# Question
Title: Are all conscious experiences stored as memories?
There are people with supermemories, called **highly superior autobiographical memory** (HSAM), i.e., the detailed recollection of events that occurred in the distant past. Although the recollection of, say the weather on this day 15 years ago may not be entirely accurate (errors occur) and may contain gaps (maybe an hour of sunshine on a predominantly rainy day is not recollected), their memories are clearly superior nonetheless.

I have heard these statements that all memories are stored in the brain and that the reason why we forget is because those memories are simply not accessible anymore. This would metaphorically be like the workings of a hard drive, where deletion of a file removes the flag, but the information is physically still stored, it is just invisible to the user and difficult to access. Following this reasoning, everyone would have HSAM in a way, barred that normally the memories can't readily be accessed.

Hypnosis seems to be capable of enhancing the *recollection of memories* in people without HSAM, and hence hypnosis is said to improve memory, indirectly indicating that memory storage indeed may generally be higher than apparent in everyday life, but that the brain needs a hand in retrieving those memories.

My question is:

* Are all conscious1 memories stored, but access is permitted only when its regularly accessed, or enhanced through hypnosis or other means? In other words, does everyone have super memory like HSAM, but do people without HSAM simply lack an efficient way to access those distant memories?

*1 With all conscious memories I mean memories of life events that were experienced while being awake and vigilant. For the sake of question focus, I suggest disregarding life events occurring during sleep, coma, anesthesia or other periods of reduced consciousness.*

# Answer
This question can be addressed in many ways. One approach that we have taken is to test memory for what has just recently happened a few seconds ago. In these experiments we ask people to find a target in a simple visual search, and report its location. For example we might show them 3 numbers and one letter and ask them to report the location of the letter. After several minutes of doing this task, we give them a surprise question in which we ask them to tell us the actual letter that they had just located in the most recent trial (which they saw just a few seconds ago). What we find is that it is easy to find situations in which our participants have very little memory of that letter. What is interesting about this is that they had just located the letter by virtue of the fact that it was a letter. We presume, therefore, that the letter had briefly entered their awareness. This can be debated, if one assumes that one can search for letters without actually experiencing the letters. However we also found the same result with digit-parity tasks (i.e. find the odd number among evens or vice versa).

We called this effect attribute amnesia, since people seem to have amnesia for a specific attribute of a stimulus they had just selected.

So while there are lots of ways to interpret this finding, the clearest result seems to be that performing a mental operation that selects a piece of visual information can leave a memory trace so weak that it cannot be remembered just a few seconds later. Our interpretation is that the memory was never created in the first place. We believe that the brain has filters on memory encoding that allow us to process information without remembering it. It is also possible that it was encoded into memory and immediately forgotten but we do not favor this view as it seems less parsimonious than the filter that prevents encoding in the first place.

Here are some articles on this phenomenon: Chen, H., & Wyble, B. (2015). Amnesia for object attributes: Failure to report attended information that had just reached conscious awareness. Psychological science, 26(2), 203-210.

Chen, H., Swan, G., & Wyble, B. (2016). Prolonged focal attention without binding: Tracking a ball for half a minute without remembering its color. Cognition, 147, 144-148.

Chen, H., & Wyble, B. (2016). Attribute amnesia reflects a lack of memory consolidation for attended information. Journal of Experimental Psychology: Human Perception and Performance, 42(2), 225.

Here are some freely-available pre-prints of related articles if you cannot access the ones above: https://psyarxiv.com/gbdcr/ https://psyarxiv.com/87yg2/

I apologize that not all of our work is available on preprint servers yet. I'd be happy to email copies of published articles if you email me at bwyble@gmail.com
> 5 votes

# Answer
This may seem far fetched at first. Give the concepts given below some time. Do your research and experiments first before disregarding the information below. In other words: You might need to put in a little effort/work for the information below to mean anything to you.

Thomas Campbell his Theory Of Everything (TOE) has a view on this. He says you can focus your intent to get any information you desire. He compares a clear focussed intent with a proper database query. You then need to `be open` to receive the outcome, and not distort it with your analytical mind, at first. He has several video's where he guides you through remote viewing what is inside boxes. I was stunned to experience accuracies in my perception, over multiple times, which has proven this mechanism to work (for me) without a doubt.

These are slides of one of his presentations. You can view the presentations on youtube. Search for "Remote Viewing by intent". http://www.my-big-toe.com/uploads/HawaiiSlides.pdf

What he mentions in his book (http://www.intradimensions.net/mybigtoe.pdf) is that your brain is the interface, but not the storage location.

I see a relation here with recollecting past memories. They might well be those intent based queries. You can get better with practise on the mechanism to query, retreive and interpret the information. Whether it are 'your' memories or other information from a past event.
> -3 votes

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Tags: memory
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# Question
Title: What is the evidence that mathematicians are more likely to have autistic traits than the rest of the population?
Baron-Cohen has conducted extensive studies \[1,2\] examining the prevalence of autism spectrum conditions (ASCs) and mathematical or scientific ability. Most of these studies, however, have focused mostly on (Cambridge) undergraduates or winners of the UK Mathematics Olympiad.

In one study, Baron-Cohen found in \[2\] that Olympiad winners scored the highest in the AQ test ($\mathrm{AQ}\colon 24.5,\mathrm{ SD}\colon 5.7$), with the second highest scoring group being the mathematics students ($\mathrm{AQ}\colon 21.5,\mathrm{ SD}\colon 6.4$).$^1$ This leads one to conjecture that autistic traits may be more prominent among individuals with higher mathematical ability.

**Question:** *What is the population evidence$^2$ around autism/autistic traits in mathematics? If possible, at the postgraduate level in professional mathematicians?*

---

**Disclaimer**: There is a another question focused on the postgraduate maths skill set: Is there any evidence for the distinction between undergrad and postgrad mathematics?.

$^1$Note however that the sample is small: $n=16$ for UK Olympiad winners, $n=85$ for mathematics students.

$^2$As in measuring the average AQ of mathematicians against other groups, such as graduate students, undergraduates, and controls.

**References**

> \[1\] Baron-Cohen, Simon, Sally Wheelwright, Amy Burtenshaw, and Esther Hobson. "Mathematical talent is linked to autism." Human nature 18, no. 2 (2007): 125-131.
>
> \[2\] Baron-Cohen, Simon, Sally Wheelwright, Richard Skinner, Joanne Martin, and Emma Clubley. "The autism-spectrum quotient (AQ): Evidence from Asperger syndrome/high-functioning autism, males and females, scientists and mathematicians." Journal of autism and developmental disorders 31, no. 1 (2001): 5-17.

# Answer
No. I can't seem to find a specific study into professional mathematicians or graduate students so far, the studies always seem to group the occupations together.

However, Baron-Cohen's team has done an impressive national survey (Ruzich et al., 2015) and recruited nearly half a million people through a UK TV show. They managed to get over 450,394 survey respondents which allowed them to analyse occupations. They found that people working in STEM scored higher in an autism screening questionnaire or AQ (Autism-Spectrum Quotient) test.

> individuals working in a STEM career (m = 21.92, SD = 8.92) scored higher than individuals non-STEM careers (m = 18.92, SD = 8.48)

Unfortunately, there wasn't a specific category for mathematicians as probably it is too specific and too small a field to analyse. The three categories (figure 3) forming STEM was Comp & IT, Engineering and Sci & Tech. Mathematicians would fit into one of those occupational roles.

**References**

Ruzich, E., Allison, C., Chakrabarti, B., Smith, P., Musto, H., Ring, H., & Baron-Cohen, S. (2015). Sex and STEM Occupation Predict Autism-Spectrum Quotient (AQ) Scores in Half a Million People. PLOS ONE, 10(10), e0141229.
> 3 votes

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Tags: autism, mathematical-ability, aspergers
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# Question
Title: Homogeneous Poisson Process of spike train
In Theoretical Neuroscience by Dayan and Abbott page 25,

> the probability $P\[t\_1, t\_2, ..., t\_n\]$ that a sequence of n spikes occurs with spike $i$ falling between times $t\_i$ and $t\_i+\Delta t$ for $i=1,2,...,n$ is given in terms of this by the relation $P\[t\_1, t\_2, ..., t\_n\]=p\[t\_1,...,t\_n\](\Delta t)^n$... the probability $P\[t\_1, t\_2, ..., t\_n\]$ can be expressed in terms of another probability function $P\_T\[n\]$, which is the probability that an arbirary sequence of exactly n spikes occurs within a trial of duration T. Assuming that the spike times are ordered so that $0 \le t\_1 \le t\_2 \le ... \le t\_n \le T$, the relationship is $$P\[t\_1, t\_2, ..., t\_n\] = n!P\_T\[n\]\big({\Delta t \over T}\big)^n$$

I get that $P\_T\[n\]$ is the probability function of $n$ spikes occurring(which later is proved to be a Poisson distribution). I'm guessing $n!$ is different ways of re-arranging the $n$ spikes. What exactly is $\big({\Delta t \over T}\big)^n$?

