# Question
Title: Basis for "we make 35,000 decisions a day" statistic
In an advertisement by Microsoft for their To-Do product they use a statistic that we "make over 35,000" decisions a day. Unsurprisingly, they don't cite a source. Is there any scholarly basis for such a figure?

Even though there are usually 86400 seconds in a day (that works out to one decision every ~2.5 seconds if you include time sleeping) you could reasonably make an argument for that number. I say that, however, without a good operational definition for "decision". Executive function researchers may outright say that figure is bunk.

**Q:** Careless usage aside, is there a source for this statistic and/or a more scholarly correct number for the "number of decisions we make each day"?

Apparently the statistic is widely "cited" (without proper citation) online. Here are a few instances (if any are left as comments I'll include them below):

This question was asked on Skeptics SE, but closed without a response:
Do people make 35000 decisions a day? \[closed\]

# Answer
> 18 votes
Concurring with the comments on the Skeptics question, I am also not aware of a standardized operationalization of "number of decisions" that could be used to produce a meaningful measure for this, and to my knowledge no (serious) research has attempted to calculate a daily tally.

This clearly poses little challenge for the numerous references to this and other unsourced/uncited statistics. While references on various blogs, social media, self-help books, and other questionable sources are not of much note, there are a few citations made on media outlets that readers might take more seriously, such as:

The Telegraph UK (2016):

> They say the average person makes 35,000 decisions a day.

Huffington Post UK (2014):

> According to newspaper ‘USA Today’ the average adult makes about 35,000 decisions each day.

Phrasings such as "they say...", "it is thought that...", "according to various online sources...", etc are not very committal about validity, and the above quotes do only appear in the "Lifestyle" sections of these newspapers, so there is not much impetus for journalistic integrity.

Articles often mention other corroborating research to make the "35,000" statistic sound more plausible. An example from a different Huffington Post UK (2011) article (found on Mirror magazine as well):

> The average Brit makes 773,618 decisions in a lifetime but lives to regret as many as 143,262 of them, a study has found. ... The study of 2,000 indecisive Brits, by Nintendo Puzzler Mind Gym 3D, found that ...

That's right, Nintendo - the game system company - purportedly conducted this apparently unpublished poll, giving a much lower number of decisions statistic (around 27 per day).

Another example on a Psychology Today (2012) article:

> According to a survey by Columbia University decision researcher, Sheena Iyengar, the average American makes approximately 70 conscious decisions every day.

Sheena Iyengar, a professor of business at Columbia, also apparently did not publish her survey findings, but she does discuss it on TED (2012):

> I recently did a survey with over 2,000 Americans, and the average number of choices that the typical American reports making is about 70 in a typical day.

Here is something from reference.com:

> Each individual is different, so it is impossible to pinpoint a specific number of daily decisions that applies to every individual, but Time magazine puts the number in the thousands.

The referenced Time Magazine article indeed says:

> Every day, we face thousands of decisions both major and minor ...

How silly. Here is another interesting item from reference.com:

> The average person has about 48.6 thoughts per minute, according to the Laboratory of Neuro Imaging at the University of Southern California. That adds up to a total of 70,000 thoughts per day.

The source cited for this amazing claim does not corroborate this ... any more, but it did!

> How many thoughts does the average person have per day? \*70,000

So let's see, 70k thoughts per day, 35k decisions per day ... that's about 1 out of every 2 thoughts is a decision? The other 1 in 2 thoughts must be the ones about sex. But wait, what's the asterisk (\*) about? Ah:

> \*This is still an open question (how many thoughts does the average human brain processes in 1 day). LONI faculty have done some very preliminary studies using undergraduate student volunteers and have estimated that one may expect around 60-70K thoughts per day. These results are not peer-reviewed/published. There is no generally accepted definition of what "thought" is or how it is created. In our study, we had assumed that a "thought" is a sporadic single-idea cognitive concept resulting from the act of thinking, or produced by spontaneous systems-level cognitive brain activations.

The most credible corroborating research I've seen so far is the Wansink & Sobal (2007) paper: "Mindless Eating: The 200 Daily Food Decisions We Overlook", published in the journal Environment and Behavior. Keeping in mind that neither author is a cognitive scientist, and that this article concerns nutritional health, not psychological measurements, and that the lead author has faced dozens of retractions and corrections of his published papers, and was barred from research due to scientific misconduct, this is nonetheless a very well cited paper. In the paper, the authors explain:

> One hundred and fifty adults ... were initially asked to estimate how many total decisions about foods and beverages they make in one day. They were then asked six questions about snacks, six questions about meals, and six questions about beverages. ... While the typical person estimated they made around 15 food and beverage decisions in a day, the average that was calculated from subsequent questioning was 219, approximately 200 more.

I'm not sure if the authors truly believe that this method conclusively sets the total number of daily food-related decisions, or if they were just pointing out that we are often not aware of many of the decisions that we make, but it is not difficult to imagine that if the survey contained more or fewer detailed "subsequent" questioning, then the total number of decisions would increase or decrease accordingly. Regardless, this paper is an important reference for the author's self-help book \- Mindless Eating (2006):

> The phrase "mindless eating" refers to the empirical finding that people make nearly 20 times more daily decisions about food than they are aware of (an average of around 200 each day).

With a range of between 27 and 35,000 decisions per day, I think you can just pick any number you want for this statistic. These types of claims are often associated with reference to research on decision fatigue and ego-depletion \- a largely discredited idea about the limits of human capacity for decision making.

Anyways, I hope you had as much fun reading this answer as I had writing it. Also, according to the Arnon Science Foundation, recent research proves that voting up this answer will make your day up to 32% better, so be sure to improve your average daily decision making by showing your support!

# Answer
> 3 votes
A serious answer exists to a sort-of-related question though, you can track the "energy budget" of the brain and see how much glucose/oxygen it's burning. 'Number of decisions' might be a silly way to talk about it, but \[metabolic\] brain effort can be quantified and it does make sense to ask how high it is and how much it changes over the course of a day. There are lots of studies comparing the level of activity associated with some task with resting-state activity: you could take the size of the difference for some reference task (it's gonna be small) and work out a plausible range for the amount of time the brain spends working at least that hard over the course of a normal day. There's a quick fact-collection on this stuff here (2002): http://www.pnas.org/content/99/16/10237

# Answer
> -1 votes
Apparently, Dr. Eva Krockow was the one to make that statement.

https://edition.cnn.com/2022/04/21/health/decision-fatigue-solutions-wellness/index.html

based on these articles.

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Tags: decision-making, executive-function
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# Question
Title: Why do fNIRS devices commonly use two different frequencies?
One of the most common techniques used for functional neuroimaging nowadays is functional near infra-red spectroscopy (fun fact: IIRC Natalie Portman worked on a research paper involving fNIRS as the modality), which shines near infrared light into the brain from a source to a detector (both called optodes) in a "banana" shape.

It's not uncommon to read that most of these devices, be they continuous wave (CW) or one of the two kinds that involve fast modulation, frequency domain (FD) or time domain (TD), require two separate frequencies to be emitted. For instance, NIRx explains it as follows on their website:

"For neuro-imaging applications it is by far most common to illuminate with two discrete wavelength, which is the minimum requirement to assess relative variations of both oxygenation states of the hemoglobin molecule independently."

Why is that the case?

I haven't delved into the intricacies of it, but no reason immediately jumps out at me. For instance, in the case of CW, the relative difference in intensity is all that matters, so why do we need two frequencies?

# Answer
> 1 votes
Basically, you have two unknowns, so you need two equations.

From Wikipedia:

> Using a dual wavelength system, measurements for HbO2 and Hb can be solved from the matrix equation

With just one measurement, you could still describe relative changes in the signal over time, but you wouldn't be able to measure the ratio of the two. That might be sufficient within a given experiment, but wouldn't result in numbers that you could compare to other recordings. Each recording is going to have a distinct signal-to-noise ratio based on things like the amount of tissue you're imaging through: most of the light is going to be lost no matter what the signal is.

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Tags: neuroimaging
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title: How does Cannabis cause psychosis?

text:
# Question
Title: How does Cannabis cause psychosis?
Whenever I research cannabis induced psychosis, I mostly get two types of results:

1) Cannabis causes psychosis directly and a bunch of other issues (mostly misleading propaganda)

2) There is no evidence that cannabis actually causes psychosis directly, rather it seems to be a correlation issue. (also misleading propaganda)

However, my two best friends experienced permanent psychosis immediately after a heavy cannabis use episode (on separate occasions).

I am convinced that cannabis is perfectly capable of causing or "unlocking" psychosis. I don't think that there is any question to this.

But how does it actually work?

In one of the cases, my friend had some very strong cannabis to smoke, after which he started to hear voices, and this never ended, even months after stopping smoking. Only after anti psychotic medication (Seroquel) did the symptoms stop, and they seem to be permanent, stopping the medication causes the symptoms to come back.

From what I understand, Seroquel suppresses dopamine, while cannabis has nothing to do with dopamine.

So how does cannabis induce a dopamine related disorder?

