What people actually run — including what didn't work

Where I started

Somewhere around 330–335 pounds. 6′3″. Fifty years old. And a problem I had misdiagnosed for two decades.

I was not eating because I was hungry. I was eating because if I did not, I would get lightheaded and start to crash — reactive hypoglycaemia, blood sugar dropping hard and taking my ability to think with it. Food was not indulgence, it was maintenance. Every couple of hours, whether I wanted it or not.

The frustrating part is that I could fix it. Ketogenic dieting worked — sustained ketosis gave my brain a fuel supply that did not spike and crash, and the compulsion to eat disappeared. I lost weight fast on it. Five pounds a week at times.

It also put me in the hospital. Twice. Both times I ran keto I ended up admitted — kidney stones and gout. Rapid fat loss dumps uric acid, and I am someone who forms stones. So the one thing that genuinely solved the underlying problem was the one thing my body would not tolerate.

My wife had the opposite problem. She ate very little. She trained hard — two hours on the elliptical at full effort, consistently, for years. Same months, same house, same commitment. I would drop five pounds a week and she would fight for one. Whatever was wrong with her was not intake and it was not effort. We never found out what it was, and research suggests that is the normal outcome rather than a failure of investigation — clinicians typically do not test for leptin resistance, and there is no routine panel for it.

Two people. Two completely different failures. One drug class that addressed both.

The foundation: GLP-1 and multi-agonist therapy

Research describes GLP-1 receptor agonists as working through the incretin and satiety pathways — decreasing appetite and increasing post-meal fullness in the hypothalamus, in effect supplying a satiety signal pharmacologically, doing the job that resistant leptin has stopped doing.

For me the relevant effect was not appetite suppression. It was glucose regulation. Blood sugar stabilised, the crashes stopped, and eating stopped being a job I had to do every two hours. The weight came off because the reason for the eating went away.

Why a combination rather than a single agent

Tirzepatide is a dual GIP/GLP-1 agonist. Retatrutide adds a third receptor — glucagon. Research describes glucagon receptor agonism as increasing energy expenditure through hepatic fatty acid oxidation and brown adipose thermogenesis, a mechanism the published literature notes is absent from GLP-1 and dual GLP-1/GIP agonists.

More than half my total loss came on tirzepatide alone. I want to be clear about that, because the marketing around triple agonists implies a different league of drug and my own experience does not support it. Tirzepatide did the heavy lifting. Retatrutide added something on top of it.

The ratio

I titrated the normal way and ended up at 12 mg of retatrutide. That is where the side effects started outweighing what I was getting for them. So rather than back the dose down, I changed its composition. I now run 12 mg total, split roughly 60/30 retatrutide to tirzepatide — same total weekly load, about two thirds reta and one third tirz.

The reasoning is receptor pharmacology, and the useful way to see it is as balance rather than raw potency. Retatrutide is roughly six times more GIP-weighted than tirzepatide; put the other way round, tirzepatide carries around six times the GLP-1 weighting that retatrutide does, measured against each molecule's own GIP activity. Retatrutide sits at about 12:1 in favour of GIP (EC50 0.064 nM GIP against 0.775 nM GLP-1). Tirzepatide sits near 1.6:1 — close to balanced. Divide one by the other and you get the six.

And retatrutide engages a third receptor that tirzepatide does not touch at all: glucagon. So when you replace part of a reta dose with tirz at the same total load, two things change at once — the stack shifts toward GLP-1 weighting, and glucagon receptor engagement comes down.

Which is exactly the pattern I found. The side effects I could not live with tracked the retatrutide dose, not the total. Capping reta below where it gets unpleasant and making up the rest with tirzepatide gave me the same total weekly load and a substantially better week.

The side effects nobody warns you about

Nausea and gut trouble get discussed endlessly. Two others do not, and in my experience they are the ones that actually make people quit.

Anorgasmia — orgasm becoming delayed, muted, or not arriving at all. It is dose-dependent and it creeps up, so people often do not connect it to the drug for weeks. Anhedonia and emotional blunting — the harder one to describe, and the one people usually reach for the phrase “I just do not care” to explain. Not sadness. Flatness. Things that should register simply do not.

