Eternal youth edition. MY CURRENT PROTOCOLDrugs:>Exemestane 6.25mg>Aspirin 300-500mg>Telmisartan 20mg>Montelukast 10mg>Finasteride 1.25mg>Bromocriptine 2.5mg>Ondansetron 4mg>Doxycycline 50mg>Tretinoin 0.1%Base:>Magnesium citrate 1g>Calcium ascorbate 2g>Vitamin E 400mg>Vitamin D 10,000IU>NAC 1g>Vitamin K3 7.5mg>MSM 4g>L-theanine 300mg>Iodine 200mcg
>>77247052>no pitavastatin>no empagliflozinngmi
>>77247052Who cares you all look like skinnyfat indians
>>77247054>pitavastatinDetrimental for muscular hypertrophy and strength. I know we had this debate before, but i can provide new studies to discuss if you want. >empagliflozinNegligible benefits if you're using low-carb diet or perform high-effort physical activity around high-carb meals. I think drugs of gliptin class provide more benefits regarding glucose metabolism by directly upregulating hormones involved in it. >>77247055>you all look like skinnyfat indiansHere's what i look like - 195cm/95kg and 100% aryan.
>>77247069>Detrimental for muscular hypertrophy and strengthWrong and I can gladly cite the MR study again.>but i can provide new studies to discuss if you want.Moreover, with high cholesterol it doesn't matter how many other things you take, you'll still die early.I bet it's another observational trial or worse.>Negligible benefits if you're using low-carb dietA keto diet kills you while empagliflozin protects your kidneys and heart.
>>77247069>Looks like a skinnyfat indian Guessed correctly
>>77247069My friend, you're ugly. Consider plastic surgery.
>>77247120>you're ugly.I'm majestic.
>>77247135Chin bone are good, the rest really need to change.I'd start with your posture, it doesn't take surgery.
>>77247075>I can gladly cite the MR study again.This study haven't showed statins are beneficial or at least neutral for muscles. >I bet it's another observational trial or worse.No. >Simvastatin impairs exercise training adaptationshttps://sci-hub.ru/https://pubmed.ncbi.nlm.nih.gov/23583255/Our findings suggest that simvastatin may mitigate improvements in fitness in response to exercise training by impairing increases in skeletal muscle mitochondrial content and function. In support of these data, physiologic doses of simvastatin disrupt mitochondrial respiration, increase oxidative stress, and activate mitochondrial apoptotic pathways in isolated skeletal muscle fibers (27). Similar observations have been reported in studies of muscle fibers taken from patients using statins (28), and high dose simvastatin (80 mg per day) has been shown to decrease skeletal muscle mitochondrial content in the absence of exercise (29,30). Statins have also been shown to reduce skeletal muscle force production (31), running capacity (17,18) and voluntary running volume (31) in rodents.>empagliflozin protects your kidneys and heart.All it does is lowering blood glucose levels. It's useless if you're not overconsuming carbs or have high level of physical activity when your muscles act as glucose sink, and can lead to hypoglycemia.
>>77247135Negative canthal tiltChud lines nasolabial foldsRecessed jawlinePudgy brow ridgePhiltrum you can play tic tac toe onOverall round potato head faceVerdict : sub5 doomed to a loveless sexless life
>>77247052"Biohacking" is even more cringe than nootropics
>>77247244So true, nattykek bro.
>>77247052The great thing about this retarded shit is that, usually, the problem takes care of itself. You just have to hope these faggots off themselves with their schizo shit before causing too much harm by convincing others to do the same.If you want to spot someone without any degree in any field of biology, or even any schooling in a single course on biology at the college level, that retard faggot list is pretty much it.
>>77247350The amount of ressentiment this threads evoke in lesser men really makes me think biohaking is the new steroids.
>>77247069oh brother
>>77247055
>>77247411True, biohacking is aryan culture.
>>77247370>resentmentFaggot, I don't envy anyone anything. It's literally my fucking job to use endocrinology and neuroscience research to shape policies. All I fucking care about is the application of biological principles to how we live our day-to-day lives in modern society, for the betterment of human functioning. My life revolves around giving people that ability.You're a dangerous schizo.
>>77247135plz fuck me daddy
>>77247435>I don't envy anyone anything.You envy me, like a lesser men should. I humiliated you several times on this board, first time discussing calpain and then discussing aspirin-triggered lipoxins. That's why you're not even trying to debate me anymore and just emotionate.>You're a dangerous schizo.I'm a great alchemist, dangerous indeed.
>>77247069how can you look like a pdf and his victim in the same time???
>>77247411>>77247423Says the slavic potatohead straight from the steppes
Taking an aromatase inhibitor with no test is some fucking retarded shit bro lol. Low estrogen symptoms are often indistinguishable from high estrogen symptoms. You don't want this shit.
>>77247052>>77247069>>77247135
>>77247650Cope.
>>77247530You're correct, look at his physique
>>77247530Exemestane has been the best addition to my stack. Your opinion is skewed by reading reports from users of exogenous androgens and breast cancer patients, as well as use of non-steroidal aromatase inhibitors. In healthy men not using exogenous androgens it acts very differently - exemestane raises total testosterone by 50%, free testosterone by more than 100% and lowers estrogen only by 40%. Here's a good explanation of the mechanism:"AIs absolutely act differently in men who are not HPTA suppressed, due to the actions of an intact negative feedback loop.In men not using exogenous androgens it goes like this...take an AI -> estradiol goes down -> pituitary gland recognizes that estradiol is decreasing -> men only have one way to create more estradiol (aromatization) -> pituitary gland increases gonadotropin production in order to create more testosterone -> this testosterone is aromatized into estradiol.That’s the negative feedback loop at work.When there is an interruption in this loop (gonadotropin production ceases when we use testosterone), that’s when it becomes very easy to drive estradiol too low. Since we are shut down, the pituitary gland is unable to ramp up gonadotropin production in its attempt to create more estradiol via aromatization.There are numerous studies of men on AI monotherapy in which they used very large doses, but did not achieve anywhere near the suppression of estradiol that we would see in somebody using testosterone as well. We’re talking 1-2mg of Arimidex per day, 2.5mg of Letrozole several times per week, etc. What occurred was a significant increase in testosterone levels, and a moderate decrease in estradiol.Here are some relevant studies:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3143915/https://academic.oup.com/jcem/article/88/12/5951/2661508https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2795655/http://press.endocrine.org/doi/10.1210/jcem.85.7.6676https://www.ncbi.nlm.nih.gov/pubmed/11397902 "
>>77247848Too many words to say you're dyel and look like shit
>>77247864>you're dyelI literally don't even lift. My body was built by intense physical labor that i get paid for. >look like shitI mog you.
>>77247530>>77247848>Relevance of anti-inflammatory and antioxidant activities of exemestane and synergism with sulforaphane for disease preventionhttps://pmc.ncbi.nlm.nih.gov/articles/PMC3839725/In conclusion, in addition to its potent mechanism-dependent inhibition of estrogen biosynthesis, exemestane has chemoprotective properties that have hitherto not been explicitly recognized. Exemestane should therefore be considered for use also in chemoprotection against mammary tumors that are not estrogen receptor-positive, and against a wide variety of nonmammary tumors (and possibly other chronic diseases) that are not estrogen-dependent but have oxidative stress, inflammation, and electrophile-damaging etiologies. The additional finding that exemestane shows powerful synergism with another widely consumed Nrf2-activator, sulforaphane, and a number of other phytochemicals, increases the attractiveness of this strategy. Our findings favor the view that use of exemestane with its broad range of actions, and its potential synergism with sulforaphane and other phytochemicals, could be a valuable chemoprotective strategy for reducing the risk of many malignancies and possibly other chronic diseases.
>>77247899>Aromatase inhibitors regenerate the thymus in aging male ratshttps://www.sciencedirect.com/science/article/pii/0192056192901152"...The thymus can be regenerated in aging rats by surgical or chemical castration and regeneration is inhibited by testosterone, which may exert this effect, at least in part, through its conversion to estradiol. An attempt has been made to regenerate the thymus in intact aging rats using inhibitors of the aromatase system, in the hope that this maneuver could lead to the use of such chemical intervention in the treatment of immunodeficiency syndromes. Young adult and aging (18-month-old) male rats were orchidectomized under ether anesthesia and 7 days later given s.c. implants of testosterone in silicone elastomer (SILASTIC) tubing. Some rats received testosterone together with a five-fold excess of the aromatase inhibitor 1,4,6-androstatriene-3,17-dione (ATD). One group of young intact rats received implants containing 25 mg ATD and group of 18-month-old intact rats received 125 mg ATD or 25 mg of another, more powerful aromatase inhibitor 4-hydroxyandrostenedione (4-OH). On the 28th day after implanting, rats were killed and the thymus, spleen, prostate gland and seminal vesicles removed for weighing and histology. In addition, estrogen receptors were measured in the thymus was enlarged after orchidectomy and greatly restored in aging rats. In aging rats, both aromatase inhibitors restored the thymus, which appeared normal histologically. In addition, ATD enlarged the thymus in young intact animals. ... It is therefore possible to restore the thymus in intact aging rats without recourse to surgical or chemical castration, and such a maneuver may possibly be of use to enhance an immune system weakened by aging or disease."
>>77247900
>>77247899>Potential repositioning of exemestane as a neuroprotective agent for Parkinson's diseasehttps://sci-hub.ru/https://pubmed.ncbi.nlm.nih.gov/28770670/The present study examined for the first time the effect of exemestane on the brain. Exemestane is highly lipophilic, and it distributes extensively into tissues, owing to its lipophilicity [59], suggesting that it can readily enter the brain. Our results demonstrated that exemestane activate the Nrf2 signalling pathway, induce gene expression of Nrf2-depensent enzyme genes, and suppress inflammatory responses. It also prevented microglial activation, dopaminergic neurodegeneration, and motor deficits in MPTP-treated mice. Therefore, exemestane repositioning for disease-modifying therapy for PD might be considered, in addition to its current usage in breast cancer.