# Answer
First of all you should notice the assumption that spikes are independent and that every sequence of spikes over an interval has the same probability. That's why you can express $P\[t\_{1}, t\_{2}, ..., t\_{n}\]$ in terms of $P\_{T}\[n\]$. Second, note that $p\[t\_{1}, t\_{2}, ..., t\_{n}\]$ is a probability density. So you can express the probability as the integral of $p\[t\_{1}, t\_{2}, ..., t\_{n}\] dt\_{1}dt\_{2}...dt\_{n}$

$\Delta t / T$ is the probability that one spike occurs in that time interval. If $\Delta t$ is small enough, only one spike is within that interval, so just let $\Delta t \rightarrow dt\_{i}$. Then $p\[t\_{1}, t\_{2}, ..., t\_{n}\] dt\_{1}dt{2}...dt{n} = n!P\_{T}\[n\]dt\_{1}dt\_{2}...dt\_{n}(\frac{1}{T})^{n}$

You should see this as a joint probability.
> 2 votes

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Tags: theoretical-neuroscience, computational-modeling
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# Question
Title: Comorbidity of Neurodevelopmental Disorders between them and Obsessive Compulsive Disorder and Obsessive Compulsive Personality Disorder
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3416662/

OCD being an anxiety disorder and OCPD being a personality disorder it is entirely possible that these two can be present on the same patient.

Autism, e.g Aspergers Syndrome and ADHD have some similarities but are distinct disorders.

We learn at university that people with Aspergers are frequently obsessive.

Based on Occam's Razor "Pluralitas non est ponenda sine necessitate" Psychiatrists and Neuropsychologists are intently parsimonious in diagnosing a patient with multiple disorders even if the examinee meets the criteria, is indeed experiencing the symptom, has the equivalent behaviour. And we are taught at university just that.

Is there any case in which the behaviour of the examinee undoubtedly suggests comorbidity of OCD,OCPD, ASD and ADHD mixed type maybe even along with an entirely distinct disorder like dysthimia? How exactly are these examinees' behaviours? As a medicine student professors do not answer these questions in their lectures ( one reason I am most probably converting to Law since they are slightly more open there).

# Answer
I found your question hard to answer because of the multiple disorders involved. I hope my answers contains some information that is usefull to you. However, it is likely not the satifsying answers you are looking for.

According to Hansen, Oerbeck, Skirbekk, Petrovski, & Kristensen (2018) about 21 percent of children with neurodevelopmental disorders (ND) have one comorbid disorder in the category of neurodevelopmental disorders. For ADHD and Autism Spectrum Disorder (ADS), tic disorder was the most common ND. 36% of ADHD patients had tic disorder as well and 44% ASD patients had a tic disorder. As for OCD, 3.3% of the patients with ADHD also had OCD and 4.0% of the patients with ASD had OCD as well. This study did not investigate the OCPD as a possible comorbid disorder for neurodevelopmental disorders. After doing some more searching, I unfortunately could not find much information about OCPD in relation to Neurodevelopmental disorders and the specific example your provided (OCD, OCDP, ADHD and ADS). However, that does not mean it is not possible, in practice all kinds of comorbidities can occur. The behavior of these patients would likely reflect the symptoms of all the disorders present in the patient.

A big problem with our current understanding/diagnosis of disorders is that most of the disorders are categorized based on their symptoms (e.g. DSM V). In practice symptoms between disorders heavily overlap resulting in comorbidity for most patients (Nolen-Hoeksema, 2014). It is often mandatory to diagnose multiple disorders. For example, if the patient meets both the criteria for ADHD and Autism Spectrum Disorder, then both disorders need to be diagnosed, same goes for OCD and OCPD (see DSM V, Chapters about Neurodevelopmental Disorders and Personality Disorders). Sometimes patients are believed to have "hybrid disorders" (multiple symptoms of multiple disorders). Therefore, it would be better to classify disorders according to their causes instead of the symptoms. That would be the first step in truly explaining disorders instead of simply describing them (Davey, 2014).

# References

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: Author.

Davey G. (2014). Psychopathology: Research, Assessment & Treatment in Clinical Psychology (2nd ed). British Psychological Association and John Wiley & Sons LTD.

Hansen, B., Oerbeck, B., Skirbekk, B., Petrovski, B., & Kristensen, H. (2018). Neurodevelopmental disorders: Prevalence and comorbidity in children referred to mental health services. Nordic Journal of Psychiatry, 72(4), 285-291. doi:10.1080/08039488.2018.1444087

Nolen-Hoeksema, S. (2014). (Ab)normal psychology (6th ed.). New York: McGraw-Hill Education
> 2 votes

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Tags: cognitive-psychology, neuroscience, learning, abnormal-psychology, clinical-psychology
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title: Brain Dynamics at the Edge of Chaos

text:
# Question
Title: Brain Dynamics at the Edge of Chaos
I've repeatedly come across the claim that brain dynamics operate near the edge of chaos, but usually they do not give any useful sources on how we actually know this.

I'm also aware that there are theoretical models that such dynamics are optimal in terms of information transfer, memory storage, etc and I find it plausible that evolution would try to get us somewhere in that region to the extent possible.

But what precise evidence do we have from brain measurements or realistic brain models that the dynamics are actually near the edge of chaos?

# Answer
Dynamical systems (basically all of them) display a wide repertoire of dynamics when tuned close to criticality (https://en.wikipedia.org/wiki/Critical\_phenomena). In this range, organized patterns of activity emerge, close to those that we find when looking at statistical dependencies between time series recording (at least partially) brain activity.

Long range correlations also emerge in this phase.

So, it's true that dynamical models tuned close to criticality better fit brain activity. On the other hand saying that "brain activity is critical" is a logical fallacy, since we are giving to the modelled system properties of the model.

(chaos is a close concept, stressing the dependency on initial conditions, but in this case I think that criticality is more relevant).

See, among other things, this scientific yet accessible paper

Beggs, J. M., & Timme, N. (2012). Being Critical of Criticality in the Brain. Frontiers in Physiology, 3. doi:10.3389/fphys.2012.00163

https://www.frontiersin.org/articles/10.3389/fphys.2012.00163/full
> 2 votes

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Tags: neuroscience, dynamic-systems
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# Question
Title: Can General Assessment of Functioning (GAF) be used to measure recovery etc. from all mental health problems?
Can General Assessment of Functioning (GAF) be used to measure recovery etc. from all mental health problems?

I know it's used with 'schizophrenia', but what about things like personality disorders, Dissociative Identity Disorder, etc.?

# Answer
> 2 votes
Yes, the General Assessment of Functioning (GAF) score can be used for all psychiatric disorders.

The GAF is not commonly used now as the DSM V has opted for the WHODAS 2.0 instead of GAF. There were fundamental problems with GAF including poor reliability with people who were less trained, cross-cultural variations and symptom severity tended to influence symptom scoring instead of functional impairment (Gold, 2014). The DSM V also commented on their concerns -

> We do not believe that a single score from a global assessment, such as the GAF, conveys information to adequately assess each of these components, which are likely to vary independently over time. Further, we are concerned about evidence that the GAF requires specific training for proper use, and that good reliability and prediction of outcomes in routine clinical practice may depend on such training (APA, 2013).

**References**:

American Psychiatric Association. (2013). Insurance Implications of DSM 5. In Diagnostic and statistical manual of mental disorders (5th ed.).

Gold, L. H. (2014). DSM-5 and the Assessment of Functioning: The World Health Organization Disability Assessment Schedule 2.0 (WHODAS 2.0). Journal of the American Academy of Psychiatry and the Law Online, 42(2), 173–181.

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Tags: measurement, abnormal-psychology
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# Question
Title: Why are people inclined to praise or fear the unknown?
Human beings are inclined to "praise" the unknown, and are often afraid of the unknown. This inclination has led to the creation of mythology and many gods. To this date we are still carrying this habit on our daily lives.

* "Oh, look at these crop circles, aliens must have created them!"
* "Oh, he can bend the spoon! He must have psychic power!"
* "Nah, earth must be standing over the oxen horns, otherwise it would fall down!"
* "It makes sense! You adjust your balance with the wrist band exerting bioenergy! Here I come!"
* "I can gain 6 pack with this Nano-Ultra-Mega-AB-Shaper. It has "nano", so it must be working, no?"
* "Since we are surrounded by energy, some chosen ones might bend it right? We call it reiki!"
* "Since you have a BS degree. You must be a heck of a genius! Now can you please answer this question of geography/history/so on?" (I usually encounter such questions from ignorant people. They regard me as Mr. Know it all, as they don't know what university infact is.)
* and most striking example of all is God of the Gaps.

To further exemplify my claim, Wikipedia quotes God of the Gaps as a variant of argument from ignorance.

> The term God-of-the-gaps argument can refer to a position that assumes an act of God as the explanation for an unknown phenomenon, which is a variant of an argument from ignorance.<sup>\[9\]\[10\]</sup> Such an argument is sometimes reduced to the following form:
>
> * There is a gap in understanding of some aspect of the natural world.
> * Therefore the cause must be supernatural.
>
> One example of such an argument, which uses God as an explanation of one of the current gaps in biological science, is as follows: "Because current science can't figure out exactly how life started, it must be God who caused life to start."

