There is a certain kind of confidence that comes from reading the original studies rather than the abstracts of the abstracts. Professor Tim Noakes has spent decades using this confidence to deconstruct one of modern medicine’s most persistent assumptions: that cholesterol is the main culprit behind heart disease.
Recently, Azza Motara, Clinical Dietitian and Science Education Specialist, sat down with Professor Noakes for a live discussion hosted by the Nutrition Network. The hour-long discussion traversed seventy years of nutritional science, the candid case for GLP-1 agonists like Ozempic, and a brand new study that pushes the ketogenic diet to the forefront of psychiatric care.
Where does the cholesterol story really begin?
Professor Noakes traces his own medical roots back to Professor Christiaan Barnard, the pioneer who performed the world’s first human heart transplant. Barnard taught his students that “a normal cholesterol is seven points five milliliters”—a number that underscores how far the goalposts have shifted since the 1970s.
Most importantly, Professor Noakes notes that Barnard’s first two transplant patients had a common diagnosis: Diabetes mellitusnot high cholesterol.
This observation forms the backbone of Noakes’ argument: insulin resistance, oxidative stress, and chronic inflammation—not dietary fat—are the real drivers of coronary heart disease. He credits the conflicted, lipophobic narrative to Ancel Keys. After World War II, Keys used a flawed WHO data set to link fat intake to heart disease.
“In science, you have to understand that a relationship like this doesn’t prove causation.” explains Noakes. While researcher John Gofman recognized that high triglycerides (driven by carbohydrate intake) were as critical as LDL levels in heart disease, the “fat is bad” narrative was the one that survived in the textbooks. By 1961, the New England Journal of Medicine cemented the claim that dietary fat—not sugar or refined carbohydrates—was the culprit, a bias that continues to dominate cardiology advice today.
What clinical trials really show
Professor Noakes challenges the theory by pointing to trials that have failed to support it.
- The Look-AHEAD Trial: Designed to test whether a low-fat, high-carbohydrate diet reduced cardiovascular events in obese diabetics, the trial was stopped early due to a lack of success.
- Women’s Health Initiative: Noakes highlights this study as a classic case of evidence of harm being concealed.
- The Statin Debate: Noakes remains critical of how statins work. “They poison the cells so the cells absorb more cholesterol from the bloodstream,” notes. Borrowing from researcher Zoë Harcombe, she reminds us: “Your liver makes cholesterol. It’s not trying to kill you. It’s trying to give you what you need to be healthy.”
How to redefine the conversation with your doctor
If you’re advised to start a statin, Professor Noakes suggests going beyond the standard blood panel. Ask your doctor to include:
- Coronary Artery Calcium (CAC) Score: A more direct measure of risk. a score of zero indicates lower short-term risk.
- Complete Lipid Panel: Specifically, looking at triglycerides, HDL-c and triglyceride to HDL ratio.
- Metabolic Health Indicators: Screening for insulin resistance.
- Individual Risk Factors: Family history, blood pressure and lifestyle factors such as smoking or vaping.
The history of insulin and a psychiatric discovery
While drugs such as Ozempic (GLP-1s) can mirror the metabolic effects of a low-carb diet, Professor Noakes urges caution about long-term use, particularly given potential side effects such as gastric paralysis and dependence on expensive, uncertain therapy.
However, the debate took a significant turn towards nutritional psychiatry. Motara and Noakes discussed a landmark randomized controlled trial published in the journal Schizophrenia Bulletin (2026). The study looked at the ketogenic diet versus a standard diet in patients with schizophrenia spectrum disorders and bipolar-1 disorders.
The results were profound:
- Participants in the keto group saw significant improvements in weight, HbA1c and insulin resistance.
- After four months, there were measurable improvements in clinical symptoms (positive, negative and depressive) and cognitive performance.
- Critical: Improvements in depression are tracked with the depth of ketosisnot the amount of weight lost, suggesting that Ketosis itself is the mechanism of action.
Wherever that leaves you
Professor Noakes’ final advice is a plea for personal empowerment: “You’re an experiment of one. You have one life, it’s your experiment, and no matter how much we say what you should do, you have to try it and find out what works for you.”
His goal is not to instill distrust in the medical establishment, but to encourage patients to ask better questions: Is my insulin resistance being treated or am I just covering up a symptom with a pill?
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