>>77247906>Association Between Hormone-Modulating Breast Cancer Therapies and Incidence of Neurodegenerative Outcomes for Women With Breast Cancerhttps://jamanetwork.com/journals/jamanetworkopen/fullarticle/2763234In this cohort study of 57843 perimenopausal- to postmenopausal-aged women with breast cancer, exposure to hormone-modulating therapy (tamoxifen and aromatase inhibitors, especially exemestane) was associated with a significant decrease in the number of women who received a diagnosis of neurodegenerative disease, most specifically Alzheimer disease.For AD, HMTs (such as estrogen therapy) have been shown to be associated with the onset of AD,34 whereas estrogen therapy has been shown to be ineffective as a treatment for those with a diagnosis of AD.35-43 Similarly, the failure of trials evaluating the use of SERMs in the treatment of AD could be due to the fact that the intervention was started past the therapeutic window for HMTs.18,44-46 Here, we show the beneficial effects of exposure to HMT as a prophylactic treatment for the potential prevention of AD.
>>77247908
>>77247487>straight from the steppesCorrect, literally straight from the land where genesis of aryan race happened.
>>77247941>Admits being indianOH NONONONO
>>77247069>>77247135Why aren't you trying to cure your autism?
>>77247848What's the function of aromatase in male physiology?
>>77248447To produce estrogen from testosterone. Estrogen is needed partly in adult life, but mostly it's needed to produce some testosterone-dependent sexual dimorphism in puberty (as evident by aromatase-null males) - after that, not so much, It's similar to DHT in that regard. Even in puberty if you have too much conversion of testosterone to estrogen via aromatase you can develop gyno or low height.
>>77247052>Finasteride
>>77248536IM SO FULL FROM FINASTERIDE YUM
>>77248536
>>77248489Dude... no...>To produce estrogen from testosterone.This is how aromatase performs its role. The role of aromatase in male physiology is to ensure testosterone homeostasis. It does this in two ways. Testosterone in circulation inhibits testosterone production by inhibiting LH in the hypothalamus. Aromatization of testosterone in circulation is one of the mechanisms that lifts this inhibition, prompting the release of GnRH and LH by the hypothalamus, which are required to stimulate cells in the male testes responsible for spermatogensis and the majority of testosterone synthesis. Inhibition of aromatase impairs GnRH and LH release, and inhibits steady testosterone levels.Aromatase is also required for testosterone to exert its effects on male brains. Throughout adulthood, key areas in the male brain involved in memory (hippocampus), sexual behaviour (pre-optic area), pain tolerance (anterior cingulate cortex) and emotional regulation (DLPFC) are regulated exclusively by estrogen receptors. Testosterone is locally aromatized, which is the only manner in which testosterone can exert its effects on male behaviour by masculinizing the architecture of the male brain (throughout adulthood).The same mechanism is responsible for controlling the suppression of LH in the hypothalamus. LH is suppressed by testosterone itself, and testosterone which is locally aromatized. Estrogen in circulation, produced through aromatization, is blocked from interacting with estrogen receptors in the hypothalamus. So, these are two different, separate mechanisms of aromatization of testosterone.
>>77247908>>77248489>>77248594Additionally, you are referencing a study of aromatase inhibition in females to allude to its suggested beneficial effects in males, but this is a grave, grave mistake.The role of aromatase in the female body is DRASTICALLY different from that of males.Aromatase in the female body is responsible for the production of estrogen. All estrogen is fabricated from testosterone, including the female body. Until methods were discovered to synthesize testosterone in vitro in the 80s, testosterone was harvested from pregnant women in the 60s and 70s, since pregnancy drastically elevates sex steroid production, for which testosterone is the precursor. In the past, pregnancy tests worked through the detection of testosterone and epitestosterone in female urine. Aromatase functions as a homeostatic control mechanism in the male nervous system. Aromatase functions as the agent for sex steroid production in females. The problem with post-menopausal females and Alzheimer's is that there are multiple forms of estrogen. Estradiol is crucial in maintaining cognitive function in female brains, and estradiol levels decline significantly with menopause. The problem is not levels of estrogen itself, its reduced levels of estradiol compared to estrone. The point of aromatase inhibitors in females in the context of Alzheimer's is to reduce levels of estrone, increasing the ratio of estradiol to estrone (which will keep being produced in the same quantities). As you can imagine, since male brain physiology is regulated through local aromatization of testosterone, estrogen in circulation is excluded from interacting with estrogen receptors, and males don't have a physiology where the management of estradiol and estrone is present, aromatase inhibitors will not interact with the neurobiological characteristics of Alzheimer's the way they do in post-menopausal women.
>>77247908>>77248489>>77248594>>77248601In general, hormonal regulation as it relates to behaviour and brain function is remarkably different in males and females.Male sex steroid regulation works predominately through negative feedback. Testosterone blocks testosterone production. Activity in estrogen receptors in the brain reduces the amount of estrogen receptors. Male sex steroid regulation is characterized by the nervous system attempting to maintain steady levels of testosterone production and testosterone in circulation, reducing peaks and dips. Testosterone's effects on male behaviour in the brain are mediated through estrogen receptors, which acts a "safeguard" to ensure that excess testosterone does not lead to changes in male physiology that further affect testosterone production. Testosterone is still required to make them happen, but the degree to which it can bring about changes is controlled by aromatization. Inhibition of aromatase not only inhibits aromatase of testosterone in the circulation (a crucial process, which in and of itself is responsible for initiating production of new testosterone), inhibition of aromatase also prevents testosterone from making male brains "more male".Female sex steroid regulation works predominately through positive feedback. Estrogens in circulation don't inhibit LH, they stimulate LH. This is how ovulation happens, because sex steroids in females stimulate the production of more sex steroids, until the system is overloaded (which initiates the process of menstruation). As you can imagine, aromatase is not a stopgap mechanism in female physiology used to maintain stable levels of sex steroids. (additionally, this is why trannies can never ovulate, because the anatomy of the female hypothalamus is different from the anatomy of the male hypothalamus, since the male hypothalamus is keyed towards sex steroids providing negative feedback, while ovulation depends on positive feedback mechanisms.
>>77247908>>77248489>>77248594>>77248601>>77248614You reference a study on the use of aromatase inhibitors in the management of Alzheimer's in post-menopausal women, in support of using aromatase inhibitors for male cognitive performance and well-being. The fact that you did reveals some serious misunderstandings about male physiology and female physiology. Long-term ingestion of various substances you've listed will lead to serious harm, if these substances are ingested based on your lack of understanding of human endocrinology, biochemistry and molecular microbiology.You don't know what you're doing. You're harming yourself. You're harming others by trying to push your ideas on them, based on serious shortcomings in your knowledge of basic human biology.All the time you've invested in looking at these articles, quoting them, you could easily have invested in actually reading a book on this subject. The same time. The same effort.Please, instead of posting your shit here, spend that same amount of time and effort just opening the book I'm linking, and start reading it. It's a really good book. If you're able to keep up with it, you can learn things you can actually use in the contexts you describe in these threads. If you're not able to keep up with the material, that should tell you how little you adequately understand the contents of the studies you list, and the workings of the substances you are listing.https://doku.pub/documents/anintroductiontobehavioralendocrinolpdf-nl31p8gdgvq1Hopefully you appreciate the effort I'm putting into writing this. I'm genuinely concerned for you or anyone who takes up your suggestions.
>>77248626What's your take on Telmisartan? I'm taking it myself to prevent cardiac remodeling from Nandrolone.
>>77248594>The role of aromatase in male physiologyHonestly, i'm not of the mindset to think of the hormones as having different "roles" in the body. It's all chaotic chemical reactions, which can sometimes produce unexpected and counterintuitive results. Speaking of them as having "roles" is either just a simplistic way of communication or creationist retardation. >Inhibition of aromatase impairs GnRH and LH release, and inhibits steady testosterone levels.It's not, in fact the opposite is true. Look into case studies of human males with genetic aromatase deficiency. >Aromatase deficiency in male and female siblings caused by a novel mutation and the physiological role of estrogens https://sci-hub.ru/10.1210/jc.80.12.3689>The role of estrogens on the sex steroid-gonadotropin feedback mechanism is clarified by the observations in patients with P450arom deficiency. The elevated levels of androgens in our two patients as well as in the female described by Conte et al. (4) failed to adequately suppress gonadotropins after the age of puberty. ... The elevated (but not castrate) concentrations of plasma FSH and LH in the brother despite the strikingly high circulating T and dihydrotestosterone levels supports an important feedback role of estrogen, either of peripheral origin or synthesized locally from Cl9 steroid precursors or from both sources as well as T, in the regulation of FSH and LH in the male>The abnormally high (-2.5 times) plasma concentration of T is probably a consequence of the high plasma LH concentrations that induced either functional hyperleydigism or an increase in Leydig cell mass in the virtual absence of local E2 synthesis and circulating E2
>>77248594>>77249124>But it's just 1 mutantFine, let's see the studies measuring effect of aromatase inhibition on GnRH, LH and testosterone in normally developed men.>Pharmacokinetics and Dose Finding of a Potent Aromatase Inhibitor, Aromasin (Exemestane), in Young Maleshttps://www.researchgate.net/publication/8963583_Pharmacokinetics_and_Dose_Finding_of_a_Potent_Aromatase_Inhibitor_Aromasin_Exemestane_in_Young_MalesSuppression of estrogen, via estrogen receptor or aromataseblockade, is being investigated in the treatment of differentconditions. Exemestane (Aromasin) is a potent and selectiveirreversible aromatase inhibitor. To characterize its suppres-sion of estrogen and its pharmacokinetic (PK) properties inmales, healthy eugonadal subjects (14–26 yr of age) were re-cruited. In a cross-over study, 12 were randomly assigned to25 and 50 mg exemestane daily, orally, for 10 d with a 14-dwashout period. Blood was withdrawn before and 24 h after the last dose of each treatment period. A PK study was per-formed (n ⴝ 10) using a 25-mg dose. Exemestane suppressed plasma estradiol comparably with either dose [25 mg, 38% (P <0.002); 50 mg, 32% (P < 0.008)], with a reciprocal increase in testosterone concentrations (60% and 56%; P < 0.003 for both).Plasma lipids and IGF-I concentrations were unaffected by treatment. The PK properties of the 25-mg dose showed the highest exemestane concentrations 1 h after administration, indicating rapid absorption. The terminal half-life was 8.9 h. Maximal estradiol suppression of 62 ⴞ 14% was observed at12 h. The drug was well tolerated. In conclusion, exemestaneis a potent aromatase inhibitor in men and an alternative to the choice of available inhibitors.
