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Protecting Your Brain on AAS
By Sadist
Thread Song:
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One of The Most Overlooked AAS Side Effects
By far, one of the most overlooked harmful effects that come with Anabolic-Androgenic steroids use is their neurotoxicity. It is very hard to notice, and unless acute - creeps up on you quite shortly - until it's already quite late.
People tend to cover all the other aspects of keeping yourself safe on gear, but greatly overlook this topic - either because it's nowhere near as spoken about - or is because it brings around yet another set of ancillaries that haven't to be regularly taken care of
However, just like with all the other ancillary stacks - this one is incredibly easy to consume and stick to, so there is absolutely no reason to not run.
All ancillaries picked on this list are as selective as possible for our task, so that the side effects are minimal.
Massive kudos to Terminid for immensely contributing to the colossal amount of research put into this thread.
Below, you'll find the Table of Contents, which not only would explain how and why each pathway occurs and damage the brain, but also how to actually prevent/treat each issue.
Within each topic, you will find the outline for each mechanism, the relevant compound, as well as all the explanations behind how each one of them fucks with your brain, how each compound unfucks it (all the scientific slop) - and the appropriate dosage protocols. I'll make sure to keep all said scientific slop as brief and to-the-point as possible though.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
Table of Contents:
I
Aβ / AMYLOID
II
EXCITOTOXICITY / NMDA
III
TAU / GSK-3β
IV
MITOPHAGY / MITOCHONDRIAL QUALITY
V
OXIDATIVE STRESS
VI
NEUROINFLAMMATION / ERβ
VII
MAO-B / DOPAMINERGIC OXIDATIVE STRESS
VIII
CIRCADIAN / MITOCHONDRIAL SIGNALING
IX
TRKB
X
IRON CHELATION
XI
INJECTION FREQUENCY / ESTER SELECTION
XII
SUMMARY
Protecting Your Brain on AAS
By Sadist
By no means is this medical advice. I am not attempting to encourage usage of AAS or any other compounds. This content is intended for educational purposes only. For more information, refer to your practitioner, or any other appropriately qualified person.
Thread Song:
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
One of The Most Overlooked AAS Side Effects
By far, one of the most overlooked harmful effects that come with Anabolic-Androgenic steroids use is their neurotoxicity. It is very hard to notice, and unless acute - creeps up on you quite shortly - until it's already quite late.
People tend to cover all the other aspects of keeping yourself safe on gear, but greatly overlook this topic - either because it's nowhere near as spoken about - or is because it brings around yet another set of ancillaries that haven't to be regularly taken care of
However, just like with all the other ancillary stacks - this one is incredibly easy to consume and stick to, so there is absolutely no reason to not run.
All ancillaries picked on this list are as selective as possible for our task, so that the side effects are minimal.
Massive kudos to Terminid for immensely contributing to the colossal amount of research put into this thread.
Below, you'll find the Table of Contents, which not only would explain how and why each pathway occurs and damage the brain, but also how to actually prevent/treat each issue.
Within each topic, you will find the outline for each mechanism, the relevant compound, as well as all the explanations behind how each one of them fucks with your brain, how each compound unfucks it (all the scientific slop) - and the appropriate dosage protocols. I'll make sure to keep all said scientific slop as brief and to-the-point as possible though.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
Table of Contents:
I
Aβ / AMYLOID
II
EXCITOTOXICITY / NMDA
III
TAU / GSK-3β
IV
MITOPHAGY / MITOCHONDRIAL QUALITY
V
OXIDATIVE STRESS
VI
NEUROINFLAMMATION / ERβ
VII
MAO-B / DOPAMINERGIC OXIDATIVE STRESS
VIII
CIRCADIAN / MITOCHONDRIAL SIGNALING
IX
TRKB
X
IRON CHELATION
XI
INJECTION FREQUENCY / ESTER SELECTION
XII
SUMMARY
I
Aβ / AMYLOID
A recurring pattern you will see with these pathways is oxidative stress. It will have its own mitigation section, but just know that it is one of the ways through which this pathway in particular damages the brain.
The other, more important one, however - is the Calcium dysregulation and excitotoxicity, thereby damaging or killing nerve cells, which will be delved into more in-depth shortly.
