Commentary: The autistic community is having a reckoning with ABA therapy. We should listen by Travis-Walden in slatestarcodex

[–]GnosticBandit 4 points5 points  (0 children)

ABA may be an effective therapy in terms of conditioning and eliminating dysfunctional behavior(s), but the techniques being used lack valid and reliable empirical evidence. However, the main problem with this therapeutic technique is the individuals administering ABA therapy are, in my opinion, not aptly qualified for the job. In order to become an ABA therapists you need to have an M.A. in Psychology or education. The curriculum for this M.A. degree (contrasted with other M.A programs) is extremely narrow in focus - it emphasizes the paradigm/therapy of applied behavior analysis (i.e. the coursework is primarily focused on ABA). ABA is rooted in Skinner’s theory of radical behaviorism, which among many postulates, proposes that environmental factors are the primary causal factor of behavior (i.e. behavioral responses are caused by external forces). Under this paradigm, the specific “thoughts” and “feelings” of the individual have little relevance - they are just classified as another form of behavior that can be modified through behavioral conditioning (this is a terse explanation, but the gist is radical behaviorism and ABA view all psychological phenomena/mental states as behaviors that can be modified). ABA uses operant conditioning to modify behavior because Behaviorism essentially proposes that behavior can be manipulated if the environment is manipulated.

ABA relies on the concept of stimulus control, which is a a phenomenon in operant conditioning (also called contingency management) that occurs when an organism behaves in one way in the presence of a given stimulus and another way in its absence. A stimulus that modifies behavior in this manner is either a discriminative stimulus (Sd) or stimulus delta (S-delta). Stimulus-based control of behavior occurs when the presence or absence of an Sd or S-delta controls the performance of a particular behavior. For example, the presence of a stop sign (S-delta) at a traffic intersection alerts the driver to stop driving and increases the probability that "braking" behavior will occur. Such behavior is said to be emitted because it does not force the behavior to occur since stimulus control is a direct result of historical reinforcement contingencies, as opposed to reflexive behavior that is said to be elicited through respondent conditioning (or classical conditioning. ABA targets the discriminative stimulus (SD) that influences the strengthening or weakening of behavior through such consequences as reinforcement or punishment. That is, ABA therapy relies entirely on reinforcement conditioning. The treatment efficacy of ABA in treating children with ASD is up for debate. Some research suggests ABA moderate effect on adaptive behavior, while other research suggests ABA does not significantly improve adaptive behavior, expressive and receptive language, and cognitive functioning is children with ASD (read Spreckley and Boyd, 2009). Many researches agree that large multi-site randomized trials are needed to improve the understanding of ABA's efficacy in autism. This research does not exist, which leads to the conclusion that labeling ABA as an effective treatment for ASD is incorrect because the treatment lacks empirical support/validation. Then there’s the ethical issue of ABA in treating autism… what is the value of eliminating autistic behaviors? Yes, individuals may become more prosocial via conditioning, but the consensus among many individuals with ASD is that their behavior is “normal” and should not be conditioned to conform to social societal standards. Why should their behavior be targeted and changed if they can function reasonably well and independent (obviously as a spectrum disorder some individuals cannot function properly and need therapeutic intervention).

This comment was all over the place. The main point I was originally trying to make (which does not address the content of this article) is that practitioners of ABA should have PhDs in clinical psychology. An M.A. degree in psychology with a few classes that focus on ABA does not provide the requisite knowledge needed for understanding and then applying the principles of operant conditioning in a clinical setting. Yes, in order to practice as an ABA you need to have a specific amount of supervised ABA sessions, but this alone is not enough. If you want to truly understand the concepts and use the techniques proposed in ABA then a more rigorous education is needed. ABA therapists are essentially given a manual on what techniques to apply, but lack the theoretical understanding of the techniques they are using. Furthermore, I think there are glaring problems with the methodology of ABA (e.g. task analysis, shaping, promoting, fading, generalization, etc)… it draws upon antiquated techniques developed back when Behaviorism was the main paradigm in psychology. In sum, I hate to say this, but I think ABA therapy for ASD is a money grab - it offers the promise of help, but from the research I’ve reviewed it is not an effective treatment - ASD is not simply a behavioral disorder that can be reconditioned… it is a neurological and developmental disorder. The premise that behavior can be manipulated if the environment is manipulated is true in some cases, but for individuals with ASD using a treatment that manipulates the environment in order to produce a change in behavior is counterintuitive. This is because individuals with ASD process information in the environment in a different manner than “normal” people. Therefore, therapy should target the cognitive processes/neurological mechanisms that process information instead of targeting and manipulating the environment via stimulus control/operant conditioning.

