tkadm30

 

Mental illness’ is terribly misleading because the ‘mental disorders’ we diagnose are no more than descriptions of what clinicians observe people do or say, not at all well established diseases — Statement of Allen Frances, Psychiatrist and former DSM-IV Task Force Chairman, 2015

A medical diagnosis and a psychiatric diagnosis are two different things.

 

“There are no objective tests in psychiatry-no X-ray, laboratory, or exam finding that says definitively that someone does or does not have a mental disorder.” “There is no definition of a mental disorder. It’s bull—. I mean, you just can’t define it.” — Allen Frances, Psychiatrist and former DSM-IV Task Force Chairman

Psychiatry, unlike medicine, is not evidence-based science. Take it or quit telling me that observations are

pure scientific evidences..

https://www.cchrint.org/psychiatric-disorders/psychiatristsphysicians-on-lack-of-any-medicalscientific-tests/

 

Note that a causal relationship between the observations and hypothesis does not exist to cause the observation to be taken as evidence,^[1] but rather the causal relationship is provided by the person seeking to establish observations as evidence.

https://en.wikipedia.org/wiki/Scientific_evidence

A model in full detail would become the thing it was modelling so obviously not that.

 

<breathless>Can AI become independent of the creators of its software (create its own path) ?

 

If its workings are too complex for the human mind to follow does that not show it can?

 

Can AI's internal processes become self referential even ? Can it operate a need to improve its own working? (going off at a bit of a tangent but what limits are there to what AI could achieve? Are there any? Where can the line be drawn? Can AI "cut the cord" ?) </ breathless>

 

Sure these may not be immediate ,or even potential concerns -but they do concern me now.

Since the binding problem of consciousness has not yet been elucidated, I think we're far from seeing mindful machines. Machine intelligence is a software program, and cannot pass the Turing test until we know how/why humans are self-aware.

AI is intrinsically limited by the intelligence of its programmers, so I guess its not possible for machines to "modelize" the unknown using

algorithms based on mathematics and physicalism. However, AI can certainly extrapolate models (I prefer the term "theories") of the universe but

could probably not produces hard scientific evidences about its validity.

A "mental illness" is not based on scientific evidences, but on the testimonial of the patient to the psychiatrist. Try to find a psychiatrist who will do brain scans to figure out the cause of the mental disorder.

Not all atypical antipsychotics are classical dopamine antagonists (blockers). For example, aripiprazole acts like a dopamine D2R antagonist under high extracellular concentration of dopamine. Under low dopaminergic tone, aripiprazole is a selective D2R ligand (agonist):

 

Under high dopaminergic tone, aripiprazole acts as a D₂-like autoreceptor antagonist rather than as an agonist. These data show that, ex vivo, alteration of dopaminergic tone by depolarization affects the actions of aripiprazole on D₂-like autoreceptors. Such unusual effects were not seen with the typical partial agonist preclamol and are consistent with the hypothesis that aripiprazole is a functionally selective D₂R ligand.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4360222/

I'm curious about how theses ex vivo alterations of dopaminergic tone may affect differential sensitivity to dopamine agonists. Could a dopamine system stabilizer like aripiprazole trigger neuroleptic malignant syndrome (NMS) ?

I haven't looked into this subject in the depth it deserves, but I'd be very surprised if marijuana does NOT cause a permanent negative effect. We know that it can induce life-altering psychosis, probably in those who are predisposed to it in the first place. We know that it affects short-term memory. We know that it lowers IQ by about four points on average, and that it does so in direct proportion to the number of days it has been used. We also know that it dramatically alters blood flow in the brain. Those seem to me to be pretty good hints.

Please provide references to support theses claims.

The genetic THC tolerance and CB1 receptor-mediated regulation of Akt/BDNF signaling trigger striatal neuroprotection: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4563779/

Seems so:

 

https://www.ncbi.nlm.nih.gov/pubmed/1130936

 

https://www.ncbi.nlm.nih.gov/pubmed/574284

 

https://www.karger.com/Article/Pdf/117686

 

Although it seems that female rats did not show any signs of hypersensitivity. Other than that, it looks to be true.

But it seems like you already knew that.

I doubt seriously atypical antipsychotics are comparable to amphetamines. Apart from that, I guess partial (inverse) dopamine agonists doesn't block dopamine receptors like dopamine antagonists.

But wait just a minute.

 

First you asked:

 

 

Then you said:

 

 

 

You just answered your own question. You said that Atypical antipsychotics ARE inverse dopamine agonists, which neccessarily means that they do inverse dopamine sensitivty. Then you stated that they:

 

 

 

So what is the question here exactly? It looks more like a statement to me than a question.

Can inverse (partial) agonism at dopamine D2 receptors trigger dopaminergic hypersensitivity?

Atypical antipsychotics (inverse dopamine agonists) are thought to cause fewer extrapyramidal symptoms than typical antipsychotics.

Can atypical antipsychotics inverse dopamine sensitivity?

How can long-term neuroleptic drug (not cannabis) usage trigger psychosis? Is it possible that atypical antipsychotics inverse chemical balance (dopamine/serotonin levels) in the brain? Can atypical antipsychotics cause dopamine hypersensitivity?

Thanks.

I'm looking for papers describing theories of quantum-like neuronal communication models. In particular, I'm interested in the biological entanglement of physical (neuronal) processes and the neurophenomenology of consciousness.

Thank you,

"Enlighten the people generally, and tyranny and oppressions of body and mind will vanish like evil spirits at the dawn of day."

-Thomas Jefferson

See this: https://en.wikipedia.org/wiki/God_gene

 

Does exercise increase dopamine or endorphin?

 

Yes. Exercise stimulate dopamine neurotransmission through calmodulin-dependent pathways in the brain: https://www.ncbi.nlm.nih.gov/pubmed/12758062

OK. Thanks for this information, jbn22.

Increasing the amount of GABA reduces seizure activity and/or anxiety.

https://www.ncbi.nlm.nih.gov/pubmed/11520315

Here's some cool papers on the science of mind wandering and the neurophenomenology of consciousness.

http://www.ini.ch/~alumit/ishai_jocn2002.pdf

https://www.ncbi.nlm.nih.gov/pubmed/25293689

http://www.mitpressjournals.org/doi/abs/10.1162/jocn_a_00656

Is it more accurate to suggest that the mind can "hop onto " any one of smorgesbord of unconscious streams?

 

There is only one conscious level (am I right?)

Yes. There is one conscious level but multiple streams of consciousness.

Unconsciousness is defined by the absence of multiple streams of conscious activity.

Thanks for the information.

It looks like the mind can switch between streams of consciousness. I have noticed smoking tobacco produces this psychological

effect.

Can terrorist attacks (or just terrorism) trigger our collective consciousness or is the medias (plural) brainwashing our thoughts with mental images about the violent nature of theses crimes? Is the term "terrorism" provoking a strong emotional response to awaken the "collective consciousness" ? How does the unity of consciousness reflect our collective mental states? Is this evidence of (quantum-like) brain-to-brain connectivity ?

What causes mind wandering?

Sleep is essential to memory consolidation, according to recent research.

Technically, I think this is called "neural representation".

https://www.ncbi.nlm.nih.gov/pubmed/10753793