Intranasal deferoxamine - Biohackers doing bio-hacker things

Ben.

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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:


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):
It sounds slightly that your manic? Which I get if your perma high. However dosent being perma high distract from cognitive benefits? Did you also notice pro cognitive effects? Or just differences in well-being?
  • 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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Jamsey

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This is really cool and matches a lot of what I’ve read related to iron. I wonder if intranasal deferoxamine would be effective for hair loss as well
 
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Ben.

Ben.

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This is really cool and matches a lot of what I’ve read related to iron. I wonder if intranasal deferoxamine would be effective for hair loss as well

Why hair loss specifically? Because it fixes organs/hormones due to fixing the brain and thus energy production or is there a more direct mechanism related to the hair folices and iron?
The whole thing at first glance looks very risky to me, putting a chelator right up the nose near the brain but maybe i just read to much fearporn information on chelators redestributing metals into even "worse" places.
 

golder

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This seems really interesting and potentially quite dangerous. Also, it seems quite hard to locate, which bizarrely makes it even more attractive to weak-minded ‘biohackers’ like me.
 

youngsinatra

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There‘s a better way to do it. (in my opinion)
1. Check iron-metabolism markers (ferritin, iron saturation index, transferrin, serum iron, hemoglobin, serum copper, ceruloplasmin)
2. Compare your blood test results with the ideal values:
(Ignore the reference range for vitamin A and D though)
3. If iron markers are elevated, then donate blood. If copper levels are below optimal go to the next step.
4. Have a sufficient intake of bioavailable copper, because nearly all facets of iron metabolism depend on copper / ferroxidase / ceruloplasmin.
Food sources are superior to oxidized copper (II) supplements. Ruminant animal liver, shellfish, oysters and mushrooms are good food sources. If you cannot tolerate or you don‘t have access to quality food sources, then you might try a copper (I) supplement like „MitoSynergy“ or „Global Healing“, taken right before a meal.
You may only lack necessary cofactors for the proper utilization of stored copper in your liver — the most important ones are riboflavin (B2), folate (B9) and cobalamin (B12).
4. If you like you can add in natural iron chelators to your diet like coffee, tea, calcium, cranberry juice, vegetables, fruits, herbs and spices, especially when eaten with a iron-rich meal.
 
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Vinny

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I read through the chat that @Ben. posted from.
pax.pharmacopoeia has been missing for some time. I don`t know what to think of this, tbh.
 

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