Retinoid

Retinoids are derivatives of vitamin A that act on nuclear retinoic acid receptors to alter gene transcription, accelerating keratinocyte turnover, normalising follicular shedding, and increasing dermal collagen synthesis over months. The active ligand is retinoic acid; the milder members are precursors that skin must convert.

The conversion chain runs retinyl ester to retinol to retinaldehyde to retinoic acid, each step enzymatic and lossy, which is the basis of the potency ladder: esters weakest, then retinol, then retinaldehyde, then tretinoin — retinoic acid itself, and prescription-only in most jurisdictions. Synthetic receptor-selective retinoids such as adapalene sit apart from the ladder: comparably effective for acne, with markedly less irritation and better light stability. Potency is not efficacy — a strong agent used twice weekly because it stings does less than a mild one used nightly.

Retinization is the adjustment period — commonly two to twelve weeks of dryness, peeling, stinging and transient flare — as turnover accelerates. It fades with continued use, buffered application, and less frequent dosing at the start.

The important correction is that irritation is a poor proxy for effect. Some of the visible peeling is barrier disruption, and treating it as a progress signal is a textbook case of Goodhart's Law; the Nociception involved reports nothing about receptor activity. Barrier repair follows the same logic as Moist Wound Healing — restore the barrier, do not chase the sting. Tretinoin also degrades in light, so evening use and daily sun protection are standard, and systemic retinoids are cleared through routes described in Xenobiotic Metabolism with teratogenicity requiring strict precautions.