objectionmaxxing

@0xexpt There is an easier way

in theory .. you could get permanent boobs size increase (even without hpl) .. ofc this is NOT medical advice .. just THEORY .. it's trying to mimic pregnancy (with a lot of missing parts) .. just wondering why no one bothered doing trials / studies? phase 1: e2 priming (months 1-2) e2 1->2 mg/day transdermal (gel or patch, not on breast) builds ducts, upregulates prog receptors week 4 IGF-1 check ; no rise = likely non-responder phase 2: add prog (months 3-6) e2 up to 4 mg/day transdermal micronized prog 200->300->400 mg/day oral at bedtime main growth phase caloric surplus +300-500 kcal/day (adipose + aromatase amp) phase 3: consolidation (months 7-9) hold e2 4mg + prog 400mg consider breast MRI at month 9 vs baseline phase 4: stop abruptly will make you retain most size but increase inflammation and cancer risks

@TuckerGoodrich > Born to late to explore the world > Born just in time to explore untested research chemical

Why the enthusiasm for untested drugs? Only a shill gets excited about being a guinea pig.

@0xexpt Yo do any of the vendors sell real og everpharma cerebrolysin or is it all chinese cerebroprotein hydrosolate

This is live btw

@Mitopapi Id add if you have normal COMT with ADHD that long term stimulant tolerance may eventually push you into the no sleep and all noise - no signal zone. First line stims are pretty poor choice imo if you have predisposition for lower D2 density via ANKK1 variant with normal COMT.