What to take:
Huperzine A
400 mcg 2x/day
Huperzine A reduces ADAM10, therefore reducing ERK1/2 signaling, leading to a decrease in BACE1. What this means is Aβ is reduced. It additionally provides direct antioxidant support against the Aβ and antagonizes the NMDA (more on this later).
Donepezil HCl
2.5 mg/EOD
Donepezil Reduces β-secretase activity, inhibits GSK-3 (which we will touch up on shortly), redirects APP cleavage/AChE-catalyzed aggregation/β-secretase activity, which are all exactly what's partially responsible for the Aβ/Amyloid activity.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
II
EXCITOTOXICITY / NMDA
Similarly to the previous, and many others pathways, besides the oxidative stress - you will see a lot of mitochondrial damage/dysregulation (which is so major it actually also has its own section). As mentioned before - excitotoxicity is the process of mitochondrial damage/death (bad stuff).
NMDA in particular selectively elevates Ca way more than a lot of other mechanisms, hence being disproportionately excitotoxic.
What to take:
Memantine HCl
2.5 mg/EOD
Memantine occupies the Mg-binding sites at the NMDA, thus preventing them from being used up by the bad stuff. It is very potent at it, more so than other such compounds (upwards of 20-fold) and does not cause dissociative side effects, like ket would.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
III
TAU / GSK-3β
GSK-3β is an extremely important aspect when it comes to Tau, as the mere activation state (not even its presence) determines whether Tau is stable - or fucks you up by collapsing into a bunch of bullshit, such as multiple different stress signals or toxic tangles. So essentially, our main goal - is to maintain the correct activation state of the former thing (mainly).
What to take:
Lithium Carbonate
150–600 mg/day
(Dose derived from low-dose studies; Serum-level guided, so be cautious of Autophagy/Proteostasis).
Directly competitively inhibits GSK-3β & phosphorylation, also lowers tau in multiple different ways.
Sulforaphane
100–200 µmol SFN-equivalent/day
Take in a complex with glucoraphanin + active myrosinase to bioactivate it.
Allows Nrf2 to bind the antioxidant elements, enabling phase II detox antioxidant genes. Not only that, but it directly suppresses GSK-3β by throttling it.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
IV
MITOPHAGY / MITOCHONDRIAL QUALITY
As discussed before, mitophagy is the process of detecting and destroying the damaged/dead mitochondria in order to avoid any toxin leakage into the system. It does so via a plethora of different mechanisms, starting off by getting flagged as fucked by PINK1 - and ultimately ending with a bunch of mechanisms bring it into autophagy.
In order for the process of the damaged mitochondria to be effectively found and recycled to be maximized, said PINK1 pathway has to be upregulated.
What to take:
Purified Urolithin A
500–1,000 mg/day (pref. Liposomal)
This does exactly that - it both elevates the PINK1 pathway, BUT also additionally restores the pathway after the Aβ-induced suppression.
Not all that much more to say here.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
V
OXIDATIVE STRESS
Good old oxidative stress is probably what's most talked about when it comes to the topic of AAS damage, and not only when it comes to neuroprotection. However, not all even know about how it actually damages the body/brain.
In short, when it takes place, different -ase compounds, alongside glutathione (the same thing used to protect you from ROS by the way) oxidative damage to the lipids, DNA and a lot of other things - leading to cell death, as well as hyperphosphorylation and inflammation (there's even more, but these are the most prevalent ones to note).
What to take:
NACET
375 mg 2x/day
N-Acetyl-Cysteine Ethyl Ether is extremely bioavailable to the brain, and acts as an amazing antioxidants as one of the main parts of the glutathione production.
Astaxanthin
12-24 mg/day
Carotenoids in general are phenomenal antioxidants, but Astaxanthin seems to be the most bioavailable to the brain, so taking it with food daily will not only yield you the neuroprotective benefits - but will also give your skin a nice gold-ish glow.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
VI
NEUROINFLAMMATION / ERβ
As the brain detects different bullshit that AAS provide - it sends inflammation signals to try and combat said bullshit. It initially is helpful, but soon becomes harmful, as ROS, nitric oxide, cytokines and other such things accumulate.
As for ERβ, estrogen in general is crucial for things like brain development, neuroprotection, anti-inflammation, etc.
What to take:
S-equol
20-30 mg/day
Yes boyos, it is unironically time to soymax. S-equol is a high-affinity, selective ERβ agonist, providing mediation antioxidative, anti-resorptive genomic and anti-inflammatory programs - all whilst its selectivity allows for it to not provide any of the actual foid-related estrogenic effects from ERα.
