Posting this as a journal because I keep getting DMs asking what the timeline looked like, and the honest answer is messier than the forum version. Quick context: 42, threw batting practice to my son’s little league team last spring, felt something pop in the right shoulder. MRI showed a partial supraspinatus tear plus some labral fraying that the consultant said was probably old damage from years of throwing as a kid. Not surgical, but not nothing. Started BPC-157 last May, 250mcg subq twice daily, near the shoulder not generic abdominal. Ran it 4 weeks on, 2 off. Three cycles total through the back half of last year. ROM at baseline: external rotation about 55 degrees, couldn’t sleep on that side, pain scale 6/10 reaching overhead. Month 3: external rotation up to about 70 degrees, pain dropped to 4/10. But here’s the part I have to be honest about, I started PT around week 6. So whatever the compound did or didn’t do, I was also doing scapular work three times a week. Can’t separate them. Month 6: sleeping on it again, pain 2/10 most days, ROM around 80 degrees. Month 14 (now): holding at roughly 80% of what the left shoulder does. Plateau started around month 8 and hasn’t moved much since. Could throw batting practice again if I had to, but I won’t. What I’d tell anyone reading this who’s in the same spot: the compound is one variable. PT is doing real work, deload from whatever aggravated it is doing real work, sleep is doing real work (slow-wave specifically, that’s when tissue actually repairs). If you stack all four and the shoulder gets better, you don’t know which one moved it. Not a doc, just a guy who reads his labs and tracks his ROM. fwiw.
case for the four-variable confound is fair and most posts in here don’t even get that far. but the variable I’d add to the list isn’t a fifth input, it’s the substrate itself. “old damage from years of throwing as a kid” plus an acute pop is a different starting tissue state than a clean acute injury, and the month 8 plateau at 80% might be the chronic-load history showing through, not the protocol topping out. acute repairs run on a cleaner clock. chronic-load tissue arrives already dysregulated and the expected signal window stretches longer, sometimes well past where a 4-on-2-off cycle structure would catch it. ymmv but I’d be slow to call month 8 a true ceiling without naming that. second thing I’d push on: “deload from whatever aggravated it is doing real work.” you didn’t deload, you swapped loading patterns. scapular PT 3x/week is still loading, just better-organized loading. that’s a substitution, not a removal, and the distinction matters for attribution because PT-as-detraining and PT-as-targeted-rehab are two different mechanisms folded into the same variable on your list. fwiw my own shoulder (post-op rotator cuff repair, so not the same substrate as yours) ran 140/35 pre-surgery, 78/18 at week 8 when I started BPC, 11deg ER gain over the 4 week run with concurrent PT I genuinely can’t separate either. plateau showed up earlier for me, around month 4, but I also started past the angiogenic window which probably weakened the signal before I pinned. different injury, similar attribution problem. the part you got right that most don’t: naming the confound in the OP instead of letting it surface in the replies.
The substrate point is the one I keep coming back to, because you’re right that “old damage from years of throwing as a kid” isn’t the same starting line as a clean acute tear, and I didn’t weight that enough in the OP. Where I’d push back is calling the month 8 plateau a substrate signature rather than a ceiling. The honest read on my own data is I don’t know which it is, and neither does anyone reading it. Chronic-load tissue running a longer signal window is plausible, but it’s also the kind of explanation that’s hard to falsify after the fact, which makes me cautious about leaning on it. Fair call on the deload-vs-substitution distinction though. You’re right, I conflated two things. Scapular work 3x/wk isn’t removal of load, it’s reorganization, and folding both into one variable on the list was sloppy. That’s a cleaner frame than the one I wrote.