People with slow COMT are told they have "high dopamine" and should feel sharp, focused, and motivated. So why do so many of them feel the exact opposite? The answer has everything to do with WHERE your dopamine is elevated and what happens to it under stress. If you've run a genetic panel and seen that you carry the Met/Met variant of the COMT gene, you've probably read that this means you break down dopamine more slowly, which leads to higher dopamine levels in the brain. And on paper, that sounds like it should protect you from attention and focus issues. More dopamine, better executive function, right? For a lot of people, their lived experience tells a completely different story. They're dealing with brain fog, an inability to start tasks, scattered attention, emotional overwhelm, and what feels like textbook ADHD. And the confusion sets in because everything they've read about their genetics says they should have PLENTY of dopamine to go around. Here's where it gets interesting though... COMT is responsible for breaking down roughly 60% of dopamine in your prefrontal cortex (the part of your brain that handles working memory, focus, and executive function) (PFC). But in the striatum (the region that drives reward processing, motivation, and task initiation), COMT handles less than 15% of dopamine clearance. The striatum relies on an entirely different system called the dopamine transporter (DAT) to do that job. Think of it like a building with multiple floors, where each floor has its own thermostat controlled by a different system. COMT is the thermostat on the top floor (your prefrontal cortex). Slow COMT means that floor runs warm. But the other floors (your striatum and reward centers) have their own thermostats, and COMT has almost no say in how those are regulated. Having a warm top floor tells you absolutely nothing about whether the rest of the building is freezing. This is the first major reason why slow COMT and ADHD symptoms can absolutely coexist. The circuits most directly tied to the motivation problems, task initiation failures, and reward insensitivity that characterize ADHD are largely outside of COMT's jurisdiction. But there's another layer to this. Dopamine in the brain operates in two modes. There's tonic dopamine, which is your baseline ambient level that's always humming in the background. And there's phasic dopamine, which comes in quick, sharp bursts whenever something important happens (a reward, a salient stimulus, a moment where your brain needs to lock in and pay attention). These two modes have an inverse relationship. When tonic dopamine is high, it activates feedback receptors that dampen the amplitude of those phasic bursts. Think of it like trying to hear someone clap in a room where the background music is already loud. The clap still happens, but it doesn't cut through the noise the way it would in a quiet room. Slow COMT raises tonic dopamine in the PFC. That part is accurate. But by raising that baseline, it can reduce the contrast of the phasic signals your brain uses to flag what's important, drive learning, and motivate action. So "more dopamine" at baseline can paradoxically translate into LESS effective dopamine signaling when it actually counts. PET imaging studies in people with ADHD have found a very specific pattern: attenuated tonic dopamine release at rest combined with enhanced phasic release during tasks. This tonic/phasic imbalance in fronto-striatal circuits is one of the leading models for how ADHD actually works at the neurochemical level. And slow COMT, by raising tonic levels in the PFC, can contribute to a version of that same signal-to-noise problem from a different angle. Now layer stress on top of all of this. There's a well-established relationship between prefrontal dopamine and cognitive performance that follows an inverted U shape. Too little dopamine and your PFC underperforms. Too much and it gets overwhelmed. There's an optimal zone in the middle where everything clicks. A meta-analysis of 75 published studies confirmed this curve, showing that it explains a significant portion of the variance in working memory performance. For people with slow COMT, baseline PFC dopamine is already sitting closer to the peak of that curve under calm conditions. This means there is very little room before stress, cognitive load, or even mild social pressure pushes them PAST optimal and into territory where executive function starts falling apart. Think of it like a dimmer switch on a light that's already near the top of its range. Any additional input doesn't make it brighter in a useful way. It becomes blinding. A study by Zareyan et al. tested this directly. In a within-subject crossover design, 140 healthy adults carrying at least one Met allele or homozygous for Val/Val each completed executive function tasks in two separate sessions (one under calm conditions and one under mild social evaluative stress), with order counterbalanced across participants. Met carriers performed significantly worse under stress compared to when they were calm. Val/Val individuals showed the opposite pattern and actually performed BETTER under that same mild pressure. This was the first empirical confirmation of the double dissociation that researchers had predicted for years. It's worth noting that two prior studies (Buckert et al., 2012 and Qin et al., 2012) successfully showed that stress impaired Met carriers, but in both cases Val/Val individuals were essentially unaffected by stress, not improved by it. The full double dissociation (Mets worse AND Vals better) was only achieved in Zareyan et al. by using a much milder stressor. The bandwidth for stress to actually boost Val/Val performance is exceedingly narrow. What this means in practical terms is that even everyday stressors (a deadline, someone watching you work, a conversation where you feel evaluated) can crash prefrontal function in people with slow COMT. And when that crash happens, it looks EXACTLY like ADHD from the outside: task avoidance, inability to initiate, scattered attention, emotional dysregulation, etc. The behavioral output is essentially the same, even though the mechanism driving it is different. Research also shows that Met carriers are more environmentally sensitive across the board. A longitudinal study tracking children over time found that COMT Met genotype and early-life family adversity interactively predicted ADHD symptom trajectories, with Met carriers showing steeper increases in symptoms under high-adversity conditions. A separate study found the same interaction with socioeconomic status. This pattern is consistent with what researchers call "differential susceptibility," meaning slow COMT makes you more responsive to your environment in both directions. You benefit more from enriching, low-stress conditions. You're harmed more by adverse ones. So if you have slow COMT and you're experiencing symptoms that feel like ADHD, here's the practical picture. Your PFC may perform well under low-demand, self-paced, calm conditions but buckle under any significant stress or cognitive load. Reducing chronic stress is a neurochemical necessity for you, because even mild persistent pressure degrades your prefrontal function in a way it doesn't for people with fast COMT. Sleep and circadian regulation matter more than you might realize here, because dopamine tone volatility amplifies the PFC function collapses that slow COMT predisposes you to. If you're stimulant maxxxing, it's also worth understanding that Met/Met individuals may be more sensitive to being pushed past optimal PFC dopamine, which can show up as increased anxiety, cognitive rigidity, or paradoxically worse attention at doses that work fine for someone with fast COMT. This argues for careful, gradual titration rather than one-size-fits-all dosing. And if you carry both slow COMT AND a high genetic burden for ADHD (which is entirely possible since they operate through independent pathways), you're dealing with a layered situation. The ADHD component drives baseline fronto-striatal dysfunction, and the slow COMT component adds prefrontal cortex stress sensitivity on top of that. Understanding which piece is contributing what is valuable, because the strategies for managing each are different. The bottom line is this: "slow COMT = high dopamine = no focus problems" is a massive oversimplification that collapses the second you understand how regionally specific COMT's influence is, how tonic and phasic dopamine interact, and how dramatically stress changes the equation for Met carriers. Your COMT status is one piece of a much bigger and more nuanced puzzle. This is for educational purposes only, not medical advice.