Note: Intranasal α-DHED could also be mogger, but fuck knows where to actually get it.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
VII
MAO-B / DOPAMINERGIC OXIDATIVE STRESS
MAO-B actively breaks down dopamine in the brain, thereby damaging it. It camps on the outside of the mitochondria's membrane and actively converts an amine into an aldehyde, reducing oxygen to peroxide - and ultimately releasing ammonia. That stuff is no good, especially the hydrogen peroxide, as it's highly membrane-permeable, and spreads rapidly, connects with neurons, converts into more damaging shit and ultimately ALSO chelates iron on top of the dopamine breakdown (we will get back to Fe chelation soon).
What to take:
Selegiline HCl
2.5 mg/EOD
Not only is the good 'ole Selegiline a pretty decent nootropic - but it's actually so due to its dopamine-preserving effects via the aforementioned inhibition of MAO-B - and whilst taken at 2.5mg EOD - it retains its guaranteed MAO-B selectivity (inb4 muh it doesn't touch MAO-A all the way up until round about >10mg ED - not only is Seleg cumulative - but is 2.5mg EOD quite literally all we need to keep our brains just that bit safer whilst running heavy AAS). Oh, and of course, it's also anti-oxidative.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
VIII
CIRCADIAN / MITOCHONDRIAL SIGNALING
BMAL1 and CLOCK are directly responsible for the transcription of the genes that control the antioxidative defense of the mitochondria (also partially responsible for NAD+). Essentially, not only will you get literal brain damage (even if sounds overexaggerated) from having a fucked up sleep schedule through multiple different ways, such as circadian oscillation of mitochondrial proteins - but will that also be greatly enhanced by the gear.
First and foremost, go fix your fucking sleep schedule. Second,
What to take:
Melatonin
40+ mg/night
People are not fucking around when you hear about them megadosing Melatonin; this is EXACTLY why they do this. It is an INSANE antioxidant for your brain with so many mechanisms through which it does so - that I won't even bother listing them. It will also make you sleep like a baby (even despite the later desensitization of the receptors - which also do re-sensitize fairly quickly, so that's not even really a worry).
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
IX
TRKB
This is the receptor for the BNDF. If you've looked into nootropics at all - you would already be very familiar with this. Brain-Derived Nootropic Factor is like the Jack-of-all-trades for your brain's goodies. In this context, however, what it helps us with is primarily PI3K/Akt (survival), Ras/MAPK-ERK (differentiation, synaptic plasticity, etc.) and PLCγ (Ca-dependent synaptic plasticity). Upregulating those three combined will not only provide you with good nootropic benefits (as mentioned 8345235 times before), but will also help you with neuroprotection.
There are even more factors, similar to BDNF that are amazing for neuroprotection - but this one is by far the most significant one. And worry not buddy boyo, as the rest will be covered by one, singular compound.
What to take:
Cerebrolysin
2ml+/pin day intravenously
Cerebro has been spoken of, by some, as this mythical compound that is either inaccessible or carries a very scary prion risk.
For those not tapped in - it's essentially a cocktail of different factors, such as BDNF, NGF, GDNF, and a LOT more of them. It easily crosses the blood-brain barrier, effortlessly binding to TrkB and providing all that yummy stuff for your brain.
Since it's derived from the pig's brain (sorry @Menas it's unironically off limits for you), you may see some people speculate its risk of giving you prion disease. It may seem that way - however first and foremost - it undergoes INSANE purification/quality control processes during its manufacture, and secondly - there has been not a SINGULAR prion disease case registered with Cerebro. Ever (we're talking decades of constant research by the way).
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
X
IRON CHELATION
Iron-driven damage and ferroptosis directly literally leads to MULTIPLE things we already covered in this thread at once: upregulation of MAO-B, amyloid, neuroinflammation and (no shit) oxidative stress.
The amyloid (APP) protein is particularly bad, as not only does it contribute to Ca homeostasis (stalls that shit) but also, if it undergoes the correct path - which more common than not it does - it gathers different (usually non-toxic) fragments straight into the dreaded Aβ we that we covered above.
What to take:
Deferoxamine Mesylate
20mg 3x/week intranasally
This totally noble formulation (which I am very proud of myself for finding) is one of the only ways that not only prevents the Aβ formation - but also actually helps revert it (hard to do).
