#understanding endogenics become a lot more easy to understand

[whatdoinose]

im gunna break this down as a pro endo traumagenic system, but know i'm interacting in good faith and for the sake of discussion. not discourse.

[responding to the second paragraph]

I think more can be said about this you're not saying so i want to add on: Anyone who was anti endo and now demonizes all anti endos as SO inherently different from them is stupid. point blank. they change their opinions and are refusing to take accountability for them it feels. like, yea, you can dislike the beliefs you had but to seperate yourself from them and act like youre so holier than thou ,, is weird. fundamentally. if theyre so evil, and you used to be one, then you don't really get to act as if youre the only moral standard ever. i think anti endos should be judged on actions purely. to insinuate theyre all so evil and harassment based and blah blah blah, but kinda shove under the rug you used to be one is laughable. like okay then why were you one? do you get what i'm saying?

im gunna offer an anecdote here:

back in 2019, when we were 11-12, we were deeply into the whole 'truscum' shit. we first learned about transness from fucking kalvin garrah and blaire white and shit, and just kinda agreed with whatever was fed to us. thats horrible! those are HARMFUL beliefs! and we recognize that! so, now, when criticizing trans inclusive radical feminists or people who don't like X type of queer people, we keep that in mind. demonizing something while you were IN those spaces is just as toxic. it implies you are more discourse oriented than discussion oriented, and atp just give up. that is unproductive. thats not to say we support those beliefs systems anymore, but it IS to say that its incredibly short sighted of you to just. act like they're inhuman. seperating yourself so far from the belief system that you could NEVER POSSIBLY believe that is absurd. it lacks critical thinking. if you know nothing better than a black and white sense of right and wrong that isn't based in anything but your current bias, thats absurdity.

When approaching people who believe what you used to, if anything it should offer you perspective on that point of view and make you better at discussion. It rubs me incredibly weird whenver i see an ex-anti endo act like all they do is harass people and shit. is that what you did? if so, what absolves you of the same critisims? it just lacks the acknowledgement it should have. i don't know how to explain, hope this makes sense.

[on the third paragraph]

You know, as ex anti endos we used to think this too. But honestly, DO they? Yea, you have this experience and whatnot. And thats valid to want a traumagen only space to talk about those issues. But are they REALLY 'invading' spaces? Endogenic systems have had their own community and have made their own terms to describe their experiences seperate from medicalized terms for decades. Endogenics have also made resources commonly used by all systems of all orgins, help support research and information on all systems of all origins, etc. I don't really see how theyre 'invading'.

What I think is lost on many is that. Endos have their own community, its just that traumegenics and them have overlap in community. So more often than not, you're talking about that overlap and unification between types of plurals than people 'invading'. The word plural? Endo. The word fictive? Endo, and not even plural specific. SP and PK? Endogenic. These are their things that we use. And many traumagens are also in their spaces because they don't mind sharing that overlap in community.

It's not that endogenics are 'taking over' disorderd spaces, its more that there's an overlap in spaces between them in the community spaces and resources used, and anti endos don't see that divide most times in think. Not their fault, its tricky. Took us ages to realize 'hey, they have their own shit we just have a similar experience so there will be overlap in discussion, terms, people finding community with each other, etc'. But endogenics don't WANT to be in disordered spaces. They don't cater to them, tho tbh as a disordered system with less distinct alters, I don't really feel they cater to me either.

ANYWAYS! yea, TLDR: they aren't claiming to be us or wanting our spaces, they've had that. for a while. Back when it was still just MPD they were creating terms for themselves. Think a lot of the issue is we use a lot of the same language and have vaguely similar experiences so people THINK they're trying to worm their way here. But in actuality theyre jst a seperate community with similar shit. Oh and also, we can't ignore the fact that there's shit stirrers on both sides and most the time anti endos (of which don't actively seek endos out to harass) interact with endos its some asshole who is just discourse hungry. So it kinda off puts that perspective.

[next para]

yea, we did. doesn't mean others of other experiences don't have their own communities tho. you cannot be so about only your own experiences you lose sight of the fact that people of other experiences will be similar to you regardless. their existence doesnt invalidate yours, nor vice versa.

[next para]

endos, DON'T say the plethora of endogenic experiences and the plethora of CDD systems' experiences are the same or 1:1. only anti endos do. nor are they demanding to be let in anywhere. its not defense when its just someone existing in their own community similar to urs. everyone has their own life shit, and sometimes it ends in similar results. doesn't mean endos are invading or they are trying to compare themselves to you. if anything, ive only ever seen a massive push from endos telling anti endos "stop trying to act like we exist for the same reasons" yk?

like everytime an anti endo brings up medical shit, you're forcing endos into the 'medicalized systemhood' box where they don't belong and don't want to be. its drawing connections and then assuming based off of that, when in actuality sometimes theres a connection and thats it. the only unifying factor is plurality of some sort. then end. you cannot see people who are similar then dislike them because theyre only similar. theyre gunna have widly different experiences. thats okay. it doesnt make yours any less there. it just means sometimes people are only similar.

anyways people with their own spaces are not taking yours, nor is people with their own experiences somehow making a mockery of yours. thats close minded thinking.

and this kinda goes into the next paragraph.

-

you are inherently close minded about what plurality can look like. you see someone who has a vague connection to you, and then get mad when theyre not the same. theyre not the same as you. stop trying to make them. yea, they may have alters or headmates or whatever you wanna call them. but that doesn't make them disordered. and it never will. you cannot say they are invading your spaces when the only ones who put them in a CDD context are people who fundamentally misunderstand them.

your trauma isn't th only thing that's ever important. sorry to say, but people go through shit. that doesn't give someone the right to insist people without trauma (for the reason of their experiences) cant have their experiences. which is it? are they people with their own experiences or not? only one forcing them into the disordered box is people who are too close minded to stop and think "hey, yea MY shit lead to this but other peoples shit may be different". plurality isn't only disordered and you don't have a right to be upset at people who recognize that.

like in your text you RECOGNIZE they have different experiences. that they aren't disordered, yet you are implying that disordered systemhood is the only valid one. why? its the same as people who say fictionkin are offensive to introjects. its not. people will have a wide variety of experiences and just because yours is related to mental health doesn't make yours the only good one.

they arent saying theyre the same as disordered systems. so stop comparing them. you are viewing it through an 'only way for plurality to exist is through medical reasons' lense. so obviously you're gunna be miffed when those non disordered people aren't disordered. this is no different than any other form of exclusion that banks on "only one who can be like me is the people who experience the same as me"

once you let go of that and understand these peoples experiences outside of a discourse perspective or the lense of disordered plurality, it starts making a lot more sense.

you aren't 'at risk' of losing spaces. mind you, non disordered systems made a lot of the shit disordered systems use and do a lot activism for plurality as a whole. you aren't at risk of shit. if people in another community than you are a 'risk' to you, thats your own problem.

also on your last note: people in a community that losely describes non disordered plurality are not to blame for people who existed decades ago that have 0 relation to them hope that helps.

-

-

anyways as a disordered system i must say, disordered spaces don't do shit for me. they are made based on being anti-endo more than they are based on being a space for disordered systems to exist. additionally, as a system who has less distinct alters, it fucking sucks! the community is largerly alter-based and theres virtually no community for those who's experiences are less alter-based. but you don't see me being all like 'grr those systems who's experiences are like XYZ instead of ABC' , thatd be absurd! everyone's different and everyone deserves their own words and spaces to describe their experiences. peace be.

Keep seeing posts of pro-endos who used to be anti-endo talking about "Ugh, anti-endo spaces are so toxic" which is not necessarily bad, there are bad anti-endo spaces out there and people are allowed to vent about how those spaces hurt them

I do have a problem when they use that as an excuse to call us all toxic and cruel. I've seen many saying things like "Anti endos are so horrible, I'm so glad I'm not one of those monsters anymore"

You need to understand we aren't the monsters you make us out to be. We're traumatized people, trying our hardest to survive with something debilitating, who can't help but see endos as mocking, whether they truly are or not. We can't help but see endos as invading our spaces.

We didn't get to have safe spaces most of the time. We didn't get to be around people who cared about us and understood us. Even those of us that did have a safe space had it poisoned by trauma elsewhere. We spent our childhoods afraid, isolated, and so agonizingly alone, feeling like we were better off dead, that we were freaks, that we were the only ones in the world going through this. This community we made for ourselves was one we had to fight through years of hell to get.

So when random people come over trying to insist that they're "just like us" and demanding to be let in, despite having only one or two things in common that we couldn't even trust they truly had, of course we'll be fucking defensive. In our eyes, you're trying to take the safe spaces we fought tooth and nail for away from us, whether you truly are or not. In our eyes you're people who know nothing about us or what we went through, and continue to go through, trying to barge into our havens and bloat it with bullshit, whether that's what you're trying to do or not.

We've been hurt so many times, by so many people, for so long. Why the fuck would we take a chance on people that are so suspect? You claim to have alters just like us, yet without any of the other symptoms of our disorders. You claim to be systems, yet without being caused by the immense trauma we had to suffer through. Hell, some of you claim that you made your alters for fun, just because you can.

Of course we're wary and defensive. We don't want to even risk losing the spaces we worked so damn hard to get.

If you've had a bad experience with anti-endo spaces, and are pro-endo now because of it, that's fine by me and I understand completely. But that doesn't make us all villians. That doesn't make us all evil monsters.

And besides, many of us have been hurt by pro-endo/mixed origin spaces too. We've seen people have horrible experiences with them. (Let's not forget endos started as natural multiples, who were notoriously shitty, cruel, and discriminatory toward any and all traumagens, and that a lot of that same rhetoric is still rampant in the community, AND that the community at large has basically just decided to pretend that never happened.

-Kaz

[sophieinwonderland]

Crafting a Conspiracy of Singlethood

I keep trying to make the erasure of plurality into a compelling conspiracy theory but I'm coming up short on some parts...

For some context, I've been thinking of ways to introduce plurality into conspiracy communities as a sort of trojan horse. When I've said I want to spread plural acceptance everywhere, I do indeed mean everywhere.

I think I can make a compelling case for endogenic plurality always existing. The imaginary friend phenomenon in children is bizarre when you look at it for more than a few minutes. About half of kids just seem to have other people in their heads they interact with, and at least two thirds of those tend to report their imaginary friends behaving in ways that are autonomous.

Due to societal pressure, children end up pushing those friends away before becoming adults.

Surely, it wouldn't be a stretch to convince conspiracy theorists that there had been some sort of mass cover-up. After all, why else would basically every institution ignore the oddities of this phenomenon and pretend it doesn't exist?

But... then that leaves a question of who and why...

For the Who... I'm thinking this can be tied back to the Church. Plurality was literally demonized and so-called imaginary friends were often seen as evil spirits to be gotten rid of. Later on, the psychiatric institutions born from predominantly Christian societies took the view that anyone else in your head simply isn't real and could be a sign of illness...

The one exception was for what they called "multiple personality" because they can't exactly ignore us when we can take over the body. But the Christian demonization of plurality carried over and resulted in all instances of "multiple personality" being seen as mental illness for a good century or so, until recent decades have called that into question with research into non-disordered plurality.

But that still leaves the other question... why?

The easy boring answer is that people fear the unknown. The Church didn't understand plurality, feared what they didn't understand, and tried to eliminate it.

While this answer is probably more true... it's also not compelling.

The idea that current plural stigma is the result of thousands of years of ignorance is boring.

No, if we want to make this conspiracy theory really stick the landing, we need an intentional coverup.

When Plurality Ruled The World...

So this is the part where I need help. I have a theory that plurality, in the form of communication with gods and spirits, would have been pretty common in pagan cultures. And the people who led these cultures would be more likely to be those communing directly with these spirits and gods, and even acting as vessels with them. In other words, the world would have been ran by plurals.

Thus, Christians who were trying to maintain control would have reason to literally demonize all instances of plurality. Establish the myth of one person per body, and that anything else has to be demonic possession.

Thus you have nearly 2000 years of parents being manipulated into believing the natural plurality of their children is a result of possession.

It's a good, compelling story. But so far, it's not much more than that.

I'm not a historian, our knowledge of pagan religions from the past is sparse at best.

I've found an article online discussing what sounds a lot like plurality with the Egyptian pharaohs having the spirits of the the gods within them, guiding them.

But I need more examples of ancient plurality, and preferably from better sources than "Tour Egypt."

If there were enough examples of this in pagan religions, we can frame the erasure and demonization of plurality as an intentional cover-up by those in power to maintain that power and control the population.

That's a good story to tell to conspiracy theorists. It just needs a stronger foundation.

[teacup-captor]

Too much bullshit syscourse on my dash also. I'm up for discussing things but I do NOT need to see ableist bullshit on my dash every day.

To any of my followers that do not know, there's a bunch of discourse in the CDD community.