>>77248594>>77249124>>77249138>The effect of testosterone aromatization on high-density lipoprotein cholesterol level and postheparin lipolytic activity.https://pismin.com/10.1016/0026-0495(93)90101-s
>>77249124>>77249138>>77249152Meta-analysis of aromatase inhibitors usage in men. >Aromatase inhibitors in men: effects andtherapeutic optionshttps://www.wellesu.com/10.1186/1477-7827-9-93
>>77248601>The point of aromatase inhibitors in females in the context of Alzheimer's is to reduce levels of estrone, increasing the ratio of estradiol to estrone (which will keep being produced in the same quantities).Exemestane, aromatase inhibitor that showed best results in preventing alzheimer's disease and related dementias in the study i cited, often reduces both estradiol and estrone to the same level, and in some studies reduces estradiol even more than estrone. >New aromatase inhibitors for the treatment of advanced breast cancer in postmenopausal womenhttps://www.sciencedirect.com/science/article/abs/pii/S0300297799000303>In healthy postmenopausal women and breast cancer patients oral doses of 0.5–800 mg o.d. suppressed plasma estradiol with 61–85%, estrone with 65–94% >Effects of exemestane and letrozole therapy on plasma concentrations of estrogens in a randomized trial of postmenopausal women with breast cancerhttps://pmc.ncbi.nlm.nih.gov/articles/PMC5429096/#S13Month-3 concentrations of E2, E1, and E1S fell below assay LLOQ in 87.9%, 85.1%, and 36.3% of patients, respectively (Table 1). The frequency of E2 suppression below LLOQ was not statistically significantly different between AIs (exemestane: 89.0%, letrozole: 86.9%, p=0.51); however, significant differences were observed for both E1 and E1S. E1 concentrations were reduced below the assay LLOQ in 90.1% of patients taking letrozole, compared to 80.1% of patients taking exemestane (p=0.005). Similarly, although 54.9% of patients taking letrozole had month-3 E1S concentrations below the assay LLOQ, this reduction was only observed in 17.4% of patients taking exemestane (p=4.34e-15).
>>77248626>You don't know what you're doing. You're harming yourself. You're harming others by trying to push your ideas on them, based on serious shortcomings in your knowledge of basic human biology.Considering you can't even double-check your own made-up assertions, i diagnose you with severe case of mental retardation, and conclude you must receive help and guidance from qualified medical professional, including prohibition of internet usage to prevent further harm to yourself or others. Perish, mortal, for the art of alchemy will forever be outside your comprehension.
>>77249236Seriously m8, did you get an official autism diagnosis? It's very obvious that you have it (I do too) and you need to work on yourself.
>>77249248>did you get an official autism diagnosis?I'm definitely not neurotypical, but it's not autism since i don't have problems at socializing when i want to or adapting to new environments - probably psychopathy, narcissism, megalomania and high trait dopamine always making me excited to go down the rabbit holes of things i'm interested in.
>>77248601>>77249207As to actually plausible explanations of beneficial effects of aromatase inhibitors in prevention of neurodegenerative diseases...>Neuroprotection from raised endogenous androgens>Neuroprotection from androgenic metabolites of aromatase inhibitors (such as 17B-hydroexemestane in case of exemestane)>Slowing of thymic involution>Decreasing of toxic metabolites of estrogen>Off-target effects (such as Nrf2 upregulation by exemestane)
>>77247052Troon general
>>77247075>with high cholesterol it doesn't matter how many other things you take, you'll still die early.There's many more healthy ways to diminish LDL and damage done by it besides statins, including drugs of sartan class, ezetimibe that prevents alzheimer's disease by improving neural protein dynamics as off-target effect, anti-inflammatory drugs (such as aspirin that also raises free thyroid hormones), and direct thyroid-mimetics such as sobetirome. >Best Sobetirome (GC-1) Protocols (Lipid-Lowering Anti-Catabolic T3 Thyroid Alternative)https://www.youtube.com/watch?v=QaWidRqxGOM
>>77247052>Magnesium>no borox or boron
>>77249834I know, i just can't source boron at a reasonable price and with certainty that it's a real product.
>>77249884just take borax its desert salt
>>77249929Are you sure it's safe and effective, anon-kun...>Soldering of copper, brass, cast iron, steel>Removal of stains and mold>Universal disinfectantThey all sell technical-grade borax. There may be impurities left from technological production process.
I take>creatine>arginine>vitamin D>olive oil>black tea>nutmeg>cumin>turmeric
>>77249951Normiest stack ever.
>>77249939The Borax Conspiracy How the Arthritis Cure has been Stopped - Walter Last
>>77249951>turmericIndian scam.
>>77247052Just made new anabolic cacao jelly full of (-)-epicatechin. Ingredients: 50g bovine collagen powder70g trehalose75g pure cacao powder>Cacao flavonoid (-)-epicatechin inhibits myostatin and strengthens muscleshttps://www.ergo-log.com/cacao-flavonoid-epicatechin-inhibits-myostatin-strengthens-muscles.htmlTreatment for 7 days with (-)-epicatechin yielded a bilateral increase in hand strength of 7%, which was accompanied by a significant increase (49.2%) in the ratio of plasma follistatin/myostatin levels"
I'm the guy from the last thread who asked about bigger balls. I don't have access to HCG or any of the other stuff that would probably make it happen faster, but I did start taking iron (27mg), D3 (5000 IU), and zinc (50mg). It's not as much as the Russian guy, but it's what I could get off the shelf.I'll let y'all know if anything comes of it, but so far I think the iron is just giving me fatigue. I don't have any other symptoms of iron toxicity so it may be some other energy problem.
>on a literal kitchen sink worth of pharmaceuticals but refuses to pin because "muh hpta"You can get all the benefits of your drug stack by just doing cardio, lifting, and having sub 15% bodyfat if you're not gonna do anabolics..kek
>>77249496Very based
>>77250741>You can get all the benefits of your drug stack by just doing cardio, lifting, and having sub 15% bodyfatNo, you can't. From my stack, only telmisartan and bromocriptine have slight exercise-mimetic properties - everything else acts trough different pathways.
>>77250793>ExemestaneLower the bodyfat and you'll have less aromatase expression, no AI needed>aspirinLower bodyfat and proper diet/hydration lowers hematocrit and thus blood thickness>montelukastUpping your VO2max through cardio increases vasodilation and lung efficiency, and effectively reduces systemic inflammation>bromocriptineThere is no reason for you to be taking a dopamine agonist. Have fun trying to get off of that when you inevitably will have to in the future>finasterideIf you're trying not to be bald then this is literally the only valid medication on hereYou are trying to pill your way out of putting the work into diet, training, and consistency. Pathetic.
>>77250842You have a trait very indicative of a low intelligence, namely - no sense of magnitude and nuance. Retards like you usually always seek natural solutions to their problems (like using saw palmetto instead of finasteride because "it inhibits 5-alpha reductase too bro!"), only to fail because they have 1/10 the power of drugs.
>>77250744Agree. Appreciating trans-women is /fit/ culture.
>>77247487you wish you were slavic, brownoid
>>77250744adorable snek drinkk
>>77247052Clomiphene / Enclomiphene, performance enhancing SERM, may be potent anti-aging drug acting through upregulation of lysosomal biogenesis. There's 2 recent chinese studies that looked at it's induction of TFEB. >>TFEB agonist clomiphene citrate activates the autophagy-lysosomal pathway and ameliorates Alzheimer's disease symptoms in micehttps://pmc.ncbi.nlm.nih.gov/articles/PMC11599454/>The TFEB activator clomiphene citrate ameliorates lipid metabolic syndrome pathology by activating lipophagy and lipolysishttps://www.sciencedirect.com/science/article/abs/pii/S0006295224006956I know those studies don't mean much alone, but there seems to be confirmatory signals from other laboratories, and they point to active TEFB inductor being the enclomiphene component. >Enclomiphene Citrate for the Treatment of Secondary Male Hypogonadismhttps://pmc.ncbi.nlm.nih.gov/articles/PMC5009465/Initial animal testing of enclomiphene was conducted by Repros Theraputics on baboons. The animals were administered 1.5 mg/kg/day of zuclomiphene, enclomiphene or clomiphene for 12 days with serum hormone measurements at 0, 12 and 19 days....Surprisingly, baboons treated with zuclomiphene also experienced 22% increases in serum cholesterol levels....enclomiphene-treated baboons had an even greater increase in testosterone (170 ng/dl to 1,144 ng/dl, p=0.03) with an 8% reduction in serum cholesterol levels.
>>77251365>TFEB; Beyond Its Role as an Autophagy and Lysosomes Regulatorhttps://pmc.ncbi.nlm.nih.gov/articles/PMC9562866/Accumulated evidence has underscored the role of TFEB as a master regulator of lysosome biogenesis and autophagy. TFEB activation positively regulates the expression of autophagy and lysosomal biogenesis-related genes that promote the clearance of intracellular substrates through lysosomal exocytosis. However, increasing evidence suggests the crucial role of the TFEB protein in the control of several other vital cellular processes, such as cellular senescence, DNA repair, ER stress, carbohydrates metabolism, lipid metabolism, and WNT signaling-related processes that position TFEB as a key regulator responding to a variety of environmental cues. The newly identified noncanonical roles of TFEB have revealed how it is able to integrate multiple upstream stimuli to mediate specific downstream responses that conceivably could have medical relevance. Therefore, pharmacological strategies for TFEB activation or mitigation might be a promising approach in specific disease conditions, as is the case of metabolic or neurodegenerative diseases, and may hold relevance for a larger number of human diseases.
