Formation of Neural Circuits in an Expanded Version of Darwin’s Theory: Effects of DNAs in Extra Dimensions and within the Earth’s Core on Neural Networks

https://pubmed.ncbi.nlm.nih.gov/31850135/

Aim: In this paper, inspiring Darwin’s theory, we propose a model which connects evolutions of neural circuits with evolutions of cosmos. In this model, in the beginning, there are some closed strings which decay into two groups of open strings.

Methods: First group couple to our universe from one side and produce matters like some genes of DNAs and couple to an anti-universe from another side with opposite sign and create anti-matters like some anti-genes of anti-DNAs.

Second group couple to the star and planet’s cores like the earth’s core from one side and produce anti-matters like stringy black anti-DNA and couple to outer layers of stars and planets like the earth from other side and produce matters like some genes of DNAs on the earth. Each DNA or anti-DNA contains some genetic circuits which act like the circuits of receiver or sender of radio waves.

To transfer waves of these circuits, some neurons emerge which some of them are related to genetic circuits of anti-DNAs in anti-universe, and some are related to genetic circuits of stringy black anti-DNA within the earth’s core. A collection of these neural circuits forms the little brain on the heart at first and main brain after some time.

Results: To examine the model, we remove effects of matters in outer layers of earth in the conditions of microgravity and consider radiated signals of neural circuits in a chick embryo. We observe that in microgravity, more signals are emitted by neural circuits respect to normal conditions. This is a signature of exchanged waves between neural circuits and structures within the earth’s core.

Conclusion: These communications help some animals to predict the time and place of an earthquake.

Discussion: This is a real(ish) paper. Whenever we imagine that scientific publishing is terribly rigorous, this is a fun article to remember it isn’t. In fact, the setup of most experiments in most papers which have the most well publicized headlines are by design unrepeatable and irreplicable.

We still do an absolutely lousy job of asking why we failed, how bad science keeps popping up, and why results continue to skew toward homogenous stews for human related work. And the reason is because quite a bit of the rigor that we assume exists in science doesn’t actually exist.

Any article that we read for example based on psychiatric conditions should be taken with exactly the level of caution and skepticism that you’d take with regard to this article as the validity of those principles is about the same as those presented in this paper. Until we can actually validate clinical “depression” for example with blind inter-rater rates above 99%, it’s impossible for any work built upon it to be any more accurate than that.

When we get bombarded with neurochemical based research that shows tiny effect sizes and completely mixed effect even in a lab setting, we should be skeptical of this rather than extending work on top of them.

No matter how confidently we believe in much of the neuroscience work being published today, in practice the overwhelming majority of it has perverted the basic science checks designed to prevent poor concepts from gaining traction into a mechanic which enables blind acceptance of the validity of that terrible science.

Science, if nothing else, must be internally and externally consistent. Science which cannot be externally consistent is probably flawed. And science which cannot be internally consistent is definitely flawed.

Edit: Dangit, should have used the full article view for the link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6910808/

Extra reading: https://retractionwatch.com/

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More Shitty Science Theater on Pubmed:

Effect of MDMA exposure during pregnancy on cell apoptosis, astroglia, and microglia activity in rat offspring striatum

Objectives: Ecstasy is a popular recreational psychostimulant with side effects on the central nervous system. This study examined the corpus striatum tissue of adult rats that received ecstasy during the embryonic period for histological and molecular studies.

Materials and methods: Rats were divided into control and ecstasy groups. The ecstasy group was given MDMA 15 mg/kg intraperitoneally twice daily at 8-hour intervals on days 7-15 of gestation. At the age of 15 weeks, adult offspring of both groups were examined for learning and memory study by the Morris water maze test. Then, ventral striatum tissue was harvested for TUNEL assay, Nissl staining, and real-time PCR for the expression of the GFAP and CD11b.

Results: Ecstasy up-regulated the GFAP and CD11b expression in the striatum of offspring (*P˂0.05). Furthermore, the Morris water maze test showed that exposure to ecstasy significantly impaired learning and spatial memory (*P˂0.05). TUNEL assay results did not show any significant change in the number of apoptotic cells in the striatum tissue of ecstasy offspring compared with controls, while Nissl staining showed a significant decrease in the number of neurons in the ecstasy group (*P˂0.05).

Conclusion: Exposure to ecstasy during pregnancy causes long-lasting changes in brain regions underlying learning and memory, including the striatum, and impaired working memory in the offspring. In addition, these data provide the first evidence that exposure to ecstasy during the embryonic period causes a persistent change in the activity of microglial cells and the number of astrocyte cells in the striatum.

Commentary: To really get an idea of how insane this study is, this would be the equivalent of me using 1.5 grams of MDMA every single day. The “therapeutic” dose employed by most MAPS-like studies top out at 125mg, and even the hardest rollers will only do 300-500mg in a day, with breaks in between. Despite that utter insanity, the MDMA rats actually outperformed the “control” rats on some of their tests, and even their best case “control” outperform was fairly low statistical reliability.

Honestly, this work to me is resoundingly supportive of the safety of MDMA once we back away from the “less neurons developed, therefore bad” conclusion the authors try to make. Especially since it was balanced by increased glial activity and low apoptosis, and components of the performance test produced better results for the MDMA group.

This type of work is pretty typical of “science” designed to support the policy aims of the funding source rather than provide actual data to help quantify the world. That stuff like this which is so obviously HARKed and HACKed, and further tied to so many unsupported assertions is so prevalent on sources like PubMed is pretty ridiculous.

Edit: Oh shit, it’s not 1.5 grams per day, they administered that dose TWICE per day so the equivalent of 3 grams per day. Like everything above times two. It’s absurd that there’s any site out there that asserts the lethal potential of MDMA if these are the results people are getting. These fucking guys are probably drug dealers using this study to cover.

Taking this at face value it seems to argue that absurd levels MDMA use during pregnancy might make rats smarter, which is generally consistent with the results most people experience on stimulants.

I’m partially amazed at this because I’m imagining what 3 grams would even feel like. I’ve sort of accidentally done a gram and a half and even though I have pretty absurd tolerances to nearly all psycho active drugs, I was fucking barely conscious on that dose. Like I remember feeling barely able to walk and there was an almost complete dissociation effect.

Thinking about this a bit more though, it does bring to mind my big/little astrocyte duality I explored in the “autism” model. It makes me wonder if the reason stimulants are so effective in “big” astrocyte individuals is because it juices the interconnecting neurons enough to balance inter-regional flow. Without that metabolic inducement, processing gets bottlenecked in circuits in which the astrocytes are “over-encoding” the local group neuron population.

This seems really consistent with a lot of work that alternatively describes some phenotypes of autism as being “under pruned” while others seem to be “low connectivity” (or probably more specifically, slow astrocytic encoding of data to local group neurons).

I need to think about this a bit more.

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