Both are consistent with blunted central dopamine and melanocortin signalling, which is also the mechanism the literature points at for the appetite suppression these drugs are prescribed for. That is the uncomfortable part: the reward pathway that makes food less interesting is not confined to food.

Shifting part of the dose to tirzepatide is what brought both back for me at the same total load — which is the single most useful thing in this entire account, because the usual advice is to reduce the dose and accept losing ground. You may not have to choose. Changing what the dose is made of is a different lever from changing how much of it there is.

Two honest caveats. These compounds are not equipotent milligram for milligram, so “12 mg total” is bookkeeping rather than a pharmacological equivalence. And there is no trial data on combining them. This is my own titration against my own side effects, and the glucagon explanation is a reasonable inference rather than something anyone has demonstrated in a study of this specific combination.

The daily stack

SuperKLOW is the one I would point at. My wife had ongoing knee pain and joint problems. Those resolved almost immediately after she started it — fast enough that neither of us had to wonder whether it was working. She has stayed on it daily since.

SuperRUSH is the daily mitochondrial shot, and the 5-Amino-1MQ in it is the single non-GLP-1 compound I would single out for effect. What I have observed personally: consistent daily energy, and — the effect I did not expect — my digestion stays regular. That matters more than it sounds on a GLP-1 protocol, since slowed gastric emptying is part of how these drugs work and constipation is among the most common complaints. I do not get it. I have no literature attributing motility effects to this compound, so I am reporting it as my own observation rather than a documented mechanism.

Potassium citrate, by prescription, is the one I would tell everyone doing aggressive fat loss to ask their doctor about. Rapid weight loss dramatically increases uric acid excretion — the same mechanism behind gout flares. Citrate alkalinises urine, which the literature describes as preventing both uric acid and calcium oxalate stone formation. I know exactly what happens without it. It is why I was hospitalised twice on keto. Nine months of losing weight faster than I ever did on keto, and not one stone.

hCG, and why it moved into the same syringe

hCG used to be its own injection twice a week. It is now split across all seven days — same weekly total, spread out — and mixed into SuperRUSH so it is not a separate shot at all. Daily microdosing at roughly 190–200 IU is described in the literature as mimicking endogenous LH pulsatility far better than a weekly bolus, which is the reason to do it that way. Folding it into a shot I was already taking is the reason it is sustainable.

That is the argument from the front of this site, applied to my own protocol. Two injections became zero additional injections, because the chemistry allowed it. Where it does not allow it, things stay separate — the GLP-1 never shares a vial with anything, and neither does SuperKLOW.

Why “in range” is not the target

The harmonised reference range for total testosterone in men aged 19–39 is 264–916 ng/dL. That is a three-and-a-half-fold span, and every value inside it is called normal. Which means a man who ran near the top of that range for his entire adult life can lose most of his own testosterone and still be told his labs are fine.

The literature is explicit: population-based reference ranges encompass men with and without symptoms across all health conditions, and are a population snapshot rather than an individual threshold. The AUA's own definition of hypogonadism requires symptoms alongside the number. So the standard target — get him to 400 or 500 because that is comfortably mid-range — is treating a population median as a personal one.

The honest caveat: most of us do not have a documented lifetime baseline to point at. I do not have decades of morning draws from my thirties. So this is reasoning from where I know I was and how I function, not from a number I can produce. Anyone making the same argument should be clear-eyed that it is an inference.

Doctors should test hormones before prescribing an SSRI

Her mental health is substantially better on hormone replacement. That is a first-hand observation, and it points at something I think is a real failure in how this gets practised. Test hormones first. Before the prescription, not after it fails.

The evidence is sharper than most people realise. A meta-analysis of 16 randomised placebo-controlled trials covering 944 subjects found a significant positive effect of testosterone on mood — with a large effect size in hypogonadal men and no statistically significant effect in eugonadal men. A second systematic review found the same pattern: the antidepressant effect is concentrated in patients with hypogonadism.