>>77250911Post your body with a timestamp and let's see how well this drug cocktail is working
>>77250954I've never seen such a thirsty snek.
>>77247052I hope you're taking a proton pump inhibitor with all of that aspirin you're taking
>>77251687I just use ginger extract for gut protection.
>>77251680>Post your bodyAlready did. >>77247069But i don't practice bodybuilding or strength training, only cardio, so it's kind of irrelevant.
>breaking news: Giving rats literally anything regrows their hair, makes their dicks a foot longer, and makes them immortal
>>77251711...And it translates to humans 86% of the times!
>>77247069Good lord.Instead of abusing pharmaceuticals, some cardio and a low carb + high protein diet would unironically achieve your 'eternal youth' faster without the brain fog and soreness in your kidneys (or the sterilized sperm cells).
Anyone else remember when biohacking meant something different than juicing?
>>77251765>some cardioI don't know why you think i have bad cardio. I can do 70 consecutive 32kg kettlebell swings to eye level at 95kg bodyweight.
>>77247052taking aspirin daily shrinks your balls the fuck is this shit.
>>77251851>taking aspirin daily shrinks your ballsOnly if you take it at doses that significantly inhibit COX-2. I take multiple low doses that inhibit only COX-1 throughout the day, which actually grows balls due to reduced estrogen, generation of which is partly dependent on PGE2. >Aspirin versus placebo on estrogen levelsin postmenopausal women: a double‑blindrandomized controlled clinical trialhttps://link.springer.com/article/10.1186/s40360-022-00571-9>Aspirin Suppresses Aromatase-Mediated Estrogen Biosynthesis to Alleviate Polycystic Ovary Syndrome by the Inhibition of Adenylate Cyclasefile:///D:/%D0%98%D0%BB%D0%BB%D1%8E%D1%81%D1%82%D1%80%D0%B0%D1%86%D0%B8%D0%B8/%D0%91%D0%B8%D0%BE%D1%85%D0%B0%D0%BA%D0%B8%D0%BD%D0%B3/Pharma/NSAIDs/Aspirin/Aspirin%20Suppresses%20Aromatase-Mediated%20Estrogen%20Biosynthesis%20to%20Alleviate%20Polycystic%20Ovary%20Syndrome%20by%20the%20Inhibition%20of%20Adenylate%20Cyclase.html
I microdose on mercury like the good ol Qin Emperor.
>>77249118>NandroloneHave you experienced negative side effects regarding dopaminergic system?
>>77250842>There is no reason for you to be taking a dopamine agonist.Dopamine agonists are good for you.
>>77251918Not him but I never experienced any bad side effects from taking deca. I was only using 100mg a week. Originally started using it in an effort to make my shoulder heal. I found that doing "TRT" with 200 test and 100 deca was giving pretty damn sick gains too
>>77251819Pathetic
>>77252468It's quite impressive, actually.
>>77247052
>>77247069You look like me and I am a 30+ dyel
>>77252923>You look like me No, i'm not.
>>77247052>"biohacking"
>>77250935Getting troons to an hero is a human past time
>>77247158You forgot: chudlips
>>77252930eat + lift is cope
>>77251819I am sure swinging a kettlebell will strengthen your heart and help to lose weight.Let me ask you this: how long have you been "biohacking", has it improved your appearance at all, and do you feel healthier?
>>77250150it is said to raise BDNF
>>77247069That face radiates pure autism. It's over. You will die a virgin.
>>77253084>how long have you been "biohacking"Around 1.5 years. >has it improved your appearance at allI always looked good, so no. >do you feel healthier?Yes. Biggest positive changes in feelings were from aspirin and exemestane.
>>77253098>That face radiates pure autism.
>>77253091>it is said to raise BDNFBy 0.0001% in mice with alzheimer's?
>>77247052>Diflunisal Shows Promise and Cost Effectiveness in ATTR-CM Carehttps://www.rarediseaseadvisor.com/insights/diflunisal-shows-promise-and-cost-effectiveness-in-attr-cm-care/>Characterizing Diflunisal as a Transthyretin Kinetic Stabilizer at Relevant Concentrations in Human Plasma using Subunit Exchangehttps://pmc.ncbi.nlm.nih.gov/articles/PMC10225472/>Diflunisal Derivatives as Modulators of ACMS Decarboxylase Targeting the Tryptophan-Kynurenine Pathwayhttps://pmc.ncbi.nlm.nih.gov/articles/PMC7856275/
this guy is biohacking REALLY hard, wowhacking his biology to pieces that is
>>77253182>Drugs are... Le dangerous!Sure, nattykek. Never take any of them without doctor's prescription.
>>77247052man if you want to take a catalog of shit just take peptides esp shit like khavinson bioregulators. Just get on rupharma and knock yourself out. Keep the apirin, fin, tret, and maybe bromo - cut everything else. You'll probably want to offset the HGH lowering effects of the bromo if you want to keep it. And your base is woefully inadequate.
>>77253190>Drugs are... Le dangerous!Put Max Verstappen in an F1 car, he'll become a world champion.Put a retard like you in an F1 car, and he'll be in a coffin if he's lucky enough not to burn to a crisp in the crash.F1 cars aren't dangerous, retards thinking they can drive them are.
>>77253194I'm literally a genius.
>>77253199How many types of energy does the human body have/use?
>>77253193>You'll probably want to offset the HGH lowering effects of the bromoBromocriptine lowers HGH only in cases of acromegaly, in healthy humans it actually elevates it.
>>77253200I'm not gonna teach you for free. Ask questions that may actually be of interest to me if you want answers.
>>77253205By not answering the question, you are conceding that you don't know. Not a genius.
>>77253210>By not answering the question, you are conceding that you don't know.Kek, is this cope really enough to lower your cortisol? Remember, i intellectually humiliated you 3 times already. You can't win while i'm playing, stupid.
>>77253213A genius would be able to answer that question quickly and effortlessly. A genius wouldn't play around evading the question. A genius wouldn't go through the effort of trying to assert himself as a genius, because he wouldn't have to.Still no answer.
>>77253218>A genius wouldn't go through the effort of trying to assert himself as a genius, because he wouldn't have to.I just have fun harassing you, retard. Remember how you tried to assert lowering testosterone aromatization will result in downregulation of FSH and LH, you stupid monkey?
>>77253193>And your base is woefully inadequate.Do you have any suggestions regarding it?
>>77253225>I just have fun harassing you, retardYou mean, trying to talk shit, evading a really basic question about human biology you would know if you were "genius", all the while wasting time talking about nothing instead of posting about your schizo stack?Please be gentle with me genius.
>>77253232>evading a really basic question about human biology you would know if you were "geniusActually in 2024 i wrote a whole lecture regarding energy systems of human body as they relate to exercise physiology, as a recap of my research. >Please be gentle with me genius.You would need to try harder than that to quell my sadistic urges, lesser being...
>>77253269STILL no answer?How many types of energy does the human body employ?
>>77247052I have been reading your replies in this thread and notice a pattern of defensiveness, self-esteem issues (insisting that you are smarter than others and visually attractive) , and the need to prove others wrong by spamming scientific articles about experiments done on mice.I suspect that the chemical cocktail you are consuming (your 'stack') has lead you to develop a hormonal imbalance alongside potentially stunted cognition since DHT is a necessary Neurosteroid for the developing brains of young men - and your reasoning behind this stack lacks sense.People here are trying to help you realize your own folly, but the only ones you respond to are the ones who dare question your stack, knowledge of substances, or simply comment on your appearance.I unironically suggest that you get help for your obvious low self-esteem and neurodivergent traits, stop poisoning yourself, actually exercise, and eat healthy. It is making you turn into a klinefelter male.This is some honest and well intentioned advice, consider it or ignore it, but do not bother making a defensive reply to me.
>>77253308>the only ones you respond to are the ones who dare question your stack, knowledge of substances, or simply comment on your appearance.Yes, because actually i'm not interested in discussing myself or hearing other's opinions about myself at all, and only write-off volatile remarks because it's a low-effort method of increasing thread engagement, keeping it on the front page and increasing the chances someone with knowledge and experience in the subject matter will contribute to the discussion i'm actually interested in - biochemistry, drugs and their uses to enhance my power.
>>77253351>knowledge and experience in the subject matter>biochemistryhttp://mvk.ch.bme.hu/oktatas/konyvek/fizkem/Biomimetikus/irodalom/Lehninger%20Principles%20of%20Biochemistry%20%202004.pdfenjoy
>>77253367>Died at 69I won't learn from noobs.
>>77247052Can gliptins be effectively used to prevent side effects and improve performance-enhancing effects of ibutamoren?DPP-IV inhibition leads to significantly increased GLP-1 and GIP secretion, so when ibutamoren raises your blood glucose, those hormones raise accordingly and stabilize it. Also, inhibition of DDP-IV prolong half-life of GHRH and IGF-1, making ibutamoren more effective.
>>77247052>Flurbiprofen enhances growth and cancellous and cortical bone accumulation in rapidly growing long boneshttps://pubmed.ncbi.nlm.nih.gov/2660884/The effects of flurbiprofen, a non-steroidal anti-inflammatory drug, on bone growth was studied by static and dynamic histomorphometry in immature (28 days old) male Sprague-Dawley rats. Flurbiprofen at 0, 0.02, 0.1, 0.5 or 2.5 mg/kg/d doses was given subcutaneously daily for 21 days. The 0.1 and 0.5 mg/kg/d doses were most effective in stimulating longitudinal and radial bone growth and enhancing the accumulation of cancellous and cortical bone. Proximal tibial longitudinal bone growth rate, growth plate thickness, and periosteal bone formation rate were increased 30-40%, while cortical bone (tibial shaft) and cancellous bone (proximal tibial metaphysis) accumulated 12% and 90% more bone than controls, respectively. Enhanced accumulation of cortical bone was attributed to stimulated periosteal bone formation without accompanying marrow cavity enlargement. Enhanced accumulation of cancellous hard tissue was postulated to be due to reduced trabecular bone resorption and no effect on bone formation. The cell counts support these conclusions. There was a decrease in osteoclast numbers (-62 to -70%), an insignificant decrease in osteoblast numbers (-5 to -30%) per mm of bone surface and a decrease in osteoclast to osteoblast ratio (-35 to -56%). The findings presented are compatible with the conclusion that flurbiprofen, induced changes in rapidly growing long bones by reducing osteoclast activity and recruitment, stimulating longitudinal and radial growth, increasing the cortical bone mass by stimulated periosteal bone growth and depressed endosteal resorption, and increasing cancellous bone mass by depressed trabecular bone resorption without affecting bone formation.
