Coming off a GLP-1.

1. Taper, don't stop. Roughly 25% off the dose every three weeks, over about twelve weeks.
2. Hit your protein target now, while the drug is still making it easy. 1.6–2.2 g/kg.
3. Start resistance training now, not after. Three to four sessions a week.
4. Buy the bridge tools before your last shot — glucomannan and berberine in the cupboard, not on order.
5. Expect the rebound in weeks two to four after the last dose, not week one.
6. Write your trip-wire number down today, while you're not hungry.

Two of those six do most of the work, and neither is a peptide: protein and lifting. Everything else on this page is scaffolding around them. If you only manage two things, manage those.

And the uncomfortable one up front: obesity behaves like a chronic condition, and stopping treatment for a chronic condition usually returns it. Coming off is a legitimate choice for plenty of reasons — cost, side effects, having reached a goal, supply. It's just worth going in knowing that the trial data on stopping is not encouraging, and that a low maintenance dose is a real alternative to a full stop.

In the STEP 1 extension, participants who stopped semaglutide 2.4 mg regained two-thirds of their lost weight within a year — about 11.6 percentage points of body weight back. Cardiometabolic improvements reverted alongside it: the blood pressure, lipids and HbA1c gains went back too, not just the number on the scale.

Cleaner design, same direction. After 36 weeks on tirzepatide, participants were randomised to continue or switch to placebo. Over the next 52 weeks the placebo group gained 14% of body weight back while the continuing group lost a further 5%. 82% of those who stopped regained more than a quarter of what they'd lost; over half regained at least half of it.

These are averages from people who stopped abruptly with no structured plan — which is exactly what this guide is trying not to be. The trials tell you what the default outcome is, not what your outcome must be. But they also mean the burden of proof is on the plan: going in with nothing is choosing the trial arm that regained.

Retatrutide has a terminal half-life of about six days (semaglutide is ~7 days, tirzepatide ~5). A fatty-acid chain binds it to albumin, which is what makes weekly dosing possible — and what makes the exit slow.

So after your last dose: day 6 you still have half of it. Day 12, a quarter. Day 18, an eighth. You don't reach negligible until somewhere past week four.

Week one feels fine. Levels are still near half of steady state, appetite is still quiet, and people conclude they've got away with it — so they don't build the habits. The rebound lands in weeks two to four, arriving as a step change into a life with no plan in it.

Tapering works because it converts that one cliff into a series of steps you can feel coming. Each reduction gives you a small, survivable increase in hunger while you still have drug on board to take the edge off — enough to rehearse the eating patterns that have to carry you afterwards. Stopping cold gives you one large increase with nothing rehearsed.

It takes roughly four to five half-lives to reach steady state at any dose — about four to five weeks for retatrutide. Steps shorter than three weeks mean you never actually find out how the new level feels before you drop again, so you're descending blind. Three weeks is the practical compromise; longer is fine, shorter is guessing.

• Weeks 1–3 — 3 mg. Baseline check. Appetite barely moves for most people. Use the easy weeks to lock the protein habit and start lifting.
• Weeks 4–6 — 2 mg. First real hunger return. This is the step that tells you how the rest will go.
• Weeks 7–9 — 1 mg. The honest test. If weight holds here, you're ready to continue. If it climbs, stay.
• Weeks 10–12 — 0.5 mg, or hold 1 mg and stretch to every 10–14 days. Either works.
• Week 13 — stop. Washout begins, and the bridge tools should already be in the cupboard.

• Semaglutide from 2.4 mg: 1.7 → 1.0 → 0.5 → 0.25, three weeks each.
• Tirzepatide from 15 mg: 10 → 7.5 → 5 → 2.5, three weeks each.

Both have licensed dose steps and pens, which makes this considerably easier to execute than with a reconstituted research compound.

Do not descend on schedule regardless of what's happening. If weight rises at any step, hold there another three weeks before continuing. If it rises again, you've found your maintenance dose — that's information, not failure. The timeline is a default, not a commitment, and the people who do badly are almost always the ones who kept to the calendar instead of the data.

1 g, 30–60 minutes before each main meal, with a full large glass of water.