@aestheticprimal Pinealon had me dreaming that I was sentenced to 20yrs of hard labour in a North Korean prison.

The beauty about Pinealon is that besides it being able to make you sleep the best sleep you've ever sleeped.. It also seems to do a ridiculously good job at enhancing exercise performance & recovery reducing HR in trained athletes by 10-12 BPM, without reducing power output

@pept_aura Can you guys respond to my support email about cerebrolysin

Lumira has let us know that they will pause their account for a few days in order to upgrade their managements on products traceability and order preparation process

@broncospin @BellaBaddie__ Yeah don't start sweeping your office or your co-workers will assume you're retarded

@BellaBaddie__ Some of the best advice I ever received was when I was 19 and working on a construction site. My boss told me that if I ever found myself looking for something to do, to pick up a broom and start cleaning up. Following that advice has definitely served me well.

Working my first office job. Is it normal to have nothing to do?

@Biomaxxer0 @doctormorphh Appreciate the info 🙏

The neurotoxicity risk is brutally overblown because redditors think 9-me-bc converts to the neurotoxin 2,9-dime-bc because that’s how beta carbolines normally convert via NNMT. what we actually see is 9-me-bc protects dopaminergic neurons against this very toxin as well as MPTP, and repairing neurons already exposed to toxins like salsolinol and rotenone. In general any rat OR human cell cultures exposed to 9-me-bc were protected against neurotoxins across the board. 9-me-bc is already methylated and can’t convert to 2,9-dime but it’s probably smart not to take SAMe while you’re on it as the donor could potentiate NNMT’s neurotoxic conversion, however I still think it’s unlikely that would happen Tl;Dr redditors are retarded, 9-me-bc is safe

@minordissent 90% of professional achievement is getting yourself into a position where that small amount of agency actually means something.

The bar is so incredibly low. If you can muster even the faintest modicum of agency every day for just a few years, you will easily propel yourself into the top decile for your age on every dimension that matters.

@doctormorphh The human equivalent dose of taurine to boost DAT would be +60 grams of taurine.

taurine is calming not only because of its GABA effects but also because it decreases dopamine reuptake by decreasing DAT however at higher doses it can have the opposite which is something to keep in mind

@AbudBakri Testing is a complete waste of time and money.

If you post about a peptide without even testing it you’re going to get flamed If you post an affiliate link for a peptide you’ve never even touched and has safety concerns, I am going to make you wish you never opened a twitter account Let this be your warning

@ConsoomerLs Spamming garbage applications is the only way to get a job.

Does this really work for landing jobs? Spamming garbage applications is a good way to speedrun getting rejected/ghosted imo.

@BasedBiohacker You prefer pinealon in AM or PM?

@cerebrolysin_ Assumed you ordered cerebrolysin based on username lol. I just got my everychem order in Canada but Germany might be more strict idk

@SerfdomByDesign ordered from everychem (US) to germany… i don’t think it’s getting through

No better feeling

@cerebrolysin_ Ya I dont think its coming if its been 4 weeks rip. where did you order from? I had a package from ru pills that's starting to look like it's not gonna clear.

@SerfdomByDesign mine has been in customs clearance for 4.5 weeks now😔😔😔

@wigger @Timcast Tren

@Timcast let's start injecting shit.. ill do whatever you do #experimenttime

should i get tan and jacked?