Read that carefully, because it is the whole argument. The treatment that works depends on which patient you have, and there is no way to tell them apart without a test. Two men walk in with identical symptoms. One is deficient and one is not. They need different medications. The only thing that distinguishes them is a blood draw that frequently never gets ordered.

For women the case is at least as strong, and it is the situation my wife is actually in — she is perimenopausal. Perimenopause is described in the literature as a window of vulnerability for depressive symptoms and major depressive episodes even in women with no prior history of depression. The antidepressant efficacy of estradiol has been examined in randomised, double-blind, placebo-controlled trials in women meeting standardised diagnostic criteria (Schmidt 2000; Soares 2001, Archives of General Psychiatry; Morrison 2004, Biological Psychiatry).

Here is what is at stake in getting it wrong. An antidepressant may help either patient feel somewhat better. But if the underlying cause is a hormone deficiency, that deficiency keeps working on bone density, muscle mass, body composition and metabolic health the entire time — none of which appears on a mood questionnaire. The score improves. The disease continues. Feeling better and being treated are not the same thing.

One thing we do not do: exercise

Neither of us trains. Not resistance training, not cardio, not walking programmes. Zero. I am stating that plainly because almost every transformation account quietly assumes a gym, and readers end up believing the drug worked because of training they cannot fit into their life.

And I have gained muscle anyway. That is not mysterious once you look at what else is in the protocol. Research on testosterone therapy in obese men with low testosterone on a hypocaloric diet found that while placebo dieters lost both fat and lean mass, weight loss in the testosterone group was almost exclusively fat — with that group regaining 3.3 kg of lean mass during maintenance against 0.8 kg in controls.

How we actually eat

Protein is the lever, and the only metric we actually track is calories per gram of protein — lower is better. Not macros, not points, not a colour-coded app. One number, and you are trying to get it down.

In practice that means batch cooking. Five pounds of ground chicken cooked down at once and portioned by weight, so a decision that would otherwise be made three times a day gets made once every four or five days. Two versions in rotation: a Chinese-style fried rice at about 9.4 calories per gram of protein, and a taco version at about 8.1 — roughly 5,400 calories and 580 grams of protein per batch, which is a bit over six days at two 300 g servings a day.

Neither batch alone reaches the daily protein target, and that is deliberate rather than an oversight — the gap gets closed with the cheapest protein available per calorie. Sliced ham runs about 6.7 calories per gram of protein and eggs about 11.4, so a couple of eggs and a few servings of ham closes a 55–60 gram gap for well under 500 calories. The alternative is simply eating larger portions of the batch and cooking more often.

And we still eat normal dinners. Hamburgers. Chicken burgers. Regular food, cooked at home, that nobody would look at and call diet food. Nothing is banned and nothing is a “compliant substitute.” The only thing that changes is that we think protein-forward — the protein gets decided first and the rest of the plate fills in around it, rather than the other way round. That is the whole discipline. It is not restriction, it is ordering.

The reason this matters on a GLP-1 protocol is that appetite is suppressed, so whatever you do eat has to carry its weight. Every calorie spent on something with a poor protein ratio is a calorie not available for the protein that preserves lean mass while you are in a deficit. Cooking in batches is how you make that a solved problem instead of a daily negotiation with yourself.

Breaking a stall: the refeed

This is the most reliable single tool I have found, and I have run it enough times to state it without hedging: it has never failed.

The situation it solves is familiar. You are adherent. The deficit is real. The scale has not moved in a week or two. Most people respond by cutting further, which is exactly wrong. Research describes what is actually happening: sustained deficits elevate cortisol by 20–40%, and cortisol drives systemic water retention that masks fat loss on the scale. Studies also document that fat cells emptied of triglycerides temporarily fill with water. The fat is leaving. The scale is lying.

Underneath that, the deficit has suppressed the machinery — published figures put leptin down 40–70% within the first week of dieting, T3 down 15–25%, and non-exercise activity thermogenesis down 200–800 kcal/day as the body unconsciously reduces spontaneous movement.

