VAT Trap Blog

Fix the food first, then move, then build muscle — and only then reach for drugs, in a sequence chosen to shrink visceral fat and flatten the glucose curve rather than simply to satisfy a cost-effectiveness threshold.

Appetite suppression is the dominant, well-evidenced mechanism behind GLP-1 and dual GIP/GLP-1 drugs. It is probably most of the story — but a patient losing a stone in six weeks on a sub-licensed dose, with almost no dietary change, sits in the part it does not comfortably explain. The grown-up response to that gap is not to pretend, but to ask better questions. This series asks one of them.

The bathroom scale has somehow become the judge of whether we're winning or losing at health. It's the wrong judge — and there's a humble £2 tool in your drawer that does the job far better.

Cardiovascular deaths fell 70–80% in sixty years — one of medicine's greatest triumphs. But progress is now slowing. Visceral fat, not LDL-C, is the upstream driver of the four real epidemic diseases: atrial fibrillation, heart failure, type 2 diabetes, and dementia. The VAT-TRAP four-pillar framework addresses all four simultaneously.

The four pillars of coronary prevention map directly onto dementia risk reduction through shared vascular mechanisms. Cardiovascular risk factors in midlife predict cognitive decline decades later, making optimal heart health our strongest defence against age-related cognitive impairment and dementia.

Learn how to measure blood pressure accurately at home using an app to calculate averages, trends, and cardiovascular risk insights.

After 60, muscle becomes deaf to protein signals. You need 3 grams of leucine per meal, not just daily totals, to flip your muscle-building switch. Same protein portions that worked at 40 barely register at 70. Threshold dosing with resistance training breaks this cycle.

Traditional weight loss approaches fail because they treat metabolism as fixed rather than dynamic. The Choice model combines weekly micro-decisions between lifestyle changes and medication adjustments, offering a flexible system that adapts to continuous metabolic changes and breaks the cycle of initial success followed by plateau and regain.

Visceral fat, strength, and metabolic precision now matter more than weight alone — redefining cardiovascular prevention without defaulting to GLP-1 therapy.

When a patient arrives breathless and unable to climb a hill, the instinct is to blame the heart. Sometimes the answer lies in the blood itself. Iron deficiency anaemia reduces oxygen delivery, forces the heart into a hyperdynamic state, and can even produce a murmur over a completely normal valve.

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.

An article by Dr Edward Leatham, Consultant Cardiologist © 2025 E. Leatham This article explores carbohydrates, visceral fat (VAT), and why adding fats to food may lower your cardiometabolic risk. Short on time? Listen to the 15-minute VAT-Trap podcast summary […]

When people think about cholesterol, they often imagine it as something floating in the blood, disconnected from body fat. In reality, the type and location of body fat — particularly visceral fat (VAT) — profoundly influence how the liver packages and clears cholesterol. Raised VAT doesn’t just sit silently around the organs; it acts like an endocrine organ, sending chemical distress signals that shift lipid metabolism in an atherogenic direction.

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.

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.

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.

In 2025, with access to low-dose CT angiography, FAI analysis, and a deeper understanding of plaque biology, it is increasingly difficult to justify CAC scoring in younger individuals.