# Answer
> 2 votes
Research into the "how" is ongoing. From the most recent review I could find, the effect of cannabis on the dopamine system is not entirely elucidated, even on a quantitative level:

> The onset of effects of THC appears to be delayed relative to the onset of other psychotomimetic drugs, suggesting that the effects of THC may be downstream to its primary site of action. Given that the endocannabinoid system is principally a neuromodulatory system, perhaps the psychosis-relevant effects of THC are related to the consequences of CB1R activation on other neurotransmitter systems implicated in the neurobiology of psychosis. Cannabinoid Dopaminergic Interactions: Single doses of dopamine (D2) receptor antagonists (olanzapine and haloperidol) have been shown to reverse the acute psychotomimetic effects of THC in healthy subjects in two HLS (5, 6) although not in the third (7). Furthermore, chronic D2 antagonist treatment failed to protect schizophrenia patients from the symptom exacerbating effects of THC (32).
>
> Preclinical studies demonstrate that THC administration increases striatal dopamine release by 25-100%, but the human data are mixed with two studies reporting no significant increase (91, 92) and one study reporting a 3.9% increase in striatal dopamine release (93). These studies had small sample sizes and differed in the THC doses, routes of administration and imaging methodology. A re-analysis combining data from two studies (91, 93) reported a significant but small increase in THC-induced dopamine release (94). Of note, in contrast to amphetamine and cocaine, which induce large increases in striatal DA release (10-30%) in humans, THC at doses that produce robust behavioral effects induces small (2-5%) increases in dopamine release. More recently, Kuepper et al, 2013 reported that individuals with psychosis as well as those with a family history of psychosis demonstrated THC-induced striatal dopamine release, but this was not observed in the controls suggesting that dopamine may be involved particularly in the effects of THC in those with an increased risk for psychosis (95).

The review also covers several genes that have been implicated in both schizophrenia and vulnerability to THC-induced psychosis:

> In the striatum, clearance of synaptic dopamine is highly dependent on the dopamine transporter (DAT). A polymorphism of the DAT1 gene is associated with lower enzymatic activity and thus, higher dopamine levels in the striatum, and has previously been associated with schizophrenia (81). Bhattacharyya et al. reported that individuals with the 9-repeat allele showed increased sensitivity to acute THC-induced psychotic symptoms (82).
>
> The enzyme AKT1 inactivates glycogen synthase kinase by phosphorylation and their interaction has been implicated in schizophrenia (83, 84). Cannabinoids stimulate the AKT1 pathway via CB1Rs and CB2Rs. Bhattacharyya et al found that a polymorphism of the AKT1 gene (the GG genotype of the SNP rs1130233) moderated sensitivity to the acute psychosisinducing effect of THC (82). Furthermore, a synergistic influence of DAT1 and AKT1 genotypes on THC-induced psychotomimetic effects was also reported.

All the DAT/AKT1 data on healthy individual using cannabis with is based on exactly one study, so I reproduce their graphical finding below:

Alas they only reported total PANSS.

In the review, there's more discussion of COMT, which has seen more attention, but suffice to say the results on that have been mixed. It remains to be seen in the DAT1/AKT1 study can be replicated. It does seem that AKT1 alone has an impact, based on more studies that found the same polymorphism of AKT1 impacts first-episode psychosis in cannabis users and psychotomimetic effects in healty cannabis smokers.

I find it interesting that yet another study on first-episode psychosis has implicated AKT1 polymorphism, however, this time with an interaction that enhanced its effect... except that the other gene involved was not DAT1 (as in the case of psychotomimetic effects on healthy individuals) but rather with DRD2.

Perhaps 10 years from now, this question will have a less tentative answer.

To further complicate the issue, cannabis has more than one active substance:

> CBD is the second most prominent cannabinoid in cannabis. Unlike THC, CBD displays CB1R antagonism/inverse agonism amongst several other modulatory effects on the endocannabinoid system. The potential antipsychotic effects of CBD have drawn increasing attention (20) and some HLS have examined the interactive effects of THC and CBD. Pretreatment with CBD is associated with lower THC-induced psychotomimetic effects, paranoia and verbal memory impairments (12, 21). Furthermore, while THC resulted in increased psychotic symptoms and skin conductance responses during processing of fearful faces; CBD, led to a reduction in anxiety and a decrease in skin conductance response (22).

For more, there's a slightly older review that's freely available in PMC.

Yet another review that focuses only on THC's effect on dopamine mentions some of the challenges in observing dopamine changes in humans following THC administration: insufficient PET camera resolution and doses that are substantially less than those used in animal models.

# Answer
> 1 votes
Cannabis induced psychosis is very prevalent. Statistically Cannabis use doubles the risk of developing psychosis in vulnerable people. There even exists a relationship regarding the dose used and the age of first use. Gene-environment interactions that modulate the association between cannabis use and the presence of psychosis have also been described.  and Cannabis is involved in approximately 50% of psychosis, schizophrenia, and schizophreniform psychosis cases.

Here are more sources on NCBI and Nature indicating that heavy cannabis use can induce psychosis.

From my perspective, the reason why cannabis can cause psychosis is because THC binds to CB1/2 receptors in the brain and directly affects dopamine transmission in the mesolimbic area. THC also causes dopamine from the VTA to be released in to the NAcc, your reward centre of the brain.

Chronic artificially elevated levels of dopamine in the mesolimbic area obviously also affect the activity of D2 receptors in the mesolimbic area where a hyperactivity is part of the condition of schizophrenia patients.

To understand why, you would want to take a look at the **D**opamine **H**ypothesis which postulates that psychotic symptoms are caused by a D2 hyperactivity in the mesolimbic area and a hypoactivity in the prefrontal cortex.

Heavy use of THC probably causes constantly elevated dopamine levels in the NAcc.

I can say from experience that heavy use of Cannabis can cause psychosis after ~3-6 months and D2 blockers completely negate the psychotic effects, suggesting that elevated dopamine levels in the NAcc/mesolimbic area might lead to sufficient D2 hyperactivity to cause positive symptoms of psychosis as postulated by the DH.

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Tags: psychosis
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title: Can schizophrenia and adhd interact?

text:
# Question
Title: Can schizophrenia and adhd interact?
So my understanding is that schizophrenia occurs when there is high dopamine activity. On the other hand adhd occurs due to low dopamine activity.

So here's my question: if the probability of someone suffering of schizophrenia is p. And the probability of someone suffering from adhd is P. Then naively assuming exclusive events one would expect the probability of having both schizophrenia and adhd to be P times p. But maybe they can interact with each other the probability of suffering from both is different? (Can someone direct me to a study?)

# Answer
There needs to be a lot more changes in the brain than just high dopamine for someone to have schizophrenia. Many people would have elevated dopamine and not be schizophrenics. For example, impulsive and aggressive people have high dopamine but are not schizophrenics. Happy people have high dopamine too!

https://my.clevelandclinic.org/health/articles/22581-dopamine

Moreover, high dopamine in schizophrenia is characterized by it being high in particular areas and particular cells, not the whole brain. Schizophrenia is also categorized by misconnected brain regions, cellular type imbalance (e/i ratio), misregulated synapses, and more! Dopamine alone is not enough to categorize schizophrenia or ADHD!

https://www.healthline.com/health/schizophrenia/schizophrenia-and-dopamine#:~:text=Increases%20in%20dopamine%20activity%20in,factors%20involved%20in%20schizophrenia%20symptoms.

Because mental illnesses are poorly understood and share a lot of commonalities between them, psychiatrists often diagnose by symptoms and expertise as opposed to biological changes. We do not know enough biology (yet) to look at a brain and say schizophrenia or adhd; we look at a person's behavior and symptoms, etc.

DSM 5 is what psychiatrists use to diagnose: if you look at the section for schizophrenia or adhd, there is not much biology, just behavior.

https://my.clevelandclinic.org/health/articles/24291-diagnostic-and-statistical-manual-dsm-5

It is not possible to calculate the probability of ADHD and schizophrenia from dopamine alone because dopamine misregulation in schizophrenia is region-specific and needs a lot more brain changes with it. Also, there is no accepted way of biologically differentiating schizophrenia or ADHD; it is only (right now) by the person's behavior and appearance etc.
> 0 votes

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Tags: schizophrenia, adhd
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# Question
Title: How big is the risk of schizophrenic delusion being mistaken for true gender dysphoria? What implications might this risk have?
I'm no expert, but below are some premises I've gleaned from my independent research.

* Schizophrenia usually does not manifest until a person's 20s. The onset is often gradual, during which time the person will have symptoms that can fly under the radar for years before rising to a level warranting a diagnosis.
* I have read mixed reports about the prevalence of gender dysphoria-like delusions among schizophrenics, but it appears that it does happen.
* Gender-affirming medical care, like hormone therapy and surgery, is sometimes provided to teenagers, the rationale being that earlier affirming care improves mental health outcomes.

I presume that gender-affirming medical professionals are aware of and on the lookout for other potential causes of gender dysphoria, including confounding mental health issues. But if schizophrenia usually cannot be diagnosed until adulthood, doesn't this mean there's a risk of a young person presenting with gender dysphoria, ultimately receiving irreversible gender-affirming care, later being diagnosed and treated for schizophrenia, then finding that the gender dysphoria was actually a delusion caused by the schizophrenia, and finally regretting their transition? This is, in fact, exactly what is described here.

So, how big of a risk is this? Is it a big enough risk to justify delaying medical transition until the patient is older? Might it justify the use of antipsychotic drugs as a test to weed out those who are likely to regret their transition later?

(I realize this question might sound like I'm fishing for a justification for medical discrimination against trans people since two of the questions in the above paragraph look an awful lot like gatekeeping, and the exploratory antipsychotics idea sounds particularly unethical to me. I assure you that's not where this is coming from. I am a trans ally and this question arose out of my various interactions with gender-critical types who often argue some variation of "transgender people are mentally ill and gender dysphoria is nothing more than a delusion.)