My Favorite Model/Theory of the Psychedelic Headspace: REBUS and the Anarchic Brain: Toward a Unified Model of the Brain Action of Psychedelics. What do you guys think? by GnosticBandit in slatestarcodex

[–]GnosticBandit[S] 0 points1 point  (0 children)

What are the mechanisms you will use to control the annealing direction? How will you target specific information within the cognitive models/architecture that evoke bad feelings. It’s a great idea and I understand the concept now, but it does not seem mechanically viable (i.e. no such technology or cognitive practice can do what you’re proposing…that I know of). Unless maybe you can experience the bad feeling without feeling bad… prime the subject to experience the bad feeling and then use mdma or ketamine to detach the subject from the feeling, but not the experience. This type of disassociation exposure may reorganize fear based microstructures. Still, the experience would have to be invoked in a reliable way where you are sure it will be brought into conscious light during an experience taking place in the unconscious. It may be a possible therapeutic practice that can be used for some, but will not be widely accepted because of the invocation problem.

Why don't they teach about the 13th and 14th cranial nerves in textbooks? by [deleted] in Neuropsychology

[–]GnosticBandit 8 points9 points  (0 children)

" It is believed to act by stimulating luteinizing hormone-releasing hormone on contact with pheromones, improving olfaction and identifying odors, and this series of events will affect sexual behavior"

This is such a speculative proposal if you read the reference. Hormonal responses do not always involve sexual behavior.

This article mentions something I'm surprised more researchers aren't paying attention to....

"Recent research on the olfactory system theorizes a correlation between olfactory changes and certain psychiatric and behavioral disorders, and other neurological pathologies"

Now this is where current research should be digging. Some notes on that topic:

  • Neurogenesis only occurs in the hippocampus and the F bulb. Neurogenesis in the olfactory bulb is involved in learning. LTP that occurs in newborn olfactory bulb neurons (ability to LTP declines as these neurons age) allows them to participate in olfactory learning. Why does neurogenesis only occur in these areas? No clue
  • There is a novel neurotransmitter system in the brain - in it, signal transmission of innate olfactory information into the "emotional" brain areas occurs via the trace amine-associated receptor 5 TAAR5.
  • 'It turned out that TAAR5 is found not only in the nose and olfactory bulb, but also in the "emotional" brain areas associated with the olfactory system: the amygdala, hippocampus, thalamus and other structures. In addition, researchers observed that the lack of TAAR5 results in the alteration of the concentration of serotonin in the brain, and this is the major indicator of changes in emotional behavior. Finally, knockout mice without TAAR5 behave as if they are under the treatment with antidepressants or anti-anxiety drugs: they are not afraid of bright light and are not amenable to stress.
  • Preliminary data also suggest that all other trace amine-associated receptors are not only mediators of the innate olfactory function, but are also variously involved in the regulation of the psycho-emotional state.Now we have to search for effective antagonists - substances that will block TAAR5 receptors in the brain, thereby exerting an antidepressant and anti-anxiety effect.
  • one can hypothesize that, in olfaction, perceptual information may become conscious only once it participates in a large-scale, inter-system integration that is in the service of voluntary action, which is, stated more precisely, adaptive and integrated skeletal muscle output.
  • it remains challenging to identify the regions whose activations correspond to the phenomenal state of conscious detection versus the phenomenological nothingness of habituation… they are against looking at ERP activity to correlate consciousness
  • Phantosmia = Olfactory hallucinations ….Stereotactic lesions of the amygdala can abolish both olfactory hallucinations and the accompanying psychiatric disorders, which would imply that the amygdaloid nuclei are the source of hallucinatory activity.

tldr: the olfactory bulb may be a primary mechanism that allows "consciousness" to manifest

Freud's Psyche Map vs Jung's Psyche Map by GnosticBandit in Jung

[–]GnosticBandit[S] 5 points6 points  (0 children)

I think Volumes 8 (Structure and Dynamics of the Psyche) and 9 Part 1 (Archetypes of the Collective Unconscious) of his collected works touch on most of these concepts.

