The SCVC Blog

Cardiovascular care news and articles from our expert team

Cholesterol, LDL, and what we learnt from PCSK9 mutations in familial hypercholesterolaemia

PCSK9 binds to LDL receptors and directs them to be destroyed within the cell, rather than allowing them to recycle to the surface. When too much PCSK9 is present, fewer LDL receptors remain available to clear LDL from the blood. The result is simple: LDL levels rise. When that happens, the liver compensates by making even more cholesterol internally. This is why around 90% of the cholesterol in your blood is made by your liver, not absorbed from your diet.

Who Can You Trust? The Rise of Anti-Statin Narratives and the Crisis of Trust in Modern Medicine

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.

Why Some People With “Normal” Cholesterol Still Get Heart Disease

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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PCSK9, visceral fat, and the modern metabolic environment

Because cholesterol is a fat-like substance, it cannot dissolve or travel freely in blood, which is mostly water. To move around, it must be packaged into microscopic transport particles called lipoproteins. One of these, LDL (low-density lipoprotein), acts as the main delivery vehicle, carrying cholesterol from the liver to cells that need it for repair or hormone production. In small amounts, LDL cholesterol is therefore completely normal and necessary. The problem only begins when too much LDL remains circulating in the blood for too long.

Why HIIT Gets Rid of Visceral Fat — The Science Behind Anaerobic Exercise

HIIT interrupts this cycle by dramatically improving insulin sensitivity and glucose uptake in skeletal muscle — particularly in the large lower-limb muscles of the thighs and glutes. A single 20-minute session of HIIT can activate GLUT-4 transporters in muscle cells for up to 24–48 hours, drawing glucose out of the bloodstream and away from storage in the liver and visceral fat depots.

MASLD/MASH -metabolic dysfunction -associated steatotic liver disease: What You Need to Know

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 usualy be stabilised or reversed — protecting not just the liver, but the heart as well.

Intervention programmes: from self-toolkits to nurse-led escalation to GLP-1 support

At Surrey Cardiovascular Clinic, we move beyond detecting risk to delivering a tiered, personalised framework for metabolic and cardiovascular prevention. Using real-time tools like CGM, the DoctorShape app, imaging, and nurse-led coaching, we help patients reduce visceral adipose tissue, improve insulin sensitivity, and restore metabolic health through lifestyle-first, data-guided care.

Transforming metabolic health: cardiometabolic services at Surrey Cardiovascular Clinic

At Surrey Cardiovascular Clinic, we focus on preventing heart disease by tackling its metabolic roots early. Using advanced imaging, metabolic phenotyping, CGM, and tailored lifestyle or pharmacological interventions, we help patients reduce visceral adipose tissue (VAT), improve insulin sensitivity, and shift from risk to resilience through precision, feedback-driven cardiometabolic care.

How to Reduce Visceral Fat Without Medication

The most effective path to reducing visceral fat without medication is not just to “eat less.” It’s to build more muscle, eat smarter, and track your progress. In this blog, which also forms one of the chapters of an ebook, I outline the programme and tools our patients use in our cardiometabolic clinic.

Understanding Cholesterol-Carrying Lipoproteins — Beyond “Good” and “Bad” Cholesterol

Small dense LDL (sdLDL) particles are the most atherogenic type of LDL. They are: Smaller and heavier Stay in the bloodstream longer. More likely to oxidise and enter artery walls. High sdLDL is typical of metabolic syndrome, diabetes, and high triglyceride states linked to visceral fat.Because sdLDL testing is specialised, the ApoB level and the LDL-C : ApoB ratio can be used to estimate particle size predominance:

Visceral Fat, Mitochondria, and the Energy Trap: Why We Store Fat Where We Shouldn’t

Visceral fat (VAT) is the dangerous, hidden fat stored around your organs that accumulates. when caloric intake exceeds energy demand, since glucose and fats that can’t be used gets stored as adipose tissue. This blog explains how ageing, muscle loss, glucose spikes and genetic factors all drive VAT accumulation — and how reversing the cycle requires restoring mitochondrial health, increasing muscle mass, and in many people, by reducing glycaemic overload.