142 replies to this topic

[jack black]

• Inositol => NDMA antagonist,

 

are you sure? this is news to me. inositol (6g dose) personally feels like serotonin boost to me.

[gamesguru]

Yeah, I'm hanging a question mark on the potency of its NMDA activity. For something else, look into Ferulic acid

[farware]

 

• Inositol => NDMA antagonist,

 

are you sure? this is news to me. inositol (6g dose) personally feels like serotonin boost to me.

 

 

I copied that over incorrectly. It should read 

 

Inositol => 5ht2a antagonist

 

5ht2a lowers glutamate release and is generally anti-autistic, anti-OCD

 

Not sure on NDMA activity, need to double check that

[farware]

I am currently researching the effects of memantine and ability to induce psychosis: 

 

Memantine is a weak, voltage-dependent, NMDA receptor antagonist that will not result in profound changes in brain glutamate levels that are theorized to cause psychosis. I would argue no, long term administration will not cause psychosis. Magnesium is also a weak NMDA receptor antagonist and long term use typically promotes brain health and does not cause psychosis.

 

 

http://www.longecity...nist-psychosis/

 

All of the amphetamines can damage the dopamine receptors long-term. If they do that longterm, I have no interest in using them shortterm either even if I could get a relief from it. Its just not how I work. I'd rather have something that works on the root causes and that is the glutamate receptor and dopamine only indirectly. 

 

Memantine seems beneficial in both SCT and ASD, lowering excess glutamate which may be beneficial in both since the hypofunctioning receptor may be trying to compensate with excess glutamate release according to one theory which makes the most sense. 

 

 

Edited by farware, 12 July 2016 - 01:18 AM.

[farware]

Also of note: 

 

In this early POC study, GLYX-13 reduced depressive symptoms within 2 hours and this effect was maintained for 7 days on average in subjects with MDD who had not responded to another antidepressant agent during the current depressive episode. The findings of this study support the hypothesis that modulation of the NMDA receptor is a valid target for the development of antidepressant drugs and the need for additional studies to further evaluate the effects of GLYX-13.

 

http://www.ncbi.nlm....pubmed/25782764

 

Looks my initial theory that modulating NMDA receptors for depression and possibly autism is the best way to go is getting more support from different studies - this one is from (2015)

 

 

[farware]

Memantine also seems to act on the dopaminergic system, mostly D2: 

 

 These data demonstrate enhanced dopamine release and metabolism after memantine treatment and support the assumption of an interaction between noncompetitive NMDA-receptor antagonists and dopaminergic systems.

 

http://www.ncbi.nlm..../pubmed/7813574

 

(1994)

 

But more importantly:

 

 In contrast, studies in our laboratory have shown that the adamantane derivative, memantine, preferentially blocks excessive NMDA receptor activity without disrupting normal activity. Memantine does this through its action as an uncompetitive, low-affinity, open-channel blocker; it enters the receptor-associated ion channel preferentially when it is excessively open, and, most importantly, its off-rate is relatively fast so that it does not substantially accumulate in the channel to interfere with normal synaptic transmission

http://www.ncbi.nlm....pubmed/15974913

 

Uncompetitive is the keyword here. It also seems to move in and out quickly so does not disrupt normal flow. 

 

So this could be the best of two worlds: Dopa + Glutamate modulation? Research continues .. 

 

 

Edit: Finding lots of problematic reports e.g. https://www.reddit.c...st_withdrawal/ 

 

Its reddit and anecdotal but still noteworthy. 

 

I think Tianeptine is probably the safest option for now. Other than that I'll look more into the Russian side especially pyritinol which seems to complement my stack 

Edited by farware, 12 July 2016 - 01:50 AM.

[jack black]

 

I copied that over incorrectly. It should read 

 

Inositol => 5ht2a antagonist

 

5ht2a lowers glutamate release and is generally anti-autistic, anti-OCD

 

Not sure on NDMA activity, need to double check that

 

 

Interesting info on that 5HT2a antagonism. I was always curious how inositol worked.

This confirms it and some more: https://selfhacked.c...blems-and-cirs/

 

They also mention 5HT2a increases glutamate release, but I see nothing on the NMDA connection (this is what you meant, right?).

 

The information about 5HT2a made me finally undestand how SSRI or similar antidepressants work. They work by flooding brain in serotonin, so the 5HT2a receptors are eventually downregulated. This is why people feel (much) worse before they feel better. But the big picture is decreased 5HT2a signaling increases BDNF. I feel strongly that BDNF is the main thing in depression and suicide.

 

Looks like serotonin is not the happy neurotransmitter like the masses belive (I used to belive too, LOL).

Edited by jack black, 12 July 2016 - 02:53 AM.

[farware]

 

 

I copied that over incorrectly. It should read 

 

Inositol => 5ht2a antagonist

 

5ht2a lowers glutamate release and is generally anti-autistic, anti-OCD

 

Not sure on NDMA activity, need to double check that

 

 

interesting info on that 5HT2a antagonism. I was always curious how inositol worked.

This confirms it and some more: https://selfhacked.c...blems-and-cirs/

 

They also mention the glutamate release, but I see nothing on the NMDA connection (this is what you meant, right?).

 

 

Yes but 5ht2a blockers are not necessarily NMDA antagonists I suppose although they might target it indirectly? Not exactly sure, need to look that up. Tianeptine definitely affects NMDA receptors 

 

According to this study 5ht2a agonists can prevent NMDA antagonist neurotoxicity: 

http://www.ncbi.nlm..../pubmed/9408919

 

This could mean that a 5ht2a antagonist could theoretically contribute to inducing psychosis in combination with NMDA antagonists - so its probably good to be careful with either one and much safer to look for modulators. Memantine looks a lot safer than the stims although I would probably not be willing to try that unless I had a proper diagnosis and maybe not even then since a misdiagnosis is likely due to the overlap of symptoms

 

For now I am doing very well on 5ht2a antagonists and glutamate modulators so why rush to the extremes? Never touch a running system

 

 

Edited by farware, 12 July 2016 - 02:44 AM.

[jack black]

 

For now I am doing very well on 5ht2a antagonists and glutamate modulators so why rush to the extremes? Never touch a running system

 

 

which ones are you taking besides inositol?

my concern is long term antagonism will increase the # of 5HT2a receptors (making the condition worse), just like long term stimulation decreases the #s.

i remember reading a human study showing inositol helping depression symptoms short term but not long term.
 

