My fiancé has been dealing with some peculiar issues that I’m trying to connect the dots on and would love input. She had lower leg swelling in the past that eventually resolved, and a remote history of Morton’s neuroma that hasn’t been symptomatic for years. Right now her main struggles are poor sleep, consistently low energy, chronic back tightness, and most notably significant thumb pain with joint locking. She describes it as if the thumb “needs to be pulled out.” Both sides were affected at first, but interestingly the untreated side resolved spontaneously while the PRP-treated side continues to be painful and lock regularly. Her job as a personal trainer and working retail means a lot of daily standing, hand and wrist loading, and repetitive strain. Emotionally, she’s carried stress since her father passed away three years ago she handled it well but still has difficult days. Nutritionally, she was vegetarian for about 40 years before introducing chicken 5–6 years ago, but otherwise eats minimal animal protein. My working thought is that this may not just be an isolated tendon or joint problem but a systemic terrain issue possibly a fibrosis-prone environment that explained the paradoxical PRP result, along with lymphatic or vascular fragility from standing all day, circadian and mitochondrial dysfunction contributing to poor energy and recovery, long-term nutrient debt from decades of vegetarianism (creatine, carnitine, B12, zinc, glycine, proline, lysine), and stress physiology from her HPA axis that stiffens fascia and keeps her in sympathetic tone. I’ve sketched out a phased protocol: first reset terrain with circadian support (melatonin or Epitalon), mitochondrial stack (SS-31, Kenetik Pro, plasmalogens), lymphatic strategies (compression, walking, electrolytes), and add Amlexanox as a fibrosis/inflammation reset. Then in phase 2, move to matrix remodeling with BPC-157, TB4, Pentosan Polysulfate, phosphatidylcholine, local tendon glides, red light, topical magnesium, and NeuFit or PEMF for fascia and back tightness, alongside nutrient repletion with collagen peptides, vitamin C, glycine/proline, zinc, copper, and manganese. Finally in phase 3, focus on integration and resilience with Epitalon cycles, MOTS-c, sauna and cold contrast, tendon-friendly strength training, strict sleep hygiene, and nutrient support like creatine, carnitine, and DHA/EPA. I’d re-evaluate with imaging if the thumb pain and locking persist or run labs if swelling recurs. My questions are: does Amlexanox make sense as a first step to rebalance the inflammatory/fibrotic terrain before PPS or repeat PRP? Is the PRP paradox more likely a redox/cellular terrain issue or immune imbalance? And am I over-attributing her back tightness and energy issues to systemic inflammation/lymphatics, or does that reasoning fit? Would love to hear how you all would think through this. @Elizabeth Yurth @Cynthia Keller @Carl Paige @Eric Fete @Eric Serrano anyone else! I’m here to learn and I want to be able to help her.

I have what I believe to be an acute strain to the plantar fascia. (36 hours) Trying NOT to throw the kitchen sink at it. Readily available to me BPC-157, TB-500 GHK-CU, KPV Cartalax Red light - R+ | NIR+ wavelengths of 480nm, 630nm, 660nm, 810nm, 830nm, 850nm and 1060nm. I believe caused by increased overuse and chronic dehydration. Also fairly certain Pickleball was invented by orthopedists.

Cerebrolysin for better brain function — has anyone tested it, and what are the recommended dosages and protocols?