First and foremost though, you'd need to craft it (very easy). Reconstitute it with BAC water to reach a 10% weight/volume conc. and use it at 10mg/nostril per intake session. Studies found the "ideal" cycle lengths to be like 18 weeks, which is perfect for us, because we can confidently run it throughout our entire cycles. It also doesn't go systemic if taken IN, so it doesn't have all the downsides it would if it were to be taken orally and whatnot.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
XI
INJECTION FREQUENCY / ESTER SELECTION
This is a shorter, but quite an important entry.
For compounds that are known for their neurotoxicity, for the love of David J. Gandy, please use the longer-acting esters, unless you're assessing your response to a roid you've never done before.
Example: Trenbolone Acetate being insanely more neurotoxic than Enanthate.
Why? It's all due to the acute accumulation of the compound in your brain peaking upon injection. This is also the reason why the entry above specifically talks about pinning the 'Lysin on injection days (although it can be done whenever and all depends on the purpose of its use, but in our context this is the case).
HOWEVER, this only mainly applies to the neurotoxic compounds, as other AAS (for example Testosterone) are actually more optimal to inject as frequent as possible due to aromatization or things of those sorts.
Aβ / AMYLOID
A recurring pattern you will see with these pathways is oxidative stress. It will have its own mitigation section, but just know that it is one of the ways through which this pathway in particular damages the brain.
The other, more important one, however - is the Calcium dysregulation and excitotoxicity, thereby damaging or killing nerve cells, which will be delved into more in-depth shortly.
What to take:
Huperzine A
400 mcg 2x/day
Huperzine A reduces ADAM10, therefore reducing ERK1/2 signaling, leading to a decrease in BACE1. What this means is Aβ is reduced. It additionally provides direct antioxidant support against the Aβ and antagonizes the NMDA (more on this later).
Donepezil HCl
2.5 mg/EOD
Donepezil Reduces β-secretase activity, inhibits GSK-3 (which we will touch up on shortly), redirects APP cleavage/AChE-catalyzed aggregation/β-secretase activity, which are all exactly what's partially responsible for the Aβ/Amyloid activity.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
II
EXCITOTOXICITY / NMDA
Similarly to the previous, and many others pathways, besides the oxidative stress - you will see a lot of mitochondrial damage/dysregulation (which is so major it actually also has its own section). As mentioned before - excitotoxicity is the process of mitochondrial damage/death (bad stuff).
NMDA in particular selectively elevates Ca way more than a lot of other mechanisms, hence being disproportionately excitotoxic.
What to take:
Memantine HCl
2.5 mg/EOD
Memantine occupies the Mg-binding sites at the NMDA, thus preventing them from being used up by the bad stuff. It is very potent at it, more so than other such compounds (upwards of 20-fold) and does not cause dissociative side effects, like ket would.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
III
TAU / GSK-3β
GSK-3β is an extremely important aspect when it comes to Tau, as the mere activation state (not even its presence) determines whether Tau is stable - or fucks you up by collapsing into a bunch of bullshit, such as multiple different stress signals or toxic tangles. So essentially, our main goal - is to maintain the correct activation state of the former thing (mainly).
What to take:
Lithium Carbonate
150–600 mg/day
(Dose derived from low-dose studies; Serum-level guided, so be cautious of Autophagy/Proteostasis).
Directly competitively inhibits GSK-3β & phosphorylation, also lowers tau in multiple different ways.
Sulforaphane
100–200 µmol SFN-equivalent/day
Take in a complex with glucoraphanin + active myrosinase to bioactivate it.
Allows Nrf2 to bind the antioxidant elements, enabling phase II detox antioxidant genes. Not only that, but it directly suppresses GSK-3β by throttling it.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
IV
MITOPHAGY / MITOCHONDRIAL QUALITY
As discussed before, mitophagy is the process of detecting and destroying the damaged/dead mitochondria in order to avoid any toxin leakage into the system. It does so via a plethora of different mechanisms, starting off by getting flagged as fucked by PINK1 - and ultimately ending with a bunch of mechanisms bring it into autophagy.
In order for the process of the damaged mitochondria to be effectively found and recycled to be maximized, said PINK1 pathway has to be upregulated.
What to take:
Purified Urolithin A
500–1,000 mg/day (pref. Liposomal)
This does exactly that - it both elevates the PINK1 pathway, BUT also additionally restores the pathway after the Aβ-induced suppression.
