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Bio.Science ∴

@1BioScience

∀ chemical transcendence ∞ for coaching, DM me

pubmed Katılım Ağustos 2025
10 Takip Edilen1.6K Takipçiler
Bio.Science ∴
Bio.Science ∴@1BioScience·
@laowaihistorian @BasedBiohacker its not contradictory, his case is an almost picture book application scenario for ISRIB. The other one is about an extreme scenario where the ISR is fundamental for the preservation of the system.
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BasedBiohacker
BasedBiohacker@BasedBiohacker·
be me > drowning in work > have a flight early tomorrow > have not even packed > many urgent things to do > stress is rising > performance getting impacted > 20mg oral ISRIB > zen. performance. getting shit done. knocking tasks out. first time ISRIB is a positive experience.
BasedBiohacker tweet mediaBasedBiohacker tweet media
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Bio.Science ∴
Bio.Science ∴@1BioScience·
Testogel and no ester solutions are one of the most underrated pre-workouts
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Bio.Science ∴@1BioScience·
@agingroy orexin agonists do not reduce your need for sleep. The functional sleep dependency is rooted in infinitely more than just a fundamental „waking signal“. All you would do is mask the symptoms of sleep deprivation to some extent, which is completely different
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Avi Roy
Avi Roy@agingroy·
If you sleep 8 hours a night, you'll spend roughly 26 years of your life asleep. People with rare short-sleeper mutations (DEC2, ADRB1) need only 4-6 hours, with no health penalty. They get back 7-13 years of waking life. The molecule that controls this is orexin. Your brain's wakefulness switch. Block it, you sleep better (3 drugs already do this). Activate it, you need less sleep. Pharma is racing to build that activator: @EliLillyandCo paid $6.3B, @TakedaPharma expects @US_FDA approval this year. Now @paulkhls and @BioProtocol designed a selective orexin activator using AI in 24 hours, for $500 in lab costs. Instead of targeting narcolepsy like everyone else, they're going after ADHD. Nobody in the pipeline is doing that. Early stage, real obstacles (peptide half-life, brain delivery), but the speed of this is remarkable. @paulkhls curious about your delivery strategy for getting a peptide past the blood-brain barrier?
Paul Kohlhaas bio/acc@paulkhls

🧵 Over 24 hours, our scientific team and AI scientist infrastructure developed a novel peptide agonist to potentially treat ADHD. Below is our paper for a pre-IND computational feasibility assessment for OX2R-004: an 18-residue peptide agonist designed as a selective OX2R agonist for ADHD. Why this matters? No approved orexin agonists exist anywhere. All marketed orexin drugs are dual OX1R/OX2R antagonists for insomnia. Clinical-stage ones are small molecules for narcolepsy only. We did this with @peptai_ a novel full 8-gate computational pipeline in one shot developed by @BioProtocol community 👇

