The Fat Loss Blueprint
16 weeks, six pathways, one pick each
Everything on this page is free. The stack, why each pick beat its alternatives, every option, the bloodwork and the safety lines. The week-by-week schedule and the decision rules are the members half.
Fat loss is not one mechanism, which is why people stall. This blueprint attacks it on six fronts at once — appetite, mitochondrial output, direct lipolysis, insulin, thyroid substrate and lean-mass protection — because the failure point moves as you get leaner. Week 1's problem is that you eat too much. Week 12's problem is that your metabolism has adapted and you are losing muscle. A protocol that only addresses the first one stops working around week 8, and that is exactly when most people quit.
Can you run all of them? Yes - and here is what it costs
This is a general protocol. You make the final call on how much of it to run — or have it built around your labs.
Which of these 6 is actually you?
This tells you where your biggest leverage is — where to start, not where to stop. Read the But line too: it is what each lane cannot do for you, which is the part a list of options never tells you.
Before any of it — the foundation
These four are not a disclaimer at the bottom of the page. They are the reason the rest of it works, and every one of them is free.
Growth hormone is released in pulses during deep sleep, insulin sensitivity is measurably worse after one bad night, and appetite regulation collapses without it. Every compound below works through a system that sleep already governs. This is not filler advice — it is the highest-leverage item on the page and it is free.
The single dietary variable with the most consistent evidence behind it for body composition, in both directions — building and preserving. Under-eating protein while running anything anabolic is paying for a signal with no substrate to act on.
Nothing here substitutes for mechanical tension. Compounds change how well you recover from and adapt to training; they do not replace the stimulus. A protocol run without training reliably produces the side effects and not the results.
Non-exercise activity is the largest and most variable component of daily energy expenditure, and it is the one that quietly falls when you start dieting. Tracking it stops the metabolic adaptation people blame on their thyroid.
The stack
Said once, so it does not have to be repeated against every item. This is the research space. Human data is limited on almost everything below — some of it has phase-2 trials, some has rodent work, some has neither. That is the honest state of the field, not a reason to rank these against each other. Unproven is not the same as ineffective, and a compound being newer does not make it worse. Every option here is presented by what it DOES — the lane it opens — so you can choose on mechanism rather than on how established it sounds. Each one's own page carries its evidence tier in full: clinical, correlative or theoretical, stated plainly.
Each pick names what it was chosen over and why. That is the difference between a blueprint and a list — if you disagree with a choice, the alternative is right there and swapping it does not break the rest.
Peptides 4
Short amino-acid chains that signal rather than force. Almost all are injected or intranasal, they need reconstituting, and they are the reason most people are on this site.
Triple GLP-1/GIP/glucagon agonism. The glucagon arm adds hepatic fat oxidation and energy expenditure on top of appetite suppression — it is the only agent here arguing on two pathways at once, which is why its phase-2 numbers outrun the duals.
Retatrutide, tirzepatide and semaglutide differ by how many receptors they engage — one, two or three. Retatrutide is the base here for the glucagon arm specifically — it is the only one adding energy expenditure rather than only reducing intake. Swapping in tirzepatide or semaglutide changes nothing else on this page, and either is a reasonable choice; they simply engage fewer receptors.
Stack this arm deeper4 optional add-ons
Each of these sits in this same pathway, so it starts the week this pathway starts. Swapping one in for the pick above does not change the schedule.
Amylin agonism — a DIFFERENT receptor from the incretins, which is why the pharma companies are developing the combination deliberately rather than as a marketing stack. It slows gastric emptying and adds satiety by a separate route.
The trade-off The nausea is NOT complementary — both slow the stomach and that effect is straightforwardly additive. If you are already struggling with GI side effects on the incretin, this makes them worse.
Dual GIP/GLP-1, and the most capable thing you can actually get a prescription for today. The GIP arm appears to change where fat is stored and how readily it mobilises, not just how much you eat — which is why its numbers outrun the GLP-1-only drugs by more than the appetite effect explains.
The trade-off Still less than the triple agonist on weight. GI side effects are the commonest reason people stop, and the titration is slow by design.
A selective amylin receptor agonist — the newest arm of this whole class and the one the next generation of combinations is being built around. Amylin governs meal termination and gastric emptying through its own receptor, so it is genuinely additive to an incretin rather than a second version of one.
The trade-off Very early — this is the least human data of anything in the arm. Almost all the trial work runs it in combination rather than alone.
Oral and not a peptide — a small molecule, so none of the food and water timing restrictions oral semaglutide carries.
The trade-off Newest of the class, with correspondingly less long-term data.
Mitochondrial & metabolic reprogrammingMOTS-c3 options
3 options — 0 to swap in, 3 to stack ontap to collapse
Direct lipolysis & adrenergic driveAOD-96044 options
4 options — 2 to swap in, 2 to stack ontap to collapse
Lean-mass protection while cuttingTesamorelin2 options
2 options — 0 to swap in, 2 to stack ontap to collapse
Health supplements & substrate
The floor underneath the compounds. Cheap, well tolerated, and the part that decides whether anything above it has a fair chance — a secretagogue on a magnesium deficiency is a rounding error.
