So on my health quest i found myself randomly in a nootropics chat website and came across a odd user (pax.pharmacopoeia) and i thought it might be interesting to share some of the claims.
From what i understood he is snorting things such as deferoxamine, insulin and a bunch of other stuff. He made waves apparantly on 4chan so take all of this with a big grain of salt because it sounds "out there". I do not advocate it and alot of posts seem like he went a somewhat "crazy". I found it interesting nonetheless. One of his theorys is the following:
The following is copy paste from the chatlog i linked above which sadly formats not well on here (hope thats ok, if not charlie can delete the thread):
From what i understood he is snorting things such as deferoxamine, insulin and a bunch of other stuff. He made waves apparantly on 4chan so take all of this with a big grain of salt because it sounds "out there". I do not advocate it and alot of posts seem like he went a somewhat "crazy". I found it interesting nonetheless. One of his theorys is the following:
Self study propelled by personal fears of aging and disease drove my pursuit towards obsession. Through studying the concepts surrounding insulin resistance, transcriptional drift, mitochondrial decline and neurological dysfunction I • have developed a strong understanding of the pathways of aging, metabolic and neurological disoders.
• Through developing this understanding of metabolic disorders, and neurological disorders both are deeply tied together with common pathology of neuronal insulin resistance, chronic endotoxicity/lipotoxicity/advanced glycation end products etc, inducing a dysfunction and decline in gabaergic/somatostatin interneurons leading to defects in gabaergic inhibition within the brain. Declines of somatostatin and other populations of inhibitory interneurons as a consequence of neuroinflammation, decline in neurotrophic supply from reduced insulin transport to the brain and decline in insulin sensitivity within the brain precipitates the development of metabolic disorder as well as declines in sensory functions and cognition with age as well as the direct progression of aging through promoting the decline of stem cell pools and the accumulation of misformed proteins within the brain and periphery(amyloid beta, etc) These misformed proteins, endotoxins, cortisol, endocannabinoids, and reactive oxygen species reduce insulin sensitivity within the brain leading to defects in gaba signalling promoting a disinhibition of glutamatergic signaling which promotes an overactivation of glutamate expressing neurons leading to excitotoxicity through an accumulation of calcium intracellularly promoting a depletion of atp within the neuron leading to cell death. A disinhibition of glutamate signaling as a consequence of diabetes and metabolic disorder.
As glutamate expressing neurons are disinhibited ,Reactive oxygen species accumulate, this leads to an aberration of endocrine functions through decline of the HPTA axis from dysfunction and decline of the hypothalamus. This leads to increased blood pressure, hyperinsulinemia/diabetes pathologies, autoimmune disorders, neurological disorders, heart arrhythmia, and ultimately decline in gene transcription called transcriptional drift all occurring due to metabolic drift, glutamate disinhibition and inflammation within the brain. I'm a independent researcher in an online syndicate of biohackers. I've proposed the development of multiple new drugs for the mitigation of these pathologies within the brain based on a self study of the decline of somatostatin interneurons within the brain in aging and its ties to all known diseases of aging. I'm working closely to meet these goals and we should see my first drug finish development which would foster the creation of a new class of drugs which would stand to cure all known neurological and metabolic disorders as well as cure all forms of intellectual disability and turn anyone into a genius.
The following is copy paste from the chatlog i linked above which sadly formats not well on here (hope thats ok, if not charlie can delete the thread):
- When we suffer from chronic inflammation the functions of the iron proteome breaks down and this promotes insulin resistance within the brain and leads to iron accumulation in the cytosol of our cells because of increased expression of DMT1,hepcidin, and ferritin heavy chain. Viruses, cortisol, glutamatergic disinhibition, endotoxins, endorphins, which are all contributing factors to insulin resistance which is mediated by the failure of insulin transport into the brain due to chronic inflammation, hyperinsulinemia, obesity, chronic mild stress etc. This insulin resistance within the brain leads to the failure of Proteostasis or the regular functions of our mitochondria supporting cellular activities. Oxidative stress reduces atp generation within the mitochondria that can't be mitigated under insulin resistance and this leads to the failure of the autophagesome. This allows iron to build up and promotes dendritic death and reduced viability of our neurons by allowing cholesterol, sphingolipids, bilrubin, and ammonia to accumulate causing defects in the lysosomal membrane
- The mitochondria in this instance is called the Endosome what's outside of mitochondria where all other organelles of our cells are is called the lysosome
- Opioids, viruses, and endotoxins promote endolysosomal deacidification
- Endolysosomal deacidification is a process which the breakdown in proteostasis through increasing endoplastic reticulum stress increases the accumulation of iron in the cytosol of our brain cells
- This is the process in which endorphins or opioids promote iron accumulation in the cell and that leads to synaptic defects and increased susceptability to excitotoxicity.