(CDD stands for "complex dissociative disorder", which means a disorder that could cause anyone to be a system).

This discourse is about whether or not "endogenic" systems exist.

(Endogenic primarily means someone who got a CDD without trauma, but it can also be used to mean someone who formed a system, but not a CDD, without trauma, or a system who got one or more alters without trauma. The opposite of this term would be traumagenic.)

Anyone who claims themselves to be and/or support endogenic systems displays their lack of understanding of the human brain, and are spreading genuinely dangerous misinformation.

I don't have the energy to give a full explanation of why this is the case, but to summarize:

A person developing alters (becoming a system) is due to the brain failing to integrate properly. It happens when a child goes through so much, their brain genuinely dysfunctions, and it doesn't develop as expected.

This is also a disorder that intentionally hides your worst trauma from you. You won't know about the things you can't handle, you'll only know about the things that are mild enough for you to be able to deal with.

A lot of systems will have been exposed to toxic environments for a long time, and grown accustomed to those environments. If you're used to trauma, you get desensitized to it. If you're used to being harassed every day, it doesn't feel like harassment. Even if you realize it's not a good thing, it's incredibly easy to brush off as "not that bad".

If you've just figured out you might be a system, it's natural to want to do research. It's natural to feel insecure that your trauma isn't "bad enough" to count. It's normal to not remember everything, or even anything you'd call traumatizing or bad at all. If you then find a community of a bunch of people telling you that nothing bad needs to have happened for you to become a system, that's comforting, of course you're inclined to trust that.

But a human brain doesn't just break in such a massive way without anything causing it. That's not how humans are built.

And anyone claiming that you can form a system without trauma is doing genuine harm. This could hinder someone from getting the help they need. This could send someone further into denial about trauma that happened to them. This could set back someone's healing process significantly.

Some people claim to be systems, but to not have a CDD. Aside form being impossible, this behavior is extremely ableist. Let's pretend for a moment that I believe this to be possible, someone could be a system without having a CDD. What's ableist about that? The problem is that they use our medical terms.

"Non-disordered" systems (systems without a CDD) enter system spaces and use system terms. If one could be both "plural" and not have a CDD, it would be a completely separate thing from being a system. These people still use our terms. They don't have a CDD, so they can't be a system, yet they still call themselves systems and plural, they still refer to their "alters" as alters, headmates, parts and more. If anyone could be "plural" and not have a CDD, they would have no place in system spaces, seeing as our spaces are for trauma survivors. They would have no business using our terms, seeing as they're medical terms.

And lastly and most offensively. Some people claim to create their alters, or to have used "t*lpamancy" (*u), which is cultural appropriation, and fucking racist. I've seen pro-endos (<- endogenic supporters) who have also been against transID (transID being people who want to transition to other identities than different genders, such as "transracial" ("transitioning" from one age to another), "transage" ("transitioning" from one age to another (most often younger from what I've seen? This is a different thing from age regression.)) and "transabled" ("transitioning" to a disabled identity, such as wanting to intentionally get PTSD, autism, epilepsy, paralysis, or DID.)

You see the irony in pro-endos, especially those who claim to create their systems, being against transabled people, right? Because it's the same thing. You can't create a system, and you cannot create alters. You can however create a persona that you roleplay as. It's incredibly offensive seeing people claiming they've created alters and systems, especially as a traumagenic system. To see a disorder that I only got to help me survive abuse be romanticized and reduced to a fun game.

To any of my followers who read this, thank you so much. I hope this made sense.

To any of my followers who read this and disagree, go outside, touch grass, and either realize you seriously think it's okay to fake a disorder, spread misinformation and hinder people's healing process, and misuse medical terms you do not have the right to use, or block me and fuck all the way off.

I keep being anxious that someone follows me and is secretly pro-endo. I hope this will scare any of them off if that's the case.

If not....

I hit pro-endo ableist shitheads with bats!!!!!!! :3 I also bite!!! Watch out!!! I could have rabies!!!!!!!!

[neuroticboyfriend]

I mean this in the best way possible but I don't understand endogenic systems... Like, how do you become plural if not through a trauma? Because blacking out and such doesn't seem like an easy way to live, and the only "resources" endos ever give me is like the plurality Wikia. I really really want to understand but it's so hard to find nonbiased resources :/

I don't know how to explain endogenic systems in general, but I can give my experience. I used to have identity delusions, but it wasn't just that I believed I was someone that I wasn't. It began that way, but as the delusions became more intense, alters would develop based on them.

It's hard to explain beyond that because I can't remember a lot. It's been years since I had these delusions and I avoid triggers... The psygenic alters have been dormant for a long time, but they were still significant (even though they were fragments).

[sysmedsaresexist]

I've tried a dozen different ways to word this response, I've given up, come back, given up, but I can't stop thinking about this post, so I'm just going to talk and I hope you'll give this consideration. It's by no means an attack on you or endogenics.

I want this to be a history lesson, and a chance to discuss the appropriateness of different arguments (???)

I think... this post is really bad. I don't think it's conveying the point you wanted to make in a way that's beneficial to anyone in syscourse.

I think it would have been a lot better to combat fusion directly, rather than make this anti vs pro. There's no indication this person is anti. It's just a person with DID, saying things that are true to them, and that are understandable based on age. Now that's not to say you shouldn't correct them, I'm glad you did, hopefully they can see the other side.

But here's the thing. Anti psych and anti fusion rhetoric are endogenic points.

So essentially what you've done here is say, "antis, look! It's not just endos, it's DID systems talking about endo ideas!"

In which case, antis are still saying fuck endos.

Saying DID isn't a disorder isn't an anti point. Saying fusion is murder isn't an anti point. Why did you make this pro vs anti?

This. Doesn't. Help. You're just confusing people more about what each side believes. And without any real way to discern how this person is anti... it just looks like you're saying that because they have DID, which is becoming a more and more common idea in endo spaces.

History is repeating itself.

Only, I don't think this had anything to do with endos, and it was a mistake to bring them into this.

Specifically in the context of this post, DID and endo history have been lost in the conversation. The endo community as we know it now developed out of the natural/empowered multiple movement (many still use those terms), which started the anti psych crap, and it largely had to do with fusion. They rejected the MPD diagnosis and therapeutic intervention, and out of this, grew the idea that systems are more than just trauma responses, and finally into no trauma required. Endogenic systems.

You say you see most anti fusion talk in CDD spaces, but as a blog that screenshots shit for a living, the most vile anti fusion talk comes from pro endos. The biggest pro endo syscourser on Twitter created an entire tag to exclude systems that fused in any way, calling any fusion murder and suicide. Anti fusion, while normal to come across in CDD spaces, is more prominent in endo spaces, and there is not a single person who will disagree with that, except for you, apparently. Final fusion has always been looked down on in endo spaces because it's rejecting that plurality is a normal, healthy state of being that doesn't need to be "fixed". It's not a disorder if it doesn't need fixing.

And it's easy to see why, fusion can be scary. It's not talked about enough in a positive way, and many fused systems are ignored and ridiculed when they try to talk.

Point is, considering this person's age, they would have been right in the middle of this original divergence of communities into natural multiples and MPD multiples, at a time when fusion was still being forced on patients. When it was the only goal in therapy.

In this way, as an older DID system myself, I don't blame them for being anti fusion.

In fact, I would even say, it's people like this that paved the way for endogenic systems in the first place.

Which is why, again, I think it would have been better to approach this from a, "myths about fusion, debunked!" post, because it would have reached both sides in a less combative, syscourse/origin-centric way. Pro endos are going to ignore the post because it's aimed at antis, and antis are going to roll their eyes because those are pro points. You've alienated any possible audience that might learn something.

Something like anti fusion is a both sides issue, very much so. But you've presented it as an anti endo issue without any actual merit behind that point, because it's not anti rhetoric.

This isn't origin discourse. You made it origin discourse. And I don't understand why. And it's not doing that very well. You've made the target audience the one that already agrees with you?? How does that help?

I don't even know that I would call most anti fusion rhetoric "misinformation" as much as I would call it fearmongering, by people who have been fearmongered themselves. It's a personal belief that only becomes a problem when they start pushing it on others.

I don't know... I hope this was coherent.

For anti-endos who think it's just mislead endos creating misinformation within the community, let me copy/paste a few juicy tidbits from a 50+yo DID System who's been rejecting treatment for over three decades that I just furiously argued with:

"I think fusion is another form of singlism. It's prejudice against multiplicities."

"You're making a case for a choice you wouldn't even choose. I don't get it. It's like stabbing yourself without knowing you are doing that." (Because I was arguing that every System should make that choice for themselves)

 "I experience it as prejudice. I'm not demonizing anyone except the people who suggest it, who are always singletons"

"That's why I think the idea of final fusion is a myth that is pushed by singletons who are not aware of how prejudiced they are against multiplicities. Worse, it's a prejudice many multiplicities have internalized."

"That's like advocating for that Christian practice for changing gay people into straight people. It doesn't work. It's not humane." (Yes he really did compare final fusion to conversion camps)

And finally, my personal favourite: "DID is not a disorder."

Pro vs anti in regards to endogenic Systems is not productive. It won't accomplish anything. The misinformation is COMING FROM BOTH SIDES.

We need to start ignoring origin as a topic to be exhaustedly argued about in a purely circular manner and start combating the misinformation on both fronts because it doesn't matter what origin someone has when it comes to validity or existence. What matters is the misinformation being spread by BOTH sides.

[dramarising-replacement]

(long post) some thoughts on the shadow discord situation from multiple points of view

i'm going to go over my thoughts on the shadow discord situation regarding DID/OSDD accessibility bots from a few different points of view. first from the point of view of a system (we are are DID system who use a similar bot to Pluralkit called Proxymaster), then from the pov of a discord server mod (both servers with and without system bots) and finally, from where i think the mods/people supporting the mods are coming from.

i would like to make a small note regarding Tupperbox, which i am aware was added as a "compromise". Tupperbox is a bot created primarily for a) roleplaying and b) endogenic ("natural" systems, who believe that trauma is not required to form a system, which i won't get into further in this post) systems. the bot prefix is tul! which is short for "tulpa", a culturally appropriative form of endogenic system. as a result, many DID/OSDD systems feel uncomfortable even using the bot in the first place. 

before i get into my actual points though, i'm going to go over a basic function of Pluralkit because it seems like some people have some misconceptions about the bot, namely regarding safety. while Pluralkit has had issues with privacy in the past (anyone with your system ID or a system member's ID could view all your info. this was one of many things that led to the creation of the SystemTime! bot, a now defunct alternative which was replaced by Proxymaster when it died) there is now the option to make all your information private, meaning the only people who can access and choose to share personal information is people from that system. 

1. from a system who uses accessibility bots as a system, having accessibility tools like Pluralkit is very helpful. not just for proxying (messages sent with a prefix that tells Pluralkit which system member is speaking and replaces the message with a webhook of their profile) but also for system organization. the bot allows the logging of switches, information on alters, and information on the system as a whole. all of that information transfers between servers, meaning any system who already has Pluralkit (which i am getting tired of writing, so will be noted as PK from now on) set up will also have a server they can log, edit, and view said information from. all of that information? irrelevant to the shadow discord. there is zero reason it would come up. it would take little effort for the mods to make a rule regarding PK asking that systems handle switches, information logging, etc. in a personal or system related server and have the bot only present for proxying. asking members of a server not to share private information would in no way be ableist, but would still allow for the accommodation provided by PK. is PK necessary to exist in a space as a system? absolutely not, but it is incredibly helpful and validating to be able to talk as yourself.

2. from a server moderator of servers with PK & similar bots setting up and moderating PK or similar bots is incredibly easy. there is virtually no actual setup required aside from disabling it in any channels it isn't wanted it, which is exactly the same as restricting any member or role using discord's channel permissions. the prefixes it comes with (pk; and pk!) would have no conflict with other bots. as far as moderating, simply implement a rule asking that anyone using the bot have their system tag (a function of PK which allows systems to set a tag, usually their system name, that attaches automatically to every member of the system) in their server nickname. PK also has a function where you can react to a proxied message with a question mark emoji to receive a DM with their main account or an exclamation mark to ping their main account. it's as easy as that to interact with PK users just like anyone else. we personally have been staff on many servers with system bots, both directly catered to systems and simply available as an accessibility tool. there is zero difficulty as a moderator as long as the rules & functions i mentioned are used.