[farware]

 

 

For now I am doing very well on 5ht2a antagonists and glutamate modulators so why rush to the extremes? Never touch a running system

 

 

which ones are you taking besides inositol?

my concern is long term antagonism will increase the # of 5HT2a receptors (making the condition worse), just like long term stimulation decreases the #s.

i remember reading a human study showing inositol helping depression symptoms short term but not long term.
 

 

 

I take very low doses to avoid such problems. Right now taking only 1g Inositol per day at most. Thats insignificant but really helps me. 

 

What is really helping me the most these days is a combination of daily Folate, physical activity and PEA from raw cacao. This combo seems to increase the blood flow to the brain which coincidentally is also what the Russians focus on. On top of that a combo mix of VitD3 +VitK2 + Calcium (best to take it in the evening). For my depression the best is Tianeptine. Tianeptine is giving me a sort of weird feeling the day after for several hours and insomnia is still an issue but as soon as I counter it with Folate and p.activity I feel much better than before with almost no depressive feelings and this effect lasts for several days. It also helps getting outside more, absorb more sunlight. 

 

http://www.ncbi.nlm....les/PMC3130317/

 

Right now at a good place with this and lots of energy. I still get tired but it doesnt last as long. 

[jack black]

 

 

 

 

 

Regarding how to figure out which vntr you have... damn hard! I just assumed I had a long variant, since I have one which implies increased susceptibility to novelty seeking - and that was supposed to be the vntr-7 and upwards. The way I've understood it until now, the 7 number is a measure of the tail end of the molecular composition of this gene, apparently the longer this number is, the more faulty your receptor will become, because the longer compositions are apparently repeats in the molecular structure, which are pointless to function, and actually makes for less correctly formed D4-receptors - it's a bunch of extra junk, and it just gets in the way.

 

This website supposedly let's you use your raw data to check this stuff right in your Firefox-browser...

 

http://www.eupedia.c...raits_snp.shtml

 

Buut... I just realized that SNP's are not the same as VNTR's, so I'm guessing you CAN'T actually see this, with your 23andme.com data! >_<

 

Apparently Familytree-DNA does do VNTR-testing, but they don't give you any interpretation, so you'd have to either plug their test-data into another service, or do some deep digging in it.

 

http://forums.family...ead.php?t=30469

 

I apologize to everyone I have misled by mentioning 23andme and getting VNTR-data... it was a GRAVE mistake. My word... I feel awful!

 

 

Actually I think there is a way to aproximate MAO fuction by a few 23andMe SNPs. The info is here:

https://selfhacked.c...e-warrior-gene/

 

But I find it confusing (in my case the info from Rs909525 conflicts with Rs6323). If you figure it out please let me know.
 

I also find rs6609257 interesting: http://www.ncbi.nlm....cles/PMC3309555

[farware]

Ok, so I'm closing in on a diagnosis. As mentioned before ASD was previously classified a subset of Schizophrenia - I still believe that. I also further assume that both autism and schizophrenia are in fact autoimmune diseases and are simply poorly understood. It's very apparent that the vast majority of cases includes gut dysbiosis and thyroid disorders. The body is attacking itself and reacts with gut and brain inflammation. This can lead to hypo or hyperglutamate receptors which in turn can either cause hallucinations, anti-social behavior, etc ... of course that is a very simplified approach and its a lot more complex but that are the links I find most plausible right now. 

 

Sources that I find highly relevant today are studies from 2002: 

 

Autism, an extreme challenge to integrative medicine. Part: 1: The knowledge base.

http://www.ncbi.nlm....pubmed/12197782

 

Is autism an autoimmune disease? 

http://www.ncbi.nlm....pubmed/15546805

 

Autism, an extreme challenge to integrative medicine. Part 2: medical management.

http://www.ncbi.nlm....pubmed/12495373

 

 

 

The supplements that help me the most are P5P, Probiotics, PEA, Folate, B2, NADH, NAC .. to support proper methylation and detoxification 

 

Its very apparent detox pathways are implicated and are not working as intended so NAC is critical. Many NAC supplements include Selen which is good too, especially for thyroid disorders. The recommended intake of P5P is 100-200mg. 

 

What Im currently researching is how Tianeptine can help with ASD symptoms. I do not understand why it works so well. It shouldnt:  

 

 Intestinal hyperpermeability manifests in autistic children as dysbiosis, food intolerances, and exorphin (opioid) intoxication http://www.ncbi.nlm....pubmed/20628438

 

 

Also dont yet understand exorphin, endorphin relations. Makes no sense to me right now so I have to do more research on that. If anyone could chime in here on how Tianeptine actually works as a mu-opioid agonist that would be great e.g. how can it be beneficial / harmful?  

 

I am also researching the effects of NADH. NADH is believed to be a cure for celiac. If that is the case, it could explain why it is also beneficial in many Schizophrenics. IN the 60's Abraham Hoffer did studies megadosing B3 with great results. For some reason they were never reproduced. I believe he was on to something and big pharma shut him down as they still do. Its not just a conspiracy theory. There are real shills and people that falsify studies for their own agenda. It's real and we have to deal with it. Hopefully when research gets published on blockchains they can no longer manipulate data so easily. 

 

Anyway, here's what I am reading right now again: 

The opioid effects of gluten exorphins: asymptomatic celiac disease

https://jhpn.biomedc...1043-015-0032-y

 

Threads on longecity:

http://www.longecity...uten-allergies/

 

 

If you read carefully, you will see that there really is a potential case for people who have illnesses like fibromyalgia, ADHD, and asperger's to have an ongoing problem with trying to live a life that is gluten and dairy free, because of how devastatingly addictive the opioid compounds are to those with compromised digestive systems, i.e. leaky gut syndrome. 

This means, that without some sort of substitution to make up for the damage done by the past unhealthy diet, ongoing psychiatric problems and digestive issues are a scientifically probable outcome.

 

 

 

 

Edited by farware, 08 August 2016 - 01:28 PM.

[Mind_Paralysis]

There is a previously unthought of possibility how Tianeptin could help in ASD: opioid receptor-down-regulation.