# Answer
Pre-syndrome schizophrenia still shows cognitive difficulties, social difficulties, etc. Perhaps the most essential characteristic of schizophrenia is cognitive difficulty, which manifests much earlier than late adolescence and schizophrenia diagnosis.

This paper: "*Elvevag, B. & Goldberg, T. E. Cognitive impairment in schizophrenia is the core of the disorder. Crit. Rev. Neurobiol. 14, 1–21 (2000)* is behind this reasoning."

So here is a paper that look at children who later develop schizophrenia "\*Childhood intellectual differences between schizophrenic adults and their siblings. https://psycnet.apa.org/record/2013-39739-017\*" and shows that even as a child, cognitive difficulties and characteristics of schizophrenia show up.

There is a lot of active research being done on UHR (ultra-high risk) individuals for psychosis, and those are pre-diagnosis but are at very high risk of descending into full-blown schizophrenia. Many studies cover this, yet there is still no reliable way to figure out who will have schizophrenia and who will not. So, in part to answer your question, we can tell who is at risk for schizophrenia pretty early on but cannot yet say for sure who will.

So if someone comes with gender delusions, one can check for cognitive difficulties and see if they're at risk for schizophrenia, but there's no way of telling, especially very early. Besides, people can have both gender delusions and schizophrenia, or a host of delusions without schizophrenia, or even hear voices and be completely healthy. In human health, you can get any combination of things and be perfectly healthy or be very ill and it's often hard to tell which you will be! This paper even looks at people who hear voices and are healthy in the sense that they do not need any medical care:

"*Toh WL, Thomas N, Robertson M, Rossell SL. Characteristics of non-clinical hallucinations: A mixed-methods analysis of auditory, visual, tactile and olfactory hallucinations in a primary voice-hearing cohort. Psychiatry Res. 2020 Jul;289:112987. doi: 10.1016/j.psychres.2020.112987. Epub 2020 May 19. PMID: 32446007.*"

In summary, the reason that gender delusions are not (usually) immediately schizophrenia is that there needs to be cognitive impairments and other changes, even when a child, to go with delusions to be at risk for schizophrenia. And we can only say 'at risk' because we do not know enough to tell. Really, as of now, we can only truly say who is schizophrenic and who is not upon full-blown manifestation, usually in late adolescence.

A good psychiatrist would explore all possible disorders and take preventive measures for all disorders the person is at risk for at each stage of development. Nutritional supplements, lifestyle changes, and better social support can help prevent a lot of mental illness at each stage of life.
> 2 votes

# Answer
Gender dysphoria is characterized by a persistent discomfort with one's assigned gender and a strong desire to be of another gender. Schizophrenia, on the other hand, is a severe mental disorder characterized by delusions, hallucinations, disorganized thinking, and impaired cognitive function.

But NOT JUST delusions. And that's what many people don't get.

A diagnosis of schizophrenia requires the presence of certain core symptoms, with careful consideration of their duration, frequency, and impact on the individual's daily life. **The symptoms are categorized into positive and negative symptoms.**

https://en.wikipedia.org/wiki/Positive\_and\_Negative\_Syndrome\_Scale

**Positive Symptoms: These symptoms involve an excess or distortion of normal functions.**

* Hallucinations: False perceptions that are not based on external stimuli. Auditory hallucinations (hearing voices) are common, but visual and other sensory hallucinations can also occur.
* Delusions: Strongly held false beliefs that are not influenced by reasoning or evidence to the contrary. Delusions can be paranoid (believing others are plotting against them), grandiose (believing in exceptional abilities), or bizarre (implausible and not based in reality).
* Disorganized Thinking: Individuals may have difficulty organizing their thoughts, leading to incoherent speech and difficulty expressing themselves logically.
* Disorganized or Abnormal Motor Behavior: This can manifest as unpredictable and inappropriate movements, agitation, catatonia (lack of movement or response), or repetitive actions.

**Negative Symptoms: These symptoms involve a decrease or loss of normal functions. They include:**

* Affective Flattening: Reduced emotional expression and responsiveness.
* Alogia: Poverty of speech; difficulty or inability to maintain normal conversation.
* Anhedonia: Reduced ability to experience pleasure from activities previously enjoyed.
* Avolition: Decreased motivation and difficulty initiating and sustaining purposeful activities.
* Social Withdrawal: Reduced interest in social interactions and a preference for isolation.

So it's not just some delusion. Otherwise you can claim 99% of human population being schizofrenic on their beliefs.
> 1 votes

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Tags: schizophrenia, transgender
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# Question
Title: Why do antipsychotics bind to D2-like instead of D1-like receptors?
My understanding is that:

1. The dopamine hypothesis of schizophrenia states that the positive symptoms are a result of excessive neurotransmission of dopamine in the mesolimbic pathway.
2. D1-like receptors have an excitatory effect on the postsynaptic neuron, while D2-like receptors have an inhibitory effect.
3. The goal of first-generation antipsychotics is to block D2-like receptors so that dopamine cannot bind to them, which prevents the typical postsynaptic response.

Given the above, I would expect that preventing dopamine from binding to D2-like receptors would lead to an increase in the probability that the postsynaptic neuron will fire, which would increase dopamine neurotransmission along the pathway. On the other hand, it would make sense to me if antipsychotics blocked D1-like receptors, since those have an excitatory effect. What am I missing here? Am I oversimplifying the effects of D2-like receptor activation?

# Answer
> 0 votes
There is a difference between the excessive transmission of dopamine and excessive neuron firing. The first can mean that a lot of dopamine will inhibit or excite neurons and cause them to fire more or less (depending on the neuron), but the second one means that the neuron is firing too much, which may be where your confusion lies!

Usually, the words misregulated or misfiring neurons are used to reduce confusion - we try to show that whatever the element of the brain is doing, it is not what it is supposed to be: too much or too little. Schizophrenia often involves a misregulated dopamine system, among other changes.

Here's a paper to describe the mechanisms of D2 receptors: *Ford CP. The role of D2-autoreceptors in regulating dopamine neuron activity and transmission. Neuroscience. 2014 Dec 12;282:13-22. doi: 10.1016/j.neuroscience.2014.01.025. Epub 2014 Jan 23. PMID: 24463000; PMCID: PMC4108583.*

And this one for the specific role of antipsychotics on d2 receptors: *Seeman P. Atypical antipsychotics: mechanism of action. Can J Psychiatry. 2002 Feb;47(1):27-38. PMID: 11873706.*

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Tags: neuroscience, schizophrenia, dopamine, psychosis
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# Question
Title: Why can some drugs make us hallucinate and think the hallucinations are reality?
The question above mainly applies to *dramamine*. I've only taken 1 tablet for carsickness, but I have read about experiences with that drug. I'm including other drugs that can make you hallucinate and think it's real.

Furthermore, **why can you still see the hallucinations as reality if you affirm to yourself that the things you see aren't real**?

# Answer
> 2 votes
In my opinion this has to do with how perception works in general.

There are many situations, where you "see" something, that is not there. Optical and other sensory illusions are a prime example. Usually these mis-perceptions result from sensory input that our organs of perception were not built to analyze. For example, the size-weight illusion stems from the fact that we don't have objects of equal size and equal outside material but differing weights in our natural habitat. You will easily recognize that all sensory illusions are induced by highly artificial stimuli such as straight and parallel lines, which have only existed in the most recent past and have as yet not had a big influence on human evolution.

In the case of drugs and hallucinations, your brain is stimulated in a way that is not meaningful for it, and it tries to make sense of what if "perceives" in the context of its evolution and experience. Obviously the stimulation by a certain drug comes close to what the stimulation would be like if outside reality were like you hallucinate it.

A drug induced hallucination is basically a sensory illusion, with the difference that you stimulate the brain directly, instead of the sensory organs.

To "break" an illusion, you need to provide a stimulus that overrides or "corrects" the misperception, e.g. a ruler to show that the lines are parallel (or not parallel) etc. Just knowing the truth (because you drew the lines yourself) doesn't change the effect.

Since drug induced hallucinations originate not in an outside sensory stimulus but in a direct manipulation of the brain, I would guess that touching the elephant head of your friend might not help to break the illusion -- you might even *feel* differently. But I have no experience with drugs and couldn't find any reports on this.

# Answer
> 0 votes
A lot of your perception / thought process and content are affected by Serotonin and Dopamine. Many drugs act on 5HT / Serotonin which augments the mechanisms / pathways which are hard wired to your thoughts and perception of reality. As of personal experience serotonin affects more of the content of thoughts whereas dopamine also affects the structure / flow of thoughts.

To illustrate this: "Serotonin is widely known for its effect on mood, but it also plays a role in memory, anger, fear, appetite, stress, addiction, sexual pleasure, sleep, pain \[...\]" which all have an effect on the content of your thoughts. As you all probably experienced in your life, a negative mood makes you inclined to negative thoughts, you all probably got angry because you were hungry.

Dopamine on the other hand is a neurotransmitter which plays a major role in psychosis. Racing thoughts, paranoia and delusions also affect the content of thoughts but its structure / flow is augmented as well.

Both play a crucial role in affecting your thought processes which in turn are part of your perception of reality.

Your perception of reality is a very complex process and a multitude of factors play into it, but the structure and content of information that flows through your brain which is a mix of thoughts and sensory input which together make up much of your constructed reality in your brain. "The brain constructs representations of what is sensed and thought about in the form of nerve impulses that propagate in circuits and network assemblies (Circuit Impulse Patterns, CIPs). CIP representations of which humans are consciously aware occur in the context of a sense of self."

