Diagrams

How to stage a new patient in clinic. Work DOWN the questions and stop at the first YES — the arrows to the right are the answers. Descending order is not a style choice: the highest stage a patient meets is their stage, so starting at the top means you never have to revisit an earlier question. And read the ladder as a state rather than a label: staging is DYNAMIC. A patient can move down it as well as up, and regression is a reported outcome rather than a technicality — which is the argument for staging at every visit rather than once at intake.

The only route by which cholesterol leaves the body. Toggle the two delivery routes \u2014 HDL straight to the liver, or the indirect handoff through CETP onto apoB particles \u2014 because which one you picture decides whether raising HDL-C sounds like a good idea.

Where every particle comes from, what shrinks it, and how it is cleared. Tap a node to trace it; tap a link for the mechanism. Switch to ORGANS to see where each step happens.

Retention through rupture, in sequence. Toggle EARLY and LATE to see which steps belong to a fatty streak and which to a plaque that can kill.

Every major LDL-lowering agent converges on one variable — hepatic LDL receptor density. Tap a drug to see how it gets there, and why combinations are more than additive.

Why dyslipidemia appears at BOTH ends of insulin resistance / type 2 diabetes — one process at different degrees, not two diseases. Tap a node to trace it; tap a link for the mechanism.

Obstructive sleep apnea satisfies two of the three claims a clinician needs and fails the third. Toggle to see which edges positive airway pressure actually interrupts — and where the randomized evidence stops.

The leptin–melanocortin pathway, and the asymmetry that determines who setmelanotide helps. Toggle to see what an MC4R agonist can and cannot rescue.

The most repeated claim about weight loss on any intervention — diet, drug or operation. Toggle between the claim as it is usually made and the anatomy underneath it. Whether the muscle protein that IS lost matters clinically — for strength, gait speed, falls or independence — has not been established by any adequately powered trial, and that is this module's closing argument.

Night eating syndrome is not a system running late. Toggle the phases to see which rhythms are delayed, which one runs AHEAD, and why the appetitive signal and the behavior stop lining up.

The defense of body weight, and why exercise leaks. Toggle to see what the system does when you take weight OFF versus when you simply burn more.

Estrogen does not act on a parallel system — it selects WHICH route adipose expansion takes. Toggle the phases to see what changes at menopause. One thing the image does not settle: whether adipose-derived estrone is protective or harmful for visceral adiposity, inflammation and insulin resistance is explicitly unsettled. The loop is well characterized; that valence is not.

The usual account says insulin suppresses SHBG. The mechanism is one step further down. Toggle EARLY and LATE for the consequence.

Where lipid goes when subcutaneous capacity is exceeded. Tap a node to trace it; tap a link for the mechanism.