Time to get technical on your ass…

Evening Gorgeous xx

How are you all doing? You OK? Good, good.

** This article needs editing, but it’s 4am and I can’t be bothered – another day **

Right. I seem to be laying things out a lot straighter than I used to, then going off on a mission explaining myself. It something I’m good at and it’s not a personality trait I intend to lose and I quite like it. This post is no different; but this post comes as a surprise, to me at least. The back story, is I was writing another post; regarding something completely different – I’ll post it after this one but this one is to be pinned. This one is important.

So I’ll go back to the beginning; way back. I was 4 years old. I was struck ill with what I was told for a long time was Epilepsy and it was treated as that. Being different anyway, I was taunted and cursed by my peers for it. For years it was a curse over me. It’s one of the two reasons I was raped – Their taunts of ‘Eppy’ and ‘He’s Gay’ pretty much prove it. But I’m not Gay and I’m not Epileptic – At the time I didn’t know what I was. This produced a great deal of depression; which persists to this day – Even now I still take Fluoxetine at 40mg daily, Depression is a killer if not managed correctly.

It took me many years to come to terms with all that, however. The final trigger being me taking drugs for several years in the early 2000’s. One single event stands out from that though. An event where I popped a pill at well known Dance Festival (Creamfields in 2001 to be precise), and everything changed. The ‘Deja-Vu’ as I’ve become accustomed to calling it began in earnest. Now I’ve written about my Deja-Vu, in a previous post, and been unable to explain the phenomenon clearly; but we will come back to it shortly. I want to move on for a reason. In 2004 I came off drugs, realised I was raped, sorted out what I could and started to move on with my life. Great. Moved to Cambridge, had a son, all seemed OK – Not. Behind the scenes something was wrong and I’ve spent the last two years trying to work out what.

I split with my son’s mum in 2016 after a troubled end to a good relationship, not without its faults mind; but it was a good time in my life. I love my son very much and I miss him dearly – I’ll see him again soon. The split, however, lead me down a path that resulted in a diagnosis of Autism Spectrum Disorder, specifically Asperger Syndrome (AS) in September of that year.

This set off a chain of events which I have written about in previous posts and I’ll not recount. The result of those events, ultimately, is this blog. This has all been born out of my diagnosis of Gender Dysphoria in 2017, the resultant transition in the December and all the changes which have happened since. I’ve talked a lot about those changes as well and won’t repeat them here either.

In amongst all of that, I’ve had a fascination with brain function; especially my own. I’ve been looking for a connection that links everything together, as I’ve always believed these events and symptoms are related in some way – They all happen to me, lets be honest. So, in that case, what’s wrong with me? Why is my brain different? Why doesn’t it work in the same way as everybody else? Well I think I’ve got a reason for that – Something I never knew about before know that appears to connect everything together.

Meet the NMDAR, or N-Methyl-D-Aspartate Receptor – I said this was technical, didn’t I?

OK, so lets get started. NMDA is an Amino Acid derivative that is very similar to Glutamate, the brains primary excitatory neurotransmitter. NMDA was developed by pharmacologists in order to activate and identify a particular subtype of neurotransmitters in the brain, ideally those involved in synaptic plasticity and memory function of the cell, or basically 1/3 of what makes it tick (No I’m not going into detail).

What’s this got to do with me? OK, well; lets start with the fact that a cell receptor is activated by two different types of drug: The cell receptor Agonist and the Antagonist. The Agonist binds to a cell receptor and fully activates that receptor; thereby allowing it to work. The Antagonist also binds to the receptor but does not activate it, and can block the action of other Agonists – stopping the receptor from working. Reference this to the NMDA Receptor and we have two lists of drugs NMDA Agonists and NMDA Antagonists. This is very simplified and the science is much more detailed and complex, much beyond the scope of what I’m talking about.

We need to know the above to understand the lightbulb moment that happened when I read this blog post: Depersonalization in gender dysphoria: widespread and widely unrecognized. Why a lightbulb moment? Well, this paragraph in particular gripped me:

Speaking personally, I noticed the lifting of depersonalization symptoms within one to two weeks after beginning HRT, and this was something that I had simply never felt before – neither during previous transition milestones such as coming out and presenting as a woman full-time, nor at any other point. Nothing has ever come close before or since. The difference felt almost undeniably chemical; merely being excited about major events in my life had never caused such a noticeable and unexpected change. Scott at Slate Star Codex has also noted that estrogen can act on NMDA receptors, which are implicated in dissociative symptoms broadly, although the potential role of such a mechanism in gender dysphoria is highly speculative.