3. from what i interpret as the perspective of the mods/those supporting them DID/OSDD, despite becoming more and more talked about on the internet over the years, is still a very unknown and misunderstood disorder. being suddenly asked to accommodate a disorder you know nothing about with a bot you know nothing about (and, from what i understood, having little knowledge and understanding of discord bots at all) would, understandably, be very overwhelming. there is a lot of misinformation of DID/OSDD in the first place, so attempting to understand something entirely new to you without any idea where to start or any idea of what's actual, credible information? is a lot to take in. 

all that said; denying and fighting an accessibility tool on the grounds that it is not useful to everyone is ableist. wheelchair ramps, subtitles, brail on signs - these are all examples of disability accommodation tools which are not useful to everyone and yet are incredibly important to the people they help. not every space is built for everyone - instead of continuing to make those spaces inaccessible, tools should be added for the people they do help, not denied because not everyone uses them. that is how accessibility works. 

apologies for the massive wall of text, but i hope this can help some people understand why this is such an issue and why many systems are upset.

[dragonclef1]

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The S glycoprotein is activated and also cleaved by host proteases, such as transmembrane protease serine 2 as well as TMPRSS11D, which enables cell surface area non-endosomal virus access at the plasma membrane. CoVs then release the viral genome RNA into the cytoplasm as well as the uncoated RNA converts 2 polyproteins, pp1a as well as pp1ab. Comprehensive autoproteolytic processing of pp1a as well as pp1ab by primary protease and also 3C-like protease create mature non-structural healthy proteins, RNA-dependent RNA polymerase as well as helicase necessary for duplication. RdRp, NSps and host aspects put together right into membrane-bound replication-transcription complexes to manufacture viral RNA. Recently created genomic RNA, nucleocapsid proteins and also envelope glycoproteins assemble as well as form viral fragment buds that fuse with the plasma membrane to release the infection. Enter your email address listed below to register for normal updates on all our latest offers, skin treatment recommendations as well as new item launches, plus receive an exclusive 10% OFF code.

Host defence peptides are produced by a large range of immune and epithelial cells in the body and also can be shared constitutively or generated during infection. They are also thought to be among one of the most old types of immune support.

Global Biosimilar Therapeutic Peptides Market Report 2020-2030 - ResearchAndMarkets.com - Manchestertimes

Global Biosimilar Therapeutic Peptides Market Report 2020-2030 - ResearchAndMarkets.com.

Posted: Fri, 08 Jan 2021 12:22:16 GMT [source]

Glucagon-like peptide 1 comes from a family of hormonal agents called the incretins, supposed since they enhance the secretion of insulin. Glucagon-like peptide 1 is a product of a particle called pre-proglucagon, a polypeptide which is divided to generate lots of hormones, including glucagon. Due to the fact that they originate from the same source, these hormones share some similarities, so are called 'glucagon-like'. Cells located in the lining of the tiny intestinal tract (called L-cells) are the major resource of glucagon-like peptide 1, although it is also produced in smaller sized amounts by the pancreas and the main nerves. Glucagon-like peptide 1 encourages the release of insulin from the pancreas, boosts the volume of cells in the pancreatic that create insulin and also holds back glucagon release. Glucagon-like peptide 1 additionally increases the sensation of volume during and also between meals by acting upon cravings centres in the brain as well as by slowing down the emptying of the stomach.

Puori Cp1 Pure Collagen Peptides (300g).

Unique peptides which assist to part the trend for the remainder of the 30% peptide mix solution to penetrate with the skin. MATRIXYL ™ 3000tricks skin cells into producing even more collagen, while Argirelox blocks signals for contraction to minimise the look of expression creases. Each "designer" peptide can be created to particularly activate a younger element of skin, as an example a peptide to make more collagen, or shut down a trouble in skin, like stop making so much unusual melanin. Hey there, I'm Paula Begoun, founder of the skincare line Paula's Option, and also today I begin my function as the Marie Claire Skincare Master. In my columns I will certainly be de-bunking skin myths, allowing you in on skin care tricks and telling you exactly which active ingredients the skincare industry is currently stressed with and why.

This is what causes the skin becoming thinner as well as tackling a crepey, extra wrinkled appearance.

As you age, protein production in the skin weakens as a result of both age as well as external environmental factors.

Numerous peptides can be incorporated in one product, as well as the majority of are discovered in anti-ageing products for skin that has actually started to show a decline in the production of those vital healthy proteins.

Various kinds of peptides have different impacts, from smoothing creases or fixing obstacle function to enhancing firmness and also hydration.

In skincare peptides are made use of to aid reinforce those proteins normally happening in the skin, consequently renewing and preserving it.

There are so many different kinds of peptide that it's hard to popularize, but some may trigger irritation for certain skin types - so do your study prior to investing, as products including them can be expensive.

On collaborating using highgrade-labs UK s4 andarine Sarms look for words that finish in "peptide"-- numerous additionally begin with "palmitoyl".

This regularly up-dated page offers a summary of the artificial processes involved in manufacturing of stomach peptides, and guideline of these procedures. Pharmaceutical items which resemble the effects of endogenous peptide ligands are call peptidomimetics. Some instances of peptidomimetics and also their matching endogenous ligand consist of desmopressin-- vasopressin, octreotide-- somatostatin, and insulin glargine-- insulin. Medicines which block the receptors for endogenous peptide ligands can be peptide or non-peptide molecules.

Call Us About This Technology.

In the context of a peptide, the amide group (Carbon Monoxide-- NH) is referred to as the peptide group. CoVs enter the host cell by means of the endosomal path and/or the cell surface area non-endosomal path and release their genome right into the target cell. The S glycoprotein assists in viral entry right into host target cell by directly binding to the angiotensin-converting enzyme 2 cellular receptor. ACE2 is a zinc metalloenzyme and also carboxypeptidase which is very expressed lungs, kidney, endothelium as well as heart.

The peptides can also be made use of to deliver cytotoxic agents to tumours with profound effectiveness. Incredibly, the peptides show very rapid tumour penetration as well as retention coupled with quick clearance from systemic blood circulation. Professor David Craik offered an interesting presentation on cyclotides - cyclic peptides generated by a selection of plants.

Required Information.

Subsequently, permitted ɸ worths will be fairly limited compared with other amino acids. The peptide bonds that connect amino acid residues in a polypeptide are developed in a condensation response in between the acidic carboxyl group of one amino acid and the basic amino group of an additional amino acid.

Eyebrows have actually grown back out and also I think it's to do with the peptides. Extra pricey that TO items but it is worth it, it's much better than the initial Buffet serum. Collagen as well as elastin production is enhanced, great lines as well as wrinkles are smoothed and also the skin's natural shops of hyaluronic acid rise.

What Are The Side Effects Of Sarms?

A beta sheet types as a result of hydrogen bonding interactions in between peptide foundations of parallel or antiparallel beta strands, which as the name recommends are primarily linear. On the other hand, the 'polar zipper' system refers to hydrogen bonding communications between the amino acid side chains on nearby beta strands. In 2019 Vapourtec developed a cooperation towards peptide synthesis with Teacher Peter Seeberger and also his Team at Max Slab Institute, Berlin. This work has actually been published in the paper shown right away listed below. The side-chain of proline is covalently bound to the N of the amino team, so in polyproline, there will certainly be much less freedom of rotation regarding the Cα-- N bond than with various other amino acids.

Extremely efficacious, its sheer power is maximised by a cutting-edge drone-based shipment system that guarantees every peptide is activated within the layer of skin that it is needed most. This packed, 30% peptide mix utilizes an introducing drone shipment system to target visible indicators of skin ageing. Neuropeptides are little proteinaceous cell-cell signaling molecules created and also launched by nerve cells. They vary from peptide hormonal agents because they are secreted from nerve cells and also act in your area on neighbouring neurons, whereas peptide hormones are secreted in to the blood by neuroendocrine cells and act at distant sites. Neuropeptides are one of the most diverse class of indicating particles in the brain, and are involved in a wide range of mind functions, consisting of analgesia, recreation, learning and also memory, benefit, food consumption and more.

Ostarine.

These peptides, consisting of three disulphide bonds that form a "knot", are both different and also durable. Prof. Craik provided a summary of these peptides and also their utility as a foundation for the shipment of therapeutic peptide epitopes. The peptides can surviving the digestion system, making oral shipment of peptide drugs a genuine possibility, although presently the bioavailability of such orally-administered peptides is reduced. If you have any inquiries or worries about the services and products provided on connected 3rd party sites, please speak to the 3rd party straight.

We are additionally offering expedited distribution times for Covid-19 related projects. Whilst the generation and also distribution of peptide rehabs represent significant difficulties, the easy storage space of peptides can be problematic. Hao Luo from Merck clarified the trouble of peptide fibrillation as well as methods for alleviating the dangers of fibrillation. It ends up that a super-fast heat and also high pH treatment making use of circulation chemistry can dramatically postpone the onset of fibrillation with no significant deterioration of the peptide. The generation of new highly discerning peptide-based medicines is being resolved by Bike Therapeutics Ltd as well as Liuhong Chen gave understandings right into the exciting advancement of Bicycle peptides. These bicycle-shaped peptides can be generated in chemically-constrained phage-display libraries, which makes it possible for the selection of peptides with high target specificity. Conjugation of the peptides to imaging representatives enables high-contrast, tissue-selective imaging.

Host support peptides are additionally referred to as anti-microbial peptides, although more lately they have actually been revealed to demonstrate a number of other immunomodulatory functions. They were initially recognized as having antibiotic results on a variety of germs, fungis as well as infections. Many HDPs are cationic, and also this is believed to moderate their anti-microbial activity by hindering microbial membrane layers.

The Best Peptide Skincare Products to Help Build Collagen and Elastin - Coveteur

The Best Peptide Skincare Products to Help Build Collagen and Elastin.

Posted: Wed, 23 Dec 2020 08:00:00 GMT [source]

Generally, attempt to liquify peptides in sterile pure water or clean and sterile dilute acetic acid (0.1%) remedy to give a stock solution at a greater concentration than that required for subsequent usage. If the peptide persists as visible bits, sonication might confirm of help as it boosts the price of dissolution. If, after sonication, the 'solution' has actually gelled, has a persistent haziness, or has a scum floating on the surface, the peptide has actually probably not liquified but is simply finely put on hold. Never be without your much-loved Boots products with our international delivery choices. UK rad 140 testolone Sarms which is anti-bacterial, making it really good for oily, spot-prone skin types, as well as any slightly a lot more fungal-type problems. I have actually written extensively concerning my love for NIOD CAIS, yet it is that excellent-- copper peptides are likewise anti-bacterial and also splendidly revitalizing on the skin. A safety peptide that is normally created in the body, carnosine blocks skin-damaging sugars from binding to collagen in the skin, protecting against the development of creases.

Nonetheless, they are additionally able to secure host tissues from proteases and also control innate as well as adaptive immunity using both pro- and anti-inflammatory activities. These activities include immune cell activation, recruitment, chemoattraction as well as guideline of immunomodulatory particles such as cytokines and also complement. Peptides help to bolster the performance of this retinol night lotion. Packed with a rich mix of ceramides, peptides and oligopeptides this glamorous moisturiser assists enhance the skin's structure while reducing the appearance of great lines as well as wrinkles. Created with a mix of 9 peptides, this giant moisturiser restores diminished and tired skin to its previous splendor. " Peptides are pieces of protein and it's these healthy proteins that are the foundation of the skin," states Dr Ewoma Ukeleghe, medical and cosmetic doctor at SKNDOCTOR. Zentraxa uses the power of engineering biology to make peptides which are as well challenging or pricey to create utilizing existing innovations.

Can you mix retinol and peptides?

Do Mix: Retinoids + Peptides Dr. Mariwalla says it's a great idea to use both a retinoid- and peptide-based night cream at bedtime. “You get the collagen-building effects of the retinoid, but it also works to improve the penetration of the peptide cream, which can help improve skin's firmness,” she explains.

The patented microbial platform presents modifications in the peptide series and also prevents several of the constraints of existing artificial chemical as well as completing biological techniques. This enables quick turnaround of new peptide layouts in addition to budget-friendly scale-up. Crucially it likewise provides the opportunity to find previously inaccessible biosuperiors. The worldwide peptide therapeutics market is anticipated to be worth $24 billion by 2020.

Serums have a lightweight structure as well as a high percentage of energetic ingredients, so they're a wonderful means to obtain a dose of peptides, attempt Radical Skin care Advanced Peptide Antioxidant Lotion. A fine example is copper-- a normally taking place mineral within our body that assists to bind collagen and elastin with each other. A copper peptide is a peptide, combined with a trace quantity of copper, which, when related to skin can help to boost the recovery procedure by delivering copper where it's needed to restore damaged skin.

[cyanpeacock]

Time for a little reductionism.

There are three paths in life.

1. It is fundamentally negative.

2. It is fundamentally neutral.

3. It is fundamentally good.

You're likely to walk all these paths, at some point or another. Think hell/purgatory/heaven, or Hekate at the triple crossroads, or the Maiden, Mother, and Crone... whichever triumverate fits your belief system.