 

It was recently shown that anxiety is caused by pathologically enhanced serotonergic activity in the brain - and not as previously assumed - low serotonin. The new proposed mode of efficacy of serotonergic drugs is then receptor-desensitization and down-regulation - by increasing serotonin even further, the receptors and production eventually down-regulate, lowering overall effects of serotonin.

 

This could explain why some report increased anxiety at the start of treatment of Anxiety /anxiety disorders, at the start of treatment. It could also explain why anxiety in general demands a higher dose for treatment, than depression.

 

One theory for the pathology of ASD is an overproduction of endogenous opioids.

 

https://en.wikipedia...d_excess_theory

 

And believe it or not... but there's quite a few ASD-ers with an opioid-addiction, who reports that the reason they're hooked, is that it seems to be the only thing that helps them.

So... what do you think? Opioid receptor down-regulation?

[farware]

Your assumption of downregulation seems to make sense. I'll have to think about that. The intuitive solution would be to take antagonists (low dose naltrexone) to counter the excess opiates but just like SSREs work better than SSRIs the solution might not be "intuitive" and as you describe the solution might be to enhance serotonin uptake to get to that "natural" downregulation. Wondering if this could lead to serotonin syndrome for some rare cases? Caution advised. 

 

So far I stayed within therapeutic doses (Tianeptine / Stablon). I am finally after weeks of battling insomnia at a stage where I tolerate therapeutic doses. Usually taking 24mg in the morning then another 12mg later in the day . I feel somewhat ok ... I still have terrible days but Im getting stuff done nearly every day now which is probably due to dopamine upregulation. I also enjoy old hobbies again, at least more than I used to which could be a result of the enhanced serotonin uptake and possible downregulation. 

 

I think we're onto something here.

 

Hyperactive ADHD cases may benefit more from LDN. I am personally higher on ASD spectrum and primarily ADHD-PI and did not do well on LDN. 

 

A recent systematic review, published in 2014^[17] showed statistically significant improvement in symptoms of irritability and hyperactivity in 77% of children treated with naltrexone.

https://en.wikipedia...d_excess_theory

 

Edited by farware, 08 August 2016 - 03:44 PM.

[Mind_Paralysis]

It may be a question about which receptors to antagonise - which receptors do the most commonly abused opiates affect, again?

 

Also, what affinity does Tianeptine have, which specific receptors? Have a look at antagonists of those - that might be the jig.

 

Maybe run a search for new ASD-meds with antagonistic effect as well.

 

 

On another note - NitroMemantine - the great white whale, the golden goose never caught, of the nootropic community, is a very powerful, yet selective NMDA-antagonist. It showed significant effects on both ADHD and ASD in mice-testing - so if you're the one who manages to organise a group buy, then that may well help. However, the reason research was halted is apparently because it's a nitrate-med - nitrate causes cancer, like nitroglycerin for instance.

The risk is low though, and is only bound to be a problem in long-term use. (read: years)

 

That's plenty of time for you to see if it helps. (except yeah, I know - it's super-hard to get the data - because there are different formulations wherein the nitrate-group is connected to the Memantine - and it was a specific bond which had the right effect.)

[farware]

Just an update on what I am taking at the moment. The stack I posted previously needs some work, so this is what Im at right now: 

 

Morning first thing empty stomach:

1. T3 20mcg - No T4 (may try T4 50 but generally T3-only seems superior)
2. Wait 5-10 minutes 
3. Pregnenolone 50mg (neuroprotection + hormone support) 
4. NADH 50mg (b3 coenzyme, serotonin support)
5. Probiotics 10 billion - rhamnosus aka the control strain that enhances other gut bacteria 

 

10-20 minutes later:

1. 2x12mg Tianeptine 
2. Eat some fiber (dates) / berries
3. Eat a little protein (shrimp, seafood, etc) 
4. Drink grape+lemon drink (not more than 100ml or it can result in stomach issues, the acid kills bacteria (PH increase) and flushes the liver, the more you drink of this the more upset your stomach, mix with water!!) 

 

Folate, P5P and NAC I take during the day. Not sure yet if its better to take it in the evening. I temporarily removed Ginkgo, seems like overkill with Tianeptine 

 

Still shuffling things around, need to do more testing to see what order works best. Any suggestions are welcome  

 

 

[jack black]

 

 

Anyway, here's what I am reading right now again: 

The opioid effects of gluten exorphins: asymptomatic celiac disease

https://jhpn.biomedc...1043-015-0032-y

 

 

 

 

 

good read, thanks for linking. this explains my life long cravings for bread and milk. on the other hand, you would think that the LDN i'm taking should make me overt celiac, but it doesn't.

 

 

Edited by jack black, 10 August 2016 - 02:05 AM.

[Mind_Paralysis]

 

 

 

Anyway, here's what I am reading right now again: 

The opioid effects of gluten exorphins: asymptomatic celiac disease

https://jhpn.biomedc...1043-015-0032-y

 

 

 

 

 

good read, thanks for linking. this explains my life long cravings for bread and milk. on the other hand, you would think that the LDN i'm taking should make me overt celiac, but it doesn't.

 

 

Hold up you guys... it may not be that simple - it seems like the opioid excess theory is on its last legs. And especially the part with the leaky gut.

 

Opioid peptides and dipeptidyl peptidase in autism.

https://www.ncbi.nlm...pubmed/12578238

 

No opioid metabolites in autism urine.

 

Absence of urinary opioid peptides in children with autism.

https://www.ncbi.nlm...pubmed/18337276

 

Gluten-free and casein-free diets in the treatment of autism spectrum disorders: A systematic review

http://www.sciencedi...750946709001111

 

 

Let's look at the problem from a different angle: what problems does autism give you, that you need to fix?

And is there an option around it, to still have the kind of life you want?

 

Perhaps individual symptoms can be fixed instead?

[farware]

 

 

Hold up you guys... it may not be that simple - it seems like the opioid excess theory is on its last legs. And especially the part with the leaky gut.

 

Opioid peptides and dipeptidyl peptidase in autism.

https://www.ncbi.nlm...pubmed/12578238

 

No opioid metabolites in autism urine.

 

Absence of urinary opioid peptides in children with autism.

https://www.ncbi.nlm...pubmed/18337276

 

Gluten-free and casein-free diets in the treatment of autism spectrum disorders: A systematic review

http://www.sciencedi...750946709001111

 

 

Let's look at the problem from a different angle: what problems does autism give you, that you need to fix?