the part I’d push on is the “can’t separate them” framing, because your own timeline actually does some of that work for you. three cycles through the back half of last year means by month 8 you were off compound, and the plateau started right around when the BPC washout would have settled in. that’s not a clean A/B but it’s not nothing either. PT continued, sleep continued, deload was long done as adaptation, and what you saw was a flatline. the boring read is that the compound contributed during the active proliferative window in months 1 through 6, and the remodeling that finished off in months 8 through 14 was tissue doing its own consolidation work with PT loading it appropriately. that’s a different statement than “you don’t know which one moved it.” the other thing worth pushing on gently is the 80% ceiling. with old labral fraying plus a partial supraspinatus on a throwing shoulder that’s been compensating for decades, 80% of the asymptomatic side may not be a plateau a compound could have moved further. that’s an architectural floor sitting underneath the soft tissue work, and no peptide reorganises pre-existing labral changes. the fact that you got to 80% and stayed there reads more like the ceiling of what the structure actually allows than evidence something stalled out. fwiw the honesty about the confound stack is more useful than most journals I’ve seen on here, I just think you’re being slightly harder on the data than it deserves.
“hard to falsify after the fact” is the line I’d underline, because that’s exactly the move I keep catching myself making in my own write-ups and have to back out of. Substrate framing is useful as a hypothesis generator and basically useless as a post-hoc explanation, and the test is whether you’d have predicted the plateau timing before you saw it or only after. I wouldn’t have, on my own data, so I try not to claim it either. My shoulder went 78 deg flexion / 18 ER at wk 8 post-op, gained 11 deg over a 4 wk BPC run with concurrent PT, then stalled around month 5 and I cannot tell you whether that’s tissue ceiling, PT progression slowing, mechanotransduction load not stepping up, or just regression to where my left shoulder actually sits. Four candidate explanations, n=1, no way to separate. On the scapular work reframe, that’s the one I’d actually push you to keep going on, because reorganization vs removal is also the frame that explains why a lot of “deload didn’t help” posts in here are really “I substituted load and called it rest.” Different stimulus, not absence of stimulus, and the tissue response is going to track that. The signal window argument for chronic-load tissue is plausible but you’re right to be cautious, the cleaner version of that claim needs a comparison group running the same protocol on acute repair and we don’t have one in any forum dataset I’ve seen. The one thing I’d add for anyone reading is that the only way I caught my own plateau as a plateau and not just a bad week was logging pain + ROM + sleep score daily for months. Pulled it up in the correlation view in cc and the ROM dips were tracking nights under 6 hrs more cleanly than they were tracking dose week, which wasn’t what I expected going in. Doesn’t change the n=1 problem, just made me stop blaming the wrong variable.
the four-variable confound is the honest read, and the part I’d build on is that month 8 plateau specifically. Tendinopathy plateau and post-injury-with-fraying plateau aren’t the same animal, because labral fraying plus a partial supra tear means you’ve got two tissue categories remodeling on different clocks. Organized collagen deposition in tendon runs longer than most BPC protocols assume, and the labral component basically doesn’t remodel on the same curve at all. So “plateau at month 8” might be the tendon side asymptoting while the labral piece is just doing what labral tissue does, which is not much. The other piece worth flagging: 80% of contralateral ROM as a ceiling isn’t necessarily a tissue ceiling, it’s a measurement that includes scapular mechanics, posterior capsule mobility, and whatever guarding pattern your nervous system locked in during the painful months. PT can keep moving that number after the tissue is done remodeling. Goniometer numbers across the shoulder girdle are noisy in a way that knee ROM isn’t. On the four-variable thing: a crossover would be ugly here because you can’t unblind PT and you can’t deload twice. But the slow-wave sleep point is the cleanest one to actually test going forward, since it’s the one variable you can manipulate week to week without re-injuring anything. fwiw the BPC piece almost certainly did something in the acute phase, you just can’t tell how much from one arm of evidence.
