number: low HDL travels with insulin resistance, raised triglycerides and adiposity, and it's those that carry the risk. §26.6.

11. b) Additive. ✅ §26.7.

12. b) Randomized evidence for hard outcomes. ⚠️ Events, not blood pressure, from a dietary substitution costing almost nothing — which is vanishingly rare in nutrition and is why it gets a section rather than a sentence. §26.7.

13. b) Advanced CKD and potassium-retaining medications. ⚠️ Hyperkalaemia risk. Check before recommending — and note this is one of §26.11's inversions. §26.7, §26.11.

14. b) Spot-urine estimation and reverse causation. ⚠️ Plus the randomized outcome evidence points the other way. Where the chapter lands: ✅ reducing sodium lowers blood pressure; 🟢 population-level reduction reduces events; 🟡 whether normotensive individuals benefit from very low intakes. ⚠️ And the practical version sidesteps most of it — most sodium comes from processed and restaurant food, not the salt cellar. §26.8.

15. b) Improve fibrosis. ⚠️ Dose-dependent: ~3–5% reduces steatosis, ~7–10% improves inflammation, ~10%+ can improve fibrosis. Same shape as §26.3, and fatty liver is the most reversible condition in the chapter. §26.9.

16. b) Alcohol. ⚠️ IARC Group 1 — breast, colorectal, oesophageal, liver, oral. Along with excess adiposity (12+ cancers), processed meat (Group 1), red meat (2A), low fibre, aflatoxin. ⚠️ And the magnitude honesty: dietary factors matter and matter considerably less than not smoking; the biggest dietary lever is alcohol. §26.10.

17. b) They invert. ⚠️ Maintain weight and lean mass · adequate energy and protein · manage side effects · eat what you can tolerate · food safety if immunosuppressed. The person most likely to be harmed by nutrition advice in this book's subject area is someone in cancer treatment given a restrictive diet by someone who meant well. §26.10.

18. c) Sodium reduction. ⚠️ The one that doesn't invert. Protein is often restricted (~0.8 g/kg in stages 3–5 not on dialysis, and REVERSING again to 1.0–1.2+ on dialysis), potassium may need limiting, and salt substitutes are contraindicated. §26.11.

19. b) Far MORE bioavailable. ⚠️ Which means someone told to "reduce phosphate" who cuts dairy and legumes while continuing to eat processed food with phosphate additives has made the problem worse and their diet poorer. Read the ingredients list — a practical, high-yield instruction rarely given. §26.11.

20. b) 8–12 weeks. ⚠️ It cannot have moved at four weeks, the result will disappoint, and people quit on a measurement that was always going to look like that. This happens constantly. ⚠️ The rule: if you want early evidence something is working, measure a fast number (triglycerides, glucose, blood pressure, liver fat). If you want to know whether it mattered, measure a slow one. §26.13b.

Scoring

Three items worth checking regardless of score.

Questions 4 and 5. ⚠️ The remission gradient is the most clinically useful thing in this book that most people with type 2 diabetes have never been told.

Question 17. ⚠️ If you got this wrong and you have a seriously ill relative, this is the correction that matters most.

Question 20. ⚠️ A four-week HbA1c ends more sustainable changes than almost anything else.