Hello my friends! I hope your Sunday is going well.
If my posts going forward for the next month or so seem a little less fun and conversational than usual please forgive me.
I’m going to bear down to fundamental efficient essentiality.
Before we get lost in the weeds of my Moonshot Project I want to emphasize something really quickly.
I’ll try to say this as succinctly as possible since I’ve already built a Major Depression Protocol and I’m going to communicate it properly, refine it, and show you guys the scientific evidence in the coming year: combine bright light therapy + ssri + Cognitive Behavioral Therapy + bibliotherapy (Burns’ Feeling Good) + my Day Frame. I’ve linked Burn’s Feeling Good here. https://www.lostfalco.com/books/ My Day Frame is at the end of this post and Satchin Panda’s work on Circadian Biology is also linked on my books page. https://www.lostfalco.com/books/
Doing all of these in combination will massively increase your probability of beating Major Depressive Disorder.
The three key historical, evidence-based cornerstones (therapy + ssri + bibliotherapy) will be WAY more effective when the realities of bright light therapy and Circadian Biology are accounted for.
This has already been shown in dozens of studies.
I’ll show you guys the evidence soon and also give you guys a temporal ordering to follow.
For example, start with Bright Light Therapy, do for one week, if symptoms abate then keep that as stand alone treatment, if BLT alone is ineffecitve, then add SSRI to Bright Light Therapy for 3 weeks, etc.
There are also other things you can simultaneously.
For example, do 30 min of bright light therapy while simultaneously reading Burns, THEN go for a 30 minute walk (exercise helps depression as pretty much everyone knows) while SIMULTANEOUSLY listening to Burns on audio book, etc, etc.
We can also combine this with Spaced Generation Learning to enhance the learning process and long term retention of concepts for patients studying Burns.
This will greatly enhance long term remission as they can continue to review Anki flashcard indefinitely on a spaced repetition schedule.
For example, instead of just reading Burns while doing bright light therapy you could 1. Read Burns AND create Anki flashcards WHILE doing Bright Light Therapy on MONDAY then, 2. Study those Anki flashcards WHILE doing Bright Light Therapy on TUESDAY, etc.
You guys get the idea.
It’s all about what you do EVERY day and the optimal ordering of the things you do each day.
If you can do things simultaneously with very low risk, then do them! (ie. bright light therapy and bibliotherapy have very few risks/side effects)
Time is our ally.
I’m going to take advantage of temporal concepts such First, Next, Eventually, Always, Until, etc. to refine and modify the protocol until it helps the most people we can possibly help.
I’m using Linear Temporal Logic to model these ideas and make sure my protocols take into account cardinality, ordinality, etc. in order to be as exact, concrete, and precise as possible.
https://en.wikipedia…_temporal_logic
There are also a lot of ‘IF-else’s’ in there so I may use computational tree logic to model various scenarios for various people but I also want to keep it simple so, we’ll see. https://en.wikipedia.org/wiki/CTL*
Clearly though, there are going to be things that just about ALL people should do ALWAYS…for example go to bed at the same time, wake up at the same time, eat at the same time, etc.
Temporal Logic concepts will allow us to tease out the ALWAYS from the conditional and design a protocol that helps the greatest number of people possible.
Wholistic, temporally ordered therapies like this have the best chance of long term success imo.
That’s coming in the next few months.
I’ll do my best to communicate that with the world as soon as I can.
Right now, I need to enhance myself so I can be the greatest force of good possible in the coming years.
So, that brings us to my Moonshot Project.
This post is getting kind of long so I’m going to just briefly mention the other core substance in my Moonshot Menagerie…MDMA.
I’ll talk more about it later but before you freak out, read the studies below in their entirety.
MDMA is currently expected to be approved for treatment in 2023.
My purpose for including MDMA is extreme, rapid synaptogenesis. (See study below)
My primary goal is to gain conscious access to the most fundamental parts of my neural architecture (whole brain efficiency and connectivity) AND to increase connectivity and efficiency in the FPN especially (frontoparietal network). (See study in my previous post).
The MDMA is going to give me massive connectivity AND the bright light is going to make that connectivity as efficient as possible.
The frontoparietal network includes areas and aptitudes typically included in IQ measurements (ie. sustained attention, complex problem-solving, working memory, etc.) and increased efficiency and connectivity between nodes in this network has the potential to increase IQ.
So, I’m going to be strengthening the connections within single networks and then I’m going to be strengthening connections from network to network.
In copying the studies I’m currently leaning towards 3 doses spread out 3 weeks apart with 100mg MDMA taken first followed by 50mg MDMA taken 2 hours later for a total of 8 hours per session and 3 total sessions.