- Morphine-Induced Modulation of Endolysosomal Iron Mediates Upregulation of Ferritin Heavy Chain in Cortical Neurons
- deferoxamine completely restores the synaptic expression that was lost to opioids
- glutamatergic activity on neurons also contributes to intake of iron from outside of the cell and that promotes increases in oxidative stress and is likely what mediates the internalization of nmda and ampa receptors from the cell surface
- iron chelation greatly potentiates glutamate induced neuron firing rate.
- Lysosomal iron modulates NMDA receptor-mediated excitation via small GTPase, Dexras1
- This is how cortisol promotes neuronal insulin resistance is by disinhibiting glutamate release and that promotes the endocytosis of gaba receptors on gaba interneurons.
- increased glutamate activity promotes iron transport into the lysosome and this is likely how glutamate exerts neurotoxicity or is partially related to reduction of synaptic complexity with chronic stimulation.
- I've snorted the equivalent of using 400kgrams of deferoxamine intravenously when doing the math comparing intranasal deferoxamine and intravenous use.
This targets the brain so incredibly well that the levels that reach the prefrontal cortex in mice is 271 fold higher than iv use.
- Intranasal Deferoxamine Provides Increased Brain Exposure and Significant Protection in Rat Ischemic Stroke
We report here that intranasal administration targets DFO to the brain and reduces systemic exposure, and that intranasal DFO prevents and treats stroke damage after middle cerebral artery occlusion (MCAO) in rats. A 6-mg dose of DFO resulted in significantly higher DFO concentrations in the brain (0.9–18.5 μM) at 30 min after intranasal administration than after intravenous administration (0.1–0.5 μM, p < 0.05). Relative to blood concentration, intranasal delivery increased targeting of DFO to the cortex approximately 200-fold compared with intravenous delivery. Intranasal administration of three 6-mg doses of DFO did not result in clinically significant changes in blood pressure or heart rate. Pretreatment with intranasal DFO (three 6-mg doses) 48 h before MCAO significantly decreased infarct volume by 55% versus control (p < 0.05). In addition, post-treatment with intranasal administration of DFO (six 6-mg doses) immediately after reperfusion significantly decreased infarct volume by 55%
- Deferoxamine promotes opioid receptor supersensitivity
- deferoxamine+NAC in mice completely prevents amphetamine induced brain damage
- intranasal deferoxamine + my next product would protect us from any metabolic stressor
Treatment with a heme oxygenase 1 inducer enhances the antinociceptive effects of µ-opioid, δ-opioid, and cannabinoid 2 receptors during inflammatory pain - PubMed
The effects of n-acetylcysteine and/or deferoxamine on manic-like behavior and brain oxidative damage in mice submitted to the paradoxal sleep deprivation model of mania
Effect of N-acetylcysteine and/or deferoxamine on oxidative stress and hyperactivity in an animal model of mania - PubMed
Heme oxygenase-1-mediated neuroprotection in subarachnoid hemorrhage via intracerebroventricular deferoxamine - PubMed
Treatment with carbon monoxide-releasing molecules and an HO-1 inducer enhances the effects and expression of µ-opioid receptors during neuropathic pain - PubMed
- adding in intranasal EPO, and intranasal igf2 or insulin would be the cure for all neurological and metabolic disorders
- Deferoxamine intranasal + inuslin and epo would put you past the need for drugs
- I'm already high enough on deferoxamine because I physically chelated iron from my brain and reduced the function of the dopamine transporter significantly
- is the intranasal insulin also required to get the effects?
they both potentiate each other by chelating iron from the brain you suppress oxidative stress, endotoxicity, and other mechanisms that downregulate insulin sensitivity so DFO increases the recycling of insulin receptors to the cell surface and growth factors like NGF, and bdnf are dependent on these insulin receptors for neurogenesis and neuroprotection
BDNF functions just like insulin in the brain so insulin is just delivering a concentration of powerful neurotrophic factors to the brain
scientists have actually done pancreatic Islet transplants into the brains of mice who've had icv streptozotocin administration to destroy the insulin receptors in the brain
icv streptozotocin perfectly mimics the amyloid beta model of cognitive decline in alzheimers and icv streptozotocin mice are also diabetic and obese
intranasal deferoxamine ameliorates icv streptozotocin induced cognitive dysfunction - Intranasal deferoxamine affects memory loss, oxidation, and the insulin pathway in the streptozotocin rat model of Alzheimer's disease - PubMed
- Intracranial pancreatic islet transplantation increases islet hormone expression in the rat brain and attenuates behavioral dysfunctions induced by MK-801 (dizocilpine) - PubMed
- Long-term effects of intracranial islet grafting on cognitive functioning in a rat metabolic model of sporadic Alzheimer's disease-like dementia - PubMed
- Intracranial Transplantation of Pancreatic Islets Attenuates Cognitive and Peripheral Metabolic Dysfunctions in a Rat Model of Sporadic Alzheimer's Disease - PubMed
- So this demonstrates that increasing insulin levels in the brain with intranasal insulin would be potentiated by intranasal deferoxamine and both would greatly ameliorate the progression of alzheimers disease and other neurodegenerative and metabolic disorders
- Intranasal deferoxamine can improve memory in healthy C57 mice, suggesting a partially non-disease-specific pathway of functional neurologic improvement - PubMed
- Reversion of age-related recognition memory impairment by iron chelation in rats - PubMed
- Deferoxamine inhibits iron induced hippocampal tau phosphorylation in the Alzheimer transgenic mouse brain - PubMed
- I've pioneered the use of so many different drugs in our group and taken many exotic drugs most have never heard of
deferoxamine beats everything
the ammount of deferoxamine i used cost $10 relative to what i paid for the whole box
this is a permanent one way change
after you take deferoxamine theres no going back to who you were before
your entire personality will change
- The mechanistic data leaves nothing to doubt.