Feelings can be physical, as in, bodily sensations, or cognitive, as in, shaped by your thoughts.

Thoughts can evolve and change. There are logical arguments for every catastrophic thought you might have, and logical arguments against.

The goal of meditation, DBT skills, therapy, counselling, even the scientific method, and so on, is to give you the ability to make these arguments yourself. You can cognitively regulate all that arises in the body or mind (allelic dysfunction omitted, because that's where psychiatry and pharmaceuticals come into it).

Say you have chronic pain, and it hurts like hell. This might lead you to believe life is fundamentally bad, and that you want an end sooner rather than later.

Pain can be managed through dissociation. Dissociation can be generated through cognition (or the controlled absence of it). Numbness of feeling leads to relaxation, which leads to the relief of pain, or at least relief from the perception of it.

Relief changes your perception of life. Sustained relief can change it profoundly.

Humans have a cycle to relief. It's a little different for everyone - we call it the circadian (approximately-24-hours) rhythm.

So, feeling the goodness in life requires identifying your cycle.

When do you wake best?

When do you work best?

On what do you work? Does it give you interest and attention?

At what times do you eat, and what do you do with your post-prandial dip (after-eating sleepiness)?

When do you sleep best?

Where do you do all these things?

How much movement do you do in a day?

Are you getting the right balance of macronutrients and micronutrients?

Are you spiritually nourished with a philosphical system(s), as well as physically nourished?

Life can be very difficult when you're young, if you aren't naturally inclined to favour attention to your bodily sensations (e.g. because of traumatic experiences, a neurodivergence, or painful genetic condition like osteoporosis or Ehlers-Danlos syndrome). Instinctively, you'd rather escape your body through cognition. Maybe you stayed up all night reading as a kid, because to try and settle down quietly was uncomfortable or painful, despite an awareness your body needs to sleep.

As kids, we don't have enough information to make the logical arguments to cognitively regulate discomfort and pain, and it's easy to either dwell on them, or dissociate from bodily sensations to a degree where your thoughts are in a spin and your mind can't calm down enough to let the body rest. Obsession vs. distraction.

As adults, we've gathered more information, and the rate of growth and hormonal change has stabilised and become familiar. We also become familiarised with our brains, and the circuits that tend to habitually fire. We get to know ourselves, and recognise our habitual patterns, shaped by the environments we have been given and sought.

Habitual patterns can be changed, once they are noticed. The thought "life is bad" can be countered with "life is good" (and yes, the precursor of "what is bad/good?" is another argument, but let's take it to be Maslow's hierarchy - it is good to self-actualize, and bad to have needs unmet or insufficiently met).

This leads you to a place of cognitive neutrality. It doesn't feel great, but it doesn't feel horrible, either. It's just a question that can be proven or disproven - a null hypothesis.

We don't like being neutral for long. We want proof or disproof of the neutral perspective. Living things want to feel good, as in, have their needs met, giving them the freedom to wander, wonder, and appreciate the beauty in their surroundings.

Over time, once the counterpoint is constructed, a mind makes the argument for life being bad less and less, until a need is unmet. One can get used to needs being unmet and maintain the "right" philosophical standpoint for survival in dire conditions, although it might not feel "good" - this might be described as ascetism. However, one probably shouldn't and won't, where needs can be met - because you have come to know "better," as in, what makes your body specifically feel better.

So, in this manner, health can be managed. OCD can be countered, BPD can be regulated, the worst of some forms of bipolar can be mitigated, anxiety can be relieved, depression can be lifted.

Growing your own neuronal networks and firing the impulses you want to (as well as getting comfortable with the ones you don't) takes time. Plenty of people will try to change you to fit their normal. Part of the process is learning that individual bodies' normals (including memories!) do not always agree, so you should find and talk to the ones who support and add to yours, rather than subtracting from it, and to hold your own when you must speak with a challenge.

That said, it may be the more effective means of coping over pharmaceutical drugs. A highly sensitive body responds better to its endogenous ligand (natural molecule) than a replacement, exogenous ligand from outside. On a physical level, the kinetics of dissociation and association of the endogenous ligand are the body's "normal." We just have to make the impulses work for our wellbeing.

If the "normal" is truly unattainable (significant allelic variation), or temporarily unattainable (environmental hardship, changes in epigenetic expression), an exogenous ligand can be applied. It won't have the same effect, because of differing chemical structures, and this is why we get side effects. The receptors get hit slightly wrong, and the pathways fire a bit funny, which has implications for the rest of your body as well as your mind.

Side effects may be bearable. They may be unbearable. You will form a perception and a judgement of the effect of application of an endogenous ligand, and pick the path that is right for your homeostasis, your maintenance of your understanding of "normal," or to fashion a path that returns you to your "normal" (your best epigenetic expression and physical patterns).

We've got a lot of language for attaining the normal, "right" perspective. There's "feeling right." There's "nirvana." There's possessing the "Sight." There's "recovery." It's all about directing energy flow to your will, and knowing the functional bounds of mind and body (which may not be the actual bounds, say, if you have a connective tissue disorder, or a predisposition to emotional intensity).

So, find the structures you have. Do you know about Wiccan practice? The Christian God? Science? Maths? Literature?

Know your language. All that you know can be related using a series of logical connectives and grammatical structures. Assume there is no mutual exclusivity here, because all of this exists, even if it hasn't been fully explained by science. Even a psychotic or psychedelic experience has basis in the physical reality of matter and energy. Your subjective, internal reality is real, because it is here.

This is hard in English, because it's often structured illogically and still understood, but remember irrationality too is part of an equation. Remember 2πr, from geometry in school? Pi is an irrational number. It's okay, and important, to be irrational sometimes! You'll find the integers, or points, that you require a return to.

You are part of the process. Numerically, you are supposed to be here. The cost-benefit analysis for your body favours you.

Hello, world.

[cambriancrew]

Did you know that the word "system" isn't in the DSM? The DSM uses the terminology "people with DID". And yes, we all agree here: DID and OSDD-1 are trauma-caused.

But "system" is not and never has been a strictly DID-exclusive term.

I witnessed the start of that myth a few years ago. Prior to that, for decades, it had been a term used almost exclusively by all plurals, by people who were accepting of all plurals, not just those whose plurality was caused by trauma, not just those with DID or OSDD-1. It meant then the same thing we insist it means now: any group of people sharing a body/head, regardless of origin or diagnostic status.

In fact, it was so universally known and acknowledged as an endogenic/endogenic-supporter term back then that antis on this very hellsite were telling their fellow people with DID or OSDD-1, "Don't call yourself a 'system'! Only fakers and faker-supporters use that term!" It's very disconcerting to see that history forgotten, and the myth accepted as long-term fact.

Also, yeah, some antis don't think we're all faking what we claim to experience. But a lot do. Some even threaten to kill us for it. And that's kinda a big deal. It's not quite as bad now, but especially back a few years ago when @systemhop and other targeted harassment blogs were big, death threats and suicide baiting and intentionally triggering imagery were all too common in people's inboxes and in the tags. Some very good people left because of it. Including a lot of people who aren't even endogenic but got harassed all the same.

So I understand why people get upset about it.

But there's literally only one person who uses the term "traumascum": ActingNT. And they're not even endogenic, and most endogenics are loudly and vocally against them and that term, as well as its derivatives plur/pluscum. (Which unfortunately, are still used by some endogenics. Like I said though, most of us are against the use of those terms too.)

As disconcerting as the "system is a DID only term for over 200 years!" myth is, the myth that the endogenic community uses and supports the use of the term "traumascum" is even more disconcerting to me. I mean, right now you can search Tumblr for "traumascum" and see all the rebuttals against it, and see that ActingNT is the only one using it. But what happens in a few months or a year when those posts disappear from the search because they're too old? What happens when this myth becomes repeated so many times that it's completely out of control and can't be refuted as easily?

What happens when we become tarnished with that term as the myth twists and becomes accepted, the same way the "System belongs strictly to people with DID" myth did?

What happens to us when a lie so often repeated becomes accepted as true, and harms our community?

Probably the same thing that happened when the system myth was.

We'll become even more vilified and hated. And some angry antis will take that as their cue to ramp up the harassment of us again. To accuse us of faking, and do whatever they can to harm us for it.

And it's horrific to see that happening right now and be unable to do much about it except scream into the void, over and over and over, "No. It's not true."

But people believe what they want to believe. And it's easy to believe we endogenics and our supporters are the villains - we're an easy target. It's easy to blame us when you're new to the community and haven't seen that we've been part of it from the very beginning, seen us be slandered, seen us defend our fellow systems of every type who got harassed just for being or supporting us. Or who are neither but people assume they are or do.

Those myths, those lies, feed into the harassment which is the plague at the core of the syscourse.

And all I can do is write the truth and hope people see it and recognize it for what it is.

[livingfitnessposts]

A COMPLETE GUIDE FOR USERS OF PRIMOBOLAN ORAL AND INJECTABLE (METHENOLONE)

Primobolan is one of the best known and most widely used anabolic steroids in the world, and its notoriety is undoubtedly due to its very beneficial positive effects compared to mild negative side effects.

This is especially true for the large number of athletes and bodybuilders who favor the notoriously smooth and gentle nature of Primobolan, although it is not the smoothest and most gentle available, Masteron, for example, is a more appropriate anabolic steroid in this regard.

Primobolan is  also known as the chemical name for Methenolone Enanthate, or Primo. It represents an androgenic anabolic steroid (AAS) that comes in both injectable and oral forms, which is quite rare in the world of anabolic steroids. As said, it is widely used by bodybuilders and athletes who want to implement a product with few side effects, no estrogenic activity at all; it is actually favored by those athletes who are primarily looking to build lean muscle mass rather than just mass.

Primobolan 200 is sometimes seen as a weak compound compared to compounds like Dianabol. This does not come as a totally inconsistent statement, given that it will not give you the ability to drop new weightlifting records or gain a lot of weight. However, it will definitely give you a great opportunity to gain some very noticeable, high-quality mass, if you are a little more patient than most bodybuilders.

It should be remembered that primobolan was a very popular anabolic steroid in the 1970s, a time known as the 'golden age' of bodybuilding, with some even saying that Arnold Schwarzenegger himself considered it his no. 1 anabolic steroid.

Whatever the legends or the facts, it is true that most of all known anabolic steroids were originally developed for medical purposes. It wasn't until later that they became big players in the bodybuilding communities, but this was not the case with Primobolan. It was actually developed in the first place, for the sole purpose of being used by bodybuilders.

However, years later, primobolan saw its huge popularity slowly decline due to the overwhelming number of fake products entering the market. Sadly, it has also been officially banned by many regulatory agencies in the major nations of the world.

Also given the high market price of primobolan, a dose of about 400 mg, good for a total cycle lasting 12 weeks, can actually cost up to $ 500; it's easy to understand why multiple users have given it up or alternatively tried using less than the recommended dosage, only to find that the product was disappointing, and for a very good reason ...

As a result, more and more athletes and bodybuilders have been changing their views on which anabolic steroid to use, turning to other alternative compounds, like trenbolone, for example, which in fact cost less and are also much less. frequent. faked that cousin.

If you only add this to the fact that looking (often without considering the much harsher negative side effects) to gain the most muscle mass in the shortest amount of time has become a widely accepted trend, few users really understand the benefits. from slowness, quality gains. With this in mind, you can easily see why Cousin has had a hard time keeping up with the competition stemming from the cheaper, faster-acting anabolic steroids.

However, there appears to be a strong comeback for this compound in recent years. Perhaps because its users have finally been able to consider the importance of avoiding the often severe side effects of many other steroids, and gaining muscle mass has become an acceptable alternative to raw bulking cycles.

All in all,  Primobolan  seems to be finally getting due consideration that it's worth it. Especially for those who have already built a strong physical base and remarkable muscle mass after many years of hard and proper training and diet. It is exactly these users who already appreciate primobolan as their icing on the cake. After all, primo really does represent one of the safest anabolic steroids: that is, it does not alter your normal blood pressure, it does not interfere with your wake / sleep cycle, and last but not least it does not encompass La at all. frequent occurrence of serious side effects such as gynecomastia.

Primobolan is  also known chemically as a compound derived from dihydrotestosterone (DHT). DHT is an androgen hormone and sex characterizing steroid that is synthesized by a particular enzyme (the 5a-reductase enzyme). Its function is basically to give men their set of masculine characteristics. Primo does not convert to estrogen, therefore its levels can increase in the body without increasing the level of estrogen. Therefore, it is quite easy for those who implement it, to avoid any estrogenic side effects.

The profile and esters of Primobolan

The oral version includes an acetate ester.