And is there an option around it, to still have the kind of life you want?

 

Perhaps individual symptoms can be fixed instead?

 

 

Autism is pretty bad because you are basically a non-functioning human being. I have no social life whatsoever and not for a lack of trying. It's also holding me back professionally. I know that if I could rely on my body to function every workday I could become a real entrepreneur instead of a solopreneur and what I really crave is a team win. I had plenty of success by myself to know its not what I am looking for. As a human you're a social being whether you like it or not and that feeling when you achieve something together rather than doing it alone is much more powerful.  

 

Especially the part with the leaky gut is receiving more and more confirmation, not sure why you are trying to discredit it. There is clear evidence that the primary comorbid symptom is gut issues. Most also suffer from celiac but dont know that they do and even when they do a test these are so unreliable that you would have to do a proper autopsy to identify it 100%.  

 

The most likely problems that arise is that due to chronic inflammation the calcium management appears to become defunct which will lead to the symptoms. Vitamin K is somewhat implicated because it controls a lot of that and seems to be deficient in autism

 

 

Vitamin K inhibits production of Interleukin-6, an inflammatory cytokine

 

 

 

1. Inflammation --> Vitamin K deficiency --> Symptomatic flare 
2. Vitamin K supplementation --> reduce inflammation --> heal gut 

 

 

I am proposing that a deficiency in Vitamin K causes unregulated calcium movement and deposition in the body of the autistic child, and that unregulated calcium is a cause of many of the symptoms associated with autism

 

 

http://www.gutresear...om/VitaminK.pdf

 

 

• So it starts with gut issues,
• then inflammation,
• then chronic inflammation of the gut,
• then via vargus nerve -> inflammation of brain -> chronic inflammation -> impaired calcium movement --> cognitive decline / anti-social behavior 

 

However, you will first have to work on rebalancing the glutamergic system which is messing with your serotonin / dopamine production before healing the gut is possible so you have to address this from multiple angles. 

 

So Vitamin K for Calcium Transmission + NADH for Serotonin Cycle + Probiotics For Gut Support + Hormone Support + Methylation Cycle (B12, Folate, B6, ...) + If Advanced Stages Glutamate Modulator

 

Several cycles are impaired and thats why "modern" medicine cant treat it. They still believe that one magic people can fix all of this. No, the only way is to address multiple systems that all work together.  

[farware]

If you need a source for Stablon, drop me a PM, not going to post it here and potentially ruin it for everyone. 

 

Highly suggest you first check whether you actually have problems with the glutamergic system first. If not, this may not be the drug for you. Same goes for P5P, only take it if you have a deficiency in B6. You can find evidence in your 23andme --> Promethease report. There are a bunch of services but I like the UI of Promethease and you can download and search it for keywords. Its how I found the genetic markers for ASD and B6 deficiency. Then look at your symptoms and try to match them, should be easy, e.g. ADHD-like symptoms are a clear sign of problems with glutamate 

 

Vitamin K is very safe, I am probably ordering from LifeExtension next, they create decent supps. 

[Mind_Paralysis]

EDIT: Wait... aren't we going completely off-topic here? Perhaps this should be its own thread? We should totally have threads only dedicated to specific disorders as well - super-ultra-mega threads, swallowing up all of the other individual ones - the board will be less cluttered then, and info will be more easily available.

 

 

 

 

 

Hold up you guys... it may not be that simple - it seems like the opioid excess theory is on its last legs. And especially the part with the leaky gut.

 

Opioid peptides and dipeptidyl peptidase in autism.

https://www.ncbi.nlm...pubmed/12578238

 

No opioid metabolites in autism urine.

 

Absence of urinary opioid peptides in children with autism.

https://www.ncbi.nlm...pubmed/18337276

 

Gluten-free and casein-free diets in the treatment of autism spectrum disorders: A systematic review

http://www.sciencedi...750946709001111

 

 

Let's look at the problem from a different angle: what problems does autism give you, that you need to fix?

And is there an option around it, to still have the kind of life you want?

 

Perhaps individual symptoms can be fixed instead?

 

 

Autism is pretty bad because you are basically a non-functioning human being. I have no social life whatsoever and not for a lack of trying. It's also holding me back professionally. I know that if I could rely on my body to function every workday I could become a real entrepreneur instead of a solopreneur and what I really crave is a team win. I had plenty of success by myself to know its not what I am looking for. As a human you're a social being whether you like it or not and that feeling when you achieve something together rather than doing it alone is much more powerful.  

 

Especially the part with the leaky gut is receiving more and more confirmation, not sure why you are trying to discredit it. There is clear evidence that the primary comorbid symptom is gut issues. Most also suffer from celiac but dont know that they do and even when they do a test these are so unreliable that you would have to do a proper autopsy to identify it 100%.  

 

The most likely problems that arise is that due to chronic inflammation the calcium management appears to become defunct which will lead to the symptoms. Vitamin K is somewhat implicated because it controls a lot of that and seems to be deficient in autism

 

 

Vitamin K inhibits production of Interleukin-6, an inflammatory cytokine

 

 

 

1. Inflammation --> Vitamin K deficiency --> Symptomatic flare 
2. Vitamin K supplementation --> reduce inflammation --> heal gut 

 

 

I am proposing that a deficiency in Vitamin K causes unregulated calcium movement and deposition in the body of the autistic child, and that unregulated calcium is a cause of many of the symptoms associated with autism

 

 

http://www.gutresear...om/VitaminK.pdf

 

 

• So it starts with gut issues,
• then inflammation,
• then chronic inflammation of the gut,
• then via vargus nerve -> inflammation of brain -> chronic inflammation -> impaired calcium movement --> cognitive decline / anti-social behavior 

 

However, you will first have to work on rebalancing the glutamergic system which is messing with your serotonin / dopamine production before healing the gut is possible so you have to address this from multiple angles. 

 

So Vitamin K for Calcium Transmission + NADH for Serotonin Cycle + Probiotics For Gut Support + Hormone Support + Methylation Cycle (B12, Folate, B6, ...) + If Advanced Stages Glutamate Modulator

 

Several cycles are impaired and thats why "modern" medicine cant treat it. They still believe that one magic people can fix all of this. No, the only way is to address multiple systems that all work together.  

