There is a particular kind of confidence that comes from having read the original studies rather than the summaries of the summaries. Prof. Tim Noakes has spent decades using that confidence to deconstruct one of modern medicine’s most stubborn assumptions: that cholesterol is the primary villain behind heart disease.
Recently, Azza Motara, Clinical Dietitian and Scientific Education Specialist, sat down with Prof. Noakes for a live discussion hosted by Nutrition Network. The hour-long conversation traversed seventy years of nutrition science, the honest case for GLP-1 agonists like Ozempic, and a brand-new study that pushes the ketogenic diet to the forefront of psychiatric care.
Where the Cholesterol Story Actually Begins
Prof. 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 point five millimoles per liter”—a figure that highlights just how much the goalposts have shifted since the 1970s.
More importantly, Prof. Noakes notes that Barnard’s first two transplant patients shared a core diagnosis: Diabetes mellitus, not high cholesterol.
This observation forms the backbone of Noakes’ argument: insulin resistance, oxidative stress, and chronic inflammation—not dietary fat—are the true drivers of coronary artery disease. He attributes the conflicting, fat-phobic narrative to Ancel Keys. After World War II, Keys utilized a flawed WHO dataset to correlate fat intake with heart disease.
“In science, you have to understand that a relationship like this does not prove causation,” Noakes explains. While researcher John Gofman identified that high triglycerides (driven by carbohydrate intake) were just as critical as LDL levels in heart disease, the “fat-is-bad” narrative was the one that survived in textbooks. By 1961, the New England Journal of Medicine solidified the claim that dietary fat—not sugar or refined carbohydrates—was the culprit, a bias that continues to dominate cardiology consults today.
What the Clinical Trials Actually Show
Prof. Noakes challenges the theory by pointing to trials that failed to support it.
- The Look-AHEAD Trial: Designed to test whether a low-fat, high-carb diet reduced cardiovascular events in obese diabetics, the trial was stopped early due to lack of success.
- The Women’s Health Initiative: Noakes highlights this study as a classic case of obscuring evidence of harm.
- The Statin Debate: Noakes remains critical of how statins function. “They poison the cells so the cells absorb more cholesterol from the bloodstream,” he notes. Borrowing from researcher Zoë Harcombe, he reminds us: “Your liver produces cholesterol. It isn’t trying to kill you. It’s trying to give you what you need to be healthy.”
How to Reframe the Conversation with Your Doctor
If you are advised to start a statin, Prof. Noakes suggests moving 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.
- Full Lipid Panel: Specifically looking at triglycerides, HDL-c, and the triglyceride-to-HDL ratio.
- Markers of Metabolic Health: Testing for insulin resistance.
- Individual Risk Factors: Family history, blood pressure, and lifestyle factors like smoking or vaping.
The Insulin Story and a Psychiatric Breakthrough
While medications like Ozempic (GLP-1s) can mirror the metabolic effects of a low-carb diet, Prof. Noakes urges caution regarding long-term use, particularly given potential side effects like gastric paralysis and the reliance on expensive, indefinite treatment.
However, the conversation took a major turn toward nutritional psychiatry. Motara and Noakes discussed a landmark randomized controlled trial published in the Schizophrenia Bulletin (2026). The study tested the ketogenic diet against a standard diet in patients with schizophrenia-spectrum 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.
- Crucially: Improvements in depression tracked with the depth of ketosis, not the amount of weight lost, suggesting that ketosis itself is the mechanism of action.
Where This Leaves You
Prof. Noakes’ closing advice is a call to personal empowerment: “You’re an experiment of one. You’ve got one life, it’s your experiment, and as much as we say what you should do, you need to try it and find out what works for you.”
His goal isn’t to foster distrust in the medical establishment, but to encourage patients to ask better questions: Is my insulin resistance being treated, or am I just masking a symptom with a pill?
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