But this answer is rather specific and not satisfying for me. I think there lies a cognitive bias that drives human beings to prefer to praise/fear the unknown over showing reasoning and critical thinking when we are faced to the unknown.

Update: This scene from The Gods Must Be Crazy is spot on! Don't miss it :)

### Questions

* Does scientific research support the claims made above about the importance of this tendency to praise or fear the unknown?
* Is there an exact term for this tendency? Is Occam's Razor the right term for this?
* What does scientific research tell us about why humans have this tendency?

# Answer
> 15 votes
In the book "Six Impossible Things Before Breakfast: The Evolutionary Origins of Belief", Wolpert (2007) discusses the evolutionary origins of belief.

Although I haven't read it yet, abc news reviewed the book.

> Wolpert argues that our wide range of beliefs, some of which are clearly false, grew out of a uniquely human trait. Alone in the animal world, **humans understand cause and effect**, and that, he says, led ultimately to the invention of tools, the rapid rise of sophisticated technology, and of course, beliefs. Even the earliest humans understood that many events that shaped their lives resulted from specific causes. Therefore, there must be a cause behind every event.
>
> ...
>
> We want to believe there is a reason for it all, and that leaves us predisposed to believe in some things for which there is little or no evidence. If a certain belief makes sense out of an otherwise senseless event, then it must be true, right?

# Answer
> 2 votes
This is speculative, but most humans are uncomfortable with not knowing, this is the root, for example, of premature cognitive commitments and of curiosity. So many people tend to adopt any available explanation to settle the discomfort of not knowing. I think a potentially more interesting question is why so many people have trouble exchanging a belief for a better explanation, anyone who has tried explaining the reasoning behind atheism to a religious person has run into this - they accept your arguments, but continue to believe as before.

# Answer
> 2 votes
I like to debate these ideas, and will share my thoughts here. But I don't know if this is really appropriate for what this site was intended for based on the "warnings" I see above. The editors should feel free to delete my comments if they run too speculative for the intent of this site.... This is all speculation despite my common writing style of talking as if it were fact....

I approach these questions from the idea that the human brain is a reinforcement learning machine. It's fairly easy to create broad explanations for theses sorts of questions by tying everything back to this idea. I'm using reinforcement learning machine in the sense of the AI machine learning use of the term, which falls fairly directly from the behaviorists ideas of classical and operant conditioning. I am an engineer and computer scientist so I talk from that perspective.

Fear, in this sense, is just (at the broadest levels) avoidance behaviors. We learn to use any behavior that allows us to stay away from the things that punish us - that cause reduced expectations of future rewards. Thoughts are just behaviors of the brain as well, which are also subject to all the same conditioning effects of our external actions. So we will naturally, be conditioned to try and avoid thoughts that produce reduced expectations of future rewards.

Let me side-bar for a moment and point out something many people who have not studded reinforcement learning fail to understand. These sorts of machines don't just learn when a "bad" event happens. They don't just learn when they are hit with a stick. There's an indirect learning at work which creates a far greater complexity to the process. They are at their core, reward prediction machines. They constantly predict expected future rewards. (Basic TD learning). The "stick" events, train their prediction system. It accumulates statistics based on every time something bad or good happens, and uses that to predict expected future rewards. Behaviors, then, our conditioned not by the sticks and carrots, but by the prediction system. Any behavior which causes a drop in the expected future rewards by the internal prediction system, is punished (it's odds of being repeated in the future drops).

So the behaviors that emergent from such indirect learning, are all about tricking the prediction system into *predicting* a better future for the agent. The complexity of the behaviors that will emerge, then are tied directly to how good the prediction system is at predicting the future. AI program attempting to use reinforcement learning often fail to look very intelligent due to the fact that they have failed, to implement high quality reward prediction system, which is itself, trained by reinforcement.

So, back to fear now. Humans understand and use cause and effect. This is a direct fall out, of having a brain that conditions behaviors based on predictions of future rewards. The behaviors that emerge from such training will use cause and effect to their advantage to control our perceived view of the future based on the things we can change now, to effect the future though that causality chain.

We don't like getting hurt. So we learn the signs in the environment that predict something bad will happen, and we change our behavior to prevent it. We see our hand moving towards a fire, and the brain is able to predict the a hand near a fire is a predictor of future pain (from being burned). We move our hand away from the fire, and it make our "predictor" produce a reduced expectation of a burn, so that action of moving the hand away from the fire is reinforced, even though we did not get burned (this time). We learn behaviors to stay away from fires in this way. Of course, there are other conflicting rewards for being near fires (like the food that results from cooking), so we end up balancing our behaviors and simply become careful around fire, vs running in fear from it.

But, in life, we are often caught off guard. We are hurt by something that we had not seen before, or that we simply failed to predict. We learn that we can use cause and effect to avoid most of these bad things in life, like keeping our hand away from wire keeps us from being burned. But when we come across a new situation, stimulus signals very different from what we have dealt with in the past, we find the odds of being hurt goes up. When dealing with a new environment we have not experienced, we do not yet now know to leverage the causality of the environment to prevent the bad things, or to acquire the good things.

Our prediction system knows, that if we wander into an something we are unfamiliar with, or odds of being hurt rises. It can use this as a cause and effect prediction. That is, the less we know about our current environment, the higher the odds that something will hurt us. Because our reward prediction system can predict this correlation between an unknown environment, and higher rewards, the system can learn behaviors, to avoid the unknown.

We will be conditioned to stay in the "safe and known environment", and stay out of the "new and unknown". This attraction to the familiar, on one side, simply become behaviors to avoid the unknown on the others. This translates to a simple "fear" of the unknown.

Now, this all works well, because our internal prediction systems are able to pick up the sensory clues from the environment to guild our actions. But, we can just as easily learn, to fool our prediction system. If the brain senses something dangerous like a fire, it will raise it's predictions of being burnt in the future. But we can also learn to close our eyes, and block the brain from seeing the danger. However, the brain is smart enough to not fall for that trick. Once it sees the fire, it understand the danger. And it understands that when we close our eyes, the fire and the danger are "still there" despite not being able to see it. However, it's not prefect, and this sort of trick does work *some*. So, when we see something really bad, we have a learned response to just look away, to close our eyes, or turn our head, exactly because this "trick" does work. It takes the stimulus away from our reward prediction hardware, and as such, makes the future look a little better than it did before.

So the system can learn behaviors, to trick its prediction system, which is only harmful in the long run, but the low level system is not advanced enough to understand that. It's where are intelligence shows it's limits. The reward prediction system is not always smart enough to recognize it's being "tricked". When it can recognize the trick, it will not fall for it. It will likely return higher expectations of future bad things happening, because it's being deceived so it can't do it's job a well. But when the trick is good enough, that it does not recognize it's a trick, such "tricks" will emerge in our learned behaviors.

All this adds up to the simple result that we learn to fear the unknown, because we learned that the more unknown there is in the world, the higher the odds of being hurt in the future becomes.

But then we find the tricks. Language behaviors are a large part of what humans do. We not only learn to deal with the environment by using our hands and body to manipulate our environmental. We also learn to talk about our environment. The better we understand some aspect of our environment, the more words and language we have to talk about it. We use our langue to guide our actions, and we now that the more we can talk about our environment, the more we are likely to be able to guide our actions in a "safe" direction.

When faced with an unknown, just talking about it, helps us better determine how to act in the situation. But it also triggers our prediction system to reduce the odds of future dangers. We just the act of talking, "tricks" our prediction system, into making us "feel better" about the future. Our talk might be nonsense (for a given situation), but if the talk is good enough to fool the prediction system, it still makes us feel better.

So we develop these behaviors of rationalizing about an known, just because it tricks our internal reward prediction system into making the future look brighter for us. The better the "story" we put together in our random talking, the better the trick works.

Superstitions, mythology, rationalizing, all emerge from such a behavior learning system just because it is able to trick the internal reward prediction system.

The learning system can't tell the difference between a behavior learned that address the real danger (like learning to move our hand away from a fire), and from the tricks that only subverts the prediction system into predicting a bright future, rather than doing what needs to actually create a real brighter future.

Humans have a very advanced prediction system. It can pick up very subtle and complex clues from the sensory environment, and produce a highly accurate prediction of the rewards, and dangers, we are likely to run into. But it is only a learning machine, with finite limits. It can be tricked. And where it can be tricked, behaviors will automatically emerge to trick the prediction system, instead of actually addressing the truth of why it was predicting something bad to start with.

The mythologies of religions are just learned behaviors that trick our own internal brain into predicting a better future for us. Just making up a name for an unknown cause, like "God" is itself a trick. Having a name for such a thing, makes us feel like we have mastered some important aspect of the unknown. That we "know the cause". But just making up a name is nothing more than a language trick to fool our internal reward prediction system.