 

 

I'm not trying to discredit the Gut-theory though  - why I posted those studies is because I - thought - it was discredited, and I figured you needed to know that.

 

Now, the review which showed that gluten-free and cassein-free diet didn't do much, if anything, to treat autism, was done in 2010 - do you know of newer reviews and studies? (which proposes other means of the gut causing inflammation)
 

Now, I suppose it doesn't discredit the gut-theory entirely - it simply discredits that gluten and cassein are the dietary villains which Autists must avoid. That certainly leaves other potential gut-problems - not sure which ones are theorized to be the most inflammatory, other then Gluten and Cassein though? Is it just that if the dietary system leaks compounds into the rest of the body, it will lead to issues, Irregardless of the composition of said compounds?

 

I believe the previous working theory which I was looking into was this:

 

Leaky gut + Gluten+Cassein ->Over-production of endogenous opiates -> Autism.

 

Now, Autists doesn't seem to have an overproduction of endogenous opiates after all (no marked difference in metabolites in urine, from neurotypicals), and it doesn't seem to be gluten and cassein doing it.

 

 

Now, if inflammation really is the most plausible basic cause, then perhaps it would be helpful to look into some of the newer, more powerful anti-inflammatories? The super-strong stuff, that's not even in use yet.

 

ASTAXANTHIN

The source of the anti-inflammatory properties of a sea-food rich diet and the orange colour in salmon as well.

 

https://en.wikipedia...iki/Astaxanthin

 

Astaxanthin, oxidative stress, inflammation and cardiovascular disease.

https://www.ncbi.nlm...pubmed/19656058

 

N-Acetylglucosamine

https://en.wikipedia...etylglucosamine

 

 

Now, these suggestions are just if the Vitamin K doesn't work, or perhaps to be used in tandem.

 

 

I think it's worth looking back at the properties of Nitro-Memantine though - since it reportedly decreased autistic symptoms in autist-rats to a great extent. NMDA-receptors are obviously a part of the glutamate network, but what would you say is the role of NMDA in Autism pathology, if any?

Edited by Stinkorninjor, 12 August 2016 - 01:31 PM.

[farware]

 

 

 

I'm not trying to discredit the Gut-theory though  - why I posted those studies is because I - thought - it was discredited, and I figured you needed to know that.

 

Now, the review which showed that gluten-free and cassein-free diet didn't do much, if anything, to treat autism, was done in 2010 - do you know of newer reviews and studies? (which proposes other means of the gut causing inflammation)
 

Now, I suppose it doesn't discredit the gut-theory entirely - it simply discredits that gluten and cassein are the dietary villains which Autists must avoid. That certainly leaves other potential gut-problems - not sure which ones are theorized to be the most inflammatory, other then Gluten and Cassein though? Is it just that if the dietary system leaks compounds into the rest of the body, it will lead to issues, Irregardless of the composition of said compounds?

 

I believe the previous working theory which I was looking into was this:

 

Leaky gut + Gluten+Cassein ->Over-production of endogenous opiates -> Autism.

 

Now, Autists doesn't seem to have an overproduction of endogenous opiates after all (no marked difference in metabolites in urine, from neurotypicals), and it doesn't seem to be gluten and cassein doing it.

 

 

Now, if inflammation really is the most plausible basic cause, then perhaps it would be helpful to look into some of the newer, more powerful anti-inflammatories? The super-strong stuff, that's not even in use yet.

 

ASTAXANTHIN

The source of the anti-inflammatory properties of a sea-food rich diet and the orange colour in salmon as well.

 

https://en.wikipedia...iki/Astaxanthin

 

Astaxanthin, oxidative stress, inflammation and cardiovascular disease.

https://www.ncbi.nlm...pubmed/19656058

 

N-Acetylglucosamine

https://en.wikipedia...etylglucosamine

 

 

Now, these suggestions are just if the Vitamin K doesn't work, or perhaps to be used in tandem.

 

 

I think it's worth looking back at the properties of Nitro-Memantine though - since it reportedly decreased autistic symptoms in autist-rats to a great extent. NMDA-receptors are obviously a part of the glutamate network, but what would you say is the role of NMDA in Autism pathology, if any?

 

I am not considering Memantine at the moment because Tianeptine seems to work for me as a modulator.  

 

Also, this nature article suggest that you'd want a NMDA modulator to improve autistic behavior not an antagonist: 

http://www.nature.co...ature11208.html

 

These findings suggest that deviation of NMDAR function in either direction contributes to the development of ASDs,

 

 

http://www.ncbi.nlm....pubmed/25636159

 

We already discussed this previously that Tianeptine is acting in a similar way and that it is a modulator - its not an agonist nor an antagonist and normalizes the NMDA channels. Thats probably how it works: Lowering neural stress reaction -> lowering inflammation -> lowering immune reaction. 

 

There is an article that suggests Memantine is a NMDA antagonist which means this is precisely what you dont want to take - we want a modulator for autism, not an antagonist 

 

http://www.sciencedi...028390899000192

 

 

===================================================================

 

 

After going through your other suggestion, I want to note that N-Acetyl-Glucosamin seems to work incredibly well on gut issues. However, I read some reports that its a sugar and can increase small intestine bacteria growth. I dont think its a supplement you want to take longterm and only as a 4-week cure. Its definitely something I need to research more since its the #2nd most popular supp for leaky gut after L-Glutamine. L-Glutamine is out of the race unless you want to get real problems, Glucosamine seems relatively well tolerated. 

 

So in conclusion, Tianeptine (modulator!) + Vitamin K (calcium channels) + hormone support (T3) seems to be the most important you can do aside from supporting your gut and methylation cycle. But as mentioned you need to work on all cycles, not just hormones, not just methylation, not just calcium, not just gluatamate - it's all together or it wont work and that's why it's so difficult because all of our current "systems" are short-sighted fabrications for short-term results. End results is obvious: Patients that get sicker and dependent on drugs ==> cash for big pharma. It disgusts me how a "sophisticated, developed" world can allow this legalized fraud scheme to continue. It's not working and everyone knows it.   

 

 

For someone with the chemical background, may be worth researching the Glycine receptor too as suggested in this thread but as suggested by one posted increasing Tianeptine dosage may be more beneficial which is also what I would suggest

http://www.longecity...ent-tianeptine/

 

Edited by farware, 12 August 2016 - 03:37 PM.

