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Continuous glucose monitors reveal how differently individuals respond to carbohydrates. We classify these responses using Glucotype, which reflects innate carbohydrate tolerance, and Current Glucose Profile (CGP), which shows a person’s present metabolic state. Combined with visceral fat grading, this system helps identify metabolic risk and guide personalised dietary or medical interventions.
Prediabetes should be viewed as an active cardiometabolic disease stage rather than a passive risk marker. Cardiovascular injury begins before overt diabetes, creating a critical window for intervention. Lifestyle therapy remains fundamental, while agents such as metformin, GLP-1 receptor agonists, dual incretin therapies, and SGLT2 inhibitors may help modify long-term cardiovascular risk.
Measuring your waist isn’t about shape or clothing size. It’s a simple health check that reflects harmful visceral fat around the organs. Measuring the narrowest point can miss risk. For meaningful results, waist must be measured at a fixed anatomical point and tracked consistently over time.
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.
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.
Ten minutes of strength training, five days a week, is enough to change metabolic health. Like brushing your teeth, it works because it’s sustainable. Keep the time fixed, increase the weights gradually, and focus on strength, not scales. Small daily habits protect muscle, reduce visceral fat, and support long-term health.
In cardiometabolic medicine, muscle is not a cosmetic tissue but a metabolic organ. Evidence consistently shows that strength, not muscle mass, predicts insulin resistance, cardiovascular risk, and survival. Many older adults are not losing muscle tissue — they are losing muscle function, and that is the pathology that matters.
A 2026 BMJ systematic review confirms that weight regain is the rule after stopping pharmacological weight-management therapy. Across drug classes, most lost weight is regained within 24 months, with parallel loss of metabolic benefit. This reflects biological defence of adiposity, not patient failure.
Smart body composition scales are not metabolic truth machines. Their value lies in engagement, not precision. During weight loss—especially with GLP-1 therapy—hydration and glycogen shifts distort “muscle” readings. Used within a tiered system that prioritises waist, strength, and function, they can support behaviour without undermining progress.
January isn’t just about weight loss. Much winter weight gain occurs as visceral fat, which drives insulin resistance and cardiovascular risk. Measuring your waist, not just your weight, gives a clearer picture of metabolic health. Building muscle and reducing visceral fat supports a healthier metabolism long after January ends.
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.
Reducing saturated fat intake is known to lower “bad” cholesterol (LDL-C) and reduce heart disease risk, but responses vary widely between individuals. Research shows that genetics strongly influence how much LDL rises when people eat foods like butter, cheese, or fatty meats compared with unsaturated fats such as olive oil, nuts, and oily fish. Even on the same diet, LDL responses can differ by up to 1 mmol/L, reflecting genetic differences in intestinal cholesterol absorption and how efficiently LDL is cleared from the bloodstream.