When people hear “tirzepatide beats semaglutide,” they assume it’s about potency.
That’s the wrong model.
The advantage comes from signal coverage, not intensity.
Semaglutide activates GLP-1 receptors. That improves satiety and insulin response. Powerful—but narrow.
Tirzepatide adds GIP. Now you’re influencing insulin secretion and nutrient partitioning simultaneously.
Retatrutide goes further. GLP-1. GIP. Glucagon.
That third signal changes the equation. Glucagon isn’t about appetite—it’s about energy availability and fat oxidation. It tells the body, “Use what you’ve stored.”
This is why early data shows triple-agonists outperforming everything before them. They don’t push harder on one lever. They pull multiple systems into alignment.
That also means more complexity. More variables. More responsibility.
Multi-pathway compounds magnify both outcomes and mistakes.
Understanding the signaling architecture is no longer optional.
PS:
“Stronger” is a lazy explanation. Biology doesn’t work that way.