[farware]

Also reading:

http://www.ncbi.nlm....les/PMC3729335/

 

 

Environmental factors, such as mercury, lead, measles, rubella virus, zinc, retinoic acid, maternal thalidomide, valproic acid, and alcohol use during pregnancy have been suggested to be involved in the etiology of autism. Increasing evidence suggests that oxidative stress plays a role in the development and clinical manifestation of autism. mitochondrial disorders often result in central nervous system (CNS) dysfunction

 

 

 

 

The multi-subunit NADH-ubiquinone oxidoreductase (complex I) is the first enzyme complex in the mitochondrial electron transport chain (ETC). Mitochondria are responsible for most of the energy production through oxidative phosphorylation, a process requiring the action of various respiratory enzyme complexes, and the mitochondrial ETC, which is located in the inner mitochondrial membrane

 

 

The kynurenine pathway (KP) is a major route of L-tryptophan catabolism, resulting in the production of the important pyridine nucleotide nicotinamide adenine dinucleotide (NAD+)

 

 

 

Ok so I supplemented both on separate days: NAD+ and NADH, of course in combination with B6/P5P. From my personal test, I conclude that NADH is more benficial and its effect is more immediate. As I understand NAD+ is the precursor and is reduced to NADH. Don't know the chemical relation yet, so how does this work?

 

NAD+ -> reduced (=gain of electrons?) -> NADH

 

 

In organisms, NAD can be synthesized from simple building-blocks (de novo) from the amino acids tryptophan or aspartic acid.

https://en.wikipedia...ne_dinucleotide

 

 

I'm still trying to catch up on basic chemistry lol so no idea what the implications are of gaining that electron, but as far as I understand it its another conversion process and by supplementing NADH directly you are simply skipping this process entirely. In theory, NAD+ conversion should happen without issues but in theory T4->T3 should also work without problems and it does NOT. The actual problem may be the ratio of NAD+/NADH and not the conversion process as far as I understand it.

 

The impaired energy pathways is supposedly the main reason why I feel so sluggish and it obviously can lead to more oxidative stress. Add to this my personal issues of less red blood cells / cells that die faster, higher turnover and you have a process that creates a lot of blood cells in a system with increased oxidative stress. Well I guess Im lucky then that this did not manifest before my 18th birthday. 

 

Edited by farware, 12 August 2016 - 05:10 PM.

[farware]

Ok so I am considering to add N-Acetyl-Glucosamine to reverse chronic inflammation since the other supps simply boost NTs and ATP it wont cure the main issue but there are some studies suggesting it may promote biofilm creation which would be bad so still doing more research. I believe once you cure the auto-immune aspect of ASD, everything else will fall into place. In my mind, ASD is an auto-immune disease, there is simply too much evidence and the comorbid symptoms speak very clearly: thyroid + IBS + B6 def. Its very apparent that the immune system is implicated. It is possible that vaccines, toxins, antibiotics, mercury, etc etc can contribute to the outbreak and thats why we see more ASD outbreaks after birth (2nd year) than in the 90s and also adults with Asperger or that develop ADHD very late. Symptoms are the same, huge overlap there that cant be easily explained away: OCD, Anti-Social, Hyperactivity, Inattentive, GAD, etc ...

 

Its very illogical to believe that an adult cant get a disease that a 2year can get. Only the symptoms will vary greatly since a developed body will respond differently. Methylation is hugely important for proper development of the body. E.g. typical signs that you were an undermethylator during childhood is tongue tie, epicanthal folds, one leg longer than the other, etc

 

 

Just to give an example of the criteria that I match personally to see how common this is: 

- Tongue tie 

- Limb length inequality (not a lot, but its visible) 

 

That is a clear sign that the methylation cycle was impaired during childhood. That's also a good sign that other processes did not work properly during childhood. I cant really explain very high-functioning autism, but it's real and the fact that I have never been diagnosed shows me how little modern medicine knows about autism and auto-immune diseases in general and it also shows me they are not ready yet to make the connections that are clearly there.  

 

 

Edited by farware, 12 August 2016 - 06:40 PM.

[farware]

So more research on biofilms:

 

What drives bacteria to produce a biofilm?

http://onlinelibrary...4.tb09643.x/pdf

 

Biofilms as “Connectors” for Oral and Systems Medicine:

http://www.ncbi.nlm....les/PMC4739346/

 

N-Acetylglucosamine-dependent biofilm formation

http://www.ncbi.nlm....pubmed/21948048

 

Biofilms work together as multicellular organisms communicating with each other via quorum sensing, allowing changes in DNA expression which benefits the entire cooperative group:

http://keithhalperin...and-Disease.pdf

 

Lactoferrin cause a “twitch” response that weakens the ability or organisms to form biofilms

 

 

Whey protein includes Lactoferrin 

 

But the best known agent to inhibit biofilm creation is probably Cranberry 

 

Here's a good list I found: https://thescienceof...biofilm-agents/

 

There are likely a number of stealthy biofilms that adversely affect the body in unknown ways. The list may include fetal development, autism, depression, chronic fatigue, Lyme disease, cognitive impairment, etc. [Janossy, 2015] Chronic Lyme disease may play a role in the development of dementia and Alzheimer’s. 

 

 

 

So - my question. Is autism an auto-immune disease caused by a virus hiding in a stealth biofilm? If so, how would you degrade this biofilm? 

 

I believe if you follow this train of thought that D-Ribose is a much better idea than NAG because D-Ribose may actually help to break down biofilms and can repair your gut. Win-win?? I therefore propose D-Ribose as a possible better alternative. 

 

More research needed. Think we are making good progress here on identifying all possible supps that are beneficial and implicated receptors and environmental factors

 

- For anyone researching anti-biofilm agents: Please note before you start taking Resveratrol, Natto, Cranberry etc and other flavonoids that they can induce a heavy immune response and worsen some forms of autoimmune. Personally I can take them without issues despite an auto-immune disease (hashimoto)  -

 

To heal your gut with NAG, it would probably be a good idea to supplement in combination with such flavonoids to avoid stealthly biofilm creation. Not going to happen after supplementing once but longterm use could support stealth biofilm creation. Havent done much research on it but that would be my suggestion

 

==> Lastly, I think QS (Quorum Sensing) is a fascinating topic of interest. If you break QS and biofilms you could significantly improve inflammation if such inflammation is caused by bacteria acting together. 

