Increase My T

After 20+ years working with men, I’ve seen it time and again: low T is often behind the statin + SSRI cycle. Optimizing to high-normal with TRT helps many improve cholesterol, mood, and even reduce or drop those meds. Eye-opening read: 👇 increasemyt.com/trt-statins-ss…

IMT client Jessie getting lean and ripped on CJC/IPAM

This powerful trio works across multiple levels: GH-driven tissue repair and metabolism, NAD+-fueled mitochondrial energy and DNA repair, and glutathione-powered antioxidant defense and detoxification. The result is a comprehensive approach that optimizes your cells from the inside out, helping men and women combat age-related decline, enhance performance, and feel their best. increasemyt.com/cjc-1295-ipamo…

BPC-157 excels at accelerating repair at existing injury sites by strongly reducing inflammation and promoting regeneration, but its potent effects may sometimes blunt the acute inflammatory signals needed for optimal muscle hypertrophy. Cibinetide (ARA-290), by contrast, offers a more balanced, preventative approach via selective activation of the innate repair receptor (IRR), modulating inflammation without excessive suppression—making it potentially superior for long-term use and supporting muscle recovery while preserving the beneficial aspects of training-induced inflammation. increasemyt.com/bpc-157-vs-cib…

Cibinetide Acetate - More commonly known as ARA-290 Added this to my program this morning, I gotta say my sciatica pain is literally gone already. Very excited to run this little known peptide. What it does: It reduces inflammation at nerve ends, so if you have pain from back or other injuries that is related to nerve pain, this did really well in studies at reducing that pain. On top of that it should do other things like: 1. Reduce muscle pain, it lowers inflammation at the cellular level and eases discomfort from training which should improve daily mobility. 2. Faster recovery from exercise. Reduces oxidative stress supporting faster muscle repair. 3. Enhances rest quality. 4. Reduces neurological inflammation. My program is all doctor prescribed and each peptide or hormone dosage is designed to bring my levels within physiological range, or a range that a human being can produce naturally. Nothing I am taking gives me supraphysiological levels, or the levels someone would have when taking a steroid cycle. The idea is to optimize levels so that it is healthy for the body, rather than bring levels up higher than that which could be produced naturally which can bring on unwanted side effects. So far I have zero side effects from the program. I will put an article going into to more detail about ARA 290 in the comments.

High protein low fat, low cost pulled chicken prep meal. Full recipe and step by step instructions inside link: increasemyt.com/cayenne-garlic…

Shocking 2026 Peptide Quality Report just dropped. Over 40% of peptides were outside label claim. Some GLP-1 products had zero active ingredient. Nearly 13% failed sterility tests. Almost 20% had dangerously high endotoxins. If you're using peptides for fat loss, TRT, or recovery — this is a serious wake-up call. At IncreaseMyT, we never take risks. All our peptides come from licensed 503A compounding pharmacies under strict USP 797 standards. Read the full breakdown here: Your health deserves better than research-grade roulette. increasemyt.com/2026-peptide-q…

@CoachPauI Very solid advice

8% body fat looks impressive in a photo. And that's about it. The mental bandwidth, the social flexibility, the food enjoyment you trade for it... It's not worth the marginal difference. 12% body fat done right is lean. It's defined. You have size. You look good with a shirt on and off. And you can actually maintain it easily.

@MartinShkreli BPC 157 is the most overhyped peptide there is, ARA 290 is much better for inflammation.

If you like “peptides” like BPC come explain why you’re not retarded

@ThatArizonaGuy1 @gregogallagher

@IncreaseMyT @gregogallagher Buddy, ok. 👍🏼

The beauty of Tirzep over Reta Tirzepatide trials show roughly 75% of weight loss coming from fat, 25% lean mass. For people who aren’t lifting heavy or prioritizing protein, that’s actually solid. And some of that lean mass loss is just glycogen and water dropping from lower calories anyway. Retatrutide is closer to 65/35. The issue is Reta’s additional mechanism, increased energy expenditure. Push the deficit too large and your body hits a ceiling on fat oxidation and starts pulling from muscle instead. The workaround is low-dose Reta. Keep the dose controlled, keep the deficit in the right range and mitigate heart rate increase. But the deeper issue is that with Reta, appetite suppression and energy expenditure are bundled. Want more? You’re getting both plus elevated heart rate. You can’t isolate the variables. With tirzepatide you have one dial. Appetite. Turn it where you want it and you know exactly what you’re adjusting. That’s why I prefer it. Cleaner. More precise.

@ThatArizonaGuy1 @gregogallagher Buddy, I am not struggling for business lol We have been around for 20 years, we don't even have to advertise anymore.

@IncreaseMyT @gregogallagher Hurry! Post again! Someone might buy your T now!