>>77247052is megadosing P5P an efficient and cheap way at inhibiting glycation?
>>77254020
>>77254020>>77254025Very limited possibility of increasing it's intracellular concentration, so no.
>>77247052Croissant diet guy here:Stalled around 175-177 for abt 3 weeks. Cut cardio on the recc of body by science by doug mcguff and what kevin richardson the naturally intense guy talks abt and reduced succinate and R-ALA supplementation in half to 5g/800mg respectively, and introduced the 10% deficit back on my two full rest days and finally broke under 175 while maintaining workout quality and feeling better energy with no cardio. Taking temp after meals, even without succ/ALA at half of reg I'm still peaking around 98.8 or 100.1f which means my body has worked through almost ALL of the pufa/o6 that was stored in my fat cells.Going for 170 but basically I want to keep quality of life and workouts and keep gaining strength like I've been doing. In other news, my T averages 800-900 but I'm feeling pushed to go from 3 rest days to 4 because I'm feeling doms and not recovered after the 3 days anymore, anything else (besides chinese roidweenie chems) I can do for recovery besides sleep?
Ive never seen an attractive or happy "biohacker".I only take advice from healthy looking people who are happy and have good lives. The nervous energy and autism surrounding this shit is really pathetic. How about you "biohack" a personality and life goals first, before you overdose on research chemicals.
>>77254335>broke under 175 while maintaining workout quality and feeling better energy with no cardio.Your current your bodyfat%?>my T averages 800-900 Impressive, very nice. Have you measured it before your cut?
>>77254366>I only take advice from healthy looking people who are happy and have good lives. Name some of the grifters you follow, i wanna have a good laugh.
>>77254386Currently probably around maybe 14%? I plugged in my DEXA stats into grok and had it run numbers and it said 11.3, but I have too much flab on my stomach for that and loose skin from being obese so I don't believe 11.3.Nah my first test was during the cut. Popped for 847 *in* the cut when I took a training layup for 2 weeks but was hammering an hour of cardio everyday and was already down 6lbs of fat. Best personal guess and what I x-reffed with a few LLMs is that the 160g+ sat fat I'm eating a day is just insanely anabolic. Now that I've cut cardio and out of regular deficit I'm hoping for closer to 1000, I've noticed I've become muskier as of late.
>>77247153>SimvastatinIs not pitavastatin. Try again.>All it does is lowering blood glucose levels.Try reading something other than Gemini synopses for once, jesus fucking christ.
>>77254601>Is not pitavastatin. It has the same mechanism of action and has neuromuscular symptoms as a side effect.>Statin-related Muscle Toxicity: An Evidence-based Reviewhttps://touchendocrinology.com/cardiovascular-risk/journal-articles/statin-related-muscle-toxicity-an-evidence-based-review/?rl=touchendocrinology.com%2Fcardiovascular-risk%2Fjournal-articles%2Fstatin-related-muscle-toxicity-an-evidence-based-review>The onset also varies with the type of statin: with pitavastatin, SRM occurs as early as 14 days, whereas, with pravastatin and fluvastatin, SRM will usually take at least 40–45 days to manifest.>Try reading something other than Gemini synopses for onceShow me the data that it is beneficial in conditions where no hyperglycemia/diabetes is present.
>>77254366>Science is autisticFucking retard.
>>77247052>Attenuation of diabetic kidney injury in DPP4 deficient rats; role of GLP-1 on the suppression of AGE formation by inducing glyoxalase 1https://www.aging-us.com/article/102643/textDipeptidyl peptidase 4 (DPP4) inactivates incretin hormone glucagon-like peptide-1. DPP4 inhibitors may exert beneficial effects on diabetic nephropathy (DN) independently of glycemic control; however, the mechanisms underlying are not fully understood. Here, we investigated the mechanisms of the beneficial effects of DPP4 inhibition on DN using DPP4-deficient (DPP4-def) rats and rat mesangial cells.Blood glucose and HbA1c significantly increased by streptozotocin (STZ) and no differences were between WT-STZ and DPP4-def-STZ. The albumin level in urine decreased significantly and the albumin/creatinine ratio decreased slightly in DPP4-def-STZ. The glomerular volume in DPP4-def-STZ significantly decreased compared with that of WT-STZ. Advanced glycation end products formation, receptor for AGE (RAGE) protein expression, and its downstream inflammatory cytokines and fibrotic factors in kidney tissue, were significantly suppressed in the DPP4-def-STZ compared to the WT-STZ with increasing glyoxalase-1 (GLO-1) expression responsible for the detoxification of methylglyoxal (MGO). In vitro, exendin-4 suppressed MGO-induced AGEs production by enhancing the expression of GLO-1 and nuclear factor-erythroid 2 p45 subunit-related factor 2, resulting in decreasing pro-inflammatory cytokine levels. This effect was abolished by GLO-1 siRNA.Our data suggest that endogenously increased GLP-1 in DPP4-deficient rats contributes to the attenuation of DN partially by regulating AGEs formation via upregulation of GLO-1 expression.
>>77247052Biojew-kun, if you had access to pharma-grade HDAC-inhibitors, would you use them? >From molecular promise to preclinical results: HDAC inhibitors in the race for healthy aging drugshttps://pmc.ncbi.nlm.nih.gov/articles/PMC6728603/Reversing or slowing the aging process brings great promise to treat or prevent age‐related disease, and targeting the hallmarks of aging is a strategy to achieve this. Epigenetics affects several if not all of the hallmarks of aging and has therefore emerged as a central target for intervention. One component of epigenetic regulation involves histone deacetylases (HDAC), which include the “classical” histone deacetylases (of class I, II, and IV) and sirtuin deacetylases (of class III). While targeting sirtuins for healthy aging has been extensively reviewed elsewhere, this review focuses on pharmacologically inhibiting the classical HDACs to promote health and longevity. We describe the theories of how classical HDAC inhibitors may operate to increase lifespan, supported by studies in model organisms. Furthermore, we explore potential mechanisms of how HDAC inhibitors may have such a strong grasp on health and longevity, summarizing their links to other hallmarks of aging. Finally, we show the wide range of age‐related preclinical disease models, ranging from neurodegeneration to heart disease, diabetes to sarcopenia, which show improvement upon HDAC inhibition.
>>77255314>Biojew-kun, if you had access to pharma-grade HDAC-inhibitors, would you use them?NTA but probably not unless cancer patient; enough OTC supplement/food HDAC inhibitors with moderate activity and minimal-to-no side effects I'd stick with those if healthy.
>>77247052>Growth Hormone, Not IGF-1 Is the Key Longevity Regulator in Mammalshttps://pmc.ncbi.nlm.nih.gov/articles/PMC9434454/Germane to this discussion, GH action is responsible for 70%–90% of circulating IGF-1 (49,50). Hepatic IGF-1 receptor gene deletion resulted in mice of normal body weight, length, and development. However, liver-specific GH receptor gene deletion produced mice with decreased body size, low IGF-1, impaired glucose metabolism, and hepatic steatosis (51). A reduction in IGF-1 signaling does not alter life span at nearly the levels observed in reduced GH signaling mutants (5% vs 40%–70%, respectively). In complete agreement, a metanalysis including 42 survival studies examined reduced somatotropic signaling (GH, IGF-1, insulin receptor substrate [IRS]) and found that mice with mutations that alter GH signaling exhibited greater relative reductions in mortality compared to those with mutations that affected either IGF-1 or IRS (52). This report concluded that reductions in GH signaling “robustly” increase median life span, exhibit low heterogeneity in the life-span response (5.6% vs IGF-1 34.1% and IRS 47.2%), and are not sex- or control strain-dependent (52). In contrast, reductions in IGF-1 signaling preferentially extend life span in females and short-lived strains of mice. Moreover, life span is not increased in transgenic mice expressing a GH antagonist where levels of circulating IGF-1 are decreased, and insulin levels and sensitivity are not altered (53). Overall, this evidence supports our work and others that strongly propose that reduced GH rather than the secondary reduction of IGF-1 provides beneficial effects on aging and is the key to longevity in mammalian systems perhaps through stress resistance, reduced inflammation, and insulin sensitivity.
>>77255518In humans, these signaling pathways are relevant to biological aging with life-span implications that reveal more intricate relationships. Briefly, it is clear that genes within the somatotropic axis and downstream targets of these pathways influence aging and longevity (54–63). For example, studies of centenarians show that enhanced insulin sensitivity is strongly correlated with longevity and that exceptional longevity is associated with reduced IGF-1 (61,64–67). There are also differences in long-lived families indicating that less GH is secreted and is under tighter regulation (68). However, while neither lifelong GH deficiency nor GH resistance consistently extends human life span, they do result in major protection from diabetes, cancer, atherosclerosis, and other age-related diseases.Although IGF-1 is likely the major determinant of life span in invertebrates, it is GH that affects multiple physiological processes that significantly affect longevity in mammals. Keys that factor into the influence of growth hormone on longevity may be the major role it plays metabolically in vertebrate organisms stemming from the wide expression of GH receptors centrally and peripherally and its regulation of circulating IGF-1 levels among others. In addition, growth hormone’s influence on aging trajectories and longevity is not limited to early- or late-life actions
>>77255518>>77255522>Significant reduction of growth hormone is required for everlasting life>Growth hormone is needed to make gains in the gym and heal wounds
>>77255539GH surprisingly activ8s some gainz goblins like the GSK3β-cyclin D3 pathway, so...>protip: look DOWNSTREAM of the GH/IGF-1 pathway for both life extension and gainz
>"BIO" hacking>It's just people taking meme supplements.