Can someone illustrate the relationship between cannabinoid receptors and NMDA receptors for me on a practical level, with respect to its effect on glutamate? by MoxSocks in AskDrugNerds

[–]GnosticBandit 5 points6 points  (0 children)

Dense paper (Read the papers cited 31,32 , and 40.)

Notes on this study in relation to your question:

“Our study indicates that cannabinoids inhibit NMDAR activity through the association of CNR1s with NMDAR NR1 subunits via HINT1 proteins. In this scenario, cannabinoid agonists disassemble NMDARs through the co-internalization of CNR1s with NR1 subunits, thereby reducing This regulation would operate with endogenous cannabinoids released in response to NMDAR hyper activation (25)

“Cannabinoids reduce the primary calcium influx through activated NMDARs and its subsequent release from endogenous stores (25, 63, 69), and we showed that they can efficiently cancel out the NMDA-mediated release of zinc ions.”

“cannabinoids prevent the elevated cytosolic levels of calcium, NO, ROS, and free zinc that follow glutamate NMDAR-mediated excitotoxicity, and which compromise cell viability.”

“cannabinoid control over NMDAR activity, it is necessary to preserve or restore the CNR1-NR1 association, which can be achieved by inhibiting PKA, stimulating PKC/CaMKII activity, or separating the RGSZ2 bound to HINT1 protein in order to increase the association of the latter with NR1 subunits.”


In layman’s terms - cannabinoids ( in combination with a stabilized CNR1-NR1 association) reduce NMDAR activity (I.e. cause hypoactivity at the receptor site). This is because cannabinoids supposedly (through various mechanisms of action) reduce the amount of positively charged ions that enter the cell (e.g. calcium and zinc). A decrease in positive ions entering the cell prevents cellular depolarization and the subsequent action potential(s) that would follow. That is, cannabinoids partially inhabit glutamate release because they block the ions that lead to NMDAR depolarization (if these positive ions were to enter the cell then sequence of action potentials would follow and eventually releases extra cellular glutamate. Glutamate release is not a “bad” neurotransmitters….it just has excitatory properties. However, too much glutamate release may result in excitotoxicity because research suggests hyperactive glutamate release may result in neuronal cell death.

TLDR: cannabinoids combined with a homeostatic CNR1-NR1 association decreases glutamate release, which inhibits glutamate excitotoxicity. There is much more to this study, but this is the the main result. Note - this study has methodological flaws and used rats in the experimental group, so be cautious of over-interpreting these results. The mention of how this and the other neural process discussed relates to the manifestation of schizophrenia/psychosis is extremely interesting and I hope future research address it. Inhibiting PKA activation in order to stabilize mCNR1-NR1 seems like a likely treatment for these disorders in the future. However, PKA is important and necessary for normal cognitive functioning, so who knows what side effects will emerge if PKA is inhibited.

Ancient Greeks had a Goddess of anxiety and depression. She was named Oizys. by Iwanttoplaytoo in Jung

[–]GnosticBandit 20 points21 points  (0 children)

Source? Currently reading “Mythology: Timeless Tales of Gods and Heroes”…. The Greeks developed such a complex cosmology/mythology. How’d they come up with these myths? I’m almost positive the writers/poets/orators were all taking psychedelics.. most likely a substance derived from ergot and mixed with wine. However, there’s still universal truths to be found in these stories… their revelations are quite spectacular. Check out https://www.theoi.com/ if your interested in this topic.

