Dyslipidaemia

Dyslipidaemia covers any abnormal lipid or lipoprotein profile, but the clinically load-bearing abnormalities are a raised burden of apolipoprotein B-containing particles and raised triglycerides. In insulin-resistant states the pattern is stereotyped: hepatic overproduction of very-low-density lipoprotein, impaired clearance, high triglycerides, low HDL cholesterol and a shift toward small dense LDL particles. That triad, sometimes called atherogenic dyslipidaemia, tracks with visceral adiposity and hepatic steatosis rather than with total cholesterol.

Fasting triglycerides above roughly 1.7 mmol per litre, or 150 mg per decilitre, are called elevated; above about 5.6 mmol per litre, or 500 mg per decilitre, pancreatitis risk becomes the dominant concern and the treatment target changes accordingly. LDL cholesterol is usually calculated, and the Friedewald equation degrades once triglycerides are high, which is why apolipoprotein B or non-HDL cholesterol is the more dependable metric in exactly the patients with the triad.

Weight loss moves these markers unevenly. Triglycerides fall substantially with visceral fat loss, HDL rises modestly and late, and LDL cholesterol often barely moves, being driven more by hepatic receptor biology than by fat mass. A trial reporting an improved lipid panel after weight loss has therefore not demonstrated a lipid-lowering mechanism, and it has not demonstrated an outcome either.

The misuse is almost always at the surrogate boundary. A rodent study showing lowered serum triglycerides gets quoted as cardiovascular benefit, when the endpoint that matters is events and the lipid change is a step removed from it. Non-fasting sampling inflates triglyceride readings, single measurements swing widely within a person, and a percentage improvement quoted from a high baseline is largely regression to the mean.