I know from personal experience that perception of reality is affected by 5HT / D2 which is probably why drugs like LSD / MDMA / THC can induce mental illnesses such as depersonalization / dissociation / paranoia / psychosis. Those are all mental states which are affected a lot by neúrotransmitters like serotonin and dopamine.

Drugs act on these receptors and mechanism and augment pathways which influence neural patterns which ultimately make up your construct of reality.

In some cases paranoid thoughts also may induce fear which makes you less likely to question it's integrity and accept it as reality because you're in fight and flight mode.

With experience you can distinguish hallucinations from reality but it's still difficult to e.g. tell paranoid thoughts apart from rational thoughts.

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Tags: cognitive-psychology, psychopharmacology, hallucinations
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# Question
Title: How is it ascertained that people treated for persecutory delusions are not indeed being persecuted?
Many people suffering from persecutory delusions have very weird, clearly improbable stories about how they are being persecuted. However - correct me if I'm wrong - in many cases these stories are, at least theoretically, *possible*.

If, for example, someone believes they are harassed by a Satanic cabal that has hacked their computers and phones, and is exfiltrating data from said devices, makes certain they will not get a job by pulling strings from behind, sends goons to stalk them and chase them down the street while leaving little tangible evidence for its actions and this is all happening without any obvious reasons then, granted, in the vast majority of cases such a person will, indeed, be delusional.

Nonetheless, it is *possible* that such a person is *not* delusional and, instead, this is precisely what is happening. Add to the above story that the Government is plotting with the coven against this person and the story will *still* be possible, even if highly improbable. It might even be the case that the persecutors are subtly convincing everyone that their victim is delusional to gaslight their victim.

Is it a real worry that a person suspected of and treated for persecutory delusions is actually really being persecuted? Even if this is a very rare case it still seems to me that treating a person who is indeed being persecuted for persecutory delusions is one of the worst things that can be done.

How is it being ascertained that this situation does not happen? That a person suspected of persecutory delusions is indeed delusional and not actually persecuted?

# Answer
> 1 votes
By checking if they have a mental illness to go with it or not and if they have any proof or evidence besides what they are saying :)

A good psychiatrist would look at evidence from other areas: does the person have cognitive difficulties? Are they coherent? Are they organized in their speech? Do they appear healthy if I ask them about everyday items, stories, and things that happened to them other than the story? Do they have a healthy memory (again, when asking about other than the story)? If they have a delusional mental illness, I would find it hard to have anyone believe them, even if what they are saying is true.

Here's DSM 5 and it's what psychiatrists use to diagnose. So they will check for symptoms of schizophrenia (disorganized speech, memory problems, etc) or any delusion-related disorders. https://repository.poltekkes-kaltim.ac.id/657/1/Diagnostic%20and%20statistical%20manual%20of%20mental%20disorders%20\_%20DSM-5%20(%20PDFDrive.com%20).pdf

Furthermore, many people believe, for example, that the government is conspiring against them and are pretty healthy in every other way. Those people might just believe in something improbable. It could be true (or not) because we humans can be perfectly healthy and believe things that are not true. An excellent way to ascertain the truth is to always ask for evidence or proof, which I think is standard police/justice procedure. This will differentiate people who believe something vs people who know something!

Here's a really nice note about the psychology of belief: https://www.psychologytoday.com/gb/blog/finding-purpose/201810/what-actually-is-belief-and-why-is-it-so-hard-change

So, in short, it is ascertained by checking that person's full mental health and if they have any real proof or evidence of the matter besides what they say. They can be mentally ill, or healthy and believing in a false story, or that everything they are saying is true and happening as they say it. It will depend on the judgment of the psychiatrists and police etc, who see them.

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Tags: abnormal-psychology, psychiatry, diagnosis, ethics
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# Question
Title: What are your thoughts on Accelerated Resolution Therapy?
Recently I came into contact with my aunt, and it seems she has been doing very well. She has been developing a therapy technique that, she claims, helps resolves psychological problems from trauma, child abuse, domestic abuse, et cetera. She calls it Accelerated Resolution Therapy.

The essential thesis of her technique is that the problems caused trauma are being dealt with incorrectly. Therapists often try to help a patient deal with the facts of the situation. They help them understand what happened, why it happened, and why what happened should not impair their life. Unfortunately, therapy can often be slow in progress and some people never fully recover from a traumatic event. My aunt's therapy technique essentially discards the old method of dealing with facts and, instead, deals with memories and pictures. Coming to terms with facts, from a rational and conscious perspective, is usually achievable. But, for my aunt, the problem aren't the facts but the images revolving around those facts. Even when a person comes to understand their trauma, they still will suffer from depression, anxiety, and other psychological problems.

What she essentially does is encourage the patient to change the images to more positive, or, at the very least, into neutral memories. She does encourage them to change their knowledge on the matter; but, rather, she simply changes the physical memory into something less traumatic. The patient will still understand that they were wronged and hurt, but the image of the pain will be removed.

Usually I'm very skeptical with new therapy techniques and any practice that claims to solve problems within 2 or 3 sessions, but it honestly makes a lot of sense. It reminds me of ghost limbs and mirror therapy, and how placing a mirror next to a limb, in tact, will help a patient be relieved of his pain. He understands, clear as day, that he is missing a limb, but the physical image of having two limbs and seeing the limbs move removes many of the psychological problems associated with ghost limbs.

She has had peer reviewed studies and is encouraging training. So, what do you all think? Does it sound like it has potential, or is it just snakeskin oil?

Here is one study showing that patients experience relief from their symptoms within 1-5 sessions.

And another study. Another study. And another.

# Answer
My concern is that there are many therapies being broadly promoted without sufficient evidence of effectiveness and this one is calling itself 'evidence-based". I worry that time and resources are being invested and that clients are being promised amazing, if not unbelievable, benefits. Clients may not be sophisticated consumers and I would hate for them to be misled by such inflated claims. I believe that we have a duty to be skeptical before jumping on board the 'next best thing' bandwagon. After all, much harm has been done in the past by advocates of sham therapies (think 'the schizophrenogenic' mother and Bateson's 'double bind' theory of schizophrenia and therapies endorsed by Jay Haley et al).

Taken directly from the ART website:

"Accelerated Resolution Therapy is a form of psychotherapy with roots in existing evidence-based therapies but shown to achieve benefits much more rapidly (usually within 1-5 sessions). Clients with depression, anxiety, panic attacks, post-traumatic stress disorder (PTSD), substance abuse, sexual abuse and many other mental and physical conditions can experience remarkable benefits starting in the first session."

It is surprising to me that this treatment - 'Accelerated Resolution Therapy' (ART) would even be recognized by SAMHSA \[https://nrepp.samhsa.gov/ProgramProfile.aspx?id=7#hide4\] as an evidence-based treatment. The data on ART is limited to 1 small sample RCT in which ART was compared to an attentional placebo, not a credible alternative treatment. Standards promulgated by APA Divison 12 based on Chambless and Hollon (1998, p.8) require at least two well controlled studies be conducted- (one ideally independent of the original investigators)

"As is the case in research in general, replication is critical, particularly replication by an independent investigatory team. The requirement of replication helps to protect the field from drawing erroneous conclusions based on one aberrant finding. Replication by an independent team of investigators also provides some protection against investigator bias or reliance on findings that prove unique to a particular setting or group of therapists. Thus, only when a treatment has been found efficacious in at least two studies by independent research teams do we consider its efficacy to have been established and label it an efficacious treatment \[highlighting added\]. If there is only one study supporting a treatment's efficacy, or if all of the research has been conducted by one team, we consider the findings promising but would label such treatments as possibly efficacious, pending replication." (p.8)

As noted in the single RCT manuscript (Kip et al., 2013) itself:

"A limitation is that the ART intervention was not compared to an active psychotherapy regimen, such as PE. Thus, no direct comparison of treatment efficacy of ART versus current firstline treatments (PE, CPT, and EMDR) can be made. Second, by design, the AC group was not parallel in contact hours to the ART intervention. " (p.1307)

This is pretty limited evidence on which to promote a new treatment. It was also surprising to me that:

1. the 'intervention' itself can be delivered delivered in as little as 2-5 60-75 minute sessions \[as little as 120 minutes of an active intervention!\]; and
2. the training and supervision of clinicians was limited as follows: "Clinicians were trained in ART over 2 days using the ART manual and supervised practice."

It is even more baffling that this intervention could be so highly effective with complex clients who have PTSD and multiple comorbid disorders. Here's what the ART website says:

Clients with depression, anxiety, panic attacks, post-traumatic stress disorder (PTSD), substance abuse, sexual abuse and many other mental and physical conditions can experience remarkable benefits starting in the first session. (highlighting added)

"In ART, the eye movements are thought to be conducive to sorting out problems quickly through increasing the integration of activities in the left and right sides of the brain. These movements also seem to help the client process information by producing a deep feeling of relaxation. Yet ART is not hypnosis. and

Importantly, clients do not even have talk about their traumas or difficult life experiences with the therapist to achieve recovery.

\[downloaded from http://acceleratedresolutiontherapy.com/.\]

Does this seem like a reasonable explanation of a therapeutic mechanism to you?

Given the fact that this was a small sample RCT compared against a non-credible attentional placebo, how do we know that these findings are not simply the result of positive investigator/clinician expectancies and essentially a placebo effect unrelated to any of the hypothesized mechanisms of treatment?

It is so attractive to belief that there are fast, easy and extremely effective treatments that require virtually no training or supervision vs. well-established treatments that are so difficult to master and deliver with fidelity and require intensive training and supervision \[in the VA, clinicians might achieve competency in CBT if they complete a 3 day workshop combined with at least six months of weekly 90 minute supervision sessions on cases with bi-weekly submissions of tapes rated on the CTS.\].