@ThatArizonaGuy1 @gregogallagher Talking about AI slop while he repeats to me the Chinese troll farm talking points

Oh please, in line citations buddy. Just because the conversation is over your head it isn't my problem. You just assumed that Reta had direct GIP effects, but you were wrong, as numerous sub data sets in phase 2 show that there was no rise in insulin sensitivity in low weight loss groups. That is just a fact, so believe whatever you want, but whoever assumed that Reta has direct GIP effects and preserves more muscle simply doesn't know how to extrapolate on medical literature. So feel free to educate yourself, or remain stupid. increasemyt.com/why-tirzepatid…

@ThatArizonaGuy1 @gregogallagher Yea because your a Retatard

@IncreaseMyT @gregogallagher I’m not reading all that 😂. If you cant sum it up then youre just fluffing your bullshit. They’re synergistic not opposing so its not countering it. And you’re still wrong. Youre welcome!!!

@ThatArizonaGuy1 @gregogallagher Let me know if you have any questions Arizona Guy, like I said, the glucagon component is counter regulatory to the GIP action. Reta has no direct GIP effects. Thanks for your attention to this matter.

Tirzepatide (Mounjaro/Zepbound) is a dual GLP-1 + GIP receptor agonist. The GIP component plays a key role in directly enhancing insulin sensitivity in adipose tissue, muscle, and liver — independent of weight loss. Preclinical and clinical studies show GIP agonism improves glucose uptake, reduces insulin resistance (via markers like HOMA-IR and adiponectin), and sensitizes tissues to insulin's effects. Retatrutide, the triple agonist (GLP-1 + GIP + glucagon), also improves insulin sensitivity dramatically (phase 2 trials: HOMA2-IR ↓ up to 52-69%, fasting insulin ↓ up to 70%), but this is primarily driven by massive weight loss (~24% body weight reduction) and increased energy expenditure/fat oxidation from glucagon receptor activation — not the same direct GIP-mediated tissue sensitization seen with tirzepatide. In short: Tirzepatide has a stronger direct mechanism for tackling insulin resistance (especially valuable in type 2 diabetes), while retatrutide excels at overall metabolic overhaul through superior fat-burning. Tirzepatide is engineered as a GIP-biased dual agonist. It has near-native (full) potency at the GIP receptor — essentially matching endogenous GIP — while being slightly less potent at GLP-1. This strong, unbiased GIP activation drives direct improvements in insulin sensitivity in adipose tissue, muscle, and liver (e.g., increased adiponectin, better Akt signaling, GLUT4 translocation, and glucose disposal) that are partially independent of weight loss. Retatrutide is a triple agonist with a GIP backbone but shows super-potency at GIP (8.9-fold greater than native GIP in some assays) while being weaker at GLP-1 and glucagon. Despite the higher raw GIP potency, the molecule is balanced differently to accommodate glucagon activation. This shifts the overall signaling profile away from pure GIP-driven effects. Tirzepatide's design as a GIP-biased (or imbalanced) dual agonist prioritizes robust GIP receptor activation—demonstrating comparable affinity and equipotency to native GIP at the GIPR, with full agonist activity—while showing reduced potency at the GLP-1R (approximately 5-fold lower affinity and 20-fold lower in low-receptor-density cAMP assays; Willard et al., 2020; Finan et al., 2016). This profile allows near-full engagement of GIP pathways, which contribute to direct, weight-independent enhancements in insulin sensitivity across tissues: in adipose (via improved glucose uptake and catabolism of glucose/lipids/BCAAs), muscle, and liver (e.g., reduced ectopic fat, better Akt/GLUT4 signaling, and adiponectin upregulation; Campbell et al., 2021; Heise et al., 2023). Preclinical data in obese insulin-resistant models confirm GIPR agonism (including from tirzepatide) boosts white adipose tissue glucose disposal independently of GLP-1R-driven weight loss, highlighting GIP's role in metabolic repair beyond calorie restriction. Clinically, this translates to superior HbA1c reductions and insulin sensitivity gains versus pure GLP-1 agonists, with potential advantages in metabolic syndrome or fatty liver contexts. Retatrutide, built on a GIP backbone as a triple agonist, achieves super-physiological GIP potency (8.9-fold greater than native GIP at the human GIPR) but balances weaker activation at GLP-1 (0.4-fold) and glucagon (0.3-fold) receptors (Jastreboff et al., 2023; Willard et al., 2023). The glucagon inclusion introduces hepatic glucose production/lipolysis and energy expenditure boosts, driving exceptional weight loss (up to ~24% in phase 2 obesity trials), but this multi-hormone synergy shifts away from the focused GIP-mediated insulin sensitization seen with tirzepatide—potentially trading some tissue-specific metabolic benefits for broader catabolic effects (e.g., enhanced fat oxidation and substrate utilization). In phase 2, retatrutide excels in profound bodyweight reduction and glycemic improvements, but the glucagon component may introduce mild counter-regulatory dynamics that dilute pure GIP-driven perks in insulin-sensitive tissues. Overall, these molecules showcase evolving incretin pharmacology: Tirzepatide optimizes native-like GIP power for targeted metabolic restoration (insulin sensitivity gains partially decoupled from weight loss), while Retatrutide's triple action pushes maximal weight shredding through synergistic energy expenditure and intake suppression. The dependence of retatrutide's insulin sensitivity improvements (primarily assessed via HOMA2-IR reductions) on weight loss, rather than being independent, can be extrapolated from multiple phase 2 trial datasets where these metabolic changes are repeatedly described as occurring in parallel with, and proportionally to, the magnitude and timeline of body weight reduction, visceral/abdominal fat loss, and liver fat clearance—without any reported dissociation or evidence of meaningful sensitivity gains in low-weight-loss subgroups. In the key MASLD substudy (Nature Medicine, 2024), HOMA2-IR improvements reached up to −69.3% at 48 weeks with higher doses (≥4 mg), but this tracked closely with dose-dependent body weight losses of 22–24% and liver fat reductions of 81–86%; the authors explicitly noted significant linear correlations (P < 0.05) between relative liver fat reduction and percent changes in insulin, C-peptide, HOMA2-IR (both insulin- and C-peptide-based), triglycerides, adiponectin, leptin, and FGF21 at both 24 and 48 weeks, indicating that sensitivity enhancements are mechanistically linked to fat mass/ectopic lipid clearance rather than a standalone direct GIP effect. Similarly, in the main phase 2 obesity trial (NEJM, 2023), fasting insulin and glycemic marker improvements aligned temporally with the progressive weight-loss trajectory (e.g., −17.1% to −24.2% at 48 weeks across doses), with no plateau in weight curves or subgroup data isolating sensitivity benefits independent of fat loss; the glucagon component's role in driving energy expenditure and catabolism further supports that the net metabolic repair is amplified by—and reliant on—the substantial fat reductions achieved.This contrasts sharply with tirzepatide, where preclinical models and select clinical analyses more explicitly demonstrate weight-decoupled GIP contributions to glucose uptake and signaling; for retatrutide, the absence of clamp-based studies, non-responder analyses, or mechanistic dissociation experiments in published reports reinforces that the observed HOMA2-IR gains appear predominantly mediated by the profound obesity-related metabolic stress relief (e.g., reduced hepatic/adipose inflammation and improved substrate handling) that weight/fat loss itself provides. Phase 3 TRIUMPH program data (emerging as of late 2025) continue to show similar tight linkages between glycemic/insulin endpoints and weight outcomes, with no clear evidence emerging of robust, weight-independent insulin sensitivity effects from the GIP agonism alone.