The injectable version contains an enanthate ester

Cousin Chemical Formula: C20H30O2

Original Manufacturer: Schering

Average effective oral dose: men = 50 mg to 100 mg per day;

Average effective oral dose: women = 10 mg to 25 mg per day

Average effective injectable dose: men = 350 mg to 600 mg per week;

Average effective injectable dose: women = 100 mg per week

Detection time: from 4 weeks to 5 weeks.

Anabolic / Androgenic Effects Ratio: 88 / 44-57

Oral Primobolan Benefits and Side Effects

Oral implementation of an anabolic steroid as a cousin can be done by means of a tablet, a pill, or a liquid suspension. Administration is usually carried out by a single dose per day, but sometimes by dividing the same dose into two parts. However, whatever your preference, it is widely known that orally administered anabolic steroids are generally more toxic and carry more negative side effects than those administered by injections, and Primobolan is no exception to this rule.

The most common possible side effects of Primobolan when taken orally include, but are not limited to, the following:

Increase in the user's blood pressure.

Headaches

A possible weakening of the osteoarticular structure, which over time can also lead to symptoms of osteoporosis.

A potentially general weakening of the body's strength levels, which may also imply an increased risk of infection, as this product can affect the immune system

A potential suppression of endogenous testosterone production, which can be avoided when proper PCT (post cycle therapy) is implemented

Possible hair loss due to its DHT properties.

The above potential negative side effects are related to normal doses in primobolan administration. In case of overdose or abuse of cousin, that is, at doses higher than one gram (1000 mg) per week, more and more severe side effects could occur (such as organ tension, for example). It's not really a good idea to assume that just because primobolan is considered a mild anabolic steroid, it should be underestimated regarding its potential side effects. Remember, it is still a respectable potent steroid and must be managed properly with a proper cycling plan.

However, a popular opinion about anabolic steroids like primobolan is that if taken orally, they will be more effective than injectables and that their action is more visible and much faster in the body. This is why some athletes and bodybuilders tend to favor the oral form, especially users who just want to see their muscle mass grow in the shortest amount of time possible.

Injectable Primobolan Benefits and Side Effects

Despite the common opinions we often hear, the opinion of most experts is that injectable steroids are by far the best form one can use to get the best results, reduce the length of an average cycle, and reduce the risk of side effects as much as possible.

Injectable primobolan is in fact superior to the oral variant of primo for many reasons and in many ways. Oral primary results can be disappointing as a substantial percentage of its active ingredient will be broken down when it arrives and is processed by the liver. Since primobolan is not 17aa in its oral form, the doses must be implemented at a considerably higher level (and potentially at considerable cost). This is why it is also recommended to use the injectable version of primobolan for the best possible results, and also to save considerable amounts of money in the long run.

If you are looking to get the fastest results, go ahead and take primo in capsules, tablets, or pills. In reality, several bodybuilders implement both forms, oral and injectable, together in the same cycle. They start with oral primobolan to maximize their muscle mass gains in the shortest amount of time, then move on to the injectable variant.

Of course, this is not the worst option, but what we recommend is to consult with your GP or a specialized health center to learn everything you can learn about the side effects of Primo. Especially with reference not only to the more severe negative side effects of the oral variant but also with regard to the prolonged use of this anabolic steroid, although in principle it is mild. Do not forget that it is highly recommended, as your doctor will also tell you, to undergo regular health checks.

What results can you expect from your Primobolan cycle?

Among the several positive effects that can take place when implementing Primobolan in the correct doses and cycles, we will indicate the following, which are however not a complete list:

Primo can help reduce breast cancer.

It does not aromatize, therefore it does not convert to estrogen. So you never really have to worry about the many estrogen-related issues like water retention, acne, and gynecomastia, to name just a few.

Primobolan is a fantastic AAS to combine with other anabolic steroids.

Doctors have found sufficient evidence to say that Primobolan is an activator of the immune system, therefore, very useful in the treatment of those diseases in which the basic reason for the disease itself is a lower activity of the "defensive system" of the body. For example, it has been shown to be beneficial in the treatment of acquired immunodeficiency syndrome (AIDS).

It is the main option for many to cut, and in fact, many athletes use it to keep their muscle mass intact while dieting on a low-calorie food intake program. Primo is really useful in this matter because it is able to make the body retain a high level of nitrogen. The higher the nitrogen level, the higher the level of muscle building and muscle mass retention in your body.

When using Primobolan in a pre-contest bodybuilding treatment, such strong maintenance of your nitrogen levels will protect your lean muscle mass and allow your diet to shed body fat deposits instead of muscle mass.

Can women use Primobolan?

There is some debate about the female use of primobolan and, in most specialized opinions, it is believed and recommended that women prefer to play it safe. The opinion is that women should never use any DHT-derived compounds due to the almost guaranteed masculinizing effects (such as the growth of facial hair, for example) that Primo may also imply unless they are very experienced users who have been tested. and approved by a specialized consultant.

Drug detection and half-life of Primobolan

Injectable primobolan has an enanthate ester   attached to it, so the half-life of this compound would be approximately 10.5 days. This does not at all mean that the compound will be completely out of your system exactly 10.5 days after your last injection. Rather, it means that after that average period of time, half of the dose you injected will be gone, but half is still circulating in your body, and therefore you can expect Primo to keep working for several weeks after your last injection before actually leaves your system completely.

On the other hand, the half-life of oral Primobolan is around 5 hours.

[sleepy-shutin]

hi i could probably help with this.

(sorry this turned out much longer than i intended.)

for starters, there's not much in the way of endogenic systems and scientific research. a lot of it is things like surveys, but there are no empirical studies or things going in-depth. i heard at the beginning of 2020 that there would be a study going into tulpa systems, but i've since heard nothing else about it, just had COVID had put it on hold. some people even (seemingly intentionally) misquote papers that are about DID/OSDD to make them seem like they are talking about endogenic systems, which makes it really important to read and pay attention to what people are sending you, not just looking at screenshots.

so when it comes to endogenic systems, right now the best thing you can do is just listen to them when they explain how their system formed and how it works. sometimes it's intentionally created, sometimes it's "spontaneous", sometimes it's that they're born like that or whatever else. there's a lot of origins.

as far as the differences between non-dissociative systems, DID/OSDD-1 and just identity problems, that can be a tough question.

telling the difference between the first two can be easy enough as non-dissociative systems are, well, not dissociative. their consciousness was not fractured into different parts of one whole consciousness due to trauma and using dissociation to cope, and as a result, their system generally will not experience the following*: amnesia, (the amnesia in DID is caused by dissociation), depersonalization (feeling as if one is not real) or derealization (feeling as if the world around one is not real), and other dissociative feelings, such as becoming disoriented/dizzy/dissociated while switching.

*(not taking into account mixed origin systems, who may have these experiences if they have a DID/OSDD-1 system plus headmates of other origins).

in DID, the root of everything is trauma-based dissociation. you have alters because of dissociation. in non-dissociative systems, it's a bit more unclear and vague as headmates can be anything from formed willingly to spiritual.

with identity problems, it can be confusing to tell whether this is dissociative parts/a system of any kind or just identity problems, and is in fact the source of many questioning people's confusion. the most you can really do is look as far into DID/OSDD-1 and other systems as you can* to get an in-depth understanding of these experiences, and come to your own conclusions. if questioning DID/OSDD-1, it may be a good idea to see a dissociative specialist if possible to help you on your journey.

*(by this i mean PLEASE read books and papers on DID/OSDD-1 if you can, they are out there, they are all over google scholar, and below i will link you to a google drive full of books and papers.)

now, i can link you to some papers and stuff relating to complex dissociative disorders, (i.e. DID and OSDD-1, the dissociative disorders that involve systems), if you want. i also have a discord server set up for discussing information on DID and OSDD-1 systems (plus a book club!) that's open to anyone who wants to join and learn about the subject, but no pressure to join.

there's a lot more information on DID and OSDD-1 than you may be thinking.

if you want a good base of knowledge on DID, here is a google drive link to a google drive full of info. the papers you'll be looking for are titled something along the lines of "examining 6 facts and myths about dissociative identity disorder" and "DID - an empirical overview". these are two relatively recent papers (as in, mid 2010s for the both of them, iirc) that go over a lot of important information relating to DID.

other things in that library i can recommend are "coping with trauma related dissociation" and "understanding and treating dissociative identity disorder - a relational approach"--two books written in relatively plain language that are pretty easy to understand, layman friendly, that go pretty in-depth on complex dissociative disorders.

if you want more books/papers/info, go to the references sections of papers you liked and look for titles that catch your eye, then paste those titles into google scholar, look for the DOI link/number and copy/paste that into sci-hub. that's how i get like all of my info. tried and true method.

anyway i hope this helps somewhat. sorry if it's somewhat incoherent, i have a migraine but if i go to bed now, i won't be able to sleep through the entire night and i have work in the morning so i have to suffer.

To all the systems out there, especially the endogenic ones, can anyone send me any legitimate scientific studies that focus on endogenic systems?

I found one study that vaguely mentioned the concept, but it was a collection of case studies of around six systems, so it’s not very reliable. Whenever I search stuff up, I don’t really find anything very useful or in-depth when it comes to how endogenic systems work, how they form, how exactly they’re medically classified, etc. I’ve seen blogs from such systems, but those aren’t really what I’m looking for. I also found a lot of people saying that endogenic systems don’t exist, but I don’t really know? I don’t think these systems are lying/misinformed?

I know that the medical community often barely acknowledges traumagenic systems, so it’s probably going to be hard to find some, but I’d really appreciate it. It helps me contextualize the whole thing, especially since I’ve just been Really Confused™️ ever since I found out that systems could (I think?) be non-traumagenic. Most of the things I’ve read when it comes to systems as a whole surrounds DID/OSDD, and it’s considered a trauma-based disorder. Also, if anyone could point me to a resource that explains the main differences between identity disturbance, just being a system, OSDD, and DID that’d be really helpful.

I want to learn as much as possible so I can make sure I never hurt anyone. Please take everything I say as literally as possible (I got ye olde ASD).

:)

(If I said anything that’s wrong, hard to understand, ignorant, or that you simply disagree with, please let me know! This also goes for anything important that I may have left out. Oh, and any grammar mistakes I may have made.)

[nostalgebraist]

Cross-posting my comment on Scott’s adult neurogenesis post:

I may just be misreading something, but it seems to me like your Part II here goes a lot further in its claims that any of the sources you link to.

Well, okay, the Neuroskeptic posts make it sound like the author is pretty convinced by the no-human-adult-neurogenesis side of the argument, but the Atlantic article makes it sound much more like there are just a lot of conflicting results, with a lot of researchers who will argue vociferously for their preferred interpretation but who will also admit that when it comes down to it, there just isn't enough data (or good enough experimental methodology) and more research is needed -- which is a very common situation in science, even in the hard sciences, and isn't any kind of crisis.

That is also the impression I get from this post by Jason Synder, which Neuroskeptic described as "excellent." Synder says things like:

In 2011 I made a list of all the human studies of adult hippocampal neurogenesis (see here, may be incomplete). The pioneering study was by Eriksson et al in 1998, where they found BrdU+ cells in cancer patients. Studies such as Knoth et al and Epp et al have used endogenous markers of immature neurons (such as DCX) to identify adult neurogenesis. Lastly, Spalding et al used another complementary and creative approach to quantify adult neurogenesis: radiocarbon dating. Individually, none of these studies are entirely convincing of adult neurogenesis in humans but, collectively, they provide strong converging evidence. They convinced me. And while the new Sorrells paper raises concerns about these previous papers, it cannot definitively refute them either.

And his post has a section heading called "We need more studies of neurogenesis in humans," describing all the complicated problems that could potentially have corrupted existing results (including the latest anti-neurogenesis ones). It definitely doesn't sound like he thinks human adult neurogenesis is dead (if it were, we wouldn't need more studies of it!).

Neuroskeptic sounds more convinced on that score, but I'm not clear on why. They write:

This result challenges previous studies, using other methods, that did report adult neurogenesis in the human hippocampus. However, the new study is consistent with another no-neurogenesis finding from a couple of years ago. For more on the methodology of these neurogenesis studies, see this excellent post by Jason Snyder. Overall, it seems to me that the evidence against adult neurogenesis is becoming pretty convincing.

I don't think this is deliberately misleading, but it is easy to misread. If you don't click through to the Synder post, it's easy to infer from the flow of the paragraph that it provides more support for the sense that adult human neurogenesis is probably dead (in fact, it does the opposite). And then, if you ignore that sentence, the rest of the paragraph isn't convincing at all -- it amounts to "there are various studies reporting the opposite result, but there's at least one that reports the same result," which does not in itself inspire strong confidence in the result.

The other Neuroskeptic post, about the earlier paper, presents an interpretation like the one in your post (under "entirely innocent, well-intentioned, and understandable") -- but it's an interpretation of that one paper, and how to reconcile it with one other paper. I don't see anyone else proposing that interpretation as a resolution of the whole dispute, and indeed, Synder and the researchers quoted in the Atlantic article all seem to think the dispute can only be truly resolved by more data and better methods.

