Retatrutide at 3 Months35 Pounds and What Came Next

I usually stay behind the data. This one is different — this is my own stack, my own year, and the notes I have been keeping in a beat-up composition book since the spring. Reader mail keeps asking the same thing: what does a real, boring, sequenced protocol actually look like over months instead of over a single flashy week? So here is mine, in order, with the reasoning I used at each turn and the places where the evidence was thinner than I wanted it to be.

Standard housekeeping first: none of this is advice, and none of it is a recommendation. I am describing what I did, not what you should do. Compounds discussed here are research compounds. Talk to a clinician who knows your labs.

Month one to three: retatrutide, and the part nobody warns you about

I started retatrutide about three months ago. Down thirty-five pounds since.

The number is the easy part to write and the least interesting thing about it. What actually happened is that my relationship with food went quiet. Not "willpower" quiet — the background noise that used to run all afternoon simply turned itself off. That matches what the triple-agonist mechanism would predict: GIP, GLP-1 and glucagon receptor activity together, with the phase 2 data in *NEJM* (Jastreboff et al., 2023) showing weight reduction at the higher doses well past what mono-agonists produced over similar windows.

What no chart prepared me for: the fatigue in weeks three through five, and the way strength training became non-negotiable rather than optional. Losing weight that fast without loading your muscles is how you end up smaller and weaker at the same time. I lifted four days a week the whole way through and I still think I left some tissue on the table.

KLOW: recovery, loose skin, and an unexpected win on my hands

Once the gym volume went up, recovery became the bottleneck. I brought in KLOW — GHK-Cu, BPC-157, TB-500 and KPV in one blend — mostly for connective tissue and for the skin question, because thirty-five pounds down leaves you with real estate that does not snap back on its own.

The skin story is honestly the most reasonable-looking evidence in my whole stack. GHK-Cu has a long dermatology literature behind it: Pickart's work on copper peptide and collagen, elastin and glycosaminoglycan synthesis goes back decades, and it is one of the few things here where the topical human data is not an afterthought. Firmness along my flanks and under my arms is better than the timeline made me expect. Not magic. Better.

The part I did not plan for: the eczema on my hands cleared up. I have had cracked, angry knuckles every winter for as long as I have been writing. Somewhere in week three of KLOW it stopped. GHK-Cu's anti-inflammatory and wound-healing profile is the obvious suspect, and KPV — the C-terminal tripeptide of α-MSH — has its own anti-inflammatory literature, mostly gut models. Is my n=1 hand eczema proof of anything? No. Is it the single most quality-of-life change in this entire log? Also yes. That is worth saying out loud.

The detour: SS-31 before MOTS-c

I wanted MOTS-c next. The pitch is energy, and after three months in a deficit, energy sounded excellent.

While researching it I kept running into the same argument, and it changed my sequencing: MOTS-c is a mitochondrial-derived peptide that signals through metabolic stress pathways — AMPK activation, the folate-methionine cycle work from Lee et al. (2015) in *Cell Metabolism*. The argument goes that if your mitochondria are already inflamed and leaky, you are shouting instructions at a machine that cannot follow them. So repair the machinery, then signal it.

That is where SS-31 (elamipretide) came in — it concentrates at the inner mitochondrial membrane and binds cardiolipin, which is the structural lipid that keeps the electron transport chain organized. There is genuine clinical work behind it in primary mitochondrial myopathy and Barth syndrome, though the trial history is mixed and the headline endpoints have not all landed.

I ran twenty-five days of SS-31, then switched to MOTS-c. Honest reporting: I cannot separate the two effects. What I can say is that the energy floor came up in the second week of MOTS-c and has stayed up, and I did not get the wired, jittery quality I was half expecting. Whether the SS-31 runway mattered or whether I simply stopped being in a savage deficit — I do not know, and I am not going to pretend the sequencing was validated. It was a reasoned bet on mechanism, not a proven protocol.

CJC-1295/ipamorelin, one cycle, then tesamorelin

My shoulder has been a problem since long before any of this. I ran one cycle of CJC-1295 with ipamorelin for it, and it did what growth-hormone secretagogues do — sleep got deeper, the joint got quieter, appetite got louder, which is a strange thing to manage while on retatrutide.

I did not renew it. When SS-31 ended and MOTS-c began, I switched that slot to tesamorelin instead, specifically because the visceral fat evidence is stronger and more specific: it is the one GHRH analog with actual FDA approval for visceral adipose reduction, with trial data (Falutz et al., *NEJM* 2007, and follow-ups) showing meaningful VAT reduction. My weight loss has been generous everywhere except the last stubborn band around my middle. That is the target.

Next up: intranasal semax

The last piece I have not started yet is semax as a nasal spray — cognitive, not physical. The literature is heavily Russian and heavily preclinical, with BDNF upregulation as the proposed mechanism. I am going in with low expectations and I will report what actually happens, including if the answer is "nothing measurable."

What I would tell past me

Three things. Lift, or the scale lies to you. Sequence deliberately instead of stacking four new things in one week, because you learn nothing from a five-variable experiment. And log everything the same day — I lost two weeks of usable notes to "I'll remember it."

Now the part I actually want from you.

If you have run a GLP-class compound and dealt with the skin question, what worked and what was oversold? If you sequenced a mitochondrial repair window before a signaling peptide, did you notice a difference, or is that whole idea just a good-sounding story we tell each other? And if anyone else has had a skin condition unexpectedly clear on a copper peptide — I want to know whether my hands are a coincidence or a pattern.

Leave it in the comments. I read all of them, and the good ones become future posts. This log continues in a few weeks with month-four numbers, tesamorelin notes, and whatever semax turns out to be.

— Nolan