it was Breiden Fehoko telling all athletes to stop taking creatine because a good diet and sleep are enough. diet and sleep matter, but food alone doesn't top off muscle creatine stores, which is why supplementing keeps showing performance gains in trials. Read his post and you’ll understand mine more lol

Looking for actual research on peptides, nootropics, metabolic compounds and more? I’ve built an extensive, and growing Compound Index on ELEVATE Research, packed with educational articles, pharmacology, mechanisms of action, clinical studies, and emerging research. No hype. No miracle claims. No “guides” Just a deeper look into the science behind compounds that deserve more attention. Whether you’re new to this space or have been researching for years, there’s plenty to explore. The index is constantly growing daily. elevateresearch.blog/compoun… #ELEVATEresearch #Peptides #Nootropics #Longevity #Research

My doc had me prescribed 150 deca and it’s been outstanding for my knees. It’s like WD-40 for real

I do 100 with my 200 trt and 350-400 with 500 test. Never any issues lol maybe a little mast on top or 25 mg anavar as a pre 😂

I leveled out after about a week, and that too was with test and deca

@PGC1a_RB @NocturnalNelly @PepMariner curious what you guys think about this one.

Could CE-123 be one of the most underrated nootropics in research? I genuinely think it deserves more attention. Everyone talks about modafinil, armodafinil, and the usual dopamine-targeting compounds, but CE-123 is an interesting molecule that rarely gets discussed. CE-123 is a synthetic modafinil analog developed as a more selective dopamine transporter (DAT) inhibitor. And its pharmacology is where things get interesting. Unlike traditional stimulants that can influence multiple neurotransmitter systems, CE-123 demonstrates relatively selective inhibition of dopamine reuptake, with minimal activity at norepinephrine and serotonin transporters in laboratory testing. Essentially, researchers were investigating whether they could improve cognitive performance through more targeted dopaminergic modulation. Here’s what makes CE-123 stand out. 1. Cognitive flexibility A 2018 study found that CE-123 improved cognitive flexibility in rats performing attentional set-shifting tasks. The animals demonstrated better ability to adapt when task rules changed. Interestingly, CE-123 didn’t produce the same increase in premature responding observed with R-modafinil under one of the study’s testing conditions. 2. Memory acquisition and retrieval Another 2018 study demonstrated improvements in spatial memory acquisition and retrieval. Researchers also observed changes in hippocampal dopamine receptor expression, particularly D1 receptors. This suggests its effects may extend beyond simply promoting wakefulness. 3. Motivation and effort A 2019 study investigated S-CE-123 in effort-based behavioral tasks. The compound increased willingness to perform demanding tasks for rewards and partially reversed motivational deficits induced by dopamine depletion. That’s particularly interesting because motivation and cognitive performance aren’t necessarily the same thing. 4. Brain penetration A 2023 pharmacokinetic study compared S-CE-123 with R-modafinil. S-CE-123 demonstrated approximately fivefold higher unbound brain-to-plasma concentration ratios. However, it was also metabolized considerably faster in liver experiments. Better brain penetration doesn’t automatically mean a better drug, but it’s an interesting pharmacokinetic distinction. 5. Aging and cognitive decline Perhaps my favorite finding comes from research involving aged rats. S-CE-123 improved performance in certain reward-motivated cognitive tasks, while younger animals didn’t demonstrate the same improvements. That raises an interesting possibility: compounds like CE-123 might have greater utility when dopaminergic function is compromised rather than already operating normally. Now the important limitations. CE-123 remains an experimental research compound. There are no established human cognitive benefits, clinical dosing standards, or comprehensive human safety data. And the results aren’t universally positive. Some studies found improvements in motivation without corresponding improvements in attention or spatial learning. We also can’t assume its selectivity eliminates cardiovascular, sleep, dependence, or other stimulant-related risks. Still, the research is fascinating. A modafinil-derived compound with selective DAT inhibition, promising preclinical findings involving memory and cognitive flexibility, and potentially interesting applications in age-related cognitive dysfunction? That’s exactly the kind of compound I think deserves more scientific attention. Not because it’s proven superior to modafinil. But because its pharmacology raises questions worth investigating. CE-123 might be one of the more overlooked experimental nootropics out there. What do you think? Underrated research compound or another promising molecule that won’t translate beyond animal studies? For research discussion only. Not medical advice. #CE123 #Nootropics #Neuroscience #CognitiveEnhancement #Dopamine #Modafinil #BrainHealth #Longevity #Elevateresearh