A soluble fibre from konjac root that absorbs many times its weight in water and forms a gel in the stomach, so you arrive at the meal already partly full and finish it sooner. Of everything non-prescription here, it's the most directly useful — it's doing a crude version of delayed gastric emptying, which is a real part of what you're losing.

Expect modest, real help: human trials support satiety and small amounts of weight loss. It is not a GLP-1 and won't feel like one.

Glucomannan expands on contact with liquid. Taken dry, with too little water, or lying down, it can swell in the throat or oesophagus — obstruction and choking cases are documented and this is the reason some countries restricted certain formats. Always a full glass, always upright, never right before bed. Skip it entirely if you have any swallowing difficulty or a known stricture. Take it two hours apart from other oral medication, because it slows their absorption too.

500 mg, two to three times daily, 20–30 minutes before meals. Start with one dose a day and build — GI upset in the first week is common and is the main reason people quit.

Genuinely useful for post-meal glucose control, which is what drives the crash-then-crave cycle once appetite suppression lifts. Worth being clear: it is not ‘nature's Ozempic’. The effect is real and modest, it's on glucose rather than appetite, and the comparison oversells it by roughly an order of magnitude.

Berberine inhibits CYP3A4 and P-glycoprotein, so it raises levels of a long list of drugs including statins, some blood-pressure medication, ciclosporin and many others. If you take anything regularly, check it against berberine specifically before starting. Combined with other glucose-lowering drugs it can push you low.

• Fibre to 30–40 g/day from food. Same mechanism as glucomannan, more of it, cheaper, and it feeds the rest of your health at the same time.
• Sleep 7–9 hours. Short sleep raises ghrelin and lowers leptin — it makes you measurably hungrier tomorrow. Coming off a GLP-1 on five hours a night is fighting yourself with one hand.
• Alcohol is the quiet one. It disinhibits eating at exactly the moment your appetite brakes are being removed, and GLP-1s were suppressing your drinking too, so intake often climbs on its own.

In STEP 1, 45% of the weight lost on semaglutide was lean mass. In SURMOUNT-1, tirzepatide came out better at 26%. Across trials the range is roughly a quarter to nearly a half.

That matters beyond appearance. Lean mass is most of your resting metabolic rate, so losing it lowers the calorie level at which you maintain — you come off the drug hungrier and needing less food than before you started. That combination is the actual engine of regain, and it's why ‘just eat less’ fails.

It is not obligatory. In case series where people did structured resistance training and hit a real protein target, lean soft tissue changes ranged from −6.9% all the way to +5.8% — some people gained lean mass while losing between 13% and 33% of their body weight.

That is the single most useful fact on this page. The muscle loss is a consequence of how the weight was lost, not of the drug. You can still change it on the way out.

1.6–2.2 g per kg body weight daily — roughly 0.7–1.0 g per pound. For a 77 kg (170 lb) person that's 120–170 g a day, which is far more than most people manage with a suppressed appetite.

Protein preserves lean mass in a deficit and is the most satiating macronutrient, so it does both jobs at once. Start hitting the number during the taper, not after — while the drug is still helping you feel full, you're building the habit on easy mode. Trying to learn it in week three of rebound hunger is the hard way round.

Three to four sessions a week, compound lifts, progressive overload. The best-evidenced way to preserve lean mass through and after weight loss, by a distance. Cardio is good for you and will not do this job. Add two easy aerobic sessions on top if you want — they help appetite regulation and sleep, which feed back into the same problem.

If you're new to it, the first eight weeks of lifting produce rapid strength gains that are mostly neural rather than muscular. Don't read that as nothing happening — it's the on-ramp.

Cheap, one of the best-evidenced supplements that exists, and directly on-task here: 3–5 g daily supports strength and lean mass during a deficit. No timing requirements, no loading needed. If the peptides below feel speculative, this is the opposite of that.

1–2 mg subcutaneous, nightly. A growth-hormone-releasing hormone analogue, and the only peptide here that is an approved medicine — FDA-approved for visceral fat reduction in HIV-associated lipodystrophy, with real imaging endpoints behind it.

Visceral fat is the compartment that drives the metabolic markers you improved on the drug, and it's the one that tends to come back first. Note what the approval actually covers though: one specific population, for one specific indication. Using it here is off-label extrapolation from a genuine evidence base, which is a better starting point than most of this category and still an extrapolation.

