Staying healthy on the weight-loss jabs.

The weight comes off. The honest question is how much of it is muscle, and what the evidence says you can do about it.

Ozempic, Wegovy, Mounjaro. The weight-loss jabs work: in the STEP 1 trial, weekly semaglutide took close to 15% of body weight off over 68 weeks (Wilding 2021, PMID 33567185), and the newer tirzepatide does more. A growing number of people in the UK are now on one, on prescription for type 2 diabetes or obesity, or bought privately for weight loss. Which is why the headline that followed landed so hard: up to 40% of what you lose on these drugs, it said, is not fat but muscle.

That is the kind of figure that makes people stop the drug, or never start it. Look closely at what it does and does not mean, though, and it is both less alarming and more useful than the headline.

Three things the headline leaves out.

The first is that "lean mass" is not the same as "muscle." On a body scan, lean mass is everything that is not fat: muscle, but also organ tissue, bone, and the water held in fat tissue itself. When you lose a lot of fat, some of the lean compartment comes down with it for reasons that have nothing to do with your muscles wasting away.

The second is that the proportion varies enormously. The most careful recent review of what the body actually loses puts the range at anywhere from 15% to 60% of total weight lost, depending on the trial, the drug, the population, and how muscle was measured (Neeland 2024, PMID 38937282). A single "40%" is the middle of a very wide spread, not a fixed rule.

The third, and the most reassuring, is that a lot of the change appears to be adaptive. A smaller body needs less muscle to carry it. When researchers used MRI rather than a simple scan, the muscle reductions were largely commensurate with the weight lost and with normal ageing, and muscle quality often improved as the fat stored inside the muscle fell (Neeland 2024). The loss is real. For most people it is not the dramatic wasting the word "muscle" conjures.

Where it does matter is at the edges. Older adults, and people who were already frail or low on muscle to begin with, have less to give up and more to lose in everyday strength if they do. That is the group where the question stops being academic, and the group most worth a conversation with a GP before and during treatment.

So if you are on one of these medications and you would rather come out the other side strong than just lighter, what does the evidence actually support? Two levers, and neither of them is a supplement.

The first is protein. Eating enough of it is the best-studied way to bias weight loss toward fat and away from muscle, on these drugs and off them. The catch is built into how the drugs work: they suppress appetite, so protein is exactly the thing people quietly stop eating enough of. Guidance for someone actively losing weight tends to land around 1.2 to 1.6g of protein per kilogram of body weight a day, which is more than most people eat and well above what a shrunken appetite delivers by default. Putting the protein at the first meal of the day, when appetite is highest, is the usual practical fix.

The second is resistance training. Asking a muscle to work against load, whether that is weights, bands, or bodyweight, is the signal that tells the body to hold on to the muscle it has while the fat comes off. The reviews of muscle preservation on GLP-1 therapy keep returning to the same pairing: adequate protein alongside resistance exercise (Neeland 2024). Walking and cardio are good for many things; they are not the muscle-sparing lever.

There is a second, quieter issue that the muscle conversation tends to crowd out. When you eat substantially less food, you take in less of everything in it, calories included. A diet that has shrunk by a third is delivering roughly a third less protein, fibre, vitamins, and minerals, unless the food that remains is chosen to work harder.

This is where the everyday basics earn more of your attention. The deficiencies worth keeping an eye on are the predictable ones for any sustained low intake: vitamin D, vitamin B12, iron, and the electrolytes. Fibre is the other casualty, and the constipation that is so common on these drugs is partly a problem of low fibre and too little water. None of this needs a cabinet of supplements. It needs the smaller amount of food to be chosen more deliberately, and anything you are low in to be confirmed on a blood test and corrected with your GP, rather than guessed at and bought in bulk.

Creatine is the one supplement with a mechanism that points straight at the muscle question, and even there the honest position is "plausible, not proven." It is among the best-evidenced compounds for supporting strength gains from resistance training in general, which is the lever that matters here. But the specific trials in people losing weight on GLP-1 drugs have not been run yet. If you are already training, it is a reasonable, cheap, well-tolerated addition. It is not a stand-in for the protein and the training, and nothing is.

The thing to take from all of this is that the drug does the weight loss, and the rest is yours. The medication lowers the number on the scale more or less whatever you do alongside it. Whether you arrive at the lower weight with your strength intact is decided by what you eat and whether you train, not by the prescription.

The jab is the easy half. Protein and resistance training are the half no one can prescribe for you, and the half that decides what kind of smaller you become.