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Seed oils rich in linoleic acid (LA), such as soybean, corn, sunflower, safflower, and canola oil, provide the exact substrate (PUFAs) that enzymes like lipoxygenase (LOX) and myeloperoxidase (MPO) use to oxidise LDL particles.

What’s actually most prone to oxidation in LDL is the fatty acid tail of the cholesteryl ester in the “oil barrel” (and the PUFA in the phospholipid shell). Cholesterol itself — the rigid steroid ring — is remarkably stable. Pure cholesterol won’t just oxidise easily in the body.

When the metabolic environment is calm — low inflammation, low oxidative stress, good insulin sensitivity — LDL particles circulate, deliver nutrients, and return to the liver without incident. But in an inflamed environment, those same particles can get trapped, oxidised, and turned into plaque.

The simple claim “saturated fat raises LDL, therefore causes heart attacks” is outdated. A more accurate view must consider biochemistry, particle quality, metabolic health, and dietary context.

Saturated fat became a convenient scapegoat, while the role of refined carbohydrates, ultra-processed foods, and chronic inflammation in driving heart disease was largely overlooked.

While GLP-1 medications may offer a quick fix for weight loss, they come with potential side effects and long-term concerns

Reality is biochemistry determines behaviour. Overeating is not a failure of willpower; it is the result of a biochemical/hormonal imbalance

Poor diet fuels stress, stress promotes sedentary behaviour, and inactivity makes the body more vulnerable to dietary harm.

There is no universal diet or lifestyle that works for everyone. Instead, solutions should be based on the root causes.

The brain, where disrupted signalling leads to a cascade of events that drive overconsumption and ultimately, system insulin resistance.