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Bio.Science ∴
Bio.Science ∴@1BioScience·
If you want to recover from Benzodiazepines, the coughing medicine Ambroxol might be one of the best things you could try Chronic benzo use does not merely downregulate GABAa receptors. It also interferes with the trafficking, expression and routing - basically, receptors are not just reduced in their number and sensitivity, but misrouted and placed in the wrong compartments/states all of which must be addressed to regain function Ambroxol - releases GABAa receptors that were literally trapped physically - restores proper synaptic placement and y2 subunit trafficking - biases internalized receptors back towards recycling rather than destruction yielding greater functional GABAa surface expression again a few examples of how it does this are its actuation of lysosomal exocytosis, inhibiting acid sphingomyelinase, being a chaperone for GCase, lysosomal biogenesis and so on
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Bio.Science ∴@1BioScience·
people using "niche" soviet Cold War Nootropics after I tell them their Semax, Selank and Noopept are straight garbage
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Bio.Science ∴@1BioScience·
a special type of lavender oil called silexan can literally give you the same anti-anxiety effects as benzodiazepines - all without the classic side effects (Addiction, Withdrawal, Dependency) Silexan was compared directly to Lorazepam. After 6 weeks, the reduction in anxiety scores was nearly identical: 45% for Silexan - 46% for Lorazepam It doesn't share the GABAergic activity, instead it inhibits VGCCs and interferes with 5ht1ar binding, which downstream basically lowers over excitation, inducing calming and anxiolytic effects
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Bio.Science ∴
Bio.Science ∴@1BioScience·
Using Tudca on Trenbolone can damage your liver Tren downregulates multiple liver transporters such as - BSEP (moves bile acids out of hepatocytes) - MRP2 (responsible for exporting waste, toxins, and things like anions (including trenbolone metabolites)) - MDR3 (exports phosphatidylcholine into bile to basically buffer bile acids) furthermore, Tudca itself is a substrate for these transporters. Since the hepatocyte can't export bile acids when Tren majorly reduced the availability of these exit transporters, TUDCA can start competing with toxic bile acids and metabolites for the remaining few exit nodes This can potentially lead to a buildup of even more toxic bile acids in the liver, worsening liver stress and or injury Tren also initiates polyamine synthesis which drains SAMe, which is required by PEMT to synthesize p-choline. As mentioned prior to this, p-choline is crucial to buffer bile acids and the lack of it induces a shift towards a damaging unbuffered milieu this can further lead to the liver downregulating NTCP, which TUDCA however, requires to enter the hepatocyte, further amplifying toxin buildup here are a few ways for you to prevent this - Sulforaphane: Nrf2 cascade starts MRP3/4 upregulation - citicoline + Betaine/TMG + Creatine for methyl-sparing) - PPARa activation which increases MDR3 expression - Polyenylphosphatidylcholine which can bypass basically the entire synthesis process - astaxanthine - Obeticholic acid or CDCA for FXR agonism, tho Tren is a transagonist which may render it basically ineffective Additionally, besides simply using lower (the usual 250mg) amounts, you can try to avoid the Cmax of both hitting the liver simultaneously to ensure they aren't hitting the same metabolic pathways or transporters at the exact same peak. Tho the effect is nothing to rely on and limited the best way is to simply not exceed doses of 250-500mg, which pretty much avoids this entirely. This mostly serves the purpose of preventing people from upping their Tudca dose on toxic compounds, thinking they will get more protection.
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c@punishedfounder·
@1BioScience you just outed yourself as a retarded grifter if you think any of those 3 compounds is a waste of money
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Bio.Science ∴
Bio.Science ∴@1BioScience·
Low dose DNP is an antioxidant and can be beneficial for your health - yes the fat burner DNP at low doses, it actually - reduced ROS - improve insulin sensitivity - increase autophagy & mitophagy while even showing neuroprotective properties crucially, you can literally die if you use it improperly
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Bio.Science ∴@1BioScience·
@BasedBiohacker dont use ISRIB if youre strongly sleep deprived tho, this will merely fry your neurons instead of providing enhancement
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BasedBiohacker
BasedBiohacker@BasedBiohacker·
> 9-Me-BC experiment begins tomorrow. > switching NAC to NACET. > ISRIB will be trialled acutely when the opportunity arises (sleep-deprived and extremely stressful/ high-stakes day). > bromantane to top up the stock. motion.
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Bio.Science ∴
Bio.Science ∴@1BioScience·
if you want to grow taller and prevent growth plate closure, then inosine will be one of the best supplements you can take Inosine is an endogenous adenosine metabolite that binds A2A receptors with a half-life of 15h vs. adenosine's mere minutes It controls multiple pathways that play into growth plate closure since A2ARs downregulate p53, a key driver of cell cycle arrest, apoptosis & cellular senescence - Inosine additionally suppresses premature stem cell exhaustion, a key driver of GP senescence and activates anti-apoptotic survival programs in chondrocytes to preserve continuous growth support - it even upregulates Δ133p53a, which is a negative p53 splice variant - theoretically making chondrocytes more stress-resistant while preserving PTHP+ stem cell proliferation in the resting zone ➣ considering that its literally a supplement, inosine can definitely be an underrated lever for height growth. It requires re-dosing it multiple times a day tho
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Bio.Science ∴
Bio.Science ∴@1BioScience·
@aestheticprimal and then it goes to the amygdala instead, put you into a state of amygdala overdrive and you rip your work apart and annihilate your setup out of rage
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Bio.Science ∴
Bio.Science ∴@1BioScience·
Most people are massively impairing their performance and potential with their Nootropic and peptide stacks, its perplexing the amount of compounds I see people throwing at themselves because they heard they were good, thinking they are making a generational transformation while damaging their progress is unfathomable Performance enhancement and optimization is a highly individual endeavor. You need something completely different than the guy next to you running uncalibrated protocols shows that most of the space has not actually understood how this should be approached
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