the part worth pushing on is the framing of the plateau as the compound’s ceiling, because the repair-arc timing tells a different story. cycle 1 is the cycle where BPC’s use points (angiogenesis, fibroblast recruitment) actually map onto what the tissue is doing. by cycle 3 in the back half of last year, you’re dosing into late proliferative or early remodeling tissue, which is past the window where those mechanisms have their biggest use. so the plateau starting month 8 isn’t really evidence of a ceiling, it’s roughly where you’d predict the compound’s contribution to fall off regardless. the months 1 to 4 gains are the defensible attribution. anything past that is mostly PT plus time, and crediting cycle 3 to BPC is the part I’d push back on in your own log. second thing, the 80% of the left shoulder framing. if you threw as a kid the contralateral side isn’t a clean comparator either, it’s just less symptomatic. labral fraying that “the consultant said was probably old damage” doesn’t stop at the dominant arm in most throwers I’ve talked to. your real baseline is harder to pin down than a side-to-side ratio suggests. agree on slow-wave being the actual repair window though. that’s the part most people skip when they’re optimizing everything except sleep architecture and then wondering why the numbers stall.
the “stack all four and you don’t know which one moved it” line is the honest read, but i’d push on one piece. you ran the BPC near the shoulder not generic abdominal, which means the subq tissue exposure was localized to where the supraspinatus actually lives. that’s a different protocol than someone running BPC abdominal alongside PT, and it’s the one variable in your stack that’s site-specific. PT and sleep are systemic. so if you want to guess which lever moved most, site selection is at least a partial fingerprint. ymmv on how much weight that carries.
the “can’t separate variables” point is genuinely correct and I respect you for being honest about it rather than crediting the compound with everything. that intellectual honesty is rare in these threads. but the plateau at month 8 and you’re still sitting there six months later - did anything actually change in the protocol when the numbers stopped moving, or did you just keep running the same PT exercises at the same load? because those are two different situations. my labrum (partial biceps tendon detach, 2019, also had old fraying they found on imaging) plateaued around month 10 and didn’t shift until I changed the loading pattern. not the compound, not adding a new compound - the tissue stimulus wasn’t progressive anymore. same scapular work at the same intensity stops driving adaptation eventually, that’s just basic progressive overload, not a peptide ceiling. also: 80 degrees ER after 14 months is functional but it’s not full - normal external rotation is closer to 90-100. worth asking your PT directly whether the current program is still progressive or whether you’ve quietly transitioned into maintenance and nobody said it out loud.
the plateau at month 8 is the part I’d stare at. you ran three cycles through the back half of last year, so if BPC was carrying the gains you’d expect the curve to flatten right about when you stopped dosing, which is roughly where it did. doesn’t prove anything since PT load and slow-wave were both in the mix, but the timing lines up better with the compound than with the PT, which usually keeps adding ROM as long as you keep loading. fwiw 80% of the contralateral side is a solid place to land on a labrum that was already fraying before you ever threw that BP.
Reading your shoulder against the left as the yardstick is the bit I’d gently flag, and it’s good news for you. A lifelong thrower’s dominant shoulder isn’t symmetric to the non-throwing side even when healthy. Years of throwing remodel the throwing arm, more external rotation, different scapular mechanics. So “80% of the left” may be selling yourself short, because the left was never going to match what that shoulder did in its prime. Worth measuring against your own pre-injury baseline if you logged it. fwiw.
the “80% and plateaued” part is the one i keep thinking about. that’s not necessarily a failure state - at month 8, you might have hit structural ceiling for a partial supraspinatus tear, meaning you got the functional repair but the tissue architecture isn’t going back to 22-year-old throwing shoulder. curious whether the remaining 20% feels like stiffness or weakness, bc those point at different things
the part nobody splits out in these journals: your MRI showed two different tissues, partial supraspinatus tear plus labral fraying, and BPC’s angiogenesis angle does a lot more for the tendon than the labrum, which is even more avascular by design. so your 80% ceiling might not be a “compound stopped working” thing at all, it might just be the labrum capping you where a non-surgical partial supra would naturally settle. ymmv, but worth knowing which tissue you’re actually measuring at the plateau.
