Accepted answer
Answering this needs the rate of weight loss and the protein intake, since those are the two modifiable contributors.
The trigger in this context is the rate of weight loss and the associated nutritional deficit, not a pharmacological property. The same phenomenon is well documented after bariatric surgery, illness and childbirth.
Gastrointestinal adverse events, indicative pooled rates
| Event | Active arm | Placebo arm | Timing |
|---|
| Nausea | 40–45 % | 15–20 % | Peaks 1–2 wk after each step |
| Vomiting | 15–25 % | 5–8 % | Follows nausea |
| Diarrhoea | 20–30 % | 10–15 % | Early, variable |
| Constipation | 20–25 % | 8–12 % | Later onset, persistent |
| Discontinuation for GI events | 4–7 % | 1–2 % | Mostly during escalation |
Ranges span agents and doses; read the specific prescribing information for a specific figure.
It is diffuse: increased shedding across the whole scalp, often noticed in the shower or on a brush, without a receding hairline or a defined crown pattern. Patterned loss is androgenetic and unrelated.
The two-to-four-month latency follows directly from the duration of the telogen phase and is the diagnostic feature of the condition.
Supplementing without a measured deficiency has no evidence behind it here and is not harmless at high doses.
The trigger is the rate of loss, not the compound. Slowing it helps future follicles.