- Protection from oxidative stress-induced apoptosis in cortical neuronal cultures by iron chelators is associated with enhanced DNA binding of hypoxia-inducible factor-1 and ATF-1/CREB and increased expression of glycolytic enzymes, p21(waf1/cip1), and erythropoietin - PubMed
- Isolated Fungal Sphenoid Sinusitis With Cavernous Sinus Thrombophlebitis: A Case Report
If you develop double vision and headache with intranasal deferoxamine take large ammounts of rapamycin intranasally
I mean large ammounts
Rapamycin Exerts Antifungal Activity In Vitro and In Vivo against Mucor circinelloides via FKBP12-Dependent Inhibition of Tor
Isolated sphenoid mucormycosis presenting as visual impairment: changing trends? - PubMed
- Chronic Energy Depletion due to Iron Deficiency Impairs Dendritic Mitochondrial Motility during Hippocampal Neuron Development
During development, neurons require highly integrated metabolic machinery to meet the large energy demands of growth, differentiation, and synaptic activity within their complex cellular architecture. Dendrites/axons require anterograde trafficking of ...
- everything feels good so I soak in everything.
- Because I'm permanently high from increased potentiation and phosporylation of my neuronal insulin receptors on all of my neuronal cell lines I'm restoring neuronal insulin sensitivity by chelating iron
- Deferoxamine doesn't work like normal drugs
- it chelates iron
- all the mechanistic effects of deferoxamine is based on removing iron that has accumulated within the cytosol of your neurons and other cell types.
- Removing iron that's accumulated by the dissociation of iron from mitochondria through endolysosomal deacidification from opioids or viruses, or from the accumulation of hepcidin or glutamatergic disinhibition reduces the healthy function of all cell types within the brain and its the main causal factor behind the degeneration of our metabolic homeostasis and our neurological functions
- This is controlling neuronal insulin resistance allowing insulin to better support the neurotrophic supply and glucose metabolism, and steroidogenesis for pregnenolone that promotes the outgrowth of microtubles on our neurons and hypothalamic inflammation that promotes neurological disorders and metabolic disease share this common contributing factor
- Neuronal insulin resistance from the accumulation of iron is the main pathological factor in the loss of proteostasis and the use of iron in protein synthesis. Excess free iron that is lost to the cytosol from endoplastic reticulum stress from LPS and saturated fat induced lipotoxicity promotes the dysfunction of mitochondria within our brain cells and promotes the functional decline of these cell types and it induces the cellular senescence and transcriptional drift in these cell lines through the dysfunction of our livers and blood brain barriers that promotes bacteria, virus, and fatty acid, ammonia and bilirubin accumulation within our brain and the reduction of cholesterol metabolism and this promotes sphingolipid accumulation in the lipid rafts of our brain cells contributing to the reduction in cell viability.
- Iron accumulation within our braincells occurs and that promotes neuronal insulin resistance
- insulin resistance leads to the breakdown and reduced insulin transport to the brain which is the root cause of all neurological and metabolic disorders
- I've removed all the iron from my brain that contributes to neuroinflammation and reduced synaptic plasticity. The data I've shared to support those observations, the observations why i'm high and the data to support why my fatigue is significantly reduced, my attention and learning is much better, my reference memory is perfect and all of that data is supported by the body of literature I've posted from the past 2 weeks
- All the data on rapamycin and neuronal cultures shows rapamycin is nontoxic in every concentration tested
- me snorting insulin with deferoxamine for the few short days may have allowed a fungal infection to occur and i took rapamycin to cure it
- Like I've said before rapamycin is non toxic and I used more rapamycin than any human alive especially by the nasal roa
- snorted some creatine too and went to sleep
- The mania is not a consequence of feeling high
- you're looking at me fully optimized
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