>>77255605>Aromatase inhibitors are meme supplements>Anti-inflammatories are meme supplements>Retinoids are mee supplementsRetarded negroid.
>>77255610I would explain to you the etymology of the word meme, but it would be wasted since you're already emotionally invested in being this upset that people aren't mainlining meme supplements.
>>77255610>totally missing the point of the post
>>77255614>>77255615Negroid, you attacked my hobby of taking biology-altering drugs used to treat life-threatening conditions without prescription by calling them "meme supplements" and think i wouldn't retaliate?
>>77255621Sorry you're so upset.
>>77255625Apology accepted...
>>77255605>"BIO" hacking>It's just people taking meme supplements.As one of the few posters ITT on more supps than Smaev; some of the meme supplements really work and do stuff confirmed by MANY clinical trials, it's just that a lot of normie brands are overpriced. Yes, some of them you can forego if you eat specific kinds of foods, but only the ESSENTIAL ones generally. If you're trying really hard to stay lean and heavy without hitting the wall however, you need to look VERY far past "what u need bro" into all the most deranged China performance-enhancing decoctions with schizo-tier fly proteomics research.
Let's say I take exemestane and enclomiphene at the same time, would these just counter each other, or would they actually have some synergy?
>>77255737Enclomiphene cancels out anti-estrogenic effects of exemestane in some tissues, so it increases SHBG and lowers IGF-1, unlike exemestane which actually lowers SHBG. Otherwise, exemestane will prevent conversion of raised testosterone to estrogen, so i predict some synergy.
>>77255562Was researching lithium for GSK3β inhibiton and found those epic studies suggesting we should absolutely megadose it... >Long-term lithium treatment in bipolar disorder is associated with longer leukocyte telomereshttps://www.nature.com/articles/tp201337Lithium-treated BD patients overall, as well as those on lithium monotherapy, had 35% longer telomeres compared with controls (P<0.0005, partial η2=0.13). TL correlated positively with lithium treatment duration of >30 months (P=0.031, R2=0.13) and was negatively associated with increasing number of depressive episodes. BD patients responding well to lithium treatment had longer telomeres than those not responding well. This is the first study to report a positive effect of long-term lithium treatment on TL. >The polygenic nature of telomere length and the anti-ageing properties of lithiumhttps://pmc.ncbi.nlm.nih.gov/articles/PMC6372618/Next, we confirmed that chronic lifetime lithium use is associated with longer telomere length in an independent sample of 384 BD patients, and in an expanded sample. This supports epidemiological data which has shown that lithium in our water supply has beneficial effects on health and longevity and suggests that lithium’s effect on telomere length may be one mechanism by which it confers its anti-ageing properties. To corroborate this theory, we tested whether lithium affects the expression of genes responsible for telomere length maintenance (identified from our gene-enrichment analyses) in a relevant model system that recapitulates the drug’s anti-ageing effects. We found that 3 out of the 13 genes identified from the gene-enrichment analysis had an assayed ortholog in a C. elegans model of lithium-induced extended longevity, where we found that lithium had an effect on all three genes. This subsequently supports the notion that genes responsible for normal telomere length regulation may play a role in mediating lithium’s anti-ageing mode of action.
>>77255562Btw, what do you think of the theory that cancer is primarily driven by mitochondrial dysfunction, and not by genetic mutations?Here's an overview of the theory:>Dr. Thomas Seyfried: Cancer as a Mitochondrial Metabolic Diseasehttps://www.youtube.com/watch?v=KusaU2taxowFound this study recently that showed positive correlation between telomere length and cancer risk, which would be strange if cancer is actually driven by mutations, since long telomeres prevent them. >Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases, A Mendelian Randomization Studyhttps://jamanetwork.com/journals/jamaoncology/fullarticle/2604820In this report, we show that genetically increased telomere length is associated with increased risk of several cancers and with reduced risk of some non-neoplastic diseases. Given the random distribution of genotypes in the general population with respect to lifestyle and other environmental factors, as well as the fixed nature of germline genotypes, these results should be less susceptible to confounding and reverse causation than those generated by observational studies. Our results could, however, reflect violations of Mendelian randomization assumptions, such as confounding by pleiotropy, population stratification, or ancestry.98 Although we cannot entirely rule out this possibility, the majority of our results persisted in sensitivity analyses that made allowance for violations of Mendelian randomization assumptions. Confounding by population stratification or ancestry is also unlikely, given the adjustments made for ancestry in the original disease GWASs (see eAppendix 1 in Supplement 1). Our results are therefore compatible with causality.
>>77247052>The Longevity Secret Hiding In Plain Sighthttps://www.youtube.com/watch?v=rOfXvTdSCtY>Risk of Alzheimer's Disease Following Influenza Vaccination: A Claims-Based Cohort Study Using Propensity Score Matchinghttps://journals.sagepub.com/doi/full/10.3233/JAD-220361>The Impact of Routine Vaccinations on Alzheimer’s Disease Risk in Persons 65 Years and Older: A Claims-Based Cohort Study using Propensity Score Matchinghttps://journals.sagepub.com/doi/10.3233/JAD-221231>For those living with dementia, new study suggests shingles vaccine could slow the diseasehttps://med.stanford.edu/news/all-news/2025/03/shingles-vaccination-dementia.html>A natural experiment on the effect of herpes zoster vaccination on dementiahttps://www.nature.com/articles/s41586-025-08800-x>Shingles Vaccine Drastically Cuts Risk of Serious Cardiac Eventshttps://www.acc.org/about-acc/press-releases/2026/03/16/19/33/shingles-vaccine-drastically-cuts-risk-of-serious-cardiac-events>Risk of Alzheimer Dementia After High-Dose vs Standard-Dose Influenza Vaccinationhttps://pmc.ncbi.nlm.nih.gov/articles/PMC13051479/>Association between shingles vaccination and slower biological aging: evidence from a US population-based cohort studyhttps://academic.oup.com/biomedgerontology/article/81/3/glag008/8430804?login=false
Who cares about these walls of text when you look like an indian lesbian
>>77256450I look significantly better than most men and also height/weight mog them.
>>77256457You wouldnt look better than 10 people if we dropped you in a mumbai slum
>>77256462Cope.
>>77256463You have klinfeleter, congrats i guess
>>77256465>You have klinfeleterNo, otherwise i wouldn't be able to work in construction where real-life strength. muscle anabolism and skill is required, which btw makes me manlier than majority of 4chan dwellers. Also, extensive knowledge of alchemy beyond any comprehension of mortals granted me unnatural beauty and immortality.
>>77256469I learned to be nice to downies at school so i wont be rubbing more salt on your wounds
>>77256472I accept your concession.
>>77256474>Concession schizo is a transgender man with klinfelter Explains a loooot
>>77256478It's a common phrase on /fit/ dating back to 2017, used in situations where an opponent doesn't have any relevant counter-argument for discussion to proceed. You're mentally impaired
>>77256492I raped your mom btw
>>77256495Your petite insults won't disprove my superiority over majority of human beings, which is evident and summarized by following data:I'm 100% aryan (light eyes, light skin, light hair)I'm way taller than most men (195cm)I'm way heavier than most men (95kg at 20%~ bodyfat)I'm smarter than most men (know 2 languages, can correctly interpret scientific research on frontier topics without formal education)I'm manlier than most men (work physically demanding job, raise testosterone with drugs)I'm richer than most men (1 hour of my work costs more than 5 hours average) I'm just an elite overall, a true aristocrat.
>>77256516Holy unc crashout
>>77247052Opinion on everolimus? Is it just better rapamycin that can actually be used for anti-aging?Also, is it reasonable to combine rapalogs with antivirals like valaciclovir? >Alternative rapamycin treatment regimens mitigate the impact of rapamycin on glucose homeostasis and the immune systemhttps://pmc.ncbi.nlm.nih.gov/articles/PMC4717280/Here, we identified an intermittent rapamycin dosing schedule with minimal effects on glucose tolerance, and we find that this schedule has a reduced impact on pyruvate tolerance, fasting glucose and insulin levels, beta cell function, and the immune system compared to daily rapamycin treatment. Further, we find that the FDA‐approved rapamycin analogs everolimus and temsirolimus efficiently inhibit mTORC1 while having a reduced impact on glucose and pyruvate tolerance. Our results suggest that many of the negative side effects of rapamycin treatment can be mitigated through intermittent dosing or the use of rapamycin analogs.
>>77256560>Opinion on everolimus? Is it just better rapamycin that can actually be used for anti-aging?I think if you have to choose between the two, evero probably mogs, but I'm generally skeptical of the FDA-approved rapalogs' safety in healthy people, especially after picrel's experience. I've looked at other ways (generally supplemental aside from meclizine) to skin the proverbial mTOR cat and knock down cytokines more selectively.
>>77256516>>77253308There is really no point of arguing with anyone here if your true goal is to learn more about "biohacking".What even is the point of this Biohacking General other than to bait people into arguing and to post photos of yourself that no one asked to see. Honestly, you would be better off ignoring bait and only responding to other "biohackers", but you instead insist on engaging in silly arguments that end in you posting a link to some scientific article about rats, or making erratic claims of genetic and intellectual superiority.>>77256469You used to be a healthy young man with a glowing and sharp look in your eyes, but now you have no facial collagen and have a glazed-over and uncanny look to your eyes, which is the complete opposite of 'biohacking' or 'eternal youth'. You could have spent those 1.5 years actually sculpting your body and spending your money from your manual labor job in more productive ways. All you have to show for your 1.5 years of biohacking is an absurd amount of saved scientific articles to argue with people on the internet, wasted money, and an uncanny appearance. I am not trying to bait you into further argument like these other dudes, I am just saying that it is pointless to make a General thread to discuss a topic if you are not even going to discuss the topic and just argue that others are wrong / inferior for questioning your logic and methods. Please stop killing threads to make this dumb general just to waste others' time. This would be better suited for looksmax desu
>>77256189Here's my theory: long telomeres correspond to stemness phenotypes and chemoresistance in cancerous cells especially with senescence-induction chemos, while short telomeres protect from cancer with easy apoptosis induction in senescent cells, but somatic mutations typically involving fusion proteins are still the most common initial carcinogenic event.