 

 

 

 

Edited by farware, 12 August 2016 - 07:19 PM.

[Mind_Paralysis]

Btw, you've mentioned a few times now that some of your current regimens are adding to your Tianeptine-results, improving even more symptoms.

 

Could you by chance break down every compound you're taking, and which specific symptoms you feel they are improving? I'm probably not the only one who's curious.

 

So more research on biofilms:

 

What drives bacteria to produce a biofilm?

http://onlinelibrary...4.tb09643.x/pdf

 

Biofilms as “Connectors” for Oral and Systems Medicine:

http://www.ncbi.nlm....les/PMC4739346/

 

N-Acetylglucosamine-dependent biofilm formation

http://www.ncbi.nlm....perative group:

http://keithhalperin...and-Disease.pdf
 

 

Lactoferrin cause a “twitch” response that weakens the ability or organisms to form biofilms

 

 

Whey protein includes Lactoferrin 

 

But the best known agent to inhibit biofilm creation is probably Cranberry 

 

Here's a good list I found: https://thescienceof...biofilm-agents/

 

There are likely a number of stealthy biofilms that adversely affect the body in unknown ways. The list may include fetal development, autism, depression, chronic fatigue, Lyme disease, cognitive impairment, etc. [Janossy, 2015] Chronic Lyme disease may play a role in the development of dementia and Alzheimer’s. 

 

 

 

So - my question. Is autism an auto-immune disease caused by a virus hiding in a stealth biofilm? If so, how would you degrade this biofilm? 

 

I believe if you follow this train of thought that D-Ribose is a much better idea than NAG because D-Ribose may actually help to break down biofilms and can repair your gut. Win-win?? I therefore propose D-Ribose as a possible better alternative. 

 

More research needed. Think we are making good progress here on identifying all possible supps that are beneficial and implicated receptors and environmental factors

 

- For anyone researching anti-biofilm agents: Please note before you start taking Resveratrol, Natto, Cranberry etc and other flavonoids that they can induce a heavy immune response and worsen some forms of autoimmune. Personally I can take them without issues despite an auto-immune disease (hashimoto)  -

 

To heal your gut with NAG, it would probably be a good idea to supplement in combination with such flavonoids to avoid stealthly biofilm creation. Not going to happen after supplementing once but longterm use could support stealth biofilm creation. Havent done much research on it but that would be my suggestion

 

==> Lastly, I think QS (Quorum Sensing) is a fascinating topic of interest. If you break QS and biofilms you could significantly improve inflammation if such inflammation is caused by bacteria acting together. 

 

How does one test for bio-films though? How do you detect it?

And, this is going to be controversial - but isn't it possible to utilize some form of steroids to heal the gut really, really fast? There's of course the untested tissue-regeneration-promoters - like SW033291 which causes ultra-fast regrowth of various forms of damage to multiple forms of tissue.

New drug triggers tissue regeneration: Faster regrowth and healing of damaged tissues

https://www.scienced...50611144438.htm

I'm not proposing any of you use SW033291, but it might be a good idea to keep a look-out for new 15-PGDH inhibitors - perhaps it's possible to create one which is specific to intestinal tissue - would definitely help a lot of people, ulcer-sufferers in particular.

 

I'm gonna' throw out some info on the actual embryonic growth of the intestines as well... perhaps we can glean some information or ideas by going back to that state? I'll admit it... I'm looking for growth-promoters and modulators - the STRONG stuff. ; )

 

(I do wonder... it's probably possible to create a SARM which does this, now isn't it? Seeing as anomalously big intestinal growth is a side-effect of some of the older anabolic steroids - the ones that are being worked on now is made to be selective for bone and muscle, but it *should* be possible to make one for intestinal growth. Should be safe for both sexes, if the selectivity is great enough.)

 

Anisotropic growth shapes intestinal tissues during embryogenesis

http://www.pnas.org/.../10525.abstract

 

duodenum morphogenesis
Many debates and biological studies are devoted to this specific morphology, which regulates the cell renewal in the intestine.

 

 

It's going to sound a bit silly... but is it possible that the Autistic gut isn't damaged, but incorrectly built? That during the fetal stage, for one reason or another, maybe mercury or something, this process is ever so slightly, slightly imprecise? Which would then result in small malformations in the intestinal organs - making them more vulnerable to damage.

 

Perhaps... it's possible to trigger and control Duodenic Morphogenesis even in an adult stage of an organism? Crazy stuff, probably super-dangerous too!

I can see a virus interupting this process, causing imperfect results - we do know that viruses alters other growth-promoters, in order to cause cancer - perhaps they can do *small* alterations as well...? Anyways, treating the virus wouldn't help much in that case - because the organ is already formed and malfunctioning.

 

Farware: you mention physical abnormalities - malformed parts of the body, most likely at the embryonic stage. What's your take on this hypothesis?

[farware]

Btw, you've mentioned a few times now that some of your current regimens are adding to your Tianeptine-results, improving even more symptoms.

 

Could you by chance break down every compound you're taking, and which specific symptoms you feel they are improving? I'm probably not the only one who's curious.

 

 

 

How does one test for bio-films though? How do you detect it?

And, this is going to be controversial - but isn't it possible to utilize some form of steroids to heal the gut really, really fast? There's of course the untested tissue-regeneration-promoters - like SW033291 which causes ultra-fast regrowth of various forms of damage to multiple forms of tissue.

New drug triggers tissue regeneration: Faster regrowth and healing of damaged tissues

https://www.scienced...50611144438.htm

I'm not proposing any of you use SW033291, but it might be a good idea to keep a look-out for new 15-PGDH inhibitors - perhaps it's possible to create one which is specific to intestinal tissue - would definitely help a lot of people, ulcer-sufferers in particular.

 

I'm gonna' throw out some info on the actual embryonic growth of the intestines as well... perhaps we can glean some information or ideas by going back to that state? I'll admit it... I'm looking for growth-promoters and modulators - the STRONG stuff. ; )

 

(I do wonder... it's probably possible to create a SARM which does this, now isn't it? Seeing as anomalously big intestinal growth is a side-effect of some of the older anabolic steroids - the ones that are being worked on now is made to be selective for bone and muscle, but it *should* be possible to make one for intestinal growth. Should be safe for both sexes, if the selectivity is great enough.)