Our behavior selection system, and our prediction system are one and the same. They work hand in hand, to both predict the future, and decide how to react to it (what behaviors to produce from second to second over our lives). The more advanced our behaviors become, the more advanced our prediction system becomes.

As we learn more advanced language behaviors, we gain an improved prediction system, that is harder to "trick" with our own language behaviors. The better we understand that we are "tricking" ourselves into feeling better, the less the tricks work to actually make us feel better. As we learn they are just tricks, our prediction system is learning at the same time, to reduce our odds of a brighter future every time it detects such a trick is being used.

So we have a natural and obvious reason to fear the unknown. That which we don't understand, is more likely to hurt us. We explore and study and experiment in life so as to reduce the dangers of the unknown (aka increase the rewards). But we also play tricks on ourselves, to make the unknown seem less unknown than it really is. But the better we understand they are tricks, the less they work, and the less we are inclined to use them.

So why do we "praise" the unknown? Well, we don't praise the unknown. We praise God, not just "the unknown". Again, it's just a trick we use to make ourselves feel better. When we were kids, we learned to trust our parents and care-givers. They were far wiser than we were, and the best way to protect ourselves, was to obey them - to turn ourselves over to their desires. If they tell us not to play with fire, and we ignored them, we got burned so we learned to value of following the desires of a "higher power" - the more experienced adults in our lives.

As we grow up, we gain our own experience, and learn that the other adults are not really a "higher power" anymore. We learn we must face the world on our own, and make our own decisions. But we still yearn for that simpler time, when there was always a far wiser force in our life to tell us what needed to be done. Praising God is all just part of that trick of allowing ourselves to believe we still have wise parents in our lives to protect us from the dangers. It's a trick to make our prediction system feel we are safer, than we really are.

Now, that said, religions have evolved over thousands of years. The customs, and rules, and beliefs, in a religion have an "intelligence" about them, that comes from a 1000 years of experience. They carry with them an evolved wisdom of the ages. So when a religion says you should not kill someone, that's a belief that has survived 1000's of years of testing. The beliefs that did not work out as well, were removed from the religion, and new beliefs were added or modified over time. So the set of beliefs and customs that make up a religion is a real type of higher intelligence. So if mixed in all those beliefs, there is a "praising God" behavior, we can also understand what is really being praised is the traditions of the religion itself. The religion asks people to turn over themselves to the traditions of the religion, just like we turned ourselves over to the wisdom of our parents when we were kids. But they make up this mythological figure they call "god" and assign him to be the root cause of everything, just because it's a great trick, to make us feel more secure about not knowing the cause of of so many things, while at the same time, giving this mythical "god" the credit for creating the time tested customs of the religion itself (the bible is the word of god and all that).

The "God" at work there is just the evolution of religious memes. It's just another process of evolution. The evolution of time tested learned behaviors. But it is a higher power, and there are valid reasons for people to respect (act according to) the traditions of such a time tested set of memes. It is actual in our interest to not kill, or steal, or lie, etc.

So I can't think of any examples where we praise the unknown. But there are standard religious memes for praising the time tested wisdom of the religion, but doing it indirectly with a "trick" by making the people believe there is a "god" that created the rules.

It's all a very complex set of learned behaviors that help people maximize their future rewards. So of the behaviors actually work to make the future better (like by not killing people we reduce the odds of others killing us), but other parts of it are just tricks we have learned to manipulate our own reward prediction system, that is, commonly talked about as, "our feelings". They are tricks to make us feel better.

Now, also, don't get me wrong about the importance of feeling better. It's what we are hard wired to do. It's our sole purpose in life - it's what we are. We are machines build for the purpose of trying to make ourselves feel better. Our low level innate rewards are wired in us by the process of evolution so that what makes us feel better, is likely to help our species survive. So at the higher more boldly abstract level, we can be seen as a survival machine (though I would argue that exists more at the level of the species than the individual). At the level of the individual, we have in effect, just been giving the "job" of making ourselves feel better, and not worrying about the bigger picture of whether that helps us to survive of not. That is beyond our pay grade. It's the job of the process of evolution, to wire us "correctly" so that the things that make us feel better, work well to help us survive. And because evolution has, in general, done a good job of that, most human behaviors do tend to lean towards maximizing our survival odds.

But evolution is not perfect, and it's constantly exploring alternatives, which is why we find so many human behaviors that seem anti-survival.

# Answer
> 2 votes
I'm going to focus on your third question:

> What does scientific research tell us about why humans have this tendency?

I use the word "focus" because, well, I can't answer that. But I can introduce you a field of research that may be able to answer that for you. It's cognitive science of religion:

> Cognitive science of religion is the study of religious thought and behavior from the perspective of the cognitive and evolutionary sciences. The field employs methods and theories from a very broad range of disciplines, including: cognitive psychology, evolutionary psychology, cognitive anthropology, artificial intelligence, neurotheology, developmental psychology, and archaeology. Scholars in this field seek to explain how human minds acquire, generate, and transmit religious thoughts, practices, and schemas by means of ordinary cognitive capacities.

Other resources to research on this topic:

# Answer
> -2 votes
I think this is slightly tautologous, because we all turn to "belief" to explain the things that we don't understand. Scientists turn to their beliefs just as much as religious people, because belief is the thing that covers those thigs we don't understand.

The real question is why do people - of all sorts - not use their beliefs as a starting point to explore and understand. Belief is the idea that everything is explicable within our existing worldview - in fact, wider than this, within the limits of our ontology - and belief is the expression of this to events we do not yet understand.

One example in cosmology is the idea of "Dark Matter". This is an extension of belief that everythign is explicable to say that there is something we do not understand. Naming it Dark Matter does nothing about explaining it, just defines it as something that is not yet understood. Defining God as He Whom Explains That Which We Do Not Understand is the same process. The real challenge is to progress into understanding that.

(and, to make my position clear, I do believe in God, but not a God of the gaps)

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Tags: cognitive-psychology, religion, cognitive-science-of-religion
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# Question
Title: Methods to find patterns or correlations in MEA spike trains
I am looking for methods currently used to analyze micro-electrode arrays spike trains and figure out patterns, as repeated sequences of activation or spacial correlations.

I know about ISI histograms, power spectrum, anda DNA-sequencing-like-algorithms, but I am looking for other methods, from statistics or machine learning. Any recommendations of papers/books exploiting these methods?

# Answer
This is a very broad question. There is a very large literature on studying MEA spike trains: some classic methods are probably already explained in books such as Dayan and Abbott's Theoretical Neuroscience.

If you're looking for "statistical modelling", i.e. describing properties of a network's activity without caring for its actual structure and dynamics, generalised linear models (GLM) are a common tool (see articles by Liam Paninski 2004, Jonathan Pillow 2008) and maximum entropy models too (Schneidman et al. 2006, Shlens et al 2006). This literature is still quite popular, although probably not as fruitful as a decade ago.

There are certainly other things that could be mentioned in this area, but I don't know them all, and it also fundamentally depends on what you're trying to do. Hope this helps.
> 1 votes

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Tags: methodology, theoretical-neuroscience
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# Question
Title: ML/Neuroscience: TensorFlow vs PyTorch vs Keras for bulding NN models of the nervous system?
I would be very grateful to people with experience in using neural network models in neuroscience for advice!

What approach would you recommend for building neural networks?

I am choosing between TensorFlow, PyTorch and Keras. An important aspect for me is to be able to easily access the params of the NN (especially the weights). I want to build encoding models of biological neurons so for me model transparency, interpretability and exploration capacity is as important (if not more) than performance metrics or efficiency.

Thanks!

# Answer
If you're looking at computational models of actual neurons and biological neural networks, there are a number of tools out there which are specifically for the purpose. The most commonly used are:

* NEST is well maintained and a common tool for network dynamics.
* Brian2 is flexible and easy to use.
* NEURON is particularly popular when one is interested in biologically detailed single neurons and their interactions.

Writing bio-plausible neural models in Tensorflow or Torch is certainly possible, but those tools are particularly useful when you want to efficiently *train* a network (normally by backpropagation), and bio-plausible models are not commonly written using these tools. However, I am aware of at least two tools that simulate *spiking* networks in Torch. These are used because the authors were interested in porting models similar to convolutional neural networks, but with spikes:

* SpykeTorch High-speed simulator of convolutional spiking neural networks with at most one spike per neuron.
* Sinabs used to port CNNs to neuromorphic hardware
> 4 votes

# Answer
If you want to build a neural network as a biological simulation, maybe none of these are the best options, since they are more suitable for deep neural networks. If you want to mimic synapses using some model as Hodgkin and Huxley, you must use some different approaches. For that, you may use NEURON environment (https://neuron.yale.edu/neuron/), which has some implementations of the theoretical models behind action potentials. It comes with a gui, but personally I don't like it, so I just code everything using their python's library.

On the other hand, if you are just looking for a way to model a network, without adding too much complexity, then any of your examples are probably are ok to build directed graphs.
> 3 votes

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Tags: theoretical-neuroscience, computational-modeling, neural-network
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# Question
Title: Is there a known reason why people feel a bit bad after other people do something for them?
There's an Thai word: kreng jai (the feeling of not wanting to disturb/inconvenience another person, or feeling uneasy due to your own request of someone)

Likewise in Burmese the word "anade" which is "a strong sense of consideration for others' feelings and a desire not to cause them to feel psychological distress, unease, or burden" and in Japanese the similar word "enryo".