Why that meal specifically

A large carbohydrate load. A large fry runs roughly 131 g of carbohydrate. Research describes the mechanism: carbohydrate triggers an insulin surge, insulin acts as a physiological antagonist to cortisol, cortisol production drops, and the kidneys release the retained water. Carbohydrate also raises leptin faster than fat or protein does, and drives T4→T3 conversion.

Roughly 2,000 mg of potassium. Those fries are hand-cut fresh potatoes with the skins on, fried in peanut oil, no artificial additives. Potassium is central to sodium and fluid balance, and it is typically depleted during a sustained deficit on low food volume. About 60 g of protein from the double burger with bacon. And it is minimally processed — potatoes, peanut oil, beef.

That last point matters more than it sounds. This is not the same intervention as ice cream and cake. Same calories, but almost no protein, no potassium, no fibre, and none of the micronutrients concentrated in potato skin. The meal is doing specific work.

What happens

The scale moves within 24 to 48 hours — either it stops climbing or it drops outright. Then, over the following one to two weeks, I will lose around ten pounds, having lost nothing at all in the week before. The published mechanisms line up with that timeline, and they stack: insulin suppressing cortisol and releasing retained water in the first 24–48 hours; leptin rising within 12–24 hours of a carbohydrate load and T4→T3 conversion improving over days one to three; then glycogen refill restoring spontaneous movement across days three to fourteen, with no conscious decision involved. Dirlewanger et al. (2000, AJCN) found three days of carbohydrate overfeeding raised leptin 28% and 24-hour energy expenditure 7%.

People ask whether I exceeded my TDEE that day. Honestly, I probably came close, and I do not know. It does not matter, because the mechanism is not caloric. Even a 1,500 calorie surplus in one sitting is under half a pound of fat. What you are buying is one to two weeks of elevated energy expenditure and restored spontaneous movement. The trade is decisively in your favour, which is why it works every time rather than sometimes.

If a single refeed does not clear a stall, the literature's answer is a longer diet break. The MATADOR study found participants taking intermittent two-week diet breaks lost 50% more fat than those dieting continuously — and kept more of it off. The refeed is a tool that buys a week or two. The diet break is the version with trial data behind it.

Her protocol

Hers is the cleanest demonstration of the whole argument, because it is the shortest. One shot a day. Two a week. That is the whole protocol.

She runs the same 60/30 split I do. Estradiol and testosterone are compounded together into a single vial — not two injections, one. The GLP-1 stays on its own, and that is deliberate: GLP-1 agonists do not share a vial with anything, ever. It is the one rule we do not bend. SuperKLOW is separate too, partly the daily schedule and partly what is in it, since copper-containing peptides do not share a vial with anything either.

Consider the conventional version of the same protocol. Estradiol on its own schedule. Testosterone separately. A GLP-1 weekly. Then whatever else gets added over time, each arriving as its own vial with its own syringe. That is how this is normally sold, because it is how it is normally made — one compound, one product, one more puncture.

That is not about convenience. Published survey data associates repeated injection into a small area with lipohypertrophy in a large share of long-term injectors, with frequency and site concentration identified as the drivers. Fewer punctures is less cumulative trauma to the tissue you need for the next decade of doses. Where the chemistry allows combining, we combine. Where it says no, they stay separate and we say so.

Where we are now

She is down over 100 pounds. I am down over 90.

I am fifty, and I feel better than I did at twenty. Labs came back in great range across the board — no issues, nothing flagged. That is the part I care about more than the scale, because it is the part that says this was done properly rather than just quickly.

We deliberately do not publish a scale reading. Weight moves daily, it moves with water, and a page that quotes a number is out of date the morning after it goes up — and then it is a page with a wrong number on it, which is worse than no number at all. What matters is not today's figure anyway. It is the direction, the duration, and the fact that it is still going.

What I would want you to take from this

Two people in one house. One of us could not stop eating and knew exactly why. One of us barely ate and never found out why. Neither problem was character, and neither responded to the advice everyone gets.

What worked was treating it as what it is — a physiological problem with a physiological solution — and then doing the unglamorous work around it. The drugs made it possible. The protocol is what made it work.