Providing independent clinical excellence since 2005
The keto and Atkins diets have profound effects on hepatic lipid metabolism, and hence on LDL cholesterol handling. Let’s unpack this carefully through the lens of the endogenous cholesterol pathway.
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.
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.
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.
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.
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.
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.
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.
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.
Small dense LDL (sdLDL) particles are the most atherogenic type of LDL. They are smaller and heavier, stay in the bloodstream longer and 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:
Mitochondria are the power stations inside every cell, converting food into energy. But in modern life, with constant carbohydrate intake and low energy demand, they become overwhelmed. Just like solar panels producing too much electricity for full batteries, mitochondria have nowhere to send surplus fuel. This triggers oxidative stress, inflammation, and early ageing. Insulin is meant to divert excess glucose to safe storage — but when that system fails, metabolic chaos follows. In this article, we explore how your mitochondria manage energy, what causes them to overload, and how lifestyle changes can help restore balance and protect long-term health
Carbohydrate Sensitive Phenotype (CSP) is not a diagnosis of diabetes or obesity. Rather, it’s a biologically driven pattern of visceral fat accumulation and carbohydrate intolerance which is highly prevalent in those with a raised waist-to-height ratio (WHtR > 0.5), triggered by aging, Western-style diet and lifestyle. More importantly, CSP gives individuals a name for their experience—one that invites support instead of judgement, and allows them to engage with food and health choices free from social shame.