>>77255562where's this lil nigga now? did they finally arrest him for killing his wife?
>>77253376It's titled Lehninger because he was involved in the first editions of what is basically the golden standard textbook for biochemistry. The guy hasn't been involved in any subsequent editions for like 30 years. We're up to the 8th edition now, and there is nothing whatsoever that Lehninger ever wrote in it anymore. The one in the link is the 4th edition and that book maybe contains like 5% of Lehninger's writings, and he was already out of the picture by then.If you had genuinely dipped your toes in the world of biochemistry, you would have known this.Just read the goddamn book. You genuinely make me sad. What are you doing to yourself dude. What is even the point of arguing about all this shit with people who actually work with biomedical research for a living, when you can't even get yourself to open the standard textbook on biochemistry and start reading it?
>>77256953>If you had genuinely dipped your toes in the world of biochemistry, you would have known this.I was just trolling you, bro.
>>77256987>talks about wanting to learn about biochemistry>starts "trolling" insteadso what did you accomplish?
>>77257001He's not trolling, he genuinely havent read a single one of those PDFs and just ran them through chatgptDude has 0 concept of biochemistry basics considering i've seen him before arguing about trying to suppress the entirety of his estrogen axis (might explain the Jacob Syndrome look)
>>77256612>>77256814Post body
>>77257059>i've seen him before arguing about trying to suppress the entirety of his estrogen axisBased. Estrogen is a trash hormone.
>>77257081>Anon self-inducing menopause symptoms to age-troonsition to a senile mtfBased !
>>77257084>self-inducing menopause symptoms Show me the dats that it is even possible when using aromatase inhibitors in healthy males. >mtfReducing estrogen raises testosterone.
>>77257088We've already established you're a menopausal woman
>>77257089I have supraphysiological levels of testosterone due to aromatase inhibition.
>>77257093You're small and dyel
>>77257097I'm significantly bigger than most men while not even training, Imagine how big and muscular i would be if i started bodybuilding. Actually i'm quite excited about it, but not planning on practicing it until i have a complete home gym and physically undemanding source of income.
>>77257100Didn't read lol you look like shit
>>77257109You're just an ordinary human, so your opinion is heavily skewed by cognitive biases - that's why i prefer external data for objective assessments of my physique, and it shows i'm larger, more muscular and beautiful than majority of world's population. You can't change opinion of a man who bases it on objective data with just your opinion.
>23 year old niggas trying to make themselves look younger
>>77257118Oh not another post by a small weak dyel i wont be reading LOL !
>>77257130It's not about looking younger, it's about looking young forever. >>77257131You will read all my posts.
>>77247052fclo 1tbspvit d 15.000 iuvit k2 mk4 45mg1 tablet cialis every 3 dayshigh dose vitamin ceating only raw seafood, raw meat and homemade focaccia
>77257135>Another weak dyel angry post at a real MAN not caring about his opinion
>>77257138>1 tablet cialis every 3 daysWhat's the point if it has half-life of 17,5 hours? You take it as a preworkout?
>>77257141I know you care about my opinion and read all my posts, because lesser men like you are literally programmed for emotional salience regarding objects of their ressentiment - that's part of your evolutionary strategy, always trying to take down and demoralize those superior to you to lessen the competition. That's why I am a tragic hero, fighting against whole of humanity.
>>77257146pre workout and also for Sexi can fuck for hours and multiple times and that's how long it keeps me goodafter 3 days i revert to normal 1 sex and then 3 to 4 hours of not wantingit just makes me feel young again and my wife is way younger than i and it's such a change of pace to my ex who never wanted sex
>>77255562This retard took growth hormone secretagogue and was surprised by worsened health and aging-related parameters. How is he not able to do even basic research we're doing here?
>>77257257
>>77247052>Reinventing Amlodipinehttps://www.sciencedirect.com/science/article/pii/S0022356526010992Attention-deficit/hyperactivity disorder (ADHD) is a prevalent neurodevelopmental disorder, and pharmacological treatments have limited mechanistic specificity. Most non-stimulants target noradrenergic tone but show modest efficacy. L-type calcium channels (LTCCs) modulate neuronal excitability, catecholaminergic transmission, cortical plasticity, and neuroinflammation, processes central to ADHD pathophysiology. This review evaluates the evidence for repurposing the LTCC blocker amlodipine as a novel ADHD therapeutic. We propose a mechanistic framework where amlodipine acts within attention/arousal circuits to stabilize dopaminergic and noradrenergic tone, restore D2-autoreceptor feedback, enhance plasticity, and reduce neuroinflammation. This systems-level model provides explanatory links between drug action and ADHD pathophysiology, highlighting therapeutic avenues not addressed by current treatments. Contrary to historical assumptions, recent evidence confirms that amlodipine penetrates the blood-brain barrier. Convergent preclinical findings show phenotype rescue in zebrafish and rat models of ADHD, accompanied by normalization of ADHD-relevant metabolic pathways. Complementary biobank analyses suggest reduced traits associated with ADHD among genetically at-risk individuals taking amlodipine. Given enantiomeric pharmacology, S-amlodipine, with higher LTCC affinity and fewer off-target liabilities than R-amlodipine, emerges as a preferred candidate. Together, these findings warrant a reappraisal of LTCC modulation in ADHD. By providing mechanistic explanations of how amlodipine engages ADHD-relevant circuits, this review clarifies its therapeutic potential and reshapes our understanding of the drug itself, with implications for repurposing, enantiomer-specific development, and broader clinical translation.
>>77257257He took the wrong secretagogue unironically
>>77257661Why?
>>77257081>Estrogen is a trash hormone.>>77257088>Show me the dats that it is even possible when using aromatase inhibitors in healthy males.Only EXCESS estro is a "trash hormone" but you shouldn't drop below the bottom quartile of the reference range or you might ACK.>https://www.courttv.com/news/wv-v-natalie-cochran-ponzi-scheme-murder-trial/One of the theories floated by the defense in that case was the victim switching up his letrozole and clomid, which is a likely contributing factor in a fairly small amount of insulin ACKing him.>>77257665Some of the small molecules do better with insulin sensitivity.
>>77257862>you shouldn't drop below the bottom quartile of the reference range or you might ACK.Agree, but i don't think it's even possible to reduce estrogen to pathologic levels unless you suppress your HPTA with non-aromatazible steroids or are hypogonadal and have low sex hormone production to begin with. In studies i seen in healthy men, aromatase inhibition quickly reaches saturation - like in this study >>77249138 where there was no difference in estrogen suppression (which was 30-40%) between 25mg and 50mg of exemestane. So it's actually pretty healthy to take aromatase inhibitors - for more testosterone, less thymic involution and neuroprotection.
>>77257516Amlodipine doubles concentration of tadalafil in the blood. >Pharmacokinetic Drug Interaction Between Amlodipine and Tadalafil: An Open-Label, Randomized, Multiple-Dose Crossover Study in Healthy Male Volunteershttps://pubmed.ncbi.nlm.nih.gov/35221673/Tadalafil is predominantly metabolized by CYP3A4, and CCBs such as amlodipine, diltiazem, and verapamil areknown to be a potent CYP3A4 inhibitor.8,9 These facts could explain why the Cmax,ss and AUCτ,ss of tadalafil wereremarkably increased in the group of tadalafil plus amlodipine in the present study. Although the plasma level of tadalafilconcentration in co-administration treatment was greater than monotherapy treatment, and the frequency of AEs such asa remarked decrease in blood pressure was not significantly different. Sildenafil, other PDE-5 inhibitor, and antihypertensive dihydropyridines such as amlodipine were metabolized by CYP3A4. However, administration of sildenafil andamlodipine did not exhibit a synergistic blood pressure-lowering action.
>>77247052>Doxycycline, Azithromycin and Vitamin C (DAV): A potent combination therapy for targeting mitochondria and eradicating cancer stem cells (CSCs)https://www.aging-us.com/article/101905/textHere, we devised a new strategy for eradicating cancer stem cells (CSCs), via a “synthetic-metabolic” approach, involving two FDA-approved antibiotics and a dietary vitamin supplement. This approach was designed to induce a “rho-zero-like” phenotype in cancer cells. This strategy effectively results in the synergistic eradication of CSCs, using vanishingly small quantities of two antibiotics. The 2 metabolic targets are i) the large mitochondrial ribosome and ii) the small mitochondrial ribosome. Azithromycin inhibits the large mitochondrial ribosome as an off-target side-effect. In addition, Doxycycline inhibits the small mitochondrial ribosome as an off-target side-effect. Vitamin C acts as a mild pro-oxidant, which can produce free radicals and, as a consequence, induces mitochondrial biogenesis. Remarkably, treatment with a combination of Doxycycline (1 μM), Azithromycin (1 μM) plus Vitamin C (250 μM) very potently inhibited CSC propagation by >90%, using the MCF7 ER(+) breast cancer cell line as a model system. The strong inhibitory effects of this DAV triple combination therapy on mitochondrial oxygen consumption and ATP production were directly validated using metabolic flux analysis. Therefore, the induction of mitochondrial biogenesis due to mild oxidative stress, coupled with inhibition of mitochondrial protein translation, may be a new promising therapeutic anti-cancer strategy. Consistent with these assertions, Vitamin C is known to be highly concentrated within mitochondria, by a specific transporter, namely SVCT2, in a sodium-coupled manner. Also, the concentrations of antibiotics used here represent sub-antimicrobial levels of Doxycycline and Azithromycin, thereby avoiding the potential problems associated with antibiotic resistance.
>>77258227Aging: Improving health-span and life-spanWe believe that the DAV triple combination therapy that we describe here may also have implications for improving health-span and life-span, as aging is one of the most significant risk factors for the development of many human cancer types [19,20]. Moreover, we have previously demonstrated that Azithromycin, by itself, is an FDA-approved drug, with remarkable senolytic activity, that targets and removes senescent fibroblasts, such as myo-fibrobasts, with great efficiency approaching nearly 97% [21]. The accumulation of pro-inflammatory senescent cells is thought to be the primary cause of many aging-associated diseases, such as heart disease, diabetes, dementia and cancer, to name only a few [21]. Since cancer-associated fibroblasts (CAFs) are senescent myo-fibroblasts, with tumor promoting activity, this triple combination approach with Azithromycin may also effectively target the glycolytic tumor stroma of aggressive and metastatic cancers, especially those bearing the metabolic hallmarks of the “Reverse Warburg Effect” [22–28].