There seems to be a common cross-cultural feeling of distress at being a burden.

Is there a psychological explanation for why people feel bad instead of good, if someone were to help them with something?

# Answer
> 2 votes
What you seem to be talking about here are cultural influences affecting your judgement on what is right and wrong to say and do in certain situations.

Ecologies shape cultures, and cultures influence the development of personalities (Triandis & Suh, 2002).

> The conceptualization of culture is by no means a simple matter. One possible way to think about culture is that “culture is to society what memory is to individuals” (Kluckhohn 1954). It includes what has worked in the experience of a society, so that it was worth transmitting to future generations.

Triandis & Suh (2002) went on to say that:

> Funder (1997) defined personality as “an individual’s characteristic pattern of thought, emotion, and behavior, together with the psychological mechanisms— hidden or not—behind those patterns” (pp.1–2)

The kind of situation you talk about would not be seen as often in Western countries, but it seems to be widespread in Eastern cultures. To use the Thai culture of เกรงใจ (Kreng Jai) you linked to in your question, as you pointed out, it is insisted that you must not cause anyone distress or discomfort. But, Kreng Jai can be vexing and cause distress in itself as the insistence can even be

> at the expense of efficiency, honesty, or one’s own interests (Thailand Family Law Center, 2012).

If you look at Fitzroy (2014), there are good aspects to Kreng Jai in business and general society.

> By demonstrating more courtesy amongst the team you show more compassion and empathy which can lead to better teamwork and better results.

However, there are many ways where if Kreng Jai was over used, it can cause all sorts of problems. For example, being too Kreng Jai to ask your boss for help can result in an important task not being completed on time. This can cause cause loss of revenue for the business, and embarrassment for both parties.

When feeling bad for *"being inconsiderate towards others feelings on the matter"*, it can cause a lot of psychological discomfort, and this is what you are describing here.

## References

Fitzroy, P. (2014). *เกรงใจ (Kreng Jai) – overused or misunderstood?* Retrieved from: https://www.linkedin.com/pulse/20141015014001-50338470-%E0%B9%80%E0%B8%81%E0%B8%A3%E0%B8%87%E0%B9%83%E0%B8%88-kreng-jai-overused-or-misunderstood

Funder D. (1997). *The Personality Puzzle*. New York, NY: Norton

Kluckhohn, C. (1954). Culture and behavior. In *Handbook of Social Psychology*, ed. G Lindzey, 2:921–76. Cambridge, MA: Addison-Wesley

Thailand Family Law Center. (2012). *Demystifying Kreng Jai*. Retrieved from: http://www.thailand-family-law-center.com/demystifying-kreng-jai/

Triandis, H. C., & Suh, E. M. (2002). Cultural influences on personality. *Annual review of psychology, 53*(1), 133-160. doi: 10.1146/annurev.psych.53.100901.135200

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Tags: cognitive-psychology, social-psychology, abnormal-psychology, psychiatry
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# Question
Title: How do I score people on the Religious Orientation Scale?
Where can I find the scoring and analysis of the intrinsic-extrinsic religious orientation scale given by Allport and Ross (1967). I'm unable to find it anywhere. There is also a religious orientation scale by Gupta and Mishra (2007).

## References

Allport, G. W., & Ross, J. M. (1967). Personal religious orientation and prejudice. *Journal of personality and social psychology, 5*(4), 432. doi: 10.1037/h0021212

# Answer
> 1 votes
I don't know about Gupta & Mishra as I cannot find the paper you are referring to, but Allport & Ross (1967) on page 436 (page 5 of the pdf) points out that the full Religious Orientation scale has been deposited with the American Documentation Institute. You need to:

> Order Document No. 9268 from ADI Auxiliary Publications Project, Photoduplication Service, Library of Congress, Washington, D.C. 20540

I couldn't find the document on the Library of Congress catalog, but it doesn't necessarily mean they don't have it.

You can have a web chat with a librarian or use their general inquiries form by going to https://www.loc.gov/rr/askalib/ask-contactus.html

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Tags: social-psychology, religion
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# Question
Title: What would make parents lose their instinct to protect their own children?
I've seen footage of the holocaust where parents and their children were shot, with the parents just standing there, doing nothing to protect their children.

I have enormous difficulty in understanding the mindset/attitude/reason for this, fatalistic?, conduct. Being a parent myself, I *know* I would just go berserk.

What would make parents act like those in the footage?

# Answer
Sounds like you have had a distressing encounter with "learned helplessness" as madsun also described. Learned helplessness is a well-studied psychological phenomenon and reaction that explains the terrible situation that you have described. It is situational and explains the "fatalism" that is so difficult to understand. The simplest explanation I can find seems to be

> a phenomenon observed in both humans and other animals when they have been conditioned to expect pain, suffering, or discomfort without a way to escape it (Ackerman blog, 2019)

Chris describes the different types of learned helplessness in an another question

**References:**

Learned Helplessness: Seligman’s Theory of Depression (+ Cure). PositivePsychology.com blog (2018, March 24).
> 3 votes

# Answer
Gas chambers were decorated as normal showers and massacres as a morning walk. They were simply not told that they are going to be executed. However, once they realized what was about to happen, their instincts typically kicked in and chaos broke out. A lot of people tried to run away and they got shot. Mothers tried to protect their children, but there was simply nothing they could do at this point. Resisting the order to stand in the line would have ended deadly - not only for the mother but also for the children. The only thing they could have done at that moment was to beg and pray for mercy.

Furthermore, there was a huge food shortage in 1944 and 1945. Staatsfeinde des Deutschen Reichs were the last priority at the food chain so most of them were extremely low on energy. This is dreadful for any kind of instinct.
> 1 votes

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Tags: abnormal-psychology
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title: Cases of psychopathy

text:
# Question
Title: Cases of psychopathy
According to this Learning-Mind website, the 3 basic behaviors of a person which indicate likely psychopathy are

* Unhealthy obsession around arson
* Cruelty to animals
* Bed wetting after the age of five years old

This has been described as the MacDonald triad.

So if 2 out of the 3 behaviors are found in one person, does that mean that he/she is certainly a psychopath? How predictive is the MacDonald triad?

How treatable is psychopathy? How can one if they have three of the MacDonald triad and have been diagnosed with psychopathy to not to behave like that?

This 2012 question discussed the definition of psychopathy - Are there any standard tests to measure psychopathy?

And so does this 2009 question - What is the proper definition of psychopathy?

# Answer
# Psychopathy and the MacDonald triad

Just keep in mind that psychopathy is often used as a more popular term for the characteristics of Anti-Social Personality Disorder (Davey, 2014). The three behaviors described by the website were indeed studied in the scientific community (see MacDonald). First of all, this research was retrospective and descriptive which in no way provides a causal link between the three factors and psychopathy. In other words, those three factors (or even two of them) are by no means the cause of psychopathy. In order to establish a true causal link between those three factors and psychopathy an experiment would be necessary (Passer, 2019) which is virtually impossible in this case.

Subsequent research has also criticized the validity of the MacDonald triad, suggesting that it likely has low predictive power for Psychopathy (Parfitt & Alleyne, 2018; Ryan, 2009). People who show all three factors of the MacDonald triad may very well not be psychopaths.

# Treatment of psychopathy

As for treatment of psychopathy, clinicians have experienced that treatment of psychopathy is very difficult if not impossible. When psychopaths are caught after a crime they often have to participate in rehabilitation programs but these are general ineffective (Butcher, Mineka & Hooley, 2017). Some studies show that treatments which are effective for other criminal offenders actually lead to higher reoffending in psychopaths (Harris & Rice, 2006). Especially treatment focused on social skills and empathy seem to have counterproductive results because it makes the psychopath even more charming and socially cunning (Vitale & Newman, 2008).

Biological treatments such as drug therapies have not been systematically studied but so far show modest changes at best, leading scientist wondering whether these are worth studying more systematically. Overall these biological treatments seem to have little impact on the indivudal with psychopathy. Also, even if these treatments could help, psychopaths are still likely to be unmotivated to take medicines for example (Butcher et al., 2017).

Lastly, cognitive behavioral therapies seem to be most promising. These therapies often focus on a few specific factors, as can be read in Butcher et al. (2014):

> Common targets of cognitive-behavioral interventions include the following: (1) increasing self-control, self-critical thinking, and social perspective taking; (2) increasing victim awareness; (3) teaching anger management; (4) changing antisocial attitudes; and (5) curing drug addiction.

However, even CBT is relatively (to other disorders) not very effective for psychopathy, as Butcher et al. (2017) write:

> Even the best of these multifaceted, cognitive- behaviorally oriented treatment programs generally produce only modest changes, although they are somewhat more effective in treating young offenders (teenagers) than older offenders, who are often hard-core, lifelong psychopaths

For further reading about treatment see chapter 10 of Butcher et al. about personality disorders.