I did find the material on the ART website rather disturbing in terms of inflated claims of efficacy with testimonials from individuals to the effect that 1 hour of ART fully resolved their longstanding complex psychological problems when no previous therapies had been effective. If I made these types of claims on my website I would be in violation of the APA ethics code.

I do have a personal 'iron in the fire' in the sense that I devote a lot of my time to training and supervising clinicians in CBT and it is a difficult , resource intensive and time consuming process to achieve competency as a CBT clinician, let alone to be able to treat highly complex patients with co-occurring illness. In my own daily therapy practice I try to adhere closely to good CBT practices and I strive to improve my efforts with results that periodically fall short of my high expectations.

I look forward to seeing additional data on ART and it would be absolutely wonderful if additional studies-- controlled trials where ART is compared to a credible alternative therapy (CPT or PE) confirm these initial findings-- because this would be wonderful for patients.

In the meantime, I worry that we are investing our time chasing mirages instead of investing in and delivering established effective evidence-based treatments to our patients.
> 2 votes

# Answer
This sounds suspiciously like *Neuro Linguistic Programming*:

> Changing the point of view from which a memory is viewed has a profound impact on a person’s understanding and emotional response to the content of the image. A variety of specific ways of changing visual perspective are presented, including the important distinction between associated images (seeing out of your own eyes) and dissociated images (seeing from an outside point of view). The therapeutic usefulness of these understandings in the treatment of phobias and couple and family problems is indicated. - Neuro-Linguistic Programming (NLP): Changing Points of View.

While NLP is now considered a pseudo-science, I do believe some of its beliefs and findings have been examined further to create some modern techniques under the framework of recent evidence based treatments.
> 0 votes

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Tags: psychology
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# Question
Title: Why do people tend to put stigma on victims of offences against the person such as rape or bullying?
**Introduction:**

Blame against victims, regarding offences against the person, such as rape or bullying, seems to be a generally consistent social phenomenon, regardless of cultural or historical context.

It is usually the victim who feels deep shame and embarrassment (to the extent of committing suicide or going insane) and it is also the public who also put them to shame and embarrassment in either explicit or implicit ways.

**Question:**

But why does the victim feel shame? Why is the public response insulting the victim for being a victim?

**Some thoughts:**

My own hypothesis is that being a victim of a humiliating offence is unconsciously perceived (on an evolutionary psychology level) as a major weakness of the individual, to the extent of becoming a vulnerability (or liability, if you will) for the whole social group.

(In contrast, the perpetrator of humiliating offence seems to be generously spared retribution by the social group and probably there are evolutionary psychology perspectives on this?)

All this being speculations, of course, I am looking for scientific research of victim blaming in the context described. Ideas for social experiments applicable to this subject-matter are also welcome.

# Answer
> 2 votes
**But why does the victim feel shame?**

Victims feel guilty for not preventing the victimization. Even going so far as to consider that they may have caused it in some way, or somehow were deserving. In the case of crimes such as sexual assault this is emphasized by the social stigma of being “impure” after an attack.

https://psycnet.apa.org/record/2021-82681-001

**Why is the public response insulting the victim for being a victim?**

One reason is because people do not want to consider it could have happened to them. By pointing out where a victim went wrong they distance themselves from the similarities between themselves and the victim.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9455198/

There is much speculation because people are not often willing to admit to victim blaming so getting at the roots of this behavior is difficult.

# Answer
> 1 votes
There are several perspectives to address this question. I personally believe they have more overlap than not, but please note the later sections of this answer may contain some less conventional opinions.

## Just World Theory

We could say that people are motivated to believe in a world that is inherently, predictably fair (the **just world hypothesis**). This allows them to predict and control their own safety and future (mis)fortune. For example, if a person endorses a just world, and they believe that they are a good person, they can believe that tragedy will not befall them as a manifestation of justice (Lerner, 1965).

If something terrible happens to a victim with no fault of their own, that serves as a contradiction to the just world hypothesis, which causes **cognitive dissonance**. To alleviate the dissonance, people can *re-appraise* the situation and assign blame to the victim--to keep the just world belief. Experiments find that just world beliefs and victim blaming are positively associated (Reichle et al., 1998).

The just world hypothesis can arguably be considered a **cognitive bias**, and it *fuels* cognitive biases such as those involved in victim blaming, such as *defensive attribution* (Shaver, 1970).

## Social incentives

When people who are dominant or similar to the observer engage in cruelty, that may lead them to justify the behaviour because people tend to conform and defend those they like. If you defend a perpetrator, you have to blame the victim to prevent cognitive dissonance. For example, studies find that men are more likely than women to blame female victims of sexual assault because of such attribution biases (Grubb & Turner, 2012).

## Moral Reasoning

Social influences aside, is belief in a "just world" causally linked to victim blaming? I believe the construct may be a bit too broadly defined. Just for some perspective, Kohlberg's theory of moral development (Kohlberg & Hersh, 1977) divides moral development into three stages (with two sub-stages each), and I think the first 'preconventional' stage aligns with the kind of just world perspective that leads to victim blaming. **Preconventional morality** follows rigid right-wrong rules that lead to reward, punishment, or at most, reciprocity; which are particularly ripe for developing beliefs that 'good' deeds are rewarded and victims are 'weak'. There is some evidence for a negative relationship between stage of moral development and the justification of aggression (Berkowitz et al., 1986).

Maybe there are some other psychological mechanisms than simply endorsements of a just world, i.e. third variables, that contribute to the experimental effects. For example, can it be that the cognitive goal / motivation behind endorsing a just world is a more important variable than the belief itself? It might be too speculative to link two different areas of research, but I did want to mention how the just world belief construct seems deceptively simple and may be imprecise.

## Object relations theory

The psychodynamic theorist Melanie Klein postulated a 'death instinct' that drives destructive impulses (Klein, 2011). The theory offers an explanation, though one difficult to demonstrate as correct, for blaming the victim: it is a case of the observer engaging in **projection** of their negative emotions and drives: fear of an unjust world, guilt for complicity, their weakness or helplessness, or their own aggressive impulses. This can fuel the many cognitive biases, motivations, or traits mentioned above as attempts to maintain ego stability and emotional equilibrium. I know this forum is not extremely enthusiastic about psychodynamic theory, but object relations has some substantial scientific support (Svrakic & Zorumski, 2021).

## References

Lerner, M. J. (1965). Evaluation of performance as a function of performer's reward and attractiveness. Journal of personality and social psychology, 1(4), 355.

Reichle, B., Schneider, A., & Montada, L. (1998). How Do Observers of Victimization Preserve Their Belief in a Just World Cognitively or Actionally? Critical Issues in Social Justice, 55–64.

Shaver, K. G. (1970). Defensive attribution: Effects of severity and relevance on the responsibility assigned for an accident. Journal of Personality and Social Psychology, 14(2), 101–113.

Grubb, A., & Turner, E. (2012). Attribution of blame in rape cases: A review of the impact of rape myth acceptance, gender role conformity and substance use on victim blaming. Aggression and violent behavior, 17(5), 443-452.

Kohlberg, L., & Hersh, R. H. (1977). Moral Development: A Review of the Theory. Theory into Practice, 16(2), 53–59.

Berkowitz, M. W., Mueller, C. W., Schnell, S. V., & Padberg, M. T. (1986). Moral reasoning and judgments of aggression. Journal of Personality and Social Psychology, 51(4), 885.

Klein, M. (2011). Envy and gratitude and other works 1946-1963. Random House.

Svrakic, D. M., & Zorumski, C. F. (2021). Neuroscience of Object Relations in Health and Disorder: A Proposal for an Integrative Model. Frontiers in Psychology, 12.

# Answer
> 0 votes
It is not as simple and straightforward as you may think. The extent of victim blaming differs case by case. Victim blaming has more to do with negative perception of the behaviour of victim in the case that is being observed.

-\>Let's take two hypothetical cases to evaluate why different situation may lead to different extent of victim blaming. I would be using different hypothetical scenerio here just so that I can reduce the level of complexity to easily explain it.

In case 1, a man with some money visibly hanging out of pocket was roaming in an alley which was infamous for crimes related to robbery. And he got attacked by someone who robbed his money and injured him sligtly.

In case 2, a man was simply sleeping at his home at night with locks on the door. Some robbers suddenly inavaded his house after breaking the locks, robbing all of his money and slightly injuring him.

In which case do you think the extent of victim blaming will be more, if it is judged by general public ? A logical evaluation would predict that victim of case 1 is more likely to be prone to victim blaming than that in case 2. A person who was roaming in alley that is infamous for crime ralated to robber, with money hanging out of his pocket at that, is more likely to be victim blamed. Why do you think that would be the case ? Let's understand that.

We humans live in a civilisation. Being cooperative and caring about others is fundamental to being civilised. When something happens that harms an individual, we as a civilisation create laws \[see criminal law\]which try to prevent that harm or at the very least minimize it. The main thing to notice is that we try to "minimize" the harm. Attempt and desire to reduce the harm to civilisation that could occur, tends to give us sense of protective environment \[see this\]and self care for ourself and those who are close to us, leading to sense of better chances of survival. Existence of criminal laws have positive effect on mental health. Remember this while I elaborate above two cases.