 

Anisotropic growth shapes intestinal tissues during embryogenesis

http://www.pnas.org/.../10525.abstract

 

duodenum morphogenesis
Many debates and biological studies are devoted to this specific morphology, which regulates the cell renewal in the intestine.

 

 

It's going to sound a bit silly... but is it possible that the Autistic gut isn't damaged, but incorrectly built? That during the fetal stage, for one reason or another, maybe mercury or something, this process is ever so slightly, slightly imprecise? Which would then result in small malformations in the intestinal organs - making them more vulnerable to damage.

 

Perhaps... it's possible to trigger and control Duodenic Morphogenesis even in an adult stage of an organism? Crazy stuff, probably super-dangerous too!

I can see a virus interupting this process, causing imperfect results - we do know that viruses alters other growth-promoters, in order to cause cancer - perhaps they can do *small* alterations as well...? Anyways, treating the virus wouldn't help much in that case - because the organ is already formed and malfunctioning.

 

Farware: you mention physical abnormalities - malformed parts of the body, most likely at the embryonic stage. What's your take on this hypothesis?

 

Not much time right now to go into everything, but you raise some interesting points and I will read through everything when I have some time

 

It's going to sound a bit silly... but is it possible that the Autistic gut isn't damaged, but incorrectly built?

 

 

Yes, I think that is a possibility e.g. that a gene is causing the gut to be more permeable than it should be. "individuals with celiac disease release significantly more zonulin" ==> one conclusion could be that epithelial cells could have a built-in defect from birth 

 

https://cdn2.omidoo....4964429copy.jpg

 

http://breakingmuscl...ing-to-our-guts

 

If that is the case, then certain supps can repair surface damage but not treat the root cause. Therefore, it is likely that you will need to supplement for life or find a way to modify your genes through gene theraphy which wont be possible for you and me and will likely cost 100k+ per theraphy and may not be covered by insurance in the future. 

 

Experimental: As for biofilm detection that can be verified by your symptoms. In my personal opinion, itching is a clear sign of biofilms but can also be a sign of poor liver health, so it is not easy to identify 100%. I would suggest drinking a  glass of cranberry juice mixed with lots of water and see what happens 1 hour after. If you notice some itching, it could be a sign of biofilm degradation - IMO you are essentially hindering QS and adhesion to gut linen with cranberry. Bacteria in the gut or even urinary tract doesnt like that. It's not very scientific so take it with a grain of salt.   

 

A lot of this is experimental and not backed by studies so I have to write about my own experience with this and as I pointed out, liver problems can cause similar problems so its best to also test with something like milk thistle, dandelion, etc to see how your liver is doing but that is heavy stuff for some people with immune disorders and needs to be treated with respect. Very tiny, tiny, tiny doses first before swallowing a full capsule. Better yet, drink a tea instead of swallowing it, that's milder. Manufacturers always try to produce high-dose capsules because thats what many consumers want, not a good idea for some! Caution.

 

Physical abnormalities: As mentioned, I think that has to do with methylation issues, not necessarily  at the embryonic stage but also during early childhood (year 1-6)

 

For a list of supps I am taking scroll up a bit. I am taking a few more and can post a complete list shortly. As mentioned I am trying to approach this a little more systematically, so it's mostly: Methylation support, hormone/endo support, Glutamate modulation, Serotonin processing support, Calcium channel support.  

 

Talking about this from a meta-perspective can help you to identify more supps and more culprits in your own biochemistry. We're all unique so supplementation also has to be unique and everyone will react differently, which is why I dont like recommending certain supplements as the "holy grail". Even Tianeptine wont work for everyone. It works for me thou. 

[farware]

Interesting sidenote: Remember how I was talking about PEA from raw cacao. Turns out cacao can also hinder QS according to some sources. 

[farware]

Another factor worth discussing in regards to inflammation is nitric oxide. Last year I made the mistake of taking L-Arginine to boost NO but as it turns out thats a bad thing for auto-immune, instead you want a modulator here too. 

 

https://drknews.com/...immune-disease/

 

Acetylcholine seems to play right into this.

 

Here's an interesting paper 

Huperzine a improves chronic inflammation and cognitive decline in rats with cerebral hypoperfusion.

http://www.ncbi.nlm....pubmed/19795377

 

So on my todo list right now: 

 

- D Ribose (ATP, Mitochondria, Gut)

- PQQ (ATP, Mitochondria)

- Huperzine A (Inflammation, NO modulator - more research on side effects)

 

I'll let you know how this works out. NADH seems to work quite well as an ATP booster but D-Ribose is a sugar and could work even better in terms of overall absorption. I will have to compare NADH to D Ribose. I dont think I will drop NADH anytime soon but cycling things may be a good strategy. PQQ seems promising as an add-on to be taken infrequently. 

 

 

 

 

 

 

 

 

 

[farware]

Re-introduced Whey protein today after months of taking it as part of a diet. Thinking about taking it with iron for enhanced iron storage. 

 

Whey also boosts all NT's - so if you have tried DMAE before and it doesnt work anymore, consider Whey protein (grassfed, not the stuff bodybuilders buy, glutenfree!). In general, you want a diet high in protein, low in carbs. However, if you develop hypoglycemia which can happen with autoimmune then you need sugar. Whey protein is rather sweet, add some coconut sugar and you have a good addition to your diet to prevent glycemic crisis e.g. when your blood sugar drops so low that you are close to fainting. This also happens when you drink certain teas, in particular green tea - so be very careful with your diet. The body needs some carbs and sugars. Beginners often take things to the extremes but that is very dangerous! 

 

I am thinking D-Ribose, NADH and Whey could be a great combination for a while. Whey also has high glutamine, however this seems to be tolerated quite well and can help repair gut lining in a more natural way than supplementing with L-Glutamine directly. 

 

Again, writing things down from my personal experiences, take with grain of salt. If you experience side effects and stuff discontinue immediately. In my opinion NADH is far more tolerable than lets say B3 as Niacin. Niacin has this stupid flush effect, I really hate that. 

 

 

Edited by farware, 13 August 2016 - 11:10 AM.