How do I tell constipation from an energy deficit on 1,100 kcal a day?

Setup, so nobody has to ask: constipation · 1,100 kcal.

This is not behaving the way I expected and I want to understand the discrepancy before I act on it.

I have photographed the current state and recorded the conditions, so I can answer follow-up questions precisely.

Is this recoverable, and how would I tell?

The mechanism explains the pattern. Delayed gastric emptying plus central appetite suppression produces early satiety, and early satiety plus a slowed transit produces exactly the symptom cluster people report.

Constipation outlasts the nausea because it has two causes and only one of them resolves. Gastric emptying accommodates over weeks; total intake, and therefore stool volume and the osmotic load reaching the colon, does not recover until intake does. This is why fibre alone can make it worse — you add bulk to a system that is short of water and short of motility.

The relevant detail is that the gallbladder signal tracks the rate of weight loss more than it tracks the drug. Rapid mobilisation of adipose tissue increases biliary cholesterol saturation and reduces gallbladder motility; that combination is lithogenic whether the loss came from a drug, a very-low-energy diet or bariatric surgery. The drug contribution on top of that is present but smaller than the rate contribution.

Telogen effluvium following substantial weight loss is documented independently of any pharmacotherapy, which is the cleanest argument that the rate of loss rather than the agent is the primary driver.

Fix the fixable causes first — fluid, electrolytes, sleep, intake — before concluding that the compound is responsible.

On the detail: the distinction worth making early is between a tolerability problem, which is unpleasant and self-limiting, and a clinical problem, which is neither. They present differently and the thresholds for each are worth writing down before you need them.

Early satiety is not a side effect; it is the mechanism being observable. The useful distinction is between satiety, where you stop eating without distress, and aversion, where the thought of food is unpleasant. The first is the intended effect. The second frequently precedes the dose being too high or escalated too fast.

Injection-site reactions are more often diluent-related than peptide-related. Benzyl alcohol sensitivity is uncommon but real, and it presents as a consistent local reaction at every site with a preserved diluent and no reaction with an unpreserved one — which is a straightforward thing to establish. Injection depth is the other common cause: intradermal placement stings and welts, subcutaneous placement usually does not.

SURMOUNT-1 reported gastrointestinal events as the most frequent adverse events, mostly mild to moderate and mostly during escalation, with discontinuation for adverse events in the single digits per cent[1].

One qualification — reported incidence in a monitored trial population is a lower bound on what happens in an unmonitored one, because trial participants were escalated to protocol and supported through it.

If the timing does not fit the escalation, look for another explanation before settling on the drug.

The incidence figures are dose-related but the timing is escalation-related, and conflating the two produces most of the bad advice in this area. Adverse events cluster in the one to two weeks following each dose increase, then decay.

Fatigue attribution is a subtraction problem. Take out the energy deficit, the dehydration, the electrolyte shortfall and the poor sleep, and what remains attributable to the drug in the trials was modest — placebo-arm fatigue rates were within a few points of active-arm rates in most of the programme. The corollary is that the fixable causes are usually the actual causes.

I would flag that attributing a symptom to a drug is a hypothesis, and the base rate of these symptoms in the general population is high enough that the hypothesis is often wrong.

A symptom diary with dates against dose steps answers most of these questions without anyone needing to guess.

The relevant detail is that the honest framing is that this is very common, usually self-limiting, and occasionally the presentation of something that is not self-limiting at all — and the differentiating features are specific enough to be worth knowing.

Pancreatitis red flags worth memorising rather than looking up: severe, persistent epigastric pain radiating to the back, worse lying flat and better sitting forward, with nausea and vomiting that does not settle. That combination is an urgent assessment, not a dose adjustment. An isolated lipase elevation without that picture is common and usually not pancreatitis.

The pooled gastrointestinal adverse-event rates across the STEP programme and the SURMOUNT programme are reported in the primary publications and in the FDA and EMA assessment reports, and the assessment reports are more useful because they give the placebo-arm rates alongside the active-arm rates in the same table.

Write down in advance which symptoms mean stop and seek care. It is a short list and it is much easier to write when you are well.