The harm that happened in above hypothetical cases is "robbery" leading to loss of asset and some body injury. When a normal human sees this case, they automatically try to think of reasons why this happened. And what should be done to reduce to such cases is the another thought many have. A logic would consider that such laws should be created that it discourage people from commiting robbery. But another logic would also discourage the behaviour of victim in the case 1. Since it's naturally more logical for a general public to percieve the idea of going in the alley that is infamous for robbery with money hanging out of your pocket at night, in a negative way. This creates a "neative perception" of the victim's behaviour is case 1. Leading people to blame the victim for being careless and often using idioms like "Shooting oneself in the foot" for the case 1. You see, victim blaming isn't baseless. It involves desire to reduce the harm which inturn requires behaviour of the victim to be appropriate too. Thus how the victim behaves also plays important role in the extent of victim blaming. Victim in case 1 was careless \[ a behaviour percieved in a negative way on general basis \]thus predictably more prone to victim blaming.

While if one consideres case 2, the victim behavior has no impact on the factor that affect the contruction of solution that can help reduce the crime. Thus there being little to no vitim blaming. Even though in the both cases same crime was committed and both victims were slightly injured. But only one was predictably more prone to victim blaming than other.

The things I've established so far are: 1.) Extent of victim blaming differ case by case. 2.) Victims behaviour may play huge role in victim blaming.

Now coming to you case, Rape crime is seen in much more negative light than robbery is, in majority of countries \[which is reflected in the severity of punishment for this crime in many courntries\]. Thus it's evident that desire to prevent it is much more strong than it is for robbery. This leads general public to be too strict upon measure that need to be taken.In turn leading people to be more strict toward victims behaviour too. If there is even a slight hint of carelessness in victims behaviour \[being alone at night wihtout a company, wearing revealing cloths,etc. which too are considered careless on general basis\], this precisely creates opening for Victim blaming in these type of cases. Leading people to precieve behaviour of victim in a negative way. Some people accuse the perpetrator, some become biased due to victims behavior and end up supproting perpetrator, while some have negative perception of both victim and perpetrator. All this differ on basis of what one is taking into consideration while judging the situation and what ideology one has. Someone else might take into consideration what you might have ignored or vice versa. Overall it mainly depends on belief when it comes to judging a situation. It can't be claimed which judgement based on which combination on belief is right or wrong. But the most obvious thing that majority agree upon is that law should exist to punish the criminal. Whether victim blaming exists or not is something that one's belief play major role in.

You can visit various sites which explain victim blaming but most don't take "perception of victims behaviour" into consideration while studying the victim balming psychology.

See this for example https://www.venthrapy.com/blog/the-psychology-of-victim-blaming/

Almost as if people just want to believe what they want. A more scientific approach would require consideration of every factor involved. Which is rarely ever done. But you have keep eye on whether factors like belief of person judging the crime take behavior of victim into consideration or not.

Again, it is not just something straight forward and much more complex process.

Edit : I found this research article which describes how "victims behavior" in hypothetical situation created difference in judgement of public. This is one of those rare article which actually put more emphasis on how victims behaviour affect the extent of victim blaming. You should give it read.

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Tags: social-psychology, evolutionary-psychology, sociology, criminology
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# Question
Title: Can a blind-from-birth individual experience vision or visual imagery during a Near-Death Experience (NDE)?
I recently watched a testimony in which a blind-from-birth individual described two NDEs they had had in which they supposedly were able to see with 20/20 vision (inside the NDEs). The person explained that normally they only have dreams in terms of sounds, smells, touch, taste, but never with visual imagery, which made the experience of sight during the NDEs quite shocking to them. Is this something that has ever been medically documented, and if so, does it have an explanation?

UPDATE:

A video with an interview is available here. Title: *Vicki Noratuk Blind Person NDE*

I also found a journal article referencing this case. Title: *Near-Death and Out-of-Body Experiences in the Blind: A Study of Apparent Eyeless Vision*, Kenneth Ring, Ph.D. Sharon Cooper, M.A. University of Connecticut. Journal of Near-Death Studies, 16(2) Winter 1997. 1997 Human Sciences Press, Inc.

In the article, the authors put forward *Eyeless Vision and Transcendental Awareness* as a possible explanation for these sorts of cases, but I don't know if this hypothesis has any merits from a scientific standpoint.

# Answer
I gather from the chat comments that this question is really about the scientific credibility of reports of visual experiences in the congenitally blind during NDEs. I cannot find any such reports in the scientific literature.

The Ring & Cooper (1997) study (re-reported in Ring & Cooper, 1999; Ring, 2001) is the only apparent exception. Other reviewers (eg, Long, 2014; Ilic et al, 2023; Beauregard, Trent, & Schwartz, 2018) seem to concur that this is indeed the only such study published. Thus, the question really comes down to the credibility of this single study.

For critical reviews of the study, see for example Irwin (2000), Fox (2003), and Augustine (2007). I'll also outline some of my own reasoning on this:

* I would generally not make any strong conclusions based on a single unreplicated study. Multiple studies, a literature review, or a meta-analysis would be better.
* This study is effectively self-published (the lead author Kenneth Ring was the chief editor of the journal it was published in). I would prefer an independent scientific journal.
* The study was small for the conclusion in question (only 14 congenitally blind participants). It's therefore unlikely to have had sufficient power for firm conclusions.
* The study quality was poor. It involved unstructured (read: easily biased) retrospective (read: unreliable memory) interviews (read: qualitative instead of quantitative) of carefully selected participants, with no hypotheses or controls, and using exploratory analyses.
* All that said, the authors don't actually conclude that congenitally blind NDEs involve visual experiences anyway!

As summarized by French (2005):

> Initial readings of such accounts often give the impression that the experience involves seeing events and surroundings in the same way that sighted people do, but closer reflection upon these cases suggests otherwise. As Ring (2001, p. 69) writes,
>
> > As this kind of testimony builds, it seems more and more difficult to claim that the blind simply see what they report. Rather, it is beginning to appear it is more a matter of their knowing, through a still poorly understood mode of generalized awareness, based on a variety of sensory impressions, especially tactile ones, what is happening around them.
>
> Ring argues that casual readers may often gain the impression that such NDEs in the blind involved literally seeing events and surroundings but that this impression is based upon having to describe these experiences, no matter how they were originally coded, in linguistic form. Our language is based largely upon the experiences of the sighted and is therefore a ‘‘language of vision’’.

I personally find it incredulous that during their very first visual experience, congenitally blind people would be able to identify objects and persons with the same expertise as sighted people, and the authors seem to agree.

There is one more nail in the coffin of this study worth mentioning just for completion. Pseudoscience is subject matter that appears on the surface to be science, but actually fails to qualify as science. This paper contains several red flags for pseudoscience:

* The study was funded by the Institute of Noetic Sciences, an organization focused on pseudoscience topics.
* The lead author Kenneth Ring's career is largely focused on pseudoscience.
* Wikipedia generally characterizes such NDE studies as pseudoscience.
* The paper itself discusses pseudoscience topics and references other pseudoscientific sources.
> 1 votes

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Tags: vision, consciousness, dreams, awareness, imagery
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title: Validity of Open Online IQ test

text:
# Question
Title: Validity of Open Online IQ test
I want to measure IQ of college students for a research project I am working on.

After searching for valid IQ test for research that is also low cost/free, I came across this site-https://openpsychometrics.org/

They have an IQ test listed as,The Full scale IQ test (https://openpsychometrics.org/tests/FSIQ/)

They also have listed some research papers that they claim have used their data (https://openpsychometrics.org/\_rawdata/cited/) but I simply used my browser search option to search for the terms "IQ" and "Intelligence" in that page, with O results.

Is the full scale IQ test valid and useable for publishable academic research work? Shall I administer their test on a sample from my target population and use it for my research work? If not, what are some other free or low cost options avaible for me?

# Answer
> 1 votes
The Full scale IQ test from that source is an online IQ test that claims to measure IQ with an overall score as well as scores for component abilities, such as short-term memory, reasoning, and verbal. The test is based on the model of intelligence proposed by Hampshire, Highfield, Parkin and Owen (2012), which they claim fits best on internet populations. The test consists of six sections, each with its own instructions, and takes about 10 to 15 minutes to complete. The test provides immediate, free results without requiring personal data or fees. There are many other free online sources that I find pretty similar to the official test like https://iqtestonline.io/.

However, the validity and reliability of this test are questionable, as there is no evidence of its psychometric properties or its alignment with other established IQ tests. The test does not provide any information about its norm group, its standard deviation, or its correlation with other measures of intelligence. The test also does not account for the possible effects of test-taking conditions, such as motivation, attention, and cheating, on the test results. The test also has some limitations and biases, such as its cultural and linguistic specificity, its narrow and abstract content, and its lack of adaptive difficulty.

Therefore, I would not recommend using this test for publishable academic research work, as it may not meet the standards of scientific rigor and validity. You may face challenges and criticisms from reviewers and peers if you use this test as a measure of intelligence for your research project.

There are some other options for IQ testing that may be more suitable for research purposes, but they may not be free or low cost. Some of the most widely used and validated IQ tests are:

• The Stanford-Binet Intelligence Scale (SBIS), which measures five factors of intelligence: fluid reasoning, knowledge, quantitative reasoning, visual-spatial processing, and working memory. It also provides a composite score, which is the overall measure of intelligence. The SBIS is suitable for ages 2 to 85, and it has a mean of 100 and a standard deviation of 15. The SBIS is administered by a trained professional and costs about 200 - 300 dollar per test.

• The Wechsler Intelligence Scale for Children (WISC), which measures four domains of intelligence: verbal comprehension, perceptual reasoning, working memory, and processing speed. It also provides a full-scale IQ score, which is the overall measure of intelligence. The WISC is suitable for ages 6 to 16, and it has a mean of 100 and a standard deviation of 15. The WISC is administered by a trained professional and costs about 200 - 300 dollar per test.