I personally believe psychopathy is one of the more serious disorders (do not get me wrong, all disorders negatively affect people), mainly because hatred and incomprehension for these individuals is very high even though in most cases there is hardly anything they can do about it.

# References

Butcher, J. N., Mineka, S., & Hooley, J. M. (2017). Abnormal psychology (17th ed.). Boston: Pearson.

Davey G. (2014). Psychopathology: Research, Assessment & Treatment in Clinical Psychology (2nd ed). British Psychological Association and John Wiley & Sons LTD.

Harris, G. T., & Rice, M. E. (2006). Treatment of psychopathy: A review of empirical findings. In C. J. Patrick (Ed.), Handbook of the psychopathy (pp. 555–72). New York: Guilford Press.

Parfitt, C., & Alleyne, E. (2018). Not the sum of its parts: A critical review of the macdonald triad. Trauma, Violence, & Abuse, (2018). doi:10.1177/1524838018764164

Passer, M. (2019). RESEARCH METHODS: Concepts and connections. S.l.: WORTH PUB.

Ryan, K. (2009). The Macdonald triad: Predictor of violence or urban myth?.

Vitale, J. E., & Newman, J. P. (2008). Psychopathy as psychopathology: Key developments in etiology, assessment, and treatment. In W. E. Craighead, D. J. Miklowitz, & L. W. Craighead (Eds.), Psychopathology: History, diagnosis, and empirical foundations (pp. 565–97). Hoboken, NJ: John Wiley & Sons.
> 3 votes

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Tags: clinical-psychology, psychology, personality-disorder
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# Question
Title: Is there a biological equivalent to the bias term used in artificial neural networks?
For the longest time, I had been thinking that the bias term used in the standard artificial neural network model (the ubiquitous one used in most machine learning implementations) can be interpreted as some kind of 'background' input, maybe similar to LFP.

However, I had previously missed the perspective that the bias term can also be interpreted as a parameter of response selectivity. For instance, a ReLu activated horizontal line detector with 0 bias will fire weakly when given a vertical line input but a sufficiently large negative bias will prevent the detector from firing (which, in the case of a horizontal line detector probably is desirable).

My question is, what would be the neural equivalent of bias and its modification mechanisms? Is the shape of the activation function known to be subject to any learning mechanisms at all?

# Answer
Let's call "response function" the function that gives a neuron's firing rate (or probability of firing) given its input. Then, different kinds of neurons have different response functions. All of them, as far as I'm aware, are nonlinear, and can usually be experimentally measured.

There are neurons that will fire a little, even for small inputs (so they're basically rectified, *non*linear units) and neurons that need a specific, non-zero threshold of input to be crossed before they fire at all (somewhat analogous to having negative bias). These used to be called Type I and Type II neurons respectively, although I've rarely heard this definition recently. There are also neurons that *always fire unless inhibited* from doing so ("tonic activity"): you can see this as implementing a positive bias.

About the second part of your question, the "modification mechanisms": there are many factors that influence a neuron's probability of firing which are *independent* both of the input and of the input weight. You can see these as changes in the bias, either temporary or long-term. The main causes of this are the neuron's recent firing history (usually neurons are less likely to fire if they've just fired, unless they like to burst) and other phenomena usually called 'intrinsic plasticity'.

I hope this gives you a bit more of an idea.
> 2 votes

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Tags: neural-network, artificial-intelligence
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title: Chomskian view on grammar

text:
# Question
Title: Chomskian view on grammar
The Chomskian view asserts that certain structural components of grammar are innate to all humans. To support the Chomskian view, the observation that we are able to omit certain pronouns in the English language without ever being taught the grammatical rules necessary is used to support the view. However, my question is, what would an example of the above observation be?

# Answer
## Summary:

It's worth noting that all languages have an oral origin so concerning the biological origins of grammar we must look for neurological structures involved in speech processing/production. However, it's worth first clarifying Chomsky's view that there are two levels of innateness: at the level of genetics i.e. biological heredity and at the level of neurological structures i.e. morphology and morphogenesis.

Based on the available evidence, it appears that specific genes and neurological structures that aid language acquisition do exist but these aren't necessarily specific for language.

## Chomsky's view:

Chomsky has historically held firm to the view expressed in 1983 \[1\]:

> QUESTION: Is the role of heredity as important for language as it is for embryology?
>
> CHOMSKY: I think so. You have to laugh at claims that heredity plays no significant role in language learning because exactly the same kind of genetic arguments hold for language learning as hold for embryological development. I’m very much interested in embryology but I’ve got just a layman’s knowledge of it. I think that recent work, primarily in molecular biology, however, is seeking to discover the ways that genes regulate embryological development. The gene-control problem is conceptually similar to the problem of accounting for language growth. In fact, language development really ought to be called language growth because the language organ grows like any other body organ.

However, Chomsky also recognised that there was little neurobiological evidence to support this view at the time beyond reasonable hunches:

> QUESTION: Is there a special place in the brain and a particular kind of neurological structure that comprises the language organ?
>
> CHOMSKY: Little enough is known about cognitive systems and their neurological basis; so caution is necessary in making any direct claims. But it does seem that the representation and use of language involve specific neural structures, though their nature is not well understood.

## Chomsky's particular hypotheses:

From the above interview we may derive two hypotheses:

1. That there might be genes for linguistic ability.
2. That the development of language may rely on neurological structures that are specific for language.

The first hypothesis is partially validated by research on the FOXP2 gene \[3\]. In 2001 it was found that in humans the mutation of this gene significantly disrupts speech and language skills.

That said, we must note that FOXP2 has other roles:

> ...FOXP2 is also expressed in defined regions of other tissues during embryo development, including the lung, the gut and the heart, as well as in several tissues of the adult organism.

Given that the heart, gut and lung developed prior to linguistic ability it's more likely that FOXP2 was initially useful for heart and lung function, and was exploited for linguistic ability rather than the other way around. This gene is actually present in other animals. The authors of \[3\] clarify this point:

> the presence of FOXP2 in other animals does not diminish its relevance for speech and language, but rather represents another example of recruitment and modification of existing pathways in evolution.

## The possibility of specific neurological structures:

Regarding the second hypothesis, this is the subject of ongoing investigation that combines AI research, cognitive science, neuroscience and morphogenesis. How language develops is a very complex and fascinating subject.

In a pioneering robot experiment \[2\], the linguist and cognitive scientist, Pierre-Yves Oudeyer showed that with basic neural equipment for adaptive holistic vocal imitation, coupling directly motor and perceptual representations in the brain, it was possible to generate spontaneously shared combinatorial systems of vocalizations in a society of babbling individuals:

> ...the transition from inarticulated vocalization systems to human-like speech codes may have been largely due to a modest biological innovation. Indeed, the model indicates that neuronal structures that encode a priori and specifically phonemic organization, as well as typical regularities of speech, do not need to be innately generated to allow the formation of such speech code. This is the second contribution of this work: it allows us to understand how the self-organizing properties of simple neural structures may have constrained the space of biological vocalization structures and how speech codes may have been generated and selected during phylogenesis. These new hypothesis may not have been identified without the use of computer models and simulations, because the underlying dynamics are complex and difficult to anticipate through uniquely verbal reasoning. This illustrates the potential importance of these new methodological tools in human and biological sciences.

Pierre-Yves' research on robot languages suggests that:

1. The specific neurological structures that aid acquisition aren't necessarily specific for language.
2. Cognitive scientists should investigate the development of the vocal tract during language acquisition.

Concerning specific neurological structures, today we know that Broca's area is heavily used for speech production but similar regions are present in other apes that have limited linguistic ability \[6\]. So it's important to consider the causal influence of Broca's region within cortical networks involved in speech production. In \[7\] the authors share that:

> Using direct cortical surface recordings in neurosurgical patients, we studied the evolution of activity in cortical neuronal populations, as well as the Granger causal interactions between them. We found that, during the cued production of words, a temporal cascade of neural activity proceeds from sensory representations of words in temporal cortex to their corresponding articulatory gestures in motor cortex. Broca’s area mediates this cascade through reciprocal interactions with temporal and frontal motor regions.

For this reason in the discussion section they infer:

> ...Broca’s area is not the seat of articulation per se, but rather is a key node in manipulating and forwarding neural information across large-scale cortical networks responsible for key components of speech production.

So far there is a lot of neurological evidence supporting Oudeyer's conjecture that *specific neurological structures that aid acquisition aren't necessarily specific for language*. As for Oudeyer's second suggestion there's still a lot we don't know. You might be interested in the work of the Max Planck Department for the Neurobiology of Language\[4,5\].