[kramlabs]

Circadian Timeline via Jack Kruse

LINK

This is the modern warm adapted human circadian cycle:

1. Our brain wakes up with a morning surge of cortisol. That is what turns our brain on at 6 AM. VIP helps do this in long light cycles. VIP is highest at 6 AM and lowest at 6 PM. Ghrelin is also highest in the morning. Ghrelin is an incretin hormone made in the stomach that has a half-life of one hour. NPY and Agouti stimulate the production of ghrelin. Ghrelin sends a signal directly to our pituitary gland and it influences our metabolism. This is why the circadian cycle in the stomach in the morning is critical to optimal health. I laid that out here in this blog and it is an important part of the Leptin Rx reset protocol.

Circadian cycles for the obese are dramatically altered compared to non-obese individuals in the morning. In the normal person, Ghrelin is high when cortisol is highest in the early morning. In them, ghrelin drops fast when food is eaten too. In the obese, ghrelin is much lower in the morning than expected. Moreover, when food is eaten, ghrelin stays elevated for an extended amount of time. This happens because of the inflammation associated with the higher leptin levels in the morning in the obese. Melatonin is known to acutely decrease ghrelin and sometimes in tough cases, I will use supplemental melatonin to demolish the morning ghrelin spikes in people with huge appetites. This is most common in the obese, eating disorders, and in those with a severe leaky gut who crave dairy and carbohydrates. It is also very common for young paleo enthusiasts because of how they embrace blue light technology gadgets of the modern world that destroy melatonin levels in the brain.  Ghrelin spikes and stimulates NPY in the hypothalamus increasing our desire and ability to eat a lot more. Leptin makes NPY decline normally, but if one is leptin resistant this does not occur and appetite is out of control at the brain level.

This is why obesity is an inflammatory brain disorder causing hormonal imbalance. Hormone imbalance implies a poor redox potential in different parts of the body.  Where the potential is destroyed a certain disease will manifest.  Obesity happens when it occurs at the leptin receptor or due to slow energy leak from the inner mitochondrial membrane.  This means the obese person is losing energy in black box radiation.  It is easy to check but few do with a thermal camera.  We see this macroscopically as major alteration is sweating and down-regulation of activity due to an inability to uncouple oxidative phosphorylation at the mitochondrial level.  It is not a disease of stress or emotion as medicine is trying to ram down media outlets.  It is a problem of an alters the quantum biology of electron/proton tunneling across our proteins.

Moreover, this should explain why the SAD breakfast is so problematic for modern humans. It is marketed as a carbohydrate fest. It is also why the Leptin Rx recommendation for protein and fat are so high in the morning. Protein is the backbone of all life.  When we are losing energy and increasing molecular chaos we need to replace our proteins to recapture our balance.  It solves this problem fast. I use protein over fat in the Leptin Rx because high-fat levels with low protein in the morning cause a spike in the gastric inhibitory peptide that can induce insulin resistance by itself. I do use high fat in certain cases, like bariatric surgery, eating disorders, hypothalamic amenorrhea, or high EMF levels.  Many people do not know this. This is why so many people do not buy Gary Taubes theory of “Why We Get Fat”. Gary has only part of the story correct, in my view, because obesity occurs on a spectrum just like autism does because it depends on how the environment affects epigenetic expression. When you understand circadian biology, you get a much more complete picture of how the system works on a 24-hour basis. It turns out electrons control the coupling of biochemistry in life and understanding this helps to make sense of why hormones are disrupted when electrons are not handled correctly.  I became a student of circadian biology when I saw the entire view from a 30,000-foot level.

2. At 6:45 AM we will expect to see the sharpest rise in blood pressure in the entire day. This is due to many activated systems in the body getting us ready to fully supply blood to all vital areas to get us motivated to begin our day and search for food. This period of rapid BP rise is why we see so many cardiac deaths occur in early morning sleep or early wakefulness. This happens when cortisol is highest.

3. At daybreak, when the sun hits the retina, the photic stimulus begins to shut off the secretion of melatonin from the pineal gland in the brain.  AM sunlight contains mostly IR light at daybreak and as we approach noon, UV light frequencies appear on the skin.

4. At 7:30 AM usually after an hour of light melatonin is completely shut off in the brain.

5. At 8:30 the gut has been awakened and peristalsis becomes more vigorous and bowel movements getting rid of yesterday’s food are very likely. This happens by protons flows to move serotonin sulfated by the light of the gut microbiome in the wall to get to the brainstem to become sulfated melatonin.  This is stimulated if food is eaten around this time as well. This is called the gastrocolic reflex.  Cortisol, aldosterone, and ghrelin are all raised at this time to drive activity, increase our blood pressure and stimulate feeding.  This is all yoked to AM sunlight stimulus.  It is blocked when we wear clothes or at work in the AM.

6. Around 9-10 AM we have the highest secretions of the sex steroid hormones in humans and these pulsatile crescendos lead to our highest alertness at around 10 AM in our day to allow us to explore our environment.

7. Our ideal muscle coordination occurs at 2:30 PM and this adapts us best to hunt for dinner at this time. An hour later we see our fastest reaction times develop from our motor systems in our CNS.

8. At 5 PM humans exhibit their greatest cardiovascular efficiency allowing for maximal exercising or hunting. This also occurs during a period of time when we have our best rates of protein synthesis in our body. This is why exercise should be optimally done in this window.

9. As the sun falls at 6 PM we begin to see a major change in the cardiovascular system about a half hour later.

10. At 6:30 PM we see our highest blood pressures due to changes in atrial natriuretic factor and antidiuretic hormone (ANF, ADH) in the renin-aldosterone axis.

11. Once this occurs over the next 30 minutes (7 PM) we begin to see a gradual rise in our body temperature as leptin (and IL-6) is released from our fat stores, with agouti’s help, slowly after dinner is eaten to signal the brain about our fat mass and inflammatory status.

12. For the next two to three hours leptin levels slowly rise as insulin levels fall. Adiponectin levels also fall during this time frame. These fat hormone signals are what activate adenosine system in our bodies. Adenosine is created over the course of the day; high levels of adenosine lead to sleepiness.

13. This peaks at 10 PM and then the circadian clock allows for melatonin secretion after 3-4 hours of total darkness. Serum leptin is rising quickly now (with agouti’s help) as it is released from the fat cells to enter the brain. Agouti is highest at this time of the day, even in a normal person.

14. As these trends continue the GI tract is slowly shut down by the circadian clocks and around 11:30 PM and bowel movements are shut down for the night. This means that the vagus nerve is quiet.

15. At midnight leptin begins to enter the hypothalamus to bind to its receptor in the hypothalamus to signal energy reserves while also yoking energy metabolism to sleep via the hypocretin neurons that control all the sleep cycles. In diurnal animals, sleepiness occurs as the circadian element causes the release of the hormone melatonin and a gradual decrease in core body temperature. This drop in temperature is the stimulus to change sulfated serotonin to sulfated melatonin.  This timing is affected by one’s chronotype.

16. It is the circadian rhythm that determines the ideal timing of a correctly structured and restorative sleep episode. Melatonin, the hormone from the pineal gland, called the “darkness hormone ” is of great importance in the functioning of the SCN. The most important target of melatonin in humans appears to be the SCN, as the SCN contains the highest density for melatonin receptors. A double effect of melatonin in the SCN, namely, an immediate effect and long-term effect, has encouraged its worldwide use against the ill effects of jet lag.  This may not be wise to do.

As an immediate effect, melatonin is found to suppress neuronal SCN activity towards night time levels. During the daytime, the SCN neurons must run faster than normal.  This is possible because the retina has more DHA in it than the brain.  In terms of long-term effect, melatonin can phase shift and amplify circadian rhythmicity of the SCN. Melatonin application has been found to be useful in synchronizing the endogenous circadian rhythms not only in people who suffer from jet lag, but also in blind individuals, patients with dementia, and in shift workers. With seasonal changes in night duration, there are parallel changes in the duration of melatonin secretion, and this leads to more secretion in winter than as compared to summer. In the cold environments of fall and winter, melatonin couples to eNOS and not to light levels. In warm adapted humans in the tropics, the light remains the focus of SCN entrainment year round.

17. After the 4 hours of darkness, melatonin secretion increases and this allows plasma leptin to enter the hypothalamus if we are sensitive to its receptor. If we are leptin resistant, this process can no longer occur.

18. Once leptin enters and binds to its receptors, it affects the lateral hypothalamic tracts to immediately send a second messenger signal to the thyroid to signal it to up-regulate thyroid function and efficiency. This is how we can raise our basal metabolic rate when we are leptin sensitive. These coupled events, matched with leptin’s actions peripherally in muscles, occur at the UCP3 sites to burn fat as we sleep at a higher basal metabolic rate.

This means electron chain transport does not make ATP as usual. When leptin allows this uncoupling to occur, we make heat and not energy from normal metabolism. This means we will burn off our excess calories as pure heat. This is one reason why calories in and calories out argument makes no biologic sense once you understand how leptin works. Humans are built to burn fat at night as we sleep to lose excess weight we don’t need.

19. The timing of the leptin action is also critical. It usually occurs between 12-3 AM and is tied to when you last ate and how much darkness your retina (SCN) have seen. This generally occurs soon after our hypothalamus releases another hormone called prolactin from our pituitary gland in the brain.

20. The surge of Prolactin is normally quite large in normal darkness but is significantly diminished in artificially lit environments after sunset. This was shown in the Jessa Gamble video HERE.

This has big implications for modern humans. The reason is that prolactin release is coordinated with sleep cycles where autophagy is at its highest efficiency and where Growth Hormone is released. If this is diminished we generally see lower DHEA levels clinically and higher IL-6 levels on cytokine arrays. This is a measure of uncoupling of sleep from normal metabolism. I base every bio hack I do on this step in circadian biology because it is the most important.

21. The normal large circadian prolactin surge we should see at around midnight after leptin enters the brain, does not happen if the patient has leptin resistance, sleep apnea, or has eaten food too close (within 3-4 hours) to bedtime. This blocks leptins ability to enter the brain because of insulin spikes. As mentioned above, this step is usually impaired if you are a post-menopausal female as well. This is often why older women sleep badly and gain weight they can not seem to lose in the gym even with a good paleo template and good habits.

This is another reason I am a big advocate for bioidentical hormone optimization in women. This need is greatest in women who are warm adapted. The need is lowest in the cold-adapted females because their leptin levels are already low due to the cold. Postmenopausal women who are cold-adapted tend to do amazingly well clinically in most disease parameters in my clinical experience. The main problem they face is that their vanity and dogma keep them from using the cold pathways to become rockstars as they age.

Exercise training tends to frustrate postmenopausal women because if their hormone response is altered they have a lot of trouble as they age. Men, on the other hand, do not lose their GH levels until 50-55 years old usually. They are also protected by their testosterone levels which persist throughout life provided that they are not suffering from inflammation which directly lowers their free and total testosterone levels. GH and testosterone keep a mans heart and muscles in tip-top shape. If inflammation destroys these levels earlier in life, it can show up even in younger people. I am finding this clinical result is an epidemic in my own practice.

What happens when step 20 is broken in modern humans?

This commonly happens in diabetics, but it is now becoming a very common finding in modern humans because of the excessive use of technology after sunset. These artificial lights also tend to be quite bright and completely un-yoke the normal circadian signals from the hormone response. Light after sunset reduces the prolactin surge we normally see in humans. When we see chronic lowered prolactin surges we also see lower growth hormone secretion during the anabolic phases of sleep.

Lowered chronic GH secretion directly affects cardiac and skeletal muscle function because the process of autophagy is made less efficient as our life continues. Lowered GH and the sex steroid hormones at sleep lead to loss of cardiac function. This is why heart failure is strongly associated with low IGF-1 and sex steroid hormone levels. When growth hormone is not released in normal amounts, it also decreases our lean muscle mass and increases our fat percentage in all our organs and in our body. This leads to slowly declining organ dysfunction and poor body composition. We can measure this process clinically by looking for falling DHEA and GH/dopamine levels as we age.

What happens in normal aging in step 21?

Aging is among the most common features found in studies on modern humans when DHEA and GH craters on hormone panels. The loss of the prolactin surge is especially prominent in postmenopausal women. Most women begin to suffer from falling DHEA and GH levels around age 35-40 while they are still in peri-menopause. The higher their HS-CRP levels, the faster they enter peri-menopause and the quicker they enter menopause. They also age faster on a cellular level because their circadian chemical clocks are sped up. As a consequence, their telomeres shorten faster as well. Women have higher levels of leptin for childbearing, so they are more prone to leptin resistant issues than men. Leptin is a sexually dimorphic hormone.