Note the highlighted words regarding NMDA receptors and you’re onto my thinking – Yeah, it’s tentative but there’s more. Off I went and followed the link and started reading about NMDA receptors and such and I found this paragraph:

Drugs that block NMDA receptors cause dissociation. The most famous dissociative anaesthetic, ketamine, is an NMDA antagonist. So is DXM, a recreational drug that causes dissociation in abusers. Wikipedia’s list of dissociative drugs is basically just fifty-five NMDA antagonists in a row. The only other category they list are kappa opioid agonists, and kappa opioid agonism probably – you guessed it – antagonize NMDA. If we take this result seriously, every substance we know of that causes dissociation is an NMDA antagonist in some way.

You dig me? Creamfields 2001 came into my head straight away – what else was in that E? That’s when the Deja-Vu started, interesting. We’re onto something here, more reading methinks… OK, read more information on disassociation and I started hitting words that I recognised; the likes of depersonalisation, derealisation and dysphoria. Hang on a second, what? Gender Dysphoria – Are you sure this link is speculative? Makes sense to me.

What tends to be the norm; is that NMDA Antagonists, at sub-anaesthetic doses cause the symptoms described above. The most famous NMDA Antagonist is Ketamine, a horse tranquiliser which is also known as the recreational drug ‘Special K’. Yeah OK, and? Well any drug worker will tell you that the most common mix of Ketamine is with Ecstacy, or E. See above.

Have I just explained my Deja-Vu, did it all come about after taking that tablet? Is it a symptom of Dysphoria? Well, possibly but there’s a problem. It should have subsided within a short space of time (maximum of two years, more likely six months). Oops, in the main it did; but mine carried on and still persists albeit VERY occasionally to this day.

So why did mine carry on? Did I miss something? Well yeah, I did. If you google NMDA, you’l come across the Wiki page for the NMDA Receptor (currently it lists just below the questions). Open up and read the page all the way down and you’ll hit this paragraph:

Cochlear NMDARs are the target of intense research to find pharmacological solutions to treat tinnitus. NMDARs are associated with a rare autoimmune disease, anti-NMDA receptor encephalitis, that usually occurs due to cross-reactivity of antibodies produced by the immune system against ectopic brain tissues, such as those found in teratoma. These are known as anti-glutamate receptor antibodies.

Hello! They told me it was Encephalitis and not Epilepsy in 2005! Are we going through another tenuous link of mine? Of course we are. But are you going to tell me there’s not something in this? Remember, it was 1976 when I had mine, and they didn’t have the technology they have today. Think.

I’m not done yet though, there’s one thing I’ve left out. And when you add it in, it all makes sense. Can you guess what it is? I’ve written about it before. Any Ideas?

Autism. Your awake then 🙂

Specifically the link between Trans Identity and Autism. Did I tell you I have Asperger Syndrome? I’m sure I did. Well, look; lets go back to that article on Slate Star Codex. You see, either I’m nuts or this article (and it’s counterparts) are answering a lot of questions. Right? OK, bear with me and go back to that article; the link is here if you missed it:

Why are Transgender People immune to optical illusions?

Oh, by the way, yes I was and in a way still am; immune to most optical illusions. It’s a problem that’s bugged me my whole life – Although I’ve noticed that it’s A LOT harder recently to see past them 🙂 Ask anyone who knows me… Right, off we go to part III of that article and we’ll do some more reading.

Read it yet? Because here’s the lightbulb moment for me:

So I wonder: is NMDA hypofunction related to transgender? That would explain the autism and schizophrenia connections. It would explain the hollow mask numbers. It would explain the dissociation. It would explain why estrogen helps the dissociation. And it would explain a lot of internal connections between all of these different conditions and factors.

And it explains the Encephalitis, fuck. It also gives an explanation to why my brother has been diagnosed with Schizophrenia after chronic, long-term Cannabis use. Could this be a genetic predisposition to NMDA Dysfunction? Who knows, but I’m off to have a chat with my GP!

Much Love,

 

Vikki xx


 

P.S. – For the sceptics:

Read section IV of the same article.

Thank you xx

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