## References:

1. Noam Chomsky. Things No Amount of Learning Can Teach. Interviewed by John Gliedman. 1983.
2. Pierre-Yves Oudeyer. Self-Organization and Complex Dynamical Systems in the Evolution of Speech. 2013.
3. Gary F. Marcus and Simon E. Fisher. FOXP2 in focus: what can genes tell us about speech and language? Elsevier. 2003.
4. Hagoort, P., & Beckmann, C. F. (in press). Key issues and future directions: the neural architecture for language. In P. Hagoort (Ed.), Human Language: From Genes and Brains to Behavior. Cambridge, MA: MIT Press.
5. Hagoort, P. (in press). Introduction. In P. Hagoort (Ed.), Human Language: From Genes and Brains to Behavior. Cambridge, MA: MIT Press.
6. Claudio Cantalupo and William D. Hopkins. Asymmetric Broca’s area in great apes. NIH Public Access. 2001.
7. Adeen Flinker, Anna Korzeniewska, Avgusta Y. Shestyuk, Piotr J. Franaszczuk, Nina F. Dronkers, Robert T. Knight, and Nathan E. Crone. Redefining the role of Broca’s area in speech. PNAS. 2015.
> 3 votes

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Tags: language
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# Question
Title: Does our consciousness die when we go to sleep or fall into a coma?
I have sometimes wondered if our consciousness dies when we go to sleep at night or perhaps when we enter a deep coma, like from brain damage, for example. When we wake, or are woken, a new consciousness is booted up with the memories of the previous consciousness, so that it gives the illusion of one continuous consciousness. This question may be partly philosophical as well as scientific, because it looks at some of the assumptions about the nature of consciousness.

A possibly unfair analogy might be to a computer, when its running it has a memory-set like a consciousness. And if you shutdown and reboot the computer, then it can continue running as it did before, as if it had never been shut down. However, once a computer is shut down, its largely inert, though I know there are unimportant edge cases exceptions to this. The computer is effectively dead when its shut down, its ram has largely dispersed. We can start the computer back up, but it will really be loading the ram from disk. The original electrical activity that made up the 'consciousness' of the computer before it was rebooted is effectively dead.

**How do we know we don't die when we go to sleep?** I mean even if our consciousness doesn't wholly die, we may suffer a partial death of sorts. I could be wrong, but I believe its possible for victims of brain damage to show minimal neural activity. Rarely, but occasionally some of these victims recover, but perhaps their brain has rebooted their mental ram (if you will). And they may not technically be the same consciousness who fell into the coma, but merely a copy of that consciousness reconstituted from data held in the brain.

Surely plenty have considered this question, **has there been any research?** Do we have any kind of answer to this question?

# Answer
**Q: Does our consciousness die when we go to sleep or fall into a coma?**

**A:** No, neuroscientifically speaking, the consciousness does not die when we are sleeping or are in a coma; it is just in a sleep mode or in a severely depressed mode. This is because the group of neural circuits that function to create consciousness (ref 1, 2, 3) does not die when we are in those conditions; it is just functioning in the mentioned modes, which are different from the mode when we are fully conscious. This is unlike the case when one actually dies or when one has a brain death. In such cases, this group of neural circuits actually dies. So, neuroscientifically speaking, the consciousness that comes from the function of this group of neural circuits dies too.

(Philosophically speaking, this question may be answered differently, depending on what one means by the word “die”, which can be different among different philosophers. But this is a neuroscience forum, so I won’t get into that discussion and use the word “die” in the neuroscientific sense.)

It should also be noted that consciousness is not an all-or-none phenomenon but is a graded phenomenon. There can be graded different levels of consciousness, such as (from high to low) heightened alertness, normal alertness, drowsiness, sleeping (from light to deep), stupor, and coma, depending on the stimulation/facilitation of the consciousness neural circuits from the ARAS (ascending reticular activating system, which arises from the rostral brainstem)(ref 4,5), and the ARAS stimulation can be affected by stimulants, physiological diurnal sleep-wake cycle, depressants, and various pathological conditions (such as trauma, brainstem hemorrhage, and tumor). Also, even if a person is/appears alert, there can be graded different consciousness states in that person. These different consciousness states have different consciousness content, such as normal conscious awareness, confusion, akinetic mutism, minimally conscious state (MCS), and vegetative state (VS), depending on the severity of damages to the consciousness neural circuits, which can be affected by similar pharmacological and pathological causes just mentioned. In these conditions, patients may appear alert (i.e, opening eyes, blinking, and chewing spontaneously) but have abnormal content of consciousness (deranged in confusion, retarded in akinetic mutism, minimal in MCS, and none or almost none in VS).(ref 6,7)

So, consciousness during sleep or coma is just consciousness in one of these various physiological/pathological states. And, as long as the consciousness neural circuits are still functioning, albeit in an abnormal mode, and living, it can be considered that, neuroscientifically, consciousness is still living too (albeit in an abnormal mode).

**Q:** When we wake, or are woken, **a new consciousness is booted up** with the memories of the previous consciousness, so that it gives **the illusion of one continuous consciousness**. …

I could be wrong, but I believe its possible for victims of brain damage to show minimal neural activity. Rarely, but occasionally some of these victims recover, but perhaps their brain has rebooted their mental ram (if you will). And **they may not technically be the same consciousness who fell into the coma, but merely a copy of that consciousness reconstituted from data held in the brain.**

**A:** You are right. And actually, technically speaking, our present-moment consciousness is just a slightly different copy of the previous-moment one. Our brain cells are in continuous metabolic activities, which continually change both their structural components and functional components. So, technically speaking, we this moment are a biologically different entity from we a moment ago. It’s been always like this since we’re born. Yet, we feel that we are the same person with same consciousness and the same “self” all along.

It can be argued that this feeling of same consciousness and same “self” is an evolved function to enhance the survival of an organism that has this feeling. Theoretically, comparing two types of animals, one with this sense, and the other without this sense, with all other things identical, the one with this sense obviously has more drive to avoid danger, to seek happiness, to stay alive, and to procreate (all for the sake of its "self") than the one without this sense. So, it is logical to conclude that the sense of same consciousness and same “self” is just the evolved function to help increase the survival chance of the being and the species that possess it. (more detailed discussion in ref 8, 9)

**References:**

1. Koch C, Massimini M, Boly M, Tononi G. Neural correlates of consciousness: progress and problems. Nature Reviews Neuroscience. 2016;17: 307-321. The full pdf file can be downloaded from **here**.
2. Song X, Tang X. An extended theory of global workspace of consciousness. Progress in Natural Science. 2008 Jul;18(7):789–793.
3. Ukachoke C. Chapter 6 – Consciousness. In: The Basic Theory of the Mind. 1st ed, 2018. p 8-18. Charansanitwong Printing Co. Bangkok, Thailand.
4. Yeo SS, Chang PH, Jang SH. The ascending reticular activating system from pontine reticular formation to the thalamus in the human brain. Front Hum Neurosci. 2013;7: 416.
5. Wikipedia. Function of the ARAS
6. Bernat JL. Chronic disorders of consciousness. Lancet 2006;367:1181–1192.
7. Cavanna AE, Cavanna SL, Servo S, Monaco F. The neural correlates of impaired consciousness in coma and unresponsive states. Discov Med. 2010 May;9(48):431-438.
8. Fabbro F, Aglioti SM,Bergamasco M,Clarici A,Panksepp J. Evolutionary aspects of self- and world consciousness in vertebrates. Front Hum Neurosci 2015; 9: 157. doi: 10.3389/fnhum.2015.00157
9. Ukachoke C. Chapter 11 Self. The Basic Theory of the Mind. 2018.
> 7 votes

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Tags: consciousness, sleep
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# Question
Title: Do people always decide to do things that they believe will provide them the maximum amount of positive feelings in their conscious life?
Is there any scientific study or theory which supports the following claim? - People always decide to act in accordance with things they believe will guarantee them the maximum amount of positive feelings in their conscious life.

Are there any other variables that play a role in the person's decision-making?

(\*Note please that I don't have a background in psychology.)

# Answer
I would say that the more compelling scientific evidence would suggest the opposite.

Daniel Kahnemann got a Nobel Prize for behavioural economics, part of which discussed that the default decision making is not a rational, thought through process. His book Thinking Fast and Slow discusses it quite well.

Dan Ariely's book Predictably Irrational discusses similar concepts, and covers some cognitive biases - specific examples of how people make decisions other than following rational decision making process.

Both of these books are readily accessible for people without a Psychology background.

One of the books suggested a way to reduce the impact of this tendency: draft out the framework for the decision making process before going into the decision environment.

I'd suggest that more decisions are made from the aspect of minimising negative feelings in the short to medium term.
> 5 votes

# Answer
Also worth having a look at Robert Sapolsky’ 2017 book Behave. There’s a good summary of all the hidden forces motivating seemingly inexplicable behaviours. For example, why does revenge taste so sweet? Turns out that one of the headiest dopamine hits our brain receives is when we punish someone. Having done so, we may feel guilty afterwards. What’s that all about? Both are evolutionary mechanisms for supporting kin co-operation (the fourth evolutionary force) and solve the ‘freeloading’ problem.

Many of our impulses are a combination of:

* Hormones and neuropeptides, such as dopamine and oxytocin, 600m years old
* Nervous system development - from 500m years BCE
* Brain development - from 500m years ago to the development of the human prefrontal cortex, c 5m years ago

What ‘feels good’ and ‘bad’ is often expressed in the brains reward system (especially the ventral striatum) using much of this very ancient apparatus. We are generally biased to following these instincts because they are what enabled our species to meet the four evolutionary challenges of survival, sexual selection, kin selection and kin co-operation.