Not all that much more to say here.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
V
OXIDATIVE STRESS
Good old oxidative stress is probably what's most talked about when it comes to the topic of AAS damage, and not only when it comes to neuroprotection. However, not all even know about how it actually damages the body/brain.
In short, when it takes place, different -ase compounds, alongside glutathione (the same thing used to protect you from ROS by the way) oxidative damage to the lipids, DNA and a lot of other things - leading to cell death, as well as hyperphosphorylation and inflammation (there's even more, but these are the most prevalent ones to note).
What to take:
NACET
375 mg 2x/day
N-Acetyl-Cysteine Ethyl Ether is extremely bioavailable to the brain, and acts as an amazing antioxidants as one of the main parts of the glutathione production.
Astaxanthin
12-24 mg/day
Carotenoids in general are phenomenal antioxidants, but Astaxanthin seems to be the most bioavailable to the brain, so taking it with food daily will not only yield you the neuroprotective benefits - but will also give your skin a nice gold-ish glow.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
VI
NEUROINFLAMMATION / ERβ
As the brain detects different bullshit that AAS provide - it sends inflammation signals to try and combat said bullshit. It initially is helpful, but soon becomes harmful, as ROS, nitric oxide, cytokines and other such things accumulate.
As for ERβ, estrogen in general is crucial for things like brain development, neuroprotection, anti-inflammation, etc.
What to take:
S-equol
20-30 mg/day
Yes boyos, it is unironically time to soymax. S-equol is a high-affinity, selective ERβ agonist, providing mediation antioxidative, anti-resorptive genomic and anti-inflammatory programs - all whilst its selectivity allows for it to not provide any of the actual foid-related estrogenic effects from ERα.
Note: Intranasal α-DHED could also be mogger, but fuck knows where to actually get it.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
VII
MAO-B / DOPAMINERGIC OXIDATIVE STRESS
MAO-B actively breaks down dopamine in the brain, thereby damaging it. It camps on the outside of the mitochondria's membrane and actively converts an amine into an aldehyde, reducing oxygen to peroxide - and ultimately releasing ammonia. That stuff is no good, especially the hydrogen peroxide, as it's highly membrane-permeable, and spreads rapidly, connects with neurons, converts into more damaging shit and ultimately ALSO chelates iron on top of the dopamine breakdown (we will get back to Fe chelation soon).
What to take:
Selegiline HCl
2.5 mg/EOD
Not only is the good 'ole Selegiline a pretty decent nootropic - but it's actually so due to its dopamine-preserving effects via the aforementioned inhibition of MAO-B - and whilst taken at 2.5mg EOD - it retains its guaranteed MAO-B selectivity (inb4 muh it doesn't touch MAO-A all the way up until round about >10mg ED - not only is Seleg cumulative - but is 2.5mg EOD quite literally all we need to keep our brains just that bit safer whilst running heavy AAS). Oh, and of course, it's also anti-oxidative.
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
VIII
CIRCADIAN / MITOCHONDRIAL SIGNALING
BMAL1 and CLOCK are directly responsible for the transcription of the genes that control the antioxidative defense of the mitochondria (also partially responsible for NAD+). Essentially, not only will you get literal brain damage (even if sounds overexaggerated) from having a fucked up sleep schedule through multiple different ways, such as circadian oscillation of mitochondrial proteins - but will that also be greatly enhanced by the gear.
First and foremost, go fix your fucking sleep schedule. Second,
What to take:
Melatonin
40+ mg/night
People are not fucking around when you hear about them megadosing Melatonin; this is EXACTLY why they do this. It is an INSANE antioxidant for your brain with so many mechanisms through which it does so - that I won't even bother listing them. It will also make you sleep like a baby (even despite the later desensitization of the receptors - which also do re-sensitize fairly quickly, so that's not even really a worry).
◆━━━━━━━━━━━━━━━━━━━━◆━━━━━━━━━━━━━━━━━━━━◆
IX
TRKB
This is the receptor for the BNDF. If you've looked into nootropics at all - you would already be very familiar with this. Brain-Derived Nootropic Factor is like the Jack-of-all-trades for your brain's goodies. In this context, however, what it helps us with is primarily PI3K/Akt (survival), Ras/MAPK-ERK (differentiation, synaptic plasticity, etc.) and PLCγ (Ca-dependent synaptic plasticity). Upregulating those three combined will not only provide you with good nootropic benefits (as mentioned 8345235 times before), but will also help you with neuroprotection.