This whole “six-stage agonist” idea reads like a playground contest where six-year-olds are trying to one-up each other without thinking through the consequences. One kid says, “I can eat the most candy,” the next says, “Well I can stay up all night,” another brags, “I can ride my bike with no hands,” and pretty soon the game spirals into chaos everybody competing, nobody coordinating, and the end result is a bunch of sick, cranky kids. That’s exactly what happens when you try to bolt GLP-1, GIP, glucagon, IGF-1, Klotho, and myostatin inhibition together into a single product. Each of these signals has real, powerful effects on metabolism, growth, and cellular resilience, but they pull in opposite directions, act on different timelines, and demand very different dosing windows. Instead of synergy, you create noisy cross-talk that leaves the body trying to follow six conflicting orders at once. True optimization doesn’t come from piling on more levers or chasing the newest shiny receptor target it comes from respecting the intelligence of the cell, reducing signal noise, and using surgically precise interventions at the right time and in the right tissue. A “GLP-1 + GIP + glucagon + IGF-1 + Klotho + anti-myostatin” cocktail is mechanistically incoherent because it stacks pathways that biochemically push in opposite directions, on different clocks, in different tissues. GLP-1R and GIPR are Gs-coupled incretin receptors that raise cAMP/PKA and potentiate β-cell insulin secretion, slow gastric emptying (GLP-1), and alter CNS appetite; GCGR is also Gs-coupled but in hepatocytes it spikes cAMP/PKA to drive glycogenolysis and gluconeogenesis, directly opposing the glucose-lowering aim of the incretins and serine-phosphorylating IRS1 to blunt insulin signaling in liver. IGF-1R is an RTK that activates IRS→PI3K→AKT→mTORC1 and MAPK/ERK to promote hypertrophy and nutrient storage, while soluble Klotho evolved as a longevity brake: it partners with FGF23 for phosphate/Vit-D control and independently dampens IGF-1/insulin signaling and shifts cells toward FoxO-mediated stress resistance and autophagy i.e., the biochemical opposite of sustained mTORC1 drive. Myostatin inhibition removes SMAD2/3 repression at ActRIIB, disinhibiting satellite cells and mTORC1 in muscle; pair that with IGF-1 and you push strong anabolism in myofibers, but the liver is simultaneously being told by glucagon to export glucose and lipids while adipose receives a GIP signal that favors storage so partitioning gets noisy. Add hard constraints from pharmacology: receptor stoichiometry and PK don’t line up. IGF-1 (IGFBP-bound) has long half-life and broad tissue exposure; GLP-1/GIP need DPP-4 protection and act over minutes to hours; glucagon clears fast but hits liver immediately; Klotho’s effects are slow, endocrine, and context-dependent; anti-myostatin requires sustained exposure for weeks to remodel transcription. One fixed dose can’t simultaneously achieve the right receptor occupancy across these targets: the concentration that meaningfully engages IGF-1R will overshoot GLP-1R CNS effects; the dose that meaningfully inhibits myostatin in skeletal muscle will not “time-match” the brief hepatic cAMP bursts from glucagon; and any hepatic PKA surge will antagonize the insulin/IGF-1 signaling you need for clean glycogen and protein synthesis. Think of it like six foremen shouting conflicting orders on a construction site: IGF-1 and anti-myostatin demand “build muscle now,” Klotho says “slow growth and repair the scaffolding first,” GLP-1/GIP say “bring in insulin and store nutrients,” glucagon yells “ship the materials back out of the warehouse,” and the clock for each foreman runs at a different speed. The “peer-reviewed” reality is that the only reason GLP-1/GIP/GCGR tri-agonists can work in trials is because they are engineered single peptides with tuned receptor bias and potency ratios to achieve a net, phase-appropriate phenotype; bolting on IGF-1, Klotho, and anti-myostatin as separate levers breaks that balance and guarantees asynchronous, tissue-mismatched signaling. The likely story arc is predictable: week 1 you feel appetite suppression and see scale weight drop from GLP-1 physiology while hepatic glucagon spikes make glucose swing; by week 2–4 IGF-1 and anti-myostatin start pushing muscle protein synthesis but collide with hepatic PKA-mediated insulin resistance and GIP-biased adipose storage, so nutrient partitioning becomes erratic; by weeks 4–8 Klotho’s brake on IGF/insulin signaling and phosphate/Vit-D shifts muddy recovery and mitochondrial quality control, leaving you with jittery glycemia, inconsistent pumps, GI side effects, possible edema or mineral issues, and a plateau where fat isn’t reliably falling and muscle isn’t cleanly accruing. Instead of a symphony you get six instruments in different keys, different tempos, and different rooms the score reads “recomp,” but the sound is chaos.

I’ve been running 250mcg SLU-PP-332 fasted AM 5x weekly. Taken with NR, Urolithin A, Fatty15. I’m going to be increasing my dose to 500mcg and curious if people are having more success going with a bolus dose and taking the full 500mcg AM, or splitting it 250 AM and 250 afternoon?