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My cholesterol came back high. Do I treat the number, or find out why it is high?

What the experts say

Mark HymanMD · family physician · functional medicine

The number is a signal, not the problem. Fix what is driving it.

What it rests onA mechanism argument running through insulin. Sugar and refined carbohydrate raise insulin; chronically elevated insulin produces insulin resistance; insulin resistance raises triglycerides, alters LDL particles and drives the inflammation that carries cardiovascular risk. His conclusion is that for many people dietary fat is not the driver and the number is downstream: 'lowering cholesterol isn't really about cholesterol.' His prescription is dietary and behavioural, with supplements including red yeast rice under guidance, and he routes to his own 10-Day Detox twice in the episode.

Simon HillMSc, BSc · nutritionist and physiotherapist · host, The Proof

Measure the causal particle and lower it

What it rests onAn outcomes-and-causality argument: ApoB counts the total number of atherogenic lipoproteins in circulation, that count is the causal exposure in the genetic, epidemiological and trial evidence, and it should be measured directly and brought below a target rather than treated as a proxy for something upstream. Recorded here as hil-apob-test and hil-apob-target.

Overview

Hyman is addressing people who have just had an unexpected result and have not yet been offered anything but a statin, and his strongest case is the metabolically unhealthy patient whose lipid picture genuinely does move with diet. Hill is reasoning about lifetime cardiovascular risk across the whole distribution, including the metabolically healthy person whose ApoB is high anyway and whose diet has little room to move it.

Neither side is describing the other's patient, and the person most likely to be harmed by picking the wrong one is the one both of them describe least: familial hypercholesterolaemia.

Where they agree

Both hold that diet, movement, sleep and body composition matter and should be addressed. Both hold that standard LDL-C alone is an incomplete picture. Both recommend more measurement rather than less, and, notably, both are commercially connected to the same testing company. Neither says do nothing.

What would settle it

For Hyman: outcome data showing that treating insulin resistance without lowering ApoB reduces events, which is the trial neither side cites. For Hill: evidence that in a metabolically healthy subgroup an elevated ApoB does not carry the risk the population data attributes to it. Both sides should re-open on any large trial of insulin-sensitising lifestyle intervention with hard cardiovascular endpoints.

Practice does not pick a winner here

You do, and your call is dated, kept, and yours to change. Follow the people you already trust and what they publish turns into a short daily practice.

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