Does hitting a plateau mean the dose needs to go up, or is that the wrong inference?

I am on tirzepatide 10 mg and have been flat for seven weeks. The reflex answer everywhere is "titrate up", and 12.5 and 15 mg exist, so the option is there. But I want to understand whether a plateau is actually evidence that the dose is insufficient, or whether that is a non-sequitur that happens to be convenient.

My reasoning for doubting it: in the trials, everyone was titrated to a target dose on a fixed schedule regardless of response, and the weight curves still flattened eventually at every dose. If the curve flattens at 15 mg too, then flattening cannot be evidence of an insufficient dose, it is just what the curve does.

Against that: I do notice appetite is much less suppressed than it was three months ago, food is interesting again, and portions have crept up. That does feel like a pharmacological change rather than a metabolic one.

Is there a principled way to decide? And what do the trial weight curves actually look like at each dose over time?

Adding a distinction that is doing invisible work in this thread: "the drug is doing less" has at least three different causes and only one of them is addressed by more drug.

1. Behavioural accommodation. You have learned to eat around the suppression. Smaller meals more often, softer and more energy-dense foods, liquid calories, grazing rather than meals. This is extremely common and it is not pharmacological at all. More drug will be accommodated around too, within a few months.
2. Restored counter-regulation. As you lose weight, orexigenic signalling rises: ghrelin goes up, leptin falls, and the drive to eat increases genuinely and physiologically. The drug is doing the same thing against a stronger opposing signal, so the net effect is smaller. More drug does help here, and this is the case where escalation is mechanistically justified.
3. Actual pharmacological tolerance at the receptor level. Least well established of the three in humans for this class, and the one most often assumed. The trial data showing sustained effect at fixed dose over two years argues against substantial receptor-level tolerance being the dominant story.

Distinguishing 1 from 2 is doable by introspection if you are honest. Are you eating more because you want to eat more, or because you have found ways to consume more within the same reduced appetite? The first is counter-regulation. The second is accommodation, and it responds to structure rather than to dose: fixed meal times, no grazing, protein first, no liquid calories.

Most people I have seen escalate on the basis of "it stopped working" were in case 1, went up a dose, got three good weeks from the nausea, and were back in the same position by week ten at a higher dose and a higher cost.

Worth stating the pharmacokinetic reason a plateau in the first eight to twelve weeks after a dose change means something different from a plateau at month seven.

These are long half-life molecules. Semaglutide has an elimination half-life of about a week, tirzepatide about five days. Reaching steady state takes roughly four to five half-lives, so:

Semaglutide: 5 x ~7 days  = ~35 days = 5 weeks to steady state
Tirzepatide: 5 x ~5 days  = ~25 days = 3.5 weeks to steady state

So exposure keeps rising for three to five weeks after every dose step, and the appetite effect keeps deepening for a while after that as the behavioural response catches up. A "plateau" observed in weeks two to four after an increase is frequently just the pre-steady-state period, and people abandon or escalate prematurely.

Conversely, at seven weeks on a stable 10 mg dose, OP is comfortably at steady state and this consideration does not apply. Their plateau is a real plateau. But it is a common enough error that it is worth having the number: give any dose four to six weeks before judging it, and judge the trend over the last three of those, not the first.