200–300 mcg subcutaneous, nightly before bed. A selective growth-hormone secretagogue, commonly paired with tesamorelin because the two raise GH by different mechanisms — GHRH analogue plus ghrelin-receptor agonist.

Its main virtue is selectivity: unlike older GHRPs it doesn't meaningfully raise cortisol or prolactin. Its main limitation is that human data is limited and short-term. Reasonable as an adjunct, not a foundation.

Both target the metabolic slowdown that follows weight loss rather than appetite — which is a real problem and a sensible thing to aim at.

• MOTS-c — a mitochondrial-derived peptide that improves insulin sensitivity and glucose handling in animal models, and behaves a bit like an exercise mimetic. Typical protocol: 5–10 mg subcutaneous, 2–3× weekly.
• 5-Amino-1MQ — an oral NNMT inhibitor. NNMT is an enzyme in fat cells; blocking it increased energy expenditure and reduced fat mass in rodents. Typical protocol: 50–150 mg oral daily.

The human evidence for both is essentially absent. Animal and cell data only. The doses circulating are convention rather than trial-derived, nobody has characterised long-term safety, and both are research chemicals sold outside any regulated supply chain — so purity and identity are a real variable on top of the pharmacology.

Treat them as an experiment you are choosing to run with your own body, and don't let them crowd out the protein and training, which are the parts that actually work. If you run them, run them one at a time so you can attribute what happens.

Tesamorelin and ipamorelin both raise IGF-1. Get a baseline IGF-1 and recheck at 8–12 weeks — persistently elevated IGF-1 is not something to run blind.

GH secretagogues can also nudge insulin resistance upward, which works against what you just achieved, so keep fasting glucose and HbA1c on the panel. Water retention, tingling hands and joint aches are the common dose-related complaints and usually mean back off.

Anyone with an active or recent cancer history should not take these without oncology input — the GH/IGF-1 axis is growth signalling, and that is the mechanism.

• Weight — weekly, same day, same conditions. Daily readings are mostly water and will make you miserable. The weekly trend is the signal.
• Waist — fortnightly. Catches visceral fat returning even when scale weight looks flat, which is the pattern when you're losing muscle and gaining fat at the same time.
• Protein — logged daily for the first month. Almost everyone overestimates it, badly. Log it until you can eyeball it accurately, then stop.

If you have access to a DEXA scan, one before and one at six months is worth more than any of the above — it tells you whether you're holding lean mass, which is the actual question.

Write the number down today: ‘if I regain more than X above my post-taper weight, I act that week.’ Five pounds / 2–3 kg is a sensible default.

Acting means going back one taper step, or restarting at a low maintenance dose. It does not mean waiting to see, and it does not mean starting again at the top dose three months later. Regain is far easier to reverse at five pounds than at twenty — and deciding the rule now, while your appetite is quiet, is the whole point.

• Protein 1.6–2.2 g/kg — consistent RCT evidence for lean-mass preservation in a deficit.
• Resistance training — the best-established intervention on this page, and the one that moved lean mass from −7% to +6% in the case series.
• Creatine — among the best-evidenced supplements in existence, directly on-task.

• Glucomannan — human trials for satiety and modest weight loss; real choking risk if taken wrong.
• Berberine — real glycaemic data, effect size wildly overstated online, meaningful drug interactions.
• Tesamorelin — FDA-approved with imaging endpoints, but for one specific population; use here is off-label extrapolation.

• Tapering itself. Clinically sensible, widely used, mechanistically sound — and no randomised trial has compared a taper against a cold stop. The withdrawal trials all stopped abruptly, so the taper is an inference from pharmacology plus clinical practice, not a proven strategy. It is the central recommendation of this guide and you should know it rests on reasoning rather than data.

• Ipamorelin — limited, short-term human data.
• MOTS-c — animal and cell data only.
• 5-Amino-1MQ — animal and cell data only.

Several compounds here are research chemicals or used off-label, and retatrutide is not an approved medicine in any market. That means no pharmacy-grade supply, no dose verification, and no one accountable for what's in the vial.