• The Wechsler Adult Intelligence Scale (WAIS), which measures the same four domains of intelligence as the WISC, but with different subtests and items. It also provides a full-scale IQ score, which is the overall measure of intelligence. The WAIS is suitable for ages 16 to 90, and it has a mean of 100 and a standard deviation of 15. The WAIS is administered by a trained professional and costs about 200 - 300 dollar per test.

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Tags: intelligence, iq
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# Question
Title: Why is Autistic Spectrum Disorder compatible with the Schizophrenia Spectrum in the DSM-V?
I am curious why DSM-V says autism spectrum disorder and schizophrenia spectrum disorder are compatible. I am geologist, and all that topic about autism smells to me like a biologic cold adaptation with a sligthy different origin than schizophrenia.

Just I am asking, as I should be missing something, but:

* In this paper it is said autists have low CB1 receptors density.
* In this other paper it is said schizophrenics have high CB1 receptors density.

Why the compatibility then? CB1 receptors are not quantum particles.

# Answer
We do not understand what causes either autism (ASD) or schizophrenia in the brain. There are some theories and ideas, but nothing conclusive and certainly nothing as simple as a single receptor. There may be gene variants that are *associated* with ASD or schizophrenia, or findings in histology or neuroimaging that *correlate* with ASD or schizophrenia.

---

In the first paper that you link, about CB1 receptor density in autism, one of the citations, reference 21, is this one:

> Purcell, A. E., Jeon, O. H., Zimmerman, A. W., Blue, M. E., & Pevsner, J. (2001). Postmortem brain abnormalities of the glutamate neurotransmitter system in autism. Neurology, 57(9), 1618-1628.

This paper includes two different genome-wide studies, each with very few individuals. For the CB1 receptor specifically, one of the studies showed more CB1 and the other showed less. It isn't clear to me why the authors have taken this to mean "CB1 is low in ASD"; the evidence they provide for this is *extremely* weak and perhaps non-existent, at least based on the given reference. You absolutely should not take this to mean "low CB1 causes autism" or that everyone with ASD has less CB1 than everyone without ASD.

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In the second paper, about schizophrenia, there are several statements that suggest higher CB1 receptor density in various brain regions, but also examples of failures to find any differences. Again, it seems there is some evidence for this but it is weak and not necessarily causal. They also mention caveats in interpreting these data:

> Assuredly, there are many confounding factors influencing the results of post-mortem studies, such as antipsychotic treatment, cannabis smoking and the heterogeneity of biochemical techniques.

Let's look into one of these papers results, Wong, D. F., Kuwabara, H., Horti, A. G., Raymont, V., Brasic, J., Guevara, M., ... & Cascella, N. (2010). Quantification of cerebral cannabinoid receptors subtype 1 (CB1) in healthy subjects and schizophrenia by the novel PET radioligand \[11C\] OMAR. Neuroimage, 52(4), 1505-1513.. Here is a figure from that paper (figure 5):

In this figure, there are 4 panels each corresponding to a different brain region. The y-axis is a measure of CB1 density (after some processing); the x-axis is age. The black symbols, solid lines, and dashed lines represent non-schizophrenic participants, the average linear relationship with age, and confidence intervals around that relationship, respectively. You could roughly consider any points between the dashed lines as "similar to normal for a given age". Notice where the red points are, indicating schizophrenia: for most brain regions and most participants, there is no real way to distinguish them from "normal" using this measure. There might be an overall group difference between schizophrenia and controls, but this is mostly due to a couple of outliers. **Many of the schizophrenia participants have lower CB1 than the average non-schizophrenia patient**: all the red points below the black lines. In this particular paper, they compared 19 brain regions and only found a significant difference (p\<0.05) in one of them, the Pons, which did not appear to be a place they expected to find a difference ahead of time. It does not appear the authors corrected for multiple comparisons. You would expect to find a significant result p\<0.05 purely by chance in one out of 20 comparisons \- that's what the 0.05 threshold means, that 5% of the time an effect that large occurs if you assume there is no actual difference; it's unlikely this result would survive correction so it should not be considered significant. They need a much larger sample to assess if there is any real difference.

That doesn't mean that there isn't some real group difference here when considering the other studies as well, but a difference between groups is not the same as saying that every individual in each group follows the same pattern, and like for ASD the evidence for a link here seems very very weak.

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In summary, the relationship between CB1 density and ASD or schizophrenia is quite weak and does not support a causal link between that receptor either condition. From the available data, it seems that most people with either ASD or schizophrenia do not have CB1 receptor densities that distinguish from the overall population distribution.
> 1 votes

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Tags: autism, evolutionary-psychology, genetics, personality-disorder, schizophrenia
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# Question
Title: Frequency band comparison between two groups
I am a beginner in signal processing. I have two resting eye closed data groups with group 1 having 40 data samples and group 2 having 100 samples. Both are taken from **different devices** with **different frequency sampling rates** (1024 vs 500), **different number of channels**(64 vs 32), **different montage system** (10-10 vs 10-20), etc but are eye closed.

*I am comparing the frequency of average of all data samples across all channels in group 1 vs frequency of average of all data samples across all channels in group 2.*

For that I have:

**Step 1.** For group 1 data(all 40 data samples): Did bandpass filtering for suggested frequency band, average re-referenced them around 32 channels.

For group 2 data(all 100 data samples): We dropped extra channels (converted from 64 to 32) keeping montage the same, cropped the data from beginning and end to make the time duration equal to group 1 data samples, resampled them from 1024 to 500Hz, did similar band pass filtering as in group 1, did not do re referencing as they were already average re-referenced around their 64 channels.

***Questions***: Instead of dropping 32 channels can we do some operation that converts 64 channels 10-10 montage to 32 channels 10-20 montage? Do we need to do re referencing again for group 2 data samples? If we will be doing wavelet denoising for each data in both groups, will we manually set wavelet, level and threshold for each sample or it will be same for all?

**Step 2.** Averaged all 40 preprocessed data for group 1 and converted it in a single data and similarly, averaged all 100 preprocessed data for group 2 and converted it in a single data.

***Questions***: Is averaging a good method, if not what other methods can we apply? What will be effects of averaging data samples before preprocessing vs after preprocessing?

**Step 3:** Comparing average of PSDs for both group's data (averaging all 32 channels) using welch.

***Questions***: Is average of power a good method to find differences in both group's frequency bands?

# Answer
I would be wary about treating your data differently. If you have 64 recording sites, you can possibly use all 64 channels to get to 32 "less noisy" channels and use *that* data optimally, but this will also give those recordings different characteristics than data based on fewer original samples (for example, if you do some sort of weighted time-averaging, you're likely to enhance lower frequencies and suppress higher frequencies because lower frequency activity tends to have greater spatial consistency and vice-versa).

> I am comparing the frequency of average of all data samples across all channels in group 1 vs frequency of average of all data samples across all channels in group 2.

**Don't do this.** Presumably, you're interested in some other characteristic besides the recording device and setup. But, your groups are *completely confounded* with these characteristics. You need a comparable control group. Unless all you want to do is compare the actual recording systems in which case nevermind what I've said. I warn you of this because I'm familiar with these sorts of data and it's common to get very different measurements **in the same participants** when using different systems (even the same physical depth electrodes connected to different recording systems!). It's okay to have data from different systems when you have both groups recorded on both systems, though you may want to adjust for recording system in the analysis.

For Step 2, I would not average directly; I would use statistical modeling (e.g. regression) to capture the variability in your data while estimating population characteristics. An alternative would be a permutation strategy. But, I would not suggest these in light of your data being recorded in different conditions because of the confounding issue described above.

For Step 3, what does "good method" mean? Appropriate methods depend on the research question and data. Average power is one method; it's going to be less appropriate if there is spatial structure to the data.
> 1 votes

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Tags: eeg, signal-processing, connectionism
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# Question
Title: Do psychiatrists take into account affects on the different serotonin receptor types and subtypes when cycling anti-depressants in patients?
If someone is going through SSRIs to find one that works, doesn't it make sense to target each receptor in turn rather than the same one with different drugs (like prozac and zoloft, for example)? Is this considered when prescribing anti-depressants?

Is it even possible?

# Answer
Short answer, no.

After lifestyle changes (optimising diet, exercise and social engagement) and psychotherapy (e.g. cognitive-behavioural therapy) have been trialled, most psychiatrists will commence a patient on selective serotonin reuptake inhibitor (SSRI), like Prozac or Zoloft. If this is trialled at a reasonably high dose for several weeks with no benefit, they'll usually switch to either another SSRI or a selective serotonin and noradrenaline reuptake inhibitor.

Most psychiatrists are not thinking about the specific receptors beyond serotonin and noradrenaline transporters because we don't have data to suggest this makes a clinical difference. For example, Prozac is an agonist at the sigma-1 receptor and the Zoloft is an antagonist at that receptor... but what that means for an individual patient, we don't know.

Some psychiatrists now consider an individual's genetic make-up when choosing a medication. This is an area called pharmacogenetics. See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5299682/ for a paper we wrote on the topic if you're interested.

Hope this helps.
> 0 votes

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Tags: clinical-psychology, depression, drugs
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# Question
Title: Does AD(H)D increase the risk of (drug induced) psychosis?
I read that patients with ADD can exhibit a hypersensitivity of dopamine in the mesolimbic area and a hyposensitivity of dopamine in the prefrontal cortex which makes them more susceptible to addictive / reward driven behaviour and IMHO also more prone to (drug induced) psychosis as those are conditions postulated by the DH.

