After a long time, I’ll be in the US again as I’m heading to the Olympia. I also got a ticket for Olympia University, and I see that at least two members of the group will be speaking there – @Elizabeth Yurth and @Eric Fete. Can’t wait :) Will anyone else be there?

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.

The TLDR feel like I’m doing “the basics” pretty well but my immunity is still terrible since being a dad - what am I missing? I’ll try keep this short but realise I need to provide enough info for context… here we go… apologies up front for the length of the post. Basically I’m a new dad to a 9 month old boy and it seems like every month or so I’m loosing a week to some bug, and then need to take it slow while recovering, get back in the groove for 2-3 weeks and then back in the trenches… pre being a dad I’d maybe be sick enough to impact training 1-2 times a year. I eat relatively healthy, 2-3 cups of berries a day, healthy fats largely from eggs, avocado, olive oil and supplementing omega 3s (I have a genetic polymorphism that apparently means I do better on monounsaturated vs saturated), plenty of meat, and when I have starches or heavier carbs I try let them have a cool down period first to get cold resistance starches and pair them with vinegar / berberine / cinnamon and / or a walk. My supplement stack is tailored primarily around addressing common deficiencies as well as personal genetic bottlenecks I have due to gene polymorphisms like MTHFR, and others related to estrogen clearing / troubles generating vitamin d / a / choline AM empty - alternate CDP choline / alpha-gpc AM with meal - methylated b vitamin complex - vit d3/k2 - Omega 3s - Artichoke extract (EOD) - Additional sublingual b12 (every 3 or 4 days) PM - tmg - Vit a (every 4 days) - Calcium d glucarate (twice a week) - DIM (twice a week) - Boron - Mag glycinate - Zinc / copper - L-theanine Also incorporate creatine, PHGG, and high dose taurine and glycine into most days as part of a smoothie… I try train 3 days strength, 2 cardio a week (when not battling flu), movement snacks through the day, I’m pretty good with sleep hygiene (baby permitting), breath practices, sun exposure, and getting 10k or more steps, intermittent fasting, cold exposure.. again much better at all these things when not sick / recovering and purposefully remove a bunch of them when I am sick so as not to go further downhill..

Would be great to hear anyone’s experience/protocols when it comes to dosing GHRP’s. I’ve been dosing tesamorelin right before bed, but lately because of my last meal being usually an hour or less before I go to sleep I’ve been concerned that the insulin spike from the carbs/fats is suppressing the GH release. What are people’s thoughts on setting an alarm and having it half way through my sleep cycle vs before bed. That way I know my stomach is empty and I’ll benefit from the full release - or will it have minimal difference either way?

One more question that’s been on my mind. I know the mechanisms and purposes of use, but I’m curious whether you have any opinions or experiences on when to use which, and how. I know that bodybuilders often use glutathione in small doses (around 150 mg three times a week), with occasional larger doses administered intravenously. My question now is whether it’s actually good to use them together on a regular basis. Too much antioxidant activity isn’t beneficial either, since it may disrupt optimal redox balance. So when should glutathione be used, and when NAC + glycine? How does the absorption of liposomal glutathione compare to intramuscular administration? Are there any markers—say in blood tests—that can guide the decision on when to use it? Or is it more a matter of adding glutathione in times of high stress, and otherwise relying on the NAC + glycine combination? I’d really like to hear your opinion. Thank you