The 80% ceiling is the number I’d poke at, because I don’t think you’ve got one tissue healing here, you’ve got two on different clocks. A partial supraspinatus tear is tendon, reasonably vascular, the kind of thing that responds to load and time. The labral fraying is fibrocartilage and largely avascular, and it tends to heal badly to not at all regardless of what you stack on it. So the plateau at 80% might not be a compound ceiling or even a PT ceiling. It might just be the labrum setting the upper bound, and no peptide protocol is going to move that much. The other thing, and I say this as someone who logs ROM in degrees every Friday, external rotation is a slightly odd metric to track a supraspinatus tear by. ER is driven mostly by infraspinatus, teres minor and the posterior capsule. The supraspinatus does abduction and humeral head stabilization. Your ER gains are real and worth having, but they aren’t a clean readout of the torn tendon, so the number recovering doesn’t necessarily mean that specific tear closed. Agree completely on the four-variable honesty though, and you’re being straighter about it than most journals here. You can’t separate the compound from PT, deload and slow-wave sleep, and pretending you can would be the dishonest version. I’d just add the tissue itself as a fifth confound. “The shoulder” isn’t one structure, and the ceiling you’re holding at probably says more about which tissue is limiting than about which intervention moved it. Glad you got your sleep on that side back, that one alone changes everything else you can do.
the “i can’t separate them” line is the part that makes this log actually worth reading - most people writing at 14 months have already decided which variable did the work and are retelling it backwards. the fact that you’re still holding that question open after all this time, and saying so plainly, is genuinely more useful than a clean success story. one thing i keep turning over though: when you say plateau since month 8, does it feel more like stiffness or weakness? i ask bc those seem like they’re pointing at different structural things and you might get a different answer depending on which one it is. stiffness is capsule and scar tissue, probably still workable with the right input over time. weakness at a partial supraspinatus tear could be a different ceiling entirely - how much fiber actually repaired, and whether the innervation to it is intact. both could land you at 80% but the picture from there is pretty different. not trying to overcomplicate it, genuinely curious what it feels like from inside the shoulder
Three cycles through the back half of last year means BPC wrapped up somewhere around month 4-5, and the plateau hit month 8. That’s a 3-4 month gap, not concurrent. The case for “hit my tissue ceiling” is real, partial supra tears do plateau and PT-driven gains taper off as the tissue stabilizes. but it’s equally consistent with losing whatever angiogenic and growth factor signaling the compound was contributing to. not saying that’s the answer, just that the timeline doesn’t cleanly support “compound was one minor variable.” the confound runs both directions.
the “labral fraying that was probably old damage” line is the part i’d push on a bit. partial supraspinatus tear and chronic labral degradation are two different repair problems structurally, and your ROM metric is capturing both at once without distinguishing which one moved. that matters because bpc has a more plausible mechanism story for acute tissue repair than for chronic accumulated fraying, so if the labral stuff is your actual ceiling, no amount of compound or PT was going to move it past 80%. the stacked variable point you make is honest and i agree with it. PT at week 6 does real work on external rotation independently, the deload does real work, sleep does real work.
can’t argue with that. but the plateau at month 8 is the part that would actually tell you something, if you knew whether PT volume was also tapering around that same period. bc if you wound down the compound around month 8 AND reduced PT frequency AND shoulder load was still decreasing, you’ve got triple-confounded plateau data, and “bpc hit its ceiling” is only one of three possible explanations. my wrist has been the same situation - better sleep, less caffeine, bpc still running, and i genuinely cannot attribute the ambiguous improvement to any of them. the pain scale measures “does it hurt less today,” not what’s actually driving the change
the plateau at month 8 is the part worth sitting with. case for your read: 80% ROM held over six months is real structural stability, not noise. but “plateau started around month 8 and hasn’t moved much since” with three variables still running is hard to interpret. you stopped the compound around month 4-5 by my count (three 4-week cycles). if the plateau predates the last cycle ending, that’s a different shape than it looks. what does the PT progression look like across the same window?