This helps explain why older women struggle with cognitive haze, loss of body composition, poor sleep, and increased levels of heart disease after menopause. Many physicians think the losses they suffer are due to the loss of estrogen from ovarian failure, but the loss of growth hormone and progesterone production are far more significant in their physiology. Progesterone is the off switch to anything that is pro-growth. Modern women are usually estrogen dominant even after menopause because of mismatches in circadian biology. Cognitive loss is especially common in post-menopausal women. They also lose on average 1% of their bone mineral density per year from menopause in large part due to the loss of progesterone, not estrogen.

Loss of progesterone also corresponds to poor sleep in these women too. Replacing progesterone in women has a major effect on their sleep and bone stock. It also dramatically improves their memories and cognitive function as well.

Snacking after dinner… Effect on circadian cycles:

If you choose to eat within 4 hours of sleep you will never see the prolactin surge you need, because any spike in insulin turns off this critical sleep time release that corresponds to the cellular maximums of the autophagic process for humans. Agouti, the incretin gut hormone also rises in the blood to higher than normal levels to block leptin from entering the brain.

Diurnal cycles for agouti are coupled to NPY and have major effects on leptin. Agouti is a gene product that normally increases the release of leptin from fat cells at night to signal the brain of what the energy status is of the body. This is great when it is working well. When it is elevated due to heavy carbohydrate use in our diet it creates a massive problem. This is why late night carbohydrate snacking is a bad thing to do.

It appears 12-3 AM are the critical hours at night are where the remnants of mammalian hibernation lie for our species. These are the anabolic times for sleep when we are rebuilding our proteins and recycling our cellular contents. They are three of the most important hours in all human biology. If you miss them, you can bet you have several neolithic diseases for sure. Why do you ask? If these three hours are not reached enough during our sleep cycle, autophagy is never optimized and cellular repair does not occur in our cells. This means we are using old broken down parts in our cells as the next day arrives at 6 AM and cortisol rises again to wake us up.

We can measure this efficiency of this process by checking DHEA and IL-6 levels. I also like to measure hormone panels to see if the inflammation has destroyed any other hormone cascades in aging men or women. This is vital in taking care of older people and treating their longevity. IL-6 levels correspond to Leptin resistant states as well. This makes sleep and metabolic coupling tightly controlled by circadian biology at all times of our life. It is magnified because sleep gets worse as we age and our DHEA, HDL, and HS CRP rise. This is where, during a bio-hack, we can see why circadian mismatches can cause neolithic diseases in humans. Often times we can find the same issues develop much earlier in a young paleo person who has a lot of mismatches in their circadian biology. I test them the same way I would an older person.

Prolactin, Doc?

You must be asking, why is this prolactin hormone so important in a warm adapted human? Prolactin is not just a hormone that secretes human milk. That is the best-known action of prolactin, but not the most important. Immediately after prolactin is released during sleep, another signal is sent to the anterior pituitary to release the largest amount of Growth Hormone as we sleep (GH). GH is stimulated only during autophagic sleep cycles in stage 3 and 4 to increase protein synthesis for muscle growth while you’re dissipating heat via the uncoupling proteins. This is where the major release of GH occurs in humans post-puberty when they are warm adapted. 99.9% reading this blog are warm adapted. If you chose to become cold adapted the GH story radically changes, as laid out in CT-6.  GH and dopamine are analog proteins.

The implications here are huge for the warm adapted human if this prolactin surge is not adequate to allow us to enter the anabolic stages of sleep. Prolactin surge is diminished by both artificial lights at night and by foods that stimulate NPY, (namely carbs and protein) when they are eaten in fall and winter when biology says they should not be available.

If you are leptin resistant for any reason, have sleep apnea, you will always have an altered body composition because of a low GH level and an altered sex steroid profiles on testing. The reason is that DHEA is the immediate precursor for those hormones and is always low in people with bad sleep efficiency. Most VLCers who are warm adapted face this very problem today. VLC diet is best used in the cold-adapted mammal and not the modern warm adapted lifestyle. In essence, this diet is a mismatch for our modern lifestyle. This is why so many bloggers think ketosis is a dirty word for performance and body composition.

This all implies that as you age you will have higher body fat %, lower muscle mass %, if autophagy is not optimized by great sleep. This is precisely what we see today in most modern humans as they age. Invariably, their sleep cycles and sleep durations are poor and decreased from their childhood levels. As they age, there is a chronic insidious erosion of circadian biology by decisions made by modern humans over and over again.

What about temperature variations in warm adapted humans?

Where does temperature enter the picture? In warm-blooded animals, homeotherms, such as humans, can change their metabolism in order to keep their heat production equal to the heat loss. Such animals have a temperature control system and thereby maintain a rather constant core temperature. Warm-blooded animals live with the advantage of an unchanged cell activity and temperature in their core. However, the human core temperature falls during the estrogen phase of the menstrual cycle (pro-growth) and during sleep (circadian rhythm by melatonin).

The lowest temperature of the day for modern humans is usually between 2 AM and 6 AM. The temperature cycle is part of the normal circadian periodicity. Our biological clock seems to be synchronized with the rotation of the globe daily. Meal composition and timing, light cycles and temperature play a role in altering normal cycles and autophagic optimization.

Ovulation releases a sharp rise in morning temperature with its estrogen surge. Progesterone effects seem to explain the higher temperature in the last phase of the menstrual cycle where it calms the pro growth effects of estrogen. In post-menopausal women, this balance is usually not ideal, and it leads to many menopausal complaints these women face today.

The reduced temperature induced by melatonin in sleep is needed for Central Nervous System autophagic repair, for another, less well-known reason. The lowered temperature sets the stage for the biologic quantum effects to be optimal on our neurons microtubules that facilitate learning and neuronal spouting that occurs brain-wide.

This is why if you don’t sleep well you feel bad the next morning and your mental performance suffers the next few days on cognitive tasks. Research also shows your learning is severely impaired because of lowered BDNF and changes in diurnal cortisol due to the sleep deficit. This is why we monitor truck drivers’ and airline pilots’ sleep and wake cycles by law!

Moreover, in hospitalized ICU patients or the elderly when this occurs, it sets the stage for the appearance of acute onset delirium. This is exacerbated when they also have a simultaneous cytokine storm from sepsis or obesity. We see this often in hospitalized patients who cannot sleep well in ICUs. Acute delirium states very much look the same as chronic sleep deprivation patients we see clinically as well. Inducing cold, using progesterone and using hypnotics helps manage these conditions. I mentioned this in my hour-long PaleoFX talk last week.

Okay, nonscientists take a breather. Geeks are up: So today we are going to look more closely at how circadian biology sculpts our species. We will assume the sun rises for us today at 6 AM. About two hours before the sunrise we are at our lowest body temperature and this signal is sent to our hypothalamus to the hypocretin neurons that link metabolism (leptin receptor) to the sleep cycle clocks. This temperature dip signals that sleep is coming to an end and that the brain needs to raise its cortisol levels to wake up the cerebral cortex not connected to the autonomic portions of the brain in the brainstem.

This is called the reticular activating system. When the reticular activating system is damaged, humans remain in a sleep-like state called coma. Neurosurgeons call this a chronic vegetative state. The release of cortisol is a neurochemical signal from the hypothalamus that allows the reticular activating system to wake up the cerebral cortex in the AM by increasing water flows from the CSF, Matrix, and cytosol.

Now we have to think about what season we are in? Is a long light cycle (summer) or is a short one that is cold (winter)?

VIP regulates the circadian rhythm in humans and most mammals. VIP is a gut hormone and is found in our taste receptors too! So if we taste the sweetness from carbs in our diet when it’s warm and they are growing in the environment, our brain is expecting us to be in a warm season rather than a cold one. So sweet means warm to the brain, not cold. If you mismatch that and eat carbs at the wrong seasonal time, you create inflammation in the brain and it throws off our chemical clocks in our cells and ages us faster. That means our telomeres get shorter. This is not good.

Even geekier: Taste perception and its relationship to glucose homeostasis begin with stimulation of taste cells located in tongue taste buds. There are five basic taste modalities: bitter, sweet, umami, salty, and sour. Taste cells are clustered into taste buds in the tongue epithelium. Mammals have four different types of taste cells (types I, II, III, and IV), exhibiting different molecular phenotypes and functional roles.

Type I cells are glial-like cells that maintain taste bud structure. Type II taste cells transduce sweet, bitter, or umami stimuli and communicate information through G-protein coupled transduction cascades. Type III cells synapse directly with afferent nerve fibers from three cranial nerves and most release serotonin upon depolarization. Type IV basal cells are rapidly dividing progenitor cells that differentiate into type I, II, and III cells. Along with biogenic amine neurotransmitters, it is becoming evident that multiple peptide hormones including glucagon-like peptide-1 (GLP-1), cholecystokinin (CCK), and neuropeptide Y (NPY) as well as VIP are located in taste cells, potentially acting as signaling modulators of multiple gustatory stimuli.

The circadian clock not only can generate its own rhythms but can also be entrained by the environmental light-dark (LD) cycle. Multiple single-cell circadian oscillators that are present in the clock can, when synchronized, generate coordinated circadian outputs which ultimately regulate the overt rhythms.

VIP is a gut polypeptide, has been identified as one of the main neurotransmitters of SCN neurons, and participates in SCN function. These SCN neurons are retino-recipient and are found in the core of the SCN. They are activated by light, and exogenous application of VIP can reset the circadian clock in a manner similar to that of light application, both in vitro and in vivo. It is estimated that 9%-24 % of SCN neurons express VIP.

Leptin was originally described as an adipocyte-derived cytokine that signals to the hypothalamus to regulate food intake and energy expenditure. Leptin signals through its receptor, which is closely related to the gp130 cytokine receptor. Leptin can induce expression of the neuropeptide gene vasoactive intestinal peptide (VIP) through the VIP cytokine response element, the same element that mediates the response to the gp130 cytokines. Leptin acts synergistically with TGF-beta to activate transcription through this element.

One of the main chemical constituents of SCN neurons is the vasoactive intestinal polypeptide (VIP). Such neurons are retino-recipient and activated by light. Exogenous application of VIP resets the SCN circadian clock in a light-like manner both in vivo and in vitro. These resetting actions appear to be mediated through the VPAC2 receptor (a type of receptor for VIP). Unexpectedly, genetically ablating expression of the VPAC2 receptor renders the circadian clock arrhythmic at the molecular, neurophysiological and behavioral levels. These findings indicate that this intrinsic neuropeptide acting through the VPAC2 receptor participates in both resettings to light and maintenance of ongoing rhythmicity of the SCN.

Neurosurgery geeks only: In mammals, the part of the nervous system responsible for most circadian behavior can be localized to the suprachiasmatic nucleus (SCN). Although previous studies suggest that each SCN neuron may be an independent oscillator, these pacemaker cells must be synchronized to each other as well as to the environment to function adaptively. Therefore, answers to questions about cell-to-cell communication within the SCN lie at the core of understanding how his timing system operates. The daily cycle of light and dark is the dominant environmental cue responsible for synchronizing this biological timing system to the environment. The SCN neurons receive photic information directly from the retinal-hypothalamic tract (RHT).  My Vermont 2017 video gets deep into the physics of the retina.

Many of the SCN neurons that receive retinal input from these cells are located in the ventrolateral (or core) region of the SCN and express GABA and, in many cases, vasoactive intestinal peptide (VIP) and the Peptide Histidine Isoleucine. These retino-recipient cells then convey this environmental information to the rest of the SCN. In brain slice preparations, application of VIP alters the firing rate of SCN neurons through a VPAC2 receptor-dependent mechanism and induces expression of mPer1 and mPer2 genes. These two genes are how the circadian cycles yoke directly to the cell cycle and are related to tumor suppressor genes and oncogenesis when mismatches occur chronically in modern man.

Functionally, the administration of VIP, and to a lesser extent PHI, can cause phase shifts of the circadian rhythms in vivo and in vitro in man.

The role of AVP (arginine/vasopressin) in circadian timekeeping has also been well established in the neurosurgery literature. Its role in the control of the circadian rhythm of food and water intake has been reported and well documented. Another intrinsic neuropeptide, VIP, acting through a VPAC2 receptor (a type of receptor for VIP), participates in both resetting to light and maintenance of ongoing rhythmicity of the SCN. NPY and GABA seem to be the neurotransmitters in the projection from the intergeniculate leaflet to the SCN adjacent to CN II. Raphe nuclei projections to the SCN contain serotonin as an NT. AVP and prokineticin 2 are seen in the outputs from the SCN as efferents.