@ironnfox Further, because of these direct GIP effects that Reta lacks, Tirzepatide is highly synergistic with IGF raising compounds.

Your wrong. Tirzepatide, because of it's strong GIP bias exerts direct action on insulin sensitivity, HPA function and inflammation. So it is therefore superior at preserving muscle, and with proper training and diet you can actually build muscle on a caloric deficit with it, much like Tren. Reta doesn't have any direct GIP effects because the glucagon component is counter regulatory to the GIP effects.

The type of glp used isn’t what determines muscle sparing or preservation. That’s resistance training and protein. Correct me if I’m wrong.

You can admit you were wrong Paul. Phase 2 trials are clear: 1) Insulin sensitivity gains occur in parallel to and in proportion with weight loss 2) Low weight loss groups had no increase in insulin sensitivity at all 3) Studies show sub 4mg Reta dosages don't really do anything at all This is in sharp contrast to Tirzepatide which directly increases insulin sensitivity, stimulates HPTA function, and directly decreases inflammation independent of weight loss even at micro dosages. Everyone just assumed Reta had direct GIP action, but the literature shows that the glucagon component is counter regulatory to the GIP effects. So everyone was wrong, and it is ok to admit that.

The issue here is the clinical trials were done on super obese sedentary people. They have zero relevance to the bro community’s Of course these people lost muscle. They ate less of the same shitty low protein high fat diet they did before. The likely didn’t workout either.

Increased insulin sensitivity is super important for bodybuilders on multiple levels. First, when using GH and androgens these increase IGF. So there is a super synergistic effect when combining them, because the increased insulin sensitivity increases nutrient partitioning efficiency. Basically it shuttles more nutrient to the muscle after IGF primes mTOR. Not to mention the decreased inflammation leads to a 25% reduction in cardiovascular disease risk, independent of weight loss. So I am not sure what you mean. Tirzepatide is just a superior peptide, because of its strong GIPA bias, unless your trying to lose 100 pounds really fast.

@LateToLongevity @gregogallagher What does that mean? Are you suggesting that bodybuilders don't benefit from increased insulin sensitivity and decreased inflammation? Maybe you don't understand what increased insulin sensitivity means.

@LateToLongevity @gregogallagher Unless your BMI is well over 35, and not because of muscle because of fat, Reta is absolutely pointless. But the Chinese trolls have sold it to everyone and everyone bought the BS hook line and sinker.

Tirzepatide is better in every way. Studies show that insulin sensitivity gains with Reta occur in parallel and in proportion to weight loss. Low weight loss sub groups had no increase in insulin sensitivity at all. Tirzepatide however, because of it's strong GIP bias, exerts direct action on insulin sensitivity, the HPA and inflammation. It is superior in every way at micro dosages for moderate fat loss.