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At Surrey Cardiovascular Clinic, we have seen a pattern: some people whose blood sugar (HbA₁c) is technically “normal” are quietly drifting towards diabetes. Their blood tests look fine — but their day-to-day glucose readings tell another story.
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Multiple studies show that low-carb, high-fat diets tend to shift LDL particles toward larger, more buoyant LDL (pattern A).
These particles are considered less atherogenic than small, dense LDL (pattern B), typical of insulin resistance.
Therefore, while LDL-C concentration may rise, LDL particle number (apoB) or non-HDL cholesterol may not rise proportionally — and inflammation markers (hs-CRP, TG/HDL ratio) often fall.
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MASLD is a silent but important marker of metabolic health and another consequence of raised Visceral Adipose Tissue (VAT). Although often discovered by chance, it carries significant implications for both liver and cardiovascular wellbeing. Through caloric restriction, physical activity, improved nutrition, and early intervention, MASLD can usually be stabilised or reversed — protecting not just the liver, but the heart as well.
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Small dense LDL (sdLDL) is the most harmful form of “bad cholesterol.” It forms when the liver overproduces VLDL — often driven by visceral fat and high insulin levels. Visceral fat sits deep around the organs and feeds directly into the liver, causing early metabolic disruption long before blood tests detect it.
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In families with inherited high cholesterol (familial hypercholesterolaemia), mutations in the PCSK9 gene have been identified which make this protein overactive. These are known as gain-of-function mutations — they increase PCSK9 activity and push LDL cholesterol to dangerous levels. For over 90% of people with raised LDL who do NOT have a mutation, there are alternative explanations outlined in a related article and for readers that are curious about this PCSK9 take a look at my technical article linked to the VAT Trap book series on LDL Cholesterol. Read blog
In the first podcast in the series, the discussion revolves around cholesterol and the fact that while your blood LDL cholesterol determines the development of coronary plaque, your levels are more about your genetics than necessarily what you eat. In contrast, what happens to coronary plaque over your lifetime and whether it causes a heart attack is more about 'inflammation', what carbohydrates and UPF's you eat and your lifestyle.
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