NPY, which is an established neurotransmitter of the geniculohypothalamic tract (GHT), was found to regulate SCN neuronal activity and to produce long-lasting suppression of firing rate of SCN neurons. When co-applied with NPY, NT (neurotensin) was found to dampen the profound inhibitory effect of NPY. So when NPY is high, which would be in equatorial or high light conditions, NPY basically makes the SCN less efficient and allows animals to perform outside their normal circadian boundaries. They stay awake longer for eating and for reproduction in high light times during summer.

All geeks reunite: VIP (along with GRP and AVP) show circadian variations in the level of mRNA in constant contact with environmental conditions from our tongue and our gut. When light becomes long-lasting in summer, NPY dominates the SCN in mammals when light becomes low and the temperature falls to 50-55 degrees constantly at our surface cold receptors, and eNOS rises and blocks all photic input to SCN and circadian rhythms are maintained by a new program. Alpha MSH induces and potentiates that seasonal change within the hypothalamus as laid out in CT-6 blog.

The moral: So the brain is wired for foods when they grow naturally, not when we feel or think we can/should eat them regardless of their availability in modern times.

Leptin sensitivity directly regulates VIP production. VIP regulates the circadian rhythm and entrains the SCN to light. When it is cold, leptin is released from fat cells in large amounts, and we begin to use eNOS to entrain our SCN to cold cycles and we should avoid carbs like the plague then. Remember from CT-6, cold empties fat cells like screaming fire would empty a crowded cinema. In cold, the pituitary-hypothalamic portal is involved in the production of lots of alpha MSH and ACTH. When MSH rises, you are allowing the brain to control everything to get you to optimal. This should make it abundantly clear that cold and warm adapted mammals are not sharing the same circadian biology. Cold selects for supreme LS and superior hormone optimization as laid out in the CT 6 blog.

In long-light summer cycles, when VIP is controlling the SCN again, androgens normalize if the mammal is leptin sensitive. VIP usually fixes our Vitamin D level to optimal too. VIP is a master controller of all inflammation for circadian cycles, but leptin is the hormone that produces VIP in the correct amounts even in light cycles. So if we are leptin resistant for any reason in long-light cycles, we have no control over our circadian cycles and this leads to neolithic diseases.

Normally, VIP lowers our cytokines as the light cycle lessens as the day progresses. At night time the cell is more reduced and not as oxidized. Reduced means better cellular health and oxidized means more cellular inflammation. The act of cellular reduction happens in autophagy during sleep with repair processes. Remember VIP is highest in the morning and this helps it elevate cortisol to wake us up. This is also why cortisol levels are highest when we start our days and lowest in the night when we sleep.

[guoposts524-blog]

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[operagheist-blog]

APOLLO’S LYRE. haha let’s talk about what the heck is physiologically or psychologically / neurologically wrong with erik, because i have a heckton of theories. PSYCHOLOGICAL CATEGORIES HERE.

ok first off, this shit all went down in the 1800s, so there was a lack of knowledge of modern medicine because it’s MODERN MEDICINE; i just want to clear that up, first. i’ll address shit in sections as follows: PHYSIOLOGICAL ISSUES, facial deformity & plausible causes. possible co-morbid illnesses or symptoms due to plausible causes of deformity. physiological capabilities & deficiencies / finding logical & plausible things in this category. effects of morphine on the human body, withdrawal symptoms, plausible causes of death via physiological complications compounded with addiction. part 2 will address PSYCHOLOGICAL / NEUROLOGICAL ISSUES, a brief overview of learning & memory. classical conditioning overview & its importance to erik’s aversion to touch initiated by another. operant conditioning overview & its importance to erik’s decision making process. stimulus / response / outcome generalization vs. discrimination of external / environmental cues, how his actions & thought processes have been affected in this manner. an overview of personality psychopathology & displayed symptoms / plausible diagnoses ft. the DSM V. emotional instability theories. opiates, endogenous opioids ( endorphins ), brief overview dopamine’s effect on biochemistry of the brain, brief clinical overview of dopamine in relativity to schizophrenic traits. morphine’s effect on brain chemistry overview + withdrawal effects on the mind. WITHOUT FURTHER ADO: 

PHYSIOLOGICAL CATEGORIES 

THE FACIAL DEFORMITY + CONCLUSIVE CAUSE FOR THIS SPECIFIC PORTRAYAL. 

i’m going to start this with LEAD POISONING while erik’s mom was pregnant because uh yeah.          lead is a hazardous substance that should be avoided at all times. it is particularly important         to avoid when pregnant as it is passed freely from mother to child via the placenta. the primary         sources of lead exposure are contaminated soil, lead-based paint & occupational exposure.         the risk of lead exposure also arises from the handling of crystal, ceramics, scented candle wicks,         plastic handle grips & arts & crafts materials also contain lead. even drinking water         can be contaminated from leaded pipes. some birth defects that can be caused by         lead exposure during pregnancy include* ( with bolded things applicable ) skin tags         & other skin markings / undescended testicles in males / shortened gestation /         premature delivery / low birth weight / premature rupture of fetal membranes (PROM) /         spontaneous abortion / miscarriage / neurological damage / developmental delays [ source ] it’s the 1800s, did they even kNOW about the hazards of lead? lead pipes were a thing, i’m fairly certain, if it could be in the soil, that could impact things. lead paint was an issue when my parents were buying a new house when i was little ( i’m 23 ), people still check for lead paint. with all of that, this is honestly one of the main things i’ll be including as a cause for the visible deformity. 

the second cause that i’ll incorporate is MERCURY POISONING during his mother’s pregnancy, however, this is less of the cause, but sure as heck didn’t help.          knowledge about the extreme vulnerability of the fetus to methylmercury began with         the minamata bay, japan experience [...] a chemical company released mercury into         minamata bay & polluted the bay heavily [...] the released mercury was methylated         in the aquatic food chain leading to high levels of mercury in fish [...] the local population         consumed high amounts of the fish. eating the fish, pregnant mothers did not only         burden themselves, but methylmercury was transferred in utero to the fetus.         this caused severe neurological complex symptoms & severe birth defects. while the mothers         were usually without symptoms of mercury poisoning, their babies were born severely         damaged with microcephaly, cerebral palsy, severe mental retardation, seizure disorders,         blindness, deafness, & other malformations. depending on the dose & timing of exposure         during gestation, the effects may be severe and immediately obvious, or subtle & delayed,          the newest findings from long-term cohort studies suggest that the cardiovascular system         is also at risk—with increased incidence of high blood pressure & decreased heart rate         variability as methylmercury exposure increases. the full expression of these health effects         of methylmercury can be delayed & deficits are often irreversible. [ source ] THE MOTHERS USUALLY WERE WITHOUT SYMPTOMS, so if mother dearest isn’t displaying anything of the sort, how could anyone know about what the heck could go wrong in the pregnancy? 

MIND YOU, i’ve seen a lot of the whole erik fretting about it being genetic; that’s completely understandable even if it isn’t a possibility ( or if the possibility is slim af ), because I REALLY DOUBT ERIK KNEW ABOUT THE EFFECTS OF THIS, EITHER, SINCE I’M PRETTY SURE IT WASN’T STUDIED ( see: mad hatters were called as such because they made their hats shiny with MERCURY ).

CO-MORBIDITY FACTORING IN HEADCANONED CONCLUSION + IMPACT ON PHYSIOLOGY, DEFICIENCIES IN SOME AREAS & THINGS THAT PROBABLY AREN’T AFFECTED AT ALL.

mmmm ok so uh even in leroux’s canon, erik still is quite capable of physical activity, despite other issues, kay’s erik has more notable health complications, because morphine. stage & 04 movie erik? do you know how much physical capability it takes to do whatever the fuck he must be doing when he’s doing basically probably the equivalent of stage rafter parkour, also here is a pbs thing on how hard it actually is to break someone’s neck. tldr, that shit isn’t easy, so the co-morbid effects likely aren’t fucking up with his muscular system in a way that would impair activity. something that likely has been affected is his nervous system, particularly sensory neurons. erik is in pain, that’s why he’s taking morphine. the issue might not be the muscular system, but then there’s the question of pain tolerance without morphine. now, being in pain does not mean that he’ll react in a way that would show that he’s in physical pain — likely, this is something he’s learned to suppress ( the reaction to physical pain ). tldr; he dodged muscular system issues from the lead / mercury combo what a miracle, but his nervous system might’ve taken a hit. 

MORPHINE EFFECTS + WITHDRAWAL + A REALLY HALFASSED PLAUSIBLE PHYSIOLOGICAL DEATH 

morphine is a painkiller that acts upon the central nervous system, morphine may be used in medical situations such as: painkilling  — morphine is used primarily to treat both acute & chronic severe pain. it is also used for pain due to myocardial infarction and for labor pains [...] concerns exist that morphine may increase mortality in the setting of non ST elevation myocardial infarction. morphine has also traditionally been used in the treatment of acute pulmonary edema [...] shortness of breath — immediate-release morphine is beneficial in reducing the symptom of shortness of breath due to both cancer and noncancer causes. in the setting of breathlessness at rest or on minimal exertion from conditions such as advanced cancer or end-stage cardiorespiratory diseases, regular, low-dose sustained-release morphine significantly reduces breathlessness safely, with its benefits maintained over time. opioid use disorder — morphine is also available as a slow-release formulation for opiate substitution therapy (OST) in austria, bulgaria, & slovenia, for addicts who cannot tolerate either methadone or buprenorphine ( but, this is modern, so ignore this ). [ source ] 

here are some signs & symptoms or morphine abuse, relevant things are bolded: symptoms that a person may have taken too much morphine. shallow breathing - it may feel like the person’s chest is barely moving and there may be few breaths each minute / feeling faint or dizzy / confusion / low blood pressure, especially when a person is also taking other medications that cause a drop in blood pressure / constricted pupils / loss of normal muscle tension / cardiac arrest / cold & clammy skin / circulatory collapse  / coma. LET’S GO REFER TO KAY’S CANON, which is where the morphine addiction really comes into play — erik has a slew of problems from that & i’ll bet he dies due to cardiac arrest. i think he’s also been noted to be colder to the touch but i’m not absolutely sure. basically these things are signs of overdose. here are some withdrawal symptoms, relevant things still bolded , italics are plausible: ( a person using morphine according to a doctor’s instruction can still become addicted to the drug, sometimes in as little as a few weeks. if a person tries to discontinue use, they will manifest some or all of these signs of withdrawal that are common to opiates: sweating / chills / tearing eyes / runny nose / restlessness / muscle aches / backache / dilated pupils / irritability / trouble sleeping / high blood pressure / rapid heart rate / vomiting / diarrhea / stomach cramps. SO UH, yeah. erik’s fucked [ source ].

OK HERE’S THE DEATH ANGST PART I AM SO SORRY. again, for my sanity & continuity, i write during plot erik between the ages of 35 & 39. factoring in travels & or circus show things & the incorporated architect’s apprentice part, the circus would be the early childhood years through at most his early teen years. his apprenticeship likely covers from his mid teen years to his early to mid twenties. the persia experience then would be his mid twenties to at most thirty, because shit went down & he had to flee. that leaves between 5 & 9 years of being the opera ghost. most likely, he’s closer to 39, especially since christine is supposed to be like 16 during the main plot & she arrives when she was 7 (?). note, erik likely fell in love with her more due to the fact that he somewhat got to know her; she probably confided in her angel of music about various things. the less innocent nature of the attraction probably wasn’t a thing until she was at least 13 or 14, giving him him 6 or 7 years to get to know her, assuming he’s 39 ( which gives 9 years of getting 30,000 francs a month or some shit + opera ghost-ing etc. ). i previously wrote about the life expectancy when erik was born, which was in the thirties at birth & if the child lived past ten, reached the fifties. i also noted that the life expectancy in 1910 when leroux published the novel was on average 51. now, let’s go back to when erik would’ve even had access to opiates, which i’m going to assume was persia. let’s say he arrives in persia at the age of 26 & works for the shah until shit goes down when he’s 30. & has access to opiates somewhere in that range of time ( quite possibly very soon after he arrived ).          opium is said to have been used for recreational purposes from the 14th century onwards in          muslim societies. ottoman & european testimonies confirm that from the 16th to the 19th          centuries anatolian opium was eaten in constantinople as much as it was exported to europe          [...] turkey supplied the west with opium long before china & india [...] extensive textual & pictorial          sources also show that poppy cultivation & opium consumption were widespread in safavid iran           & mughal india. even today, iran ( persia ) has very easy access to opium, where it is less          expensive than beer [ source ]. ok ok so, i’ll give him the benefit of the doubt, but even if the addiction began at the end of his time in persia, & a person can end up addicted in as little as a few weeks, that’s still 10 or so years of addiction. so, factoring in withdrawal ( say, he somehow doesn’t have access to it, imports to europe don’t line up etc ) or the possibility of overdose, it’s unlikely that erik would live past his mid forties & this is disregarding psychological factors. 

[healthstoresnow-blog]

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