What if blocking a single inflammatory signaling molecule could extend lifespan by approximately 25%? That’s exactly what researchers observed in mice. A 2024 study published in Nature by Widjaja and colleagues investigated interleukin-11 (IL-11), an inflammatory signaling protein associated with aging, fibrosis, and metabolic dysfunction. The results were impressive. Researchers used two different approaches. First, mice genetically lacking IL-11 lived approximately 24.9% longer on average. Second, normal mice receiving an IL-11-blocking antibody beginning at 75 weeks of age experienced substantial increases in median lifespan. Males lived approximately 22.5% longer. Females lived approximately 25% longer. And lifespan wasn’t the only improvement. Researchers observed better metabolic health, improved muscle function, reduced frailty, and fewer visible tumors at autopsy. Mechanistically, IL-11 inhibition influenced ERK, AMPK, and mTORC1 signaling. That last pathway should sound familiar to anyone following rapamycin and longevity research. But here’s where things get interesting. IL-11-targeting therapies have already entered human clinical development. However, those trials are investigating fibrotic diseases, including pulmonary fibrosis, not aging or lifespan extension. That’s an important distinction. We currently have compelling mouse data, but no evidence that IL-11 inhibition extends human lifespan. The longevity findings also need independent replication. And while reducing excessive inflammatory signaling sounds beneficial, IL-11 has physiological functions. Chronically suppressing it could introduce consequences that short-term studies won’t detect. This is why the ongoing human trials are worth watching. Not because they’ll establish IL-11 inhibition as an anti-aging treatment, but because they’ll help clarify its safety profile and biological effects in humans. A 25% lifespan extension in mice is remarkable. Translating that into safe, meaningful benefits for humans is an entirely different challenge. Promising target? Absolutely. Proven longevity intervention? Not even close. #IL11 #Longevity #AgingResearch #Inflammation #mTOR #Rapamycin #Biotechnology #Biohacking #LifeExtension #ElevateBiohacking

Metformin has been around for nearly 70 years, but new research suggests this old diabetes medication might have some interesting effects on the aging brain. A randomized, double-blind trial from Mayo Clinic, published October 27 in the Journal of Clinical Investigation, examined 40 older adults with insulin resistance over 40 weeks. Participants received either metformin or placebo, with both groups receiving vitamin B12. Here’s what researchers observed: Metformin improved BMI, body fat, fasting glucose, and HbA1c. Brain glucose uptake increased relative to placebo in four regions rich in insulin receptors, including areas of the prefrontal cortex, retrosplenial cortex, and thalamus. Whole-brain glucose uptake showed a positive trend but didn’t reach statistical significance (p = 0.086). A composite score combining processing speed and working memory also improved. Sounds promising, right? Here’s where the details matter. There were only 20 participants per group. The cognitive composite was constructed post hoc, and the other cognitive measures didn’t demonstrate significant differences. A conference abstract from the same trial also reported reductions in leg lean mass and a small decline in VO2 peak among participants receiving metformin. And importantly, this wasn’t a dementia prevention trial. Researchers measured metabolic changes, brain imaging, and cognitive performance over approximately 10 months. My takeaway? Not a fan. The brain glucose findings are genuinely interesting. Improving metabolic dysfunction may influence how certain brain regions utilize energy. But improved glucose uptake isn’t automatically improved cognition, and improved cognition over several months isn’t proof of dementia prevention. We also shouldn’t ignore potential tradeoffs involving skeletal muscle and aerobic capacity, especially in older adults. Metformin remains an interesting longevity research candidate for many, but interesting mechanisms aren’t the same as demonstrated longevity benefits. But yeah personally, I’m not a fan at all. The research continues. #Metformin #Longevity #BrainHealth #Neuroscience #InsulinResistance #CognitiveHealth ##AgingResearch #Elevateresearch

Agreed

Cagrilintide: What the Research Shows elevateresearch.blog/2026/10…

Yeah it’s always seemed like the perfect dose, i did a split 2x2 am/pm for a bit but 4 before bed was better. Sleep was outstanding

glad you're into it. the research so far is mostly mitochondria and heart stuff, haven't seen anything on ADHD yet

never smoked is the key detail. can't blame old cigarette damage when there wasn't any

whatever you think of his timelines, his computing calls aged way better than most. Which of his health predictions do you think lands first?

wearable data can't really separate the workout from why people train late, like stress or late dinners. the 4 hour cutoff is easy enough to try tho

the six months in bed part is what nobody thinks about. kinda why leg strength and balance seem just as important as the bone scan

thanks for flagging the post hoc composite. the brain glucose uptake part is more convincing to me than the memory score with 20 per arm

7,731 pigs left in 1946 and then they survey the diet in 1949 lol. That timing kinda wrecks the whole sweet potato story

people eating under 0.6 g/kg might just be sicker or eating less overall tho. curious how they adjusted for that