Substrate partitioning & insulin controlMyo-Inositol4 options
4 options — 1 to swap in, 3 to stack ontap to collapse
Thyroid & thermogenic substrateIodine3 options
3 options — 1 to swap in, 2 to stack ontap to collapse
Thyroid & thermogenic substrateSelenium
The 16-week schedule
What goes in, what comes out, and when. The exact doses for each phase are inside the Academy — the structure below is free because it is the part you need to decide whether this fits your life.
| 1–4 | 5–8 | 9–16 | 17+ | Ongoing | |
|---|---|---|---|---|---|
| Iodine | |||||
| Selenium | |||||
| Retatrutide | |||||
| Magnesium | |||||
| Vitamin D | |||||
| Omega-3 (Fish Oil) | |||||
| Creatine | |||||
| Tesamorelin | |||||
| AOD-9604 | |||||
| MOTS-c | |||||
| Myo-Inositol |
Each bar is a week block that compound is running. The shape is free — it is what tells you whether this fits your life. The doses for each phase are the members half.
Lock the substrate floor and get the appetite arm working. Nothing else goes in until this is stable.
Titrate slowly. Almost every bad GLP-1 experience is a dose escalated faster than the gut adapted. Nausea is not a sign it is working — it is a sign you went too fast. If you are still nauseated at the end of a week, hold the dose rather than climbing. Iodine and selenium go in from day one because they are a floor, not a lever — they do nothing dramatic and they cost almost nothing.
Appetite is handled. Now change what the cell does with the fuel, and release it directly.
Two arms at once is the most I would add in one step, and only because they act by unrelated mechanisms — if something goes wrong you can still tell them apart. Add myo-inositol only if your baseline fasting insulin came back high; if it was normal, this arm has nothing to fix.
Rate of loss slows here and that is expected. Nothing new goes in - the lean-mass and mitochondrial arms started early precisely so they are working by now.
If weight has not moved for three weeks, do not add anything. Re-check steps and protein first — NEAT falls silently in a deficit and it is the usual culprit. Adding another compound to a stall you have not diagnosed is how people end up on six things that each do nothing.
Run the after-panel before deciding anything about round two.
Weight regain after stopping a GLP-1 is the norm, not a personal failure — the appetite signal was borrowed, not bought. What you keep is what the foundation built. That is the honest reason the foundation is at the top of this page rather than the bottom.
Everything above is easy compared with holding it.
Most of this reverses on stopping unless the diet and training changed with it. Plan the exit before the entry — a GLP-1 discontinued without a maintenance plan reliably regains, and that is a protocol failure rather than a personal one.
The doses for each phase are inside
Every compound above, dosed week by week, plus the reconstitution numbers and Coach Cam's notes on running it. $10/mo.
Unlock the schedule →Bloodwork
The before-panel is not a formality — fasting insulin is what tells you whether this blueprint is even the right one. High fasting insulin with normal glucose means appetite is being driven hormonally and the appetite arm will work. Genuinely low insulin with the same complaint means the driver is behavioural, and no compound on this page addresses that. The mid-protocol panel exists mostly for ferritin and B12 — the most commonly missed consequence of a GLP-1 working well. Hair shedding and muscle loss on a good response is very often a nutrition problem wearing a drug's name.
Before you start
Everything, drawn before you start. This is the one that decides which pathway is actually yours - and the only one you cannot go back and collect later.
Around week 8
The short list, drawn while you are running it. Not a progress report - it is the draw that catches the things that go wrong quietly.
After
Drawn at the end, against your own baseline. This is what turns the protocol into information rather than a feeling.
All three are drawn at Quest, 2,000+ US locations, no doctor visit, HSA/FSA eligible. Prefer to pick and choose? Every marker above links to its own page, and the panel builder assembles any combination.
Adjusting it
A protocol you cannot adjust is a protocol you abandon. Four situations come up on nearly every run of this — nausea that will not settle, a three-week stall, hair shedding, glucose moving the wrong way. Each one has a specific answer, and the wrong answer to a stall is the reason most people end up on six compounds that each do nothing.
The four decision rules are inside
What to change, what to leave alone, and how to tell a real stall from a water shift. $10/mo.
Unlock the decision rules →The lines I'd stop at
- Severe, persistent abdominal pain radiating to the back. That is the pancreatitis picture and it is not one to wait out. A mildly raised lipase with no symptoms is common and not the same thing — symptoms decide here, not the number.
- Any new lump, or a change in a mole. Nothing on this page is established as causing that, and none of it is worth running while an unexplained finding is unexplained.
- Vomiting that stops you keeping fluids down. That becomes an electrolyte problem faster than people expect.
- Persistent severe upper abdominal pain radiating to the back on any incretin. That is the pancreatitis presentation.
- Resting heart rate persistently above 100, palpitations, or chest tightness on any adrenergic compound.
- Losing more than about 1% of bodyweight per week for several weeks. Beyond that the loss is increasingly lean tissue, and it is the thing that makes the weight come back.
It is built for the common case, not for you specifically. Compound selection and dosing genuinely do change person to person — training age, bloodwork, what you have run before, what you react to. Adjust it against your own numbers using the panels above, or if you want it built around your labs rather than the average, that is what 1-on-1 coaching is for.