Providing independent clinical excellence since 2005
What if the heart works like a hybrid engine? Continuously switching between fatty acids, glucose, and ketones, it optimises fuel use for efficiency and demand. But in metabolic disease, this flexibility is lost. The result: poorer fuel, narrowed supply lines, and a strained engine — a new way to understand cardiovascular risk.
N-of-1 medicine shifts the focus from population averages to personal biology. This blog series explores how individuals can run simple, safe self-experiments — using themselves as the control — to test plausible health hypotheses, track meaningful outcomes, and discover what genuinely improves their own health and wellbeing over time.
Coronary heart disease often presents without warning, making early prevention essential. This article outlines a personalised approach to identifying individual risk, detecting underlying coronary inflammation and plaque, and implementing structured preventive strategies. Combining risk scoring, advanced imaging and holistic management, we help patients reduce the likelihood of future heart events.
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.
A coronary stent treats a narrowed artery, not the biology that caused it. Insulin resistance driven by visceral fat promotes inflammation and abnormal healing, increasing restenosis risk. Diabetes is the end stage, but waist size often reveals risk much earlier — making metabolic health central to long-term outcomes after stenting.
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.
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.
Epigenetics is the molecular bridge between lifestyle and disease. It explains why two people eating the same meal can have very different glucose spikes, and why decades of stress or sleep loss can push one individual towards metabolic syndrome while another remains resilient.
Semaglutide’s cardiovascular benefits extend beyond weight loss — it powerfully reduces visceral adipose tissue (VAT), the internal fat that drives inflammation, insulin resistance and small dense LDL. At SCVC, our GLP-1 programme targets VAT directly using personalised VAT scans and flexible dosing to improve long-term heart health.
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.
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.