GLP-1 drugs seem paradoxical: they enhance insulin action yet shrink dangerous belly fat. The explanation lies in restoring normal insulin timing, reducing chronic insulin exposure, and reversing fat “spillover” from liver to abdomen. Real patient cases show rapid visceral fat loss alongside smoother glucose profiles and lower cardiovascular risk.

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Adequate protein and resistance training are essential for healthy ageing and reducing visceral fat. As we grow older, muscles become less responsive, making higher protein intake vital to preserve strength, metabolism, and independence. Building and feeding muscle is the most effective way to improve insulin sensitivity, raise metabolic rate, and burn harmful VAT.

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Raised visceral fat quietly disrupts thyroid chemistry, increasing reverse T3 and lowering active T3 inside tissues. This pushes the body into metabolic “conservation mode” — slowing energy, mood and fat loss despite normal blood tests. Reducing VAT gradually restores healthy thyroid activation and metabolic resilience.

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One of the greatest challenges in the online world is investigator bias. Any “expert” with a strong conviction — whether pro- or anti-statin — can easily find studies that appear to confirm their view. The internet is full of such cherry-picked data. When presented with confident authority, this can sound utterly convincing to a lay audience. The reality is that true medical understanding does not come from one paper, one YouTube video, or one self-proclaimed authority.

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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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