New stuff arrived including the no clinic data MK-777. Hopefully no turbo cancer. Trying out nasal spray Pinealon too
>>77258241Nice, are you planning on doing bloodwork?
>>77258244Maybe once since I need a new doctor anyways otherwise this is all rather mild stuff, should be fine on the MK doing it week days only.Also poly-cell is fucking awesome, no alcohol burn or weird taste, other providers need to copy this shit asap
>>77247052>Sitagliptin elevates plasma and CSF incretin levels following oral administration to nonhuman primates: relevance for neurodegenerative disordershttps://link.springer.com/article/10.1007/s11357-024-01120-4The endogenous incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) possess neurotrophic, neuroprotective, and anti-neuroinflammatory actions. The dipeptidyl peptidase 4 (DPP-4) inhibitor sitagliptin reduces degradation of endogenous GLP-1 and GIP, and, thereby, extends the circulation of these protective peptides. The current nonhuman primate (NHP) study evaluates whether human translational sitagliptin doses can elevate systemic and central nervous system (CNS) levels of GLP-1/GIP in naive, non-lesioned NHPs, in line with our prior rodent studies that demonstrated sitagliptin efficacy in preclinical models of Parkinson’s disease (PD). PD is an age-associated neurodegenerative disorder whose current treatment is inadequate. Repositioning of the well-tolerated and efficacious diabetes drug sitagliptin provides a rapid approach to add to the therapeutic armamentarium for PD. The pharmacokinetics and pharmacodynamics of 3 oral sitagliptin doses (5, 20, and 100 mg/kg), equivalent to the routine clinical dose, a tolerated higher clinical dose and a maximal dose in monkey, were evaluated. Peak plasma sitagliptin levels were aligned both with prior reports in humans administered equivalent doses and with those in rodents demonstrating reduction of PD associated neurodegeneration. Although CNS uptake of sitagliptin was low (cerebrospinal fluid (CSF)/plasma ratio 0.01), both plasma and CSF concentrations of GLP-1/GIP were elevated in line with efficacy in prior rodent PD studies. ... In conclusion, this study provides a supportive translational step towards the clinical evaluation of sitagliptin in PD and other neurodegenerative disorders for which aging, similarly, is the greatest risk factor.
Sardine, Egg, Red Onion, Carrot, Sprouts, Parsley, Pomegranate, Strawberry, Blueberry, Grapefruit, Beet, Cacao, Green Tea, Olive Oil
>>77258403Axle bench, viking press, green moose, lava juice. Dumbbell raise, birthday cake, large fries, chocolate shake
>>77258241Did the first dose of 777Will update mid morning if the hunger feels different from 677
is we takin recombinant human lactoferrin
Bros... Red Wine at night is all you need
>>77257273>>77257257what a stupid retard. he measured his actual blood growth hormone.GH is pulsatile, it should be near 0 most of the day and then spike massively every 3 hours or so. You can't get any meaningful information just measuring a random GH blood draw
>>77247484>in the same time
>>77247052>Body-wide multi-omic counteraction of aging with GLP-1R agonismhttps://pubmed.ncbi.nlm.nih.gov/41265449/Identifying practical ways to counteract aging and associated degenerative disorders is urgently needed. We performed deep molecular profiling and functional assessments in aging male mice to show that glucagon-like peptide-1 receptor agonist (GLP-1RA) treatment broadly counteracts age-related changes. In mice treated with a GLP-1RA from 11 months for 30 weeks, we observed strong body-wide multi-omic age-counteracting effects and improved selected physical functions. Importantly, the effects were specific to aged mice, not young adults, and were attained with a relatively low dose that minimally affected food intake or body weight. With GLP-1RA treatment beginning at 18 months for 13 weeks, the molecular age-counteracting effects were even stronger and largely dependent on hypothalamic GLP-1R, pointing to a brain-body axis of aging modulation. Comparison with mammalian target of rapamycin (mTOR) inhibition, a proven anti-aging strategy, revealed strong multi-omic similarities. Our findings have broad implications for the mechanisms behind GLP-1RAs' pleiotropic benefits, guiding clinical trials, and informing development of anti-aging-based therapeutics.
>>77258883https://www.cell.com/cell-metabolism/fulltext/S1550-4131(25)00474-7
>>77258883>>77258886Anti-aging properties of GLP-1 are a scam. Research on incretin-elevating drugs showed no extension of lifespan in healthy organisms. Example: >DPP-4 inhibition with linagliptin ameliorates the progression of premature aging in klotho−/− micehttps://pmc.ncbi.nlm.nih.gov/articles/PMC5709858/ The major findings of our present study were that linagliptin significantly ameliorated the progression of premature aging phenotypes, as shown by the amelioration of cognitive impairment, alopecia, body weight gain–loss, and hypoglycemia. Furthermore, there was a trend for linagliptin to prolong survival of klotho−/− mice. These effects of linagliptin in klotho−/− mice were not observed in control wild-type mice, thereby showing that these beneficial effects of linagliptin were specific for klotho−/− mice.
Absolute state of this thread kek we need the IP count back. Kill yourself OP
>>77258905Yes, i argue with myself. It's a secret of my power.
>>77258906Yes you're the only who cares about this tranny shit. I can tell aside from the bryan schizo that every other poster is clowning you or telling you to get help
>>77258913Don't you dare bring my beloved bryan schizo into this...
>>77258772>Red Wine at night is all you needDisrupts sleep architecture.
>>77256612>I'm generally skeptical of the FDA-approved rapalogs' safety in healthy people, especially after picrel's experience. I decided to investigate situation just a bit, and it seems it's more complicated than that. First of all, he decided to megadose it for some reason. Rapamycin is more selective for mTORC1 then mTORC2 at lower doses, and it has long half-life, so it accumulates.
>>77256612>>77258951Then there's this video, critiquing his decision to stop rapamycin based on research (study link - https://www.biorxiv.org/content/10.1101/2024.10.22.619522v1.full.pdf) showing it accelerates epigenetic clocks. >Bryan Johnson Stopped Taking RAPAMYCIN & It DOESN'T Make Sense...https://www.youtube.com/watch?v=PmdQv8Wu-yoVideo author argues it was a mistake, since other longevity intervention, similarly to rapamycin, haven't showed positive influence on epigenetic clock. Then there's this comments from primary investigator in the study regarding interpretation of the research:
>>77256612>>77258951>>77258958What i think it actually means in practice is that HDAC-inhibitors are necessary for anti-aging at some point.
>>77247052New video on rapamycin from Brad Stanfield. https://www.youtube.com/watch?v=Rcgiv8PoNBc
>>77258550Well nothing to report really, some light hunger was felt but it was basically nothing.
>>77259489Have you used MK-677 before to compare?
>>77259493Yes I forgot to type that part. The ravenous feeling of 677 didn't start until a few days later for me on that, so I'll give this a few days as well. So far I don't think it's even close as my morning coffee was more than enough to make the feeling "disappear" (not quite an accurate word since the feeling is still there). For me MK-677 had a genuine empty stomach feeling, so far 777 does not have that. It's like my body can tell it's just the receptors being activated
>>77247052>Study finds erectile dysfunction medications associated with significant reductions in deaths, cardiovascular disease, dementiahttps://www.utmb.edu/news/article/utmb-news/2024/11/19/study-finds-erectile-dysfunction-medications-associated-with-significant-reductions-in-deaths--cardiovascular-disease--dementiaThe study utilized the United States Collaborative Network, which includes data from over 50 million men within the TriNetX global database. For the study, researchers evaluated more than 500,000 men aged 40 or older diagnosed with erectile dysfunction between February 2004 and February 2021. Outcomes in men prescribed tadalafil or sildenafil were compared to those diagnosed with erectile dysfunction who did not receive the medications. Key findings include:>Mortality: 34% reduction with tadalafil, 24% with sildenafil>Heart Attack: 27% reduction with tadalafil, 17% with sildenafil>Stroke: 34% reduction with tadalafil, 22% with sildenafil>Venous Thromboembolism: 21% reduction with tadalafil, 20% with sildenafil>Dementia: 32% reduction with tadalafil, 25% with sildenafil>Benefits of Tadalafil and Sildenafil on Mortality, Cardiovascular Disease, and Dementiahttps://www.amjmed.com/article/S0002-9343(24)00705-8/fulltext
hey, is there a thing that decreases the left side of the heart in case of enlargement? Mainly left ventricle and aorta
>>77259664>New drugs in hypertrophic cardiomyopathyhttps://www.escardio.org/communities/councils/cardiology-practice/education/cardiopractice/new-drugs-in-hypertrophic-cardiomyopathy/
>>77258241>Hopefully no turbo cancer.There is no evidence it's a mutagen, but it could "turbo-charge" an existing cancer; doing some medically unnecessary cancer screening and chemoprophylaxis stacking is probably the smartest, but I ran MK-677 fora few months with just metformin as an adjuvant over a decade ago, and didn't ACK of some rare sarcoma or anything.>>77259664>>77260096Picrel is one of the most interesting quasi-recent discoveries. Lot of research on both of picrel compounds recently, especially Paeoniflorin in oncology, but warning it's an anti-androgen aromatase inducer.
>>77260445Post body
>>77260447Bet you haven't even read the latest zebrafish/C2C12 assays on deranged East-Asian anabolic algae upregulating both myogenic regulatory factors and the notorious AkT/mTOR pathway:>Pro-myogenic and anti-atrophic effects of Padina arborescens extract through Akt/mTOR signaling in dexamethasone-induced C2C12 cells and zebrafish model>https://link.springer.com/article/10.1007/s11626-026-01181-zPost research.
>>77260452>Blah blah blahI can tell you look even worse than the faggot OP kek
so do you guys actually take any of this