I am not entirely sure if recreational drugs release Dopamine in the NAcc and if that can cause positive symptomatic behaviour of schizophrenia / psychosis in conjunction with a hypersensitivity in affected brain regions.

Does this suggest that a patient with ADD and heavy recreational THC use is more likely to evolve psychotic symptoms if balance of D2 activity is not artificially secured?

# Answer
Having ADHD does increase the risk of drug-induced psychosis. This may be because many of the medications used to treat ADHD are stimulants and stimulants can contribute to the development of psychosis. A recent paper in the New England Journal of Medicine (a top tier medical journal) found that the risk is greatest with amphetamine-based medications (https://pubmed.ncbi.nlm.nih.gov/30893533/). As to the molecular basis of this relationship - I don't think there is a robust explanation.

If someone had ADHD, they certainly should not be using THC. They may wish to be re-assessed after extended abstinence from the THC (plus any other substances) and they may find they don't have ADHD afterall.

One additional note is that psychosis has considerable heterogeneity. There's a lot of focus on dopamine networks but glutamine, GABA, NA, ACh and serotonin may all play some role. It's easy to get caught up with excessive reductionism and cause-effect oversimplification.
> 1 votes

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Tags: adhd, dopamine, psychosis
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title: How do SSRIs interact with MDMA?

text:
# Question
Title: How do SSRIs interact with MDMA?
I'm not sure if I understand the synergetic effects of MDMA and SSRIs correctly.

According to PMC81503 "It is clear, however, that the increase in the net release of serotonin (and possibly dopamine) is the major mechanism of action underlying the distinctive mental effects of MDMA" but it also states "MDMA does not act by directly releasing serotonin but, rather, by binding to, and thus blocking, the transporter involved in its reuptake."

Do SSRIs interfere with MDMA? Do both bind to SERT, do they compete? Do SSRIs prevent the serotonin released by MDMA from being reuptaken? Do SSRIs increase the net release of MDMA when taken together compared to MDMA alone?

# Answer
**Do SSRIs interfere with MDMA?** Yes, a 2022 systematic review by Saparast et al found that SSRIs and duloxetine attenuated the subjective effects of MDMA.

**Do they both bind to SERT?** Yes, but they act slightly differently. From the same systematic review, MDMA results increases neurotransmitter levels in the synaptic cleft by reversing their transport and promoting their release, while antidepressants do so by preventing the reabsorption (reuptake) of these neurotransmitters, thereby increasing their availability in the synaptic cleft.

**Do SSRIs prevent the serotonin released by MDMA from being reuptaken (sic)?** Theoretically, I think they would. However, things can get very complicated at both pharmacokinetic and pharmacodynamic levels and I'm not aware of a study that has demonstrated this finding.

**Do SSRIs increase the net release of MDMA when taken together compared to MDMA alone?** Theoretically, yes. Further, some SSRIs are inhibitors of the cytochrome P450 enzyme CYP2D6 which breaks down MDMA. So you would expect higher plasma concentrations. However, this doesn't accord with the results of studies showing that individuals taking SSRIs had attenuated subjective effects from MDMA.

There's limited literature on this topic and it's challenging to extrapolate from small studies of volunteers.
> 1 votes

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Tags: drugs, neuro-transmitters, serotonin
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# Question
Title: What is the difference between "avolition" and "abulia"
The Wikipedia articles are confusing especially the first one https://en.wikipedia.org/wiki/Abulia https://en.wikipedia.org/wiki/Avolition

If you google "abulia avolition" the first entry ("Verywell Health") says "Aboulia is the lack of will rather than motivation" which contradicts wiki's article that puts abulia under "Disorders of Diminished Motivation" umbrella. This Verywell Health's author is not even a psychiatrist but a patient lol.

# Answer
Abulia has been defined as: "(1) difficulty to initiate and sustain purposeful movements; (2) poverty of spontaneous movements; (3) reduced spontaneous speech; (4) increased response time to queries; (5) passivity; (6) reduced emotional responsiveness and spontaneity; (7) reduced social interaction; and (8) reduced interest in usual pastimes."

Avolition has been defined as, "reduced initiation and persistence of goal directed activity".

There is considerable overlap between the two concepts, as well as the related concept of apathy. The pathological basis probably involves the same neural circuits. As I noted in a previous post that was deleted, there is considerable disagreement among experts as to what many of these terms mean. If you're interested, see this paper from only 22 years ago attempting to find consensus on the term abulia.
> 0 votes

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Tags: terminology, psychiatry
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# Question
Title: What is the source for Feynman describes the learning technique named by his name?
There is a lerning technique by Richard Feynman, which is known as "Feynman learning technique", and consists of four steps:

1. Select a concept to learn.
2. Teach it to a child. (Or maybe an adult who have zero knowledge in that field.)
3. Identify gaps in your explanation. Go back to the source material to better understand it.
4. Organize and simplify.

You can find its description, for example, here or here.

But where can I find its original description, that is, the description provided by Richard Feynman himself?

# Answer
As noted by Bryan, Feynman didn't coin this technique. It was developed by Scott Young (see the comments section here - https://www.scotthyoung.com/blog/2011/09/01/learn-faster/) and named in honour of Feynman:

> The technique is loosely inspired by an account in Richard Feynman's biography about understanding the Yang-Mills mass gap. But he didn't follow the exact structure I'm doing (explaining as if teaching it to someone else), his was more like a close reading. So in that sense, the technique is mine (although, self-explanations have a long tradition in educational psychology as well, so I can't take credit for the overall concept).

I've read Feynman's autobiography and several of his lecture series. If he had any educational philosophy, it's probably best encapsulated in this quote from his biography: "We must remove the rigidity of thought... We must leave freedom for the mind to wander about in trying to solve the problems... The successful user of mathematics is practically an inventor of new ways of obtaining answers in given situations. Even if the ways are well known, it is usually much easier for him to invent his own way - a new way or an old way - than it is to try to find it by looking it up."
> 5 votes

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Tags: learning, reference-request
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# Question
Title: Can motor or muscle actions actually be conscious?
Of course I can think of performing actions, but all of that seems to be part of sensory feedback or memory. The implementation of how the action itself is done feels unconscious. I've also heard of a study saying we're aware of our voluntary actions after the start. And seeing as most of our CNS(edit: interneurons) is inhibitory neurons, it makes sense that consciousness is some sort of feedback mechanism rather than some "doer".

# Answer
Motor control is pretty complicated; I'd say with a bit of hand-waving that it involves about 80-90% of your entire central nervous system (CNS): brain and spinal cord (of course that's not to say that "everything else" only has 10-20% of the brain to work with; there's a lot of overlap in sensory and motor systems!). Here's an online textbook on motor control that you might be interested in:

https://wisc.pb.unizin.org/kines531/chapter/what-are-some-of-the-complexities-involved-in-the-control-of-movement/

Consider one of the diagrams from this online book, borrowed from Purves' textbook *Neuroscience*:

(Figure originally from *Neuroscience. (2010). (D. Purves, G. J. Augustine, D. Fitzpatrick, W. C. Hall, A.-S. Lamantia, J. O. Mcnamara, & S. M. Williams Eds. 4th ed.). Sunderland, Massachusetts U.S.A.: Sinauer Associates, Inc.*)

We're still figuring out what exactly "consciousness" is, but most neuroscientists focus on the cerebral cortex as the place where consciousness happens, perhaps with some influence of the thalamus. All the other features on this diagram like the basal ganglia, cerebellum, brain stem, spinal cord are CNS areas that are absolutely critical for motor control but don't seem to involve conscious processing. Another page from the book talks about some of the motor deficits observed when there are problems with some of these areas.

The signals generated in premotor and even motor cortex that you are conscious of are more like a "plan" for an overall movement rather than the specific instructions. During development, connections between these various regions work to translate between the "plan" and the actual motor actions. This is a *learning* process; it works by starting from somewhat random connections and pruning them until the instruction produces the desired action. Conscious cognitive control of muscles would be very undesirable; you need to contract and relax dozens to hundreds of muscles to perform most actions. It's not as simple as reaching your arm out in front of you, when you do that you also need to shift muscle contractions throughout your whole trunk to prevent the change in balance from tipping you over.
> 1 votes

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Tags: consciousness
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# Question
Title: Do beta-blockers prevent ability to learn by reducing neuroplasticity?
Learning is fundamentally linked to epinephrine, acetylcholin and dopamine.

Do heart pressure medication like beta blockers block these processes to some extent by reducing epinephrine?

# Answer
> 1 votes
Your question has the implicit assumption that beta-blockers prevent or impair the ability to learn new information. This is incorrect. There were a series of studies done in the 1980s addressing this topic. These were reviewed in an Archives of Internal Medicine (now JAMA Internal Medicine) study that concluded: "There is a suggestion in the literature that such agents \[beta-blockers\] may actually improve performance on complex tasks requiring well-controlled anxiety plus coordinated input from memory, perceptual motor functioning, and learning." Subsequent studies have looked at the effect of lipophilic beta-blockers like propranolol that can cross the blood-brain barrier and arrived at similar conclusions.

If your question was referring to memory consolidation during stressful situations, there's a recent meta-analysis that suggests that propranolol has limited utility in preventing traumatic memory reconsolidation.

Learning involves a complex system beyond the three neurotransmitters you've listed, one that is still being investigated. Complex systems can rarely be understood from first principles e.g. if X, then Y.

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Tags: learning, stress
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