I’m tentatively setting my dates for Dec 25th, Jan 14th, and Feb 4th.
I’ll do 8 hours each moonshot day, study my Anki flashcards the whole session if I’m able, and post here periodically (maybe every 15 minutes or half hour) while I’m dosing.
I’ll keep you guys updated as I do more research.
All things are currently flexible and open to change.
There are so many more substances I’m thinking about adding.
Bottom line though is that I’ll keep doing bright light therapy during the moonshot sessions and between the moonshot sessions since the whole brain network effects were shown after 4 weeks of daily bright light therapy in the study I linked in my last post.
This pretty much perfectly aligns with the 6 week, 3 dose plan of MDMA.
Beautiful.
Ok, gotta run. So much more to share in the coming days!
btw, If I get shut down on Longecity in the future you guys know my website address (see links below). I’ll just start posting everything over there. Peace!
3,4-Methylenedioxymethamphetamine (MDMA)-Assisted Therapy in Hawaii: A Brief Review
Abstract
The Food and Drug Administration (FDA) granted breakthrough therapy status to 3,4-methylenedioxymethamphetamine-assisted therapy (MDMA-AT) in 2017 due to preliminary evidence supporting its efficacy and safety in treating post-traumatic stress disorder (PTSD). A series of six phase-II clinical trials studying MDMA-AT for treatment-resistant PTSD found that 54% of MDMA-AT full-dose participants no longer met the diagnosis of PTSD after two MDMA sessions, compared to 23% in the control group. In the first phase-III clinical trial, 67% no longer met the criteria for PTSD after three sessions. The effects are durable, with 67% no longer diagnosable after one year and 74% at nearly four years. The MDMA-AT is being fast-tracked for potential FDA approval by 2023. In 2021, Hawaii’s Senate Bill 738 unsuccessfully proposed that psilocybin be removed from the Schedule I controlled substances list due to its clinical efficacy for major depressive disorder. Methylenedioxymethamphetamine is also a Schedule I controlled substance and has proven to be a treatment option that could potentially benefit the people of Hawaii.
https://www.scienced…211124718307551Psychedelics Promote Structural and Functional Neural Plasticity
Highlights
•Serotonergic psychedelics increase neuritogenesis, spinogenesis, and synaptogenesis
•Psychedelics promote plasticity via an evolutionarily conserved mechanism
•TrkB, mTOR, and 5-HT2A signaling underlie psychedelic-induced plasticity
•Noribogaine, but not ibogaine, is capable of promoting structural neural plasticity
Summary
Atrophy of neurons in the prefrontal cortex (PFC) plays a key role in the pathophysiology of depression and related disorders. The ability to promote both structural and functional plasticity in the PFC has been hypothesized to underlie the fast-acting antidepressant properties of the dissociative anesthetic ketamine. Here, we report that, like ketamine, serotonergic psychedelics are capable of robustly increasing neuritogenesis and/or spinogenesis both in vitro and in vivo. These changes in neuronal structure are accompanied by increased synapse number and function, as measured by fluorescence microscopy and electrophysiology. The structural changes induced by psychedelics appear to result from stimulation of the TrkB, mTOR, and 5-HT2A signaling pathways and could possibly explain the clinical effectiveness of these compounds. Our results underscore the therapeutic potential of psychedelics and, importantly, identify several lead scaffolds for medicinal chemistry efforts focused on developing plasticity-promoting compounds as safe, effective, and fast-acting treatments for depression and related disorders.
Towards an understanding of psychedelic-induced neuroplasticity
Abstract
Classic psychedelics, such as LSD, psilocybin, and the DMT-containing beverage ayahuasca, show some potential to treat depression, anxiety, and addiction. Importantly, clinical improvements can last for months or years after treatment. It has been theorized that these long-term improvements arise because psychedelics rapidly and lastingly stimulate neuroplasticity. The focus of this review is on answering specific questions about the effects of psychedelics on neuroplasticity. Firstly, we review the evidence that psychedelics promote neuroplasticity and examine the cellular and molecular mechanisms behind the effects of different psychedelics on different aspects of neuroplasticity, including dendritogenesis, synaptogenesis, neurogenesis, and expression of plasticity-related genes (e.g., brain-derived neurotrophic factor and immediate early genes). We then examine where in the brain psychedelics promote neuroplasticity, particularly discussing the prefrontal cortex and hippocampus. We also examine what doses are required to produce this effect (e.g., hallucinogenic doses vs. “microdoses”), and how long purported changes in neuroplasticity last. Finally, we discuss the likely consequences of psychedelics’ effects on neuroplasticity for both patients and healthy people, and we identify important research questions that would further scientific understanding of psychedelics’ effects on neuroplasticity and its potential clinical applications.
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