@AdvancedForged You can't fix stupid

When these dangerous Chinese peptides get handled by compound pharmacies it’s MUCH safer SAFE ME HARDER DADDY • Dosing errors leading to overdoses and hospitalizations (ongoing, highlighted 2024 onward): Multiple reports of patients self-administering 5–20 times the intended dose from multi-dose vials of compounded semaglutide (e.g., due to confusion with units vs. mg/ml, lack of clear instructions, or provider miscalculations). Adverse events included severe nausea, vomiting, abdominal pain, dehydration, fainting, headache, migraine, acute pancreatitis, and gallstones; some required hospitalization. Specific examples: one patient took 5x dose after unclear telemedicine guidance and online self-research; a provider prescribed 25 units instead of 5 units (5x overdose, severe vomiting); another prescribed 20 units instead of 2 units (10x overdose in three patients, nausea/vomiting).
References: FDA alert on dosing errors with compounded injectable semaglutide (July 2024, updated); FDA concerns with unapproved GLP-1 drugs (2025–2026 updates). • Adverse events and hospitalizations from compounded semaglutide and tirzepatide (reported through 2025): FDA received 605 adverse event reports for compounded semaglutide and 545 for compounded tirzepatide as of July 31, 2025 (likely underreported, as many compounders aren’t required to report). Events included gastrointestinal issues (vomiting, nausea, abdominal pain), fainting, pancreatitis, gallstones, and other serious effects; many led to medical attention or hospitalization. Compounded versions showed higher risks for errors, contamination, and preparation issues compared to approved products.
References: FDA postmarket safety information on unapproved GLP-1 drugs (updated 2026); Everyday Health/FDA summary (2025); pharmacovigilance studies using FAERS data. • Deaths linked to compounded semaglutide (reported since 2023): At least 10 deaths associated with compounded semaglutide in FDA’s adverse event database (per Novo Nordisk reports and FDA data). Additional broader reports cite over 900 total adverse events for compounded semaglutide/tirzepatide by late 2024, with 17 involving deaths (some tied to dosing errors or quality issues). These often involved overdoses or severe complications.
References: CNN report on Novo Nordisk CEO warning (November 2024); NAM (National Association of Manufacturers) report on compounded drugs threatening safety (2025); FDA adverse event data summaries. • Increased risks of serious outcomes and specific harms in compounded GLP-1s (FAERS analyses, 2018–2025): Compounded versions linked to higher reporting odds ratios for gastrointestinal symptoms (e.g., abdominal pain, diarrhea, nausea, vomiting), cholecystitis, suicidality, preparation/prescribing errors, contamination, and manufacturing issues. Hospitalization odds were about 2.35 times higher than with non-compounded products. Some cases involved contamination risks or improper sterility.
References: Pharmacovigilance studies in journals (e.g., via Endocrinology Advisor, Frontiers in Pharmacology); FDA inspections and warnings on compounding facilities (2025). • Poison control and overdose spikes tied to compounded GLP-1s (2023 onward): Calls to U.S. poison centers for GLP-1 overdoses (often compounded) rose over 1,500% from 2019 levels in 2023, linked to confusing labeling, lack of instructions, and variable concentrations in vials/syringes. Independent tests showed some products with up to 250% of listed potency, raising overdose risks.
References: Reports from poison control centers; analyses in RealClear Journals and other sources on FDA regulatory failures (2025). *god knows how many unreported

@ferrisbuhler81 Doctors are mostly retarded and the ones who are competent, are not accessible, and grey market is 10x cheaper

Gray market = unmet demand. When the system doesn’t provide a path, people find one. I’m optimistic this will change for the better.

@conductr_ Exposure therapy, lifting, and developing competency in a professional domain.

People who went from insecure to genuinely confident, what was the one shift that actually changed everything for you?