There are even more factors, similar to BDNF that are amazing for neuroprotection - but this one is by far the most significant one. And worry not buddy boyo, as the rest will be covered by one, singular compound.
What to take:
Cerebrolysin
2ml+/pin day intravenously
Cerebro has been spoken of, by some, as this mythical compound that is either inaccessible or carries a very scary prion risk.
For those not tapped in - it's essentially a cocktail of different factors, such as BDNF, NGF, GDNF, and a LOT more of them. It easily crosses the blood-brain barrier, effortlessly binding to TrkB and providing all that yummy stuff for your brain.
Since it's derived from the pig's brain (sorry @Menas it's unironically off limits for you), you may see some people speculate its risk of giving you prion disease. It may seem that way - however first and foremost - it undergoes INSANE purification/quality control processes during its manufacture, and secondly - there has been not a SINGULAR prion disease case registered with Cerebro. Ever (we're talking decades of constant research by the way).
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X
IRON CHELATION
Iron-driven damage and ferroptosis directly literally leads to MULTIPLE things we already covered in this thread at once: upregulation of MAO-B, amyloid, neuroinflammation and (no shit) oxidative stress.
The amyloid (APP) protein is particularly bad, as not only does it contribute to Ca homeostasis (stalls that shit) but also, if it undergoes the correct path - which more common than not it does - it gathers different (usually non-toxic) fragments straight into the dreaded Aβ we that we covered above.
What to take:
Deferoxamine Mesylate
20mg 3x/week intranasally
This totally noble formulation (which I am very proud of myself for finding) is one of the only ways that not only prevents the Aβ formation - but also actually helps revert it (hard to do).
First and foremost though, you'd need to craft it (very easy). Reconstitute it with BAC water to reach a 10% weight/volume conc. and use it at 10mg/nostril per intake session. Studies found the "ideal" cycle lengths to be like 18 weeks, which is perfect for us, because we can confidently run it throughout our entire cycles. It also doesn't go systemic if taken IN, so it doesn't have all the downsides it would if it were to be taken orally and whatnot.
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XI
INJECTION FREQUENCY / ESTER SELECTION
This is a shorter, but quite an important entry.
For compounds that are known for their neurotoxicity, for the love of David J. Gandy, please use the longer-acting esters, unless you're assessing your response to a roid you've never done before.
Example: Trenbolone Acetate being insanely more neurotoxic than Enanthate.
Why? It's all due to the acute accumulation of the compound in your brain peaking upon injection. This is also the reason why the entry above specifically talks about pinning the 'Lysin on injection days (although it can be done whenever and all depends on the purpose of its use, but in our context this is the case).
HOWEVER, this only mainly applies to the neurotoxic compounds, as other AAS (for example Testosterone) are actually more optimal to inject as frequent as possible due to aromatization or things of those sorts.
XII
SUMMARY
SUMMARY
Compound Name | Dosage | Intake Frequency |
| Huperzine A | 400 mcg | 2x/day |
| Donepezil HCl | 2.5mg | EOD |
| Memantine HCl | 2.5mg | EOD |
| Lithium Carbonate | 150–600 mg | Daily |
| Sulforaphane | 100–200 µmol | Daily |
| Purified Urolithin A | 500–1,000 mg | Daily |
| NACET | 375 mg | 2x/day |
| Astaxanthin | 12-24 mg | Daily |
| S-equol | 20-30 mg | Daily |
| Melatonin | 40mg+ | Nightly |
| Cerebrolysin | 2ml+ | Pin days, intravenously |
| Deferoxamine Mesylate | 20mg | 3x/week, intranasally @ 10mg/nostril |
| Fix your sleep schedule |
| Inject neurotoxic compounds, such as 19nor-derivatives as infrequently as possible, and thereby using the longest-acting esters |
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Inb4 yes I personally do ALL this shit, maybe except for sleep, that I do slack on just a tad (for now
)Inb4 2.0 "muh cba to take allat" here's a generally amazing ancillary lifehack for you:
just get a fucking XL pillbox:
And as always thank you all for reading! Stay safe!
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Tags:
@Orka @Volpa @SlayerJonas @imontheloose
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