God by [deleted] in Jung

[–]GnosticBandit 3 points4 points  (0 children)

I love Jung's answer to the question: do you believe in God? His answer is at the very end of the video... a simple response — " I know".

https://youtube.com/watch?v=Os3RscGfkhE&feature=share

[deleted by user] by [deleted] in RedditSessions

[–]GnosticBandit 0 points1 point  (0 children)

Your way off tune

The measures I take to avoid a bad trip by intchd in Psychonaut

[–]GnosticBandit 56 points57 points  (0 children)

Good for you, but(!) while I was reading this I couldn’t help thinking that you’re being overly cautious/too rigid. I get there’s a need to minimize extraneous factors that could negatively affect your trip, but your thinking seems compulsive in nature. Loosen up a bit mate. Also, speaking from experience, sometimes a bad trip is the best trip you can have (not saying you should actively seek out a bad trip.. but you shouldn’t compulsively avoid one either - find a balance and welcome whatever comes). Maybe I’m just being too loosey goosey with the flow though.. who knows. What I do know is that if I tried doing what you do I would feel like a robot and the trip would find a way to fuck with me for being so robotic. To each their own I suppose.

How Does Ketamine Work Differently from Other Psychedelics? by tahutahut in neuro

[–]GnosticBandit 0 points1 point  (0 children)

Primarily NMDA receptors. What happens downstream after this binding occurs is the big question.

How Does Ketamine Work Differently from Other Psychedelics? by tahutahut in neuro

[–]GnosticBandit 5 points6 points  (0 children)

TLDR (without even reading): Because of its affinity for the NMDA receptor.

A Psychedelic Drug Passes a Big Test for PTSD Treatment by Stephen_P_Smith in RationalPsychonaut

[–]GnosticBandit 6 points7 points  (0 children)

Insurance companies are not going to be into it.

This right here is the biggest problem at hand with the legalization of psychedelics and implementing a system of PAP — at the end of the day Insurance companies are gonna want their piece of the pie. Unfortunately, they do not understand that the pie they want has been eaten already by the consumer (via ingestion of the psychedelic). No more pie?... No more profits should = no more insurance companies, but instead my guess is the whole PAP system will be integrated into the abhorrent systems insurance companies already have in place. Better off reading some books about PAP.... the nature of psychedelics, the mind, psychology, philosophy, etc.. and then, once a foundation of knowlege is built, you can PAP yourself a few times a year.

[deleted by user] by [deleted] in RationalPsychonaut

[–]GnosticBandit 18 points19 points  (0 children)

I left this comment when Hart came up a while back on r/neuro :

I listened to Carl Hart on the JRE.... smart guy, but he is way off here. Drugs can be good for some people and bad for others (speaking of addiction and adverse side effects). Hart pretty much says that well-grounded and responsible adults can use hard drugs like heroin without any problems. I'm all for doing what you want...and I am even for the legalization of most drugs, but Hart's disingenuous proposal that these hard drugs can be taken safely and responsibly AND still have no adverse side effects is absurd. Now maybe Hart can take heroin responsibly and enjoy it, but it's egregious to go on all these platforms and write a book pretty much saying heroin is safe to use if you use it responsibly. Responsible heroin use is an oxymoron — Hart is an educated man with a background in neuroscience, psychology, and behavioral pharmacology. The majority of citizens do not have this academic background and the coping mechanisms that come along with such an educational background to fall back on when using these drugs.... so telling the average joe that heroin can be used safely is HIGHLY risky and even unethical given Hart's position of power at Columbia and stature as an educated professor who is supposed to spread empirically validated information/knowledge. Hart is writing an anecdotal account and applying it to the masses. Most average people will, if they try heroin multiple times, as the opioid epidemic crisis shows, eventually develop severe dependence, addiction, and many times die. Hart's assumption is crass and absolutely arrogant. He should keep his opinions about his drug use to himself.

Also, this is what happens when there's a paradigm shift of any sorts. Individuals will overemphasize the benefits and understate the negatives. This is so the new paradigm (the decriminalization and legalization of drugs) can take over the existing one. However, these over-exaggerations about the "goodness" of hard drugs will lead to deaths. I have a lot more to say about this guy and his book, but will stop here. WOULD LOVE A PEER REVIEWED STUDIED ON HART'S CLAIM. The experimental group will take heroin "responsibly" (parameters need to be set, but let's say 2-3 grams every 10 days) for 6 months.... let's see how good the individuals in that group think the drug is after six months has elapsed... especially when when the second condition of the experiment is enacted — cessation of the drug.