Alot Of People Link Gut Issues With Autism, Would A Sterile Gut Do The Job For These Linked Symptoms

[TreasureVibe]

Hey everyone. As most of you know, Ray Peat simply recommends a sterile and clean gut, as there is no consensus on what a healthy gut should be. As autism and autism symptoms are linked to gut issues, would a sterile and clean gut get rid of the symptoms?

 

[General Orange]

Interesting. I think that could work, partially. But you also have to repartition certain neurotransmitters in the brain.

 

[TreasureVibe]

Interesting. I think that could work, partially. But you also have to repartition certain neurotransmitters in the brain.

How would one do that?

 

[General Orange]

Some herbs are known to alter neuronal connections.
Ayahuasca for example: Edit oops wrong link:http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0118143
GABA http://news.mit.edu/2015/altered-brain-chemistry-autism-1217
Ashwadangha, Bacopa Monnieri.

 

[TreasureVibe]

Some herbs are known to alter neuronal connections.
Ayahuasca for example: Edit oops wrong link:The Psychedelic State Induced by Ayahuasca Modulates the Activity and Connectivity of the Default Mode Network
GABA http://news.mit.edu/2015/altered-brain-chemistry-autism-1217
Ashwadangha, Bacopa Monnieri.

Thanks man. Could you post your opinion on the safety of IP6/inositol/IP3 on the heart?

What Do You Know About IP6/IP-6/inositol Hexaphosphate/phytate/phytic Acid?

Or are you not specialized in that.

 

[General Orange]

I know a guy with "autism" and he takes adderal. It makes him able to concentrate on one thing greatly. But multitasking becomes worse.
I do not really believe in the autistic spectrum diagnosis. But I do see were they could benefit with certain nootropics and herbs.
I think I would treat them with Ayurveda. Something that contains bacopa would be profitable for them.

 

[General Orange]

I treated myself while I was still on SSRI, with Ashwagandha to prevent libido and erectile dysfunction.
I then discovered I could take multiple serotonin boosters like rhodiola, st johns wort, nootropics etc. when I just combine them with ashwagandha, because of its serotonin repartitioning and gaba positive effect that prevents excessive serotonin or syndrome.

So ashwagandha is a safe herb to combine with substances or herbs in treating neurological disorders.
This has been done for long time in India.
For example: Ayurveda and Autism

 

[TreasureVibe]

I treated myself while I was still on SSRI, with Ashwagandha to prevent libido and erectile dysfunction.
I then discovered I could take multiple serotonin boosters like rhodiola, st johns wort, nootropics etc. when I just combine them with ashwagandha, because of its serotonin repartitioning and gaba positive effect that prevents excessive serotonin or syndrome.

So ashwagandha is a safe herb to combine with substances or herbs in treating neurological disorders.
This has been done for long time in India.
For example: Ayurveda and Autism

That's actually really coincidental as a relative of mine with autism uses Ashwagandha currently and has improved alot in behavior and stress and overall mind as far as I can tell. I recall though reading that Bacopa was not so good for the brain long term or something like that, is this true?

 

[General Orange]

Bacopa is an Nitric Oxide inducer, so used alone chronically is not so good, unless it is combined with ashwagandha as neuroprotector that mediates NO production in the brain.

 

[General Orange]

Together, the main mechanism underlying the neuroprotective effects of WS can be attributed to its role in the down regulation of nNOS and neurochemical alterations of specific neurotransmitter systems. These observations thus suggest that WS root extract could be developed as a potential preventive or therapeutic drug for stress induced neurological disorders.

Neuroprotective effects of Withania somnifera dunal.: A possible mechanism. - PubMed - NCBI

 

[TreasureVibe]

Bacopa is an Nitric Oxide inducer, so used alone chronically is not so good, unless it is combined with ashwagandha as neuroprotector that mediates NO production in the brain.

Bacopa raises serotonin though, isn't that a bad thing for autism?

 

[General Orange]

I think these psychobiotic gutmicrobes can be a problem in neurological disorders.
Hence certain foods you eat have effect on them, and they make a neurotransmitter in response and this affects mood and inflammatory markers in the brain. I suppose a dysfunctional microbiome can maybe sustain a neurological disorder.

 

[General Orange]

Bacopa raises serotonin though, isn't that a bad thing for autism?

The raising and lowering of transmitters is a overrated thing. It does not interest me so much, I think it is more important what the relative change in behavior of these groups of transmitters do, the repartitioning of serotonin and modulation of them.

 

[General Orange]

this for example with bacopa:

6. Activation of Neurotransmitter Systems by Bacoside
...As a first step, Rajan et al. [41] estimated the level of neurotransmitters to understand the effect of BME treatment. They found that BME treatment during postnatal period significantly upregulated the level of 5-HT, ACh, GABA, and Glu. In contrast, it reduced the level of dopamine (DA). Notably, the reported inhibitory effects of cholinesterase activity of BME may possibly increase the level of ACh and enhance memory [33, 40]. On the other hand, 5-HT receptors present in the GABAergic neuron [57] may activate the GABAergic neurons [58, 59], which enhances the release of GABA. In fact, increased GABA level in hippocampus could activate the inhibitory GABA receptors on cholinergic system that leads to inhibition of ACh release [60, 61], but 5-HT receptors may directly act on the cholinergic system and increase release of Ach [62]. ...

 

[General Orange]

and

8. Activation of 5-HT Receptor by BME Treatment
In view of these reports, expression of 5-HT receptors (5-HT1A, 5-HT2A, 5-HT4, 5-HT5A, 5-HT6, and 5-HT7) after BME treatment was examined. Notably, 5-HT3A receptor expression was increased compared to all other receptors. It is the only metabotropic receptor, and its expression could be stimulated by endogenous 5-HT which may facilitate the hippocampal-dependent task [73, 74]. ...

The upregulated 5-HT3A receptor might regulate serotonergic system and may interact with other neurotransmitters that are involved in learning and memory [58, 67, 81]. It should be noted that 5-HT3A is a heteroreceptor; its stimulation by means of mCPBG has been reported to enhance GABA and DA levels and inhibit the release of ACh [74]. The activation of 5-HT3 receptors in dopaminergic neuron could facilitate the release of DA [82, 83], and mCPBG inhibits dopamine uptake by binding with dopamine transporter [84], thereby increasing the synaptic dopamine level. On the other hand, the anticholinesterase activity of BME [40] and other regulatory mechanisms of BME are also involved in the regulation of ACh level and memory enhancement [33, 85].

A noteworthy point is that it did not alter the level of Glu. This suggests that glutamate neurons in the hippocampus may not colocalize with 5-HT3A receptor [59]. The observed changes are indication of the facilitatory effect of BME on long-term and intermediate forms of memory through 5-HT3A receptor.

 

[TreasureVibe]

and

Fascinating, but what is the actual outcome of such activation and how can you predict that?