Reference: David Buss ed Evolutionary Psychology, Fifth Edition
> 0 votes

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Tags: decision-making
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# Question
Title: Biologically plausible models for causal inference in the human brain
## Introduction:

In ‘Is coding a relevant metaphor for the brain?’(2018) Romain Brette argues that *the causal structure of neural codes (linear, atemporal) is incongruent with the causal structure of the brain (circular, dynamic).* While he clearly explains how neural codes are inappropriate theoretical constructs for behavioural neuroscience experiments it's immediately clear what he means by *causal structure*.

On the 18th page he explains that:

> The causal structure of the brain is sketched on Figure 9A. At a coarse description level, the brain is a dynamical system coupled to the environment by circular causality. At a finer description level, the brain is itself made of neurons, which are themselves dynamical systems coupled together. To a first approximation, the coupling is mediated by spikes, which are timed events. In a dynamical system, state variables have a causal role by construction; examples of state variables in this physical system are membrane potential and the state of ionic channels. Spikes have causal effect, but being events they are not state variables; a spike is something that happens, not a property of the system.

which is incongruent with concept of a neural code since:

> Neural codes abstract time away, but temporality is critical to the operation of a dynamical system.

It's worth noting that Judea Pearl and other computer scientists have developed practical methods for causal inference \[2\] but no rigorous notion of causality. For this reason, I think evidence of the brain's causal structure would require a practical dynamical model of the brain on which we can perform causal inference to answer questions in behavioural neuroscience.

## Questions:

This leads me to a couple questions:

1. Are there biologically-plausible dynamical systems models that would qualify? (Might brain network models be sufficient? Ex: \[3\])
2. Assuming such models exist, what methods may we use to perform causal inference on these dynamical systems?

After further reflection upon comments due to Bryan Krause I think these two questions may be combined to form a single question:

*Are there biologically plausible models for causal inference in the human brain?*

## Discussion:

### Dynamical Systems that build upon neural coding theory:

Brette's notion of causal structure for the brain appears to be in direct opposition with that of Karl Friston's *Free Energy Principle* \[4\] whose formalism builds upon neural coding theory:

> Learning under the free-energy principle can be formulated in terms of optimizing the connection strengths in hierarchical models of the sensorium. This rests on associative plasticity to encode causal regularities and appeals to the same synaptic mechanisms as those underlying cell assembly formation.

However, in \[5\] Karl Friston argues that a dynamical system like the brain can encode sequences of events via attractors:

> ...the basic idea is that the environment unfolds as an ordered sequence of spatio-temporal dynamics, whose equations of motion induce attractor manifolds that contain sensory trajectories. Critically, the shape of the manifold generating sensory data is itself changed by other dynamical systems that could have their own attractors. If we consider the brain has a generative model of these coupled attractors, then we would expect to see attractors in neuronal dynamics that are trying to predict sensory input. In a hierarchical setting, the states of a high-level attractor enter the equations of motion of a low-level attractor in a nonlinear way, to change the shape of its manifold.

This is a plausible hypothesis which suggests that a more sophisticated notion of encoding might be used by the brain where state variables emerge from temporal sequences via attractors. Having said that, Brette's critique of the conventional interpretation of neuronal codes by the majority of behavioural neuroscientists still holds.

### Causal Inference vs the metaphysics of Causality:

We can't know the brain itself, only models of the brain that we may use to do experiments. To clarify my first question: Brette says that models based on notions of neural coding wouldn't qualify so what are concrete examples of dynamical systems models that do? My questions are very much designed to move the discussion beyond theory and what could be useful to behavioural neuroscientists. Furthermore, I suspect that it's not possible to define causality without going into metaphysics. This is probably why Judea Pearl chose to develop a theory of causal inference and not a theory of causal methods. Using methods from causal inference you can argue that two causal structures are distinct if: (1) there is a method for causal inference that is applicable to struct A but not struct B (2) there is a method for causal inference for which struct A and struct B give different answers.

## References:

1. Romain Brette. Is coding a relevant metaphor for the brain? BioArxiv. 2018.
2. Robert R. Tucci. Introduction to Judea Pearl's Do-Calculus. 2013.
3. Christopher W. Lynn & Danielle S. Bassett. The physics of brain network structure, function and control. Nature. 2019.
4. Karl Friston. The free-energy principle: a unified brain theory? 2010.
5. Karl Friston and Stefan Kiebel. Predictive coding under the free-energy principle. Phil. Trans. R. Soc. B. 2009.
6. The Metaphysics of Causation. Stanford Encyclopedia of Philosophy. 2016.

# Answer
> 1 votes
From the literature I have found on biologically plausible models for causal inference in the human brain, experimental validation appears to be constrained by a lack of data. In the case of causal inference models for multisensory perception, the authors of \[2\] say that:

> ...the specific computations underlying the frontal multisensory representations, and their specific role in driving behaviour, have remained elusive.

But, the path to biologically plausible models first starts with cognitive plausibility.

## Cognitively plausible models:

In \[1\], Kording et al. come up with a time-bounded model and compute-efficient cognitive model for multisensory perception:

> Perceptual events derive their significance to an animal from their meaning about the world, that is from the information they carry about their causes... The brain should thus be able to efficiently infer the causes underlying our sensory events. ...We formulate an ideal-observer model that infers whether two sensory cues originate from the same location and that also estimates their location(s). This model accurately predicts the nonlinear integration of cues by human subjects in two auditory-visual localization tasks. ...By combining insights from the study of causal inference with the ideal-observer approach to sensory cue combination, we show that the capacity to infer causal structure is not limited to conscious, high-level cognition; it is also performed continually and effortlessly in perception.

Their causal model may be succinctly described as follows:

1. One cause may be reponsible for both sensory cues(audio and visual).
2. Two separate causes may be responsible for each cue.

They then go on to define a Causal Bayesian model which may be described using Bayes rule:

\begin{equation} P(C|x\_v,x\_a) = \frac{P(x\_v,x\_a|C)P(C)}{P(x\_v,x\_a)} \end{equation}

where $C$ denotes a type of cause and $x\_v, x\_a$ represent the visual signals and auditory signals respectively which are modelled as univariate Gaussian variables.

If $C=1$ there is a single cause and if $C=2$ there are distinct causes. Although this model is simple the authors find that the model's predictions actually match the behaviour of the participants in the experiment. This experiment is very useful but the authors recognise:

> This leaves the question of what neural processes underlie the causal inference computations that emerge at the behavioural level as close to Bayes-optimal.

## Finding a neural description of multisensory causal processes:

Building upon \[1\], the authors of \[2\] combined a multivariate analysis approach to MEG data with computational modelling of behaviour, to infer where in the brain and when neural signals predicted by models of sensory fusion and causal inference emerge during multisensory perception. They reasoned that causal inference would rely at least in part on the frontal cortex, a structure that is thought to subserve causal reasoning and sensory conflict resolution.

This is an important step forward as they managed to find a neural description using MEG data that is consistent with their hypotheses and a refinement of Kording et al. causal model:

> Using a multisensory rate-categorisation task, we show that flexible multisensory behaviour is best described by a Bayesian causal inference model. The neural representations of sensory fusion and inference unfold hierarchically in time and across distinct brain regions. This comprises a cascade from early unisensory encoding at the primary cortical level, to reliability-weighted fusion in the parietal-temporal cortices, and to causal inference primarily in the frontal lobe. We found that neural representations within the dorsomedial and ventrolateral PFC were directly predictive of categorical choices, and that the vlPFC subserves a particular behavioural benefit of inferring sensory causes to minimise perceptual bias in discrepant crossmodal contexts. Our results thereby reconcile previous rival computational models of multisensory integration (Figure 1), by showing that distinct computational strategies are orchestrated in temporal sequence and along a parietal-frontal hierarchy.

Perhaps greater progress can be made modelling the probabilistic behaviour of populations of neurons \[3,4\]. But, as pointed out by Brette these would have to be neural dynamics models where the method for inferring population codes accounts for temporal dynamics in a biologically plausible manner.

## References:

1. Konrad P. Körding , Ulrik Beierholm , Wei Ji Ma , Steven Quartz, Joshua B. Tenenbaum, and Ladan Shams. Causal Inference in Multisensory Perception. PLOS. 2007.
2. Yinan Cao, Christopher Summerfield, Hame Park, Bruno L. Giordano, Christoph Kayser. Causal inference in the multisensory brain. biorxiv. 2018.
3. Zemel RS, Dayan P, Pouget A. Probabilistic interpretation of population codes. Neural Comput 10: 403–430. 1998.
4. Pouget A, Dayan P, Zemel RS. Inference and computation with population codes. Annu Rev Neurosci 26: 381–410. 2003.
5. Karl Friston and Stefan Kiebel. Predictive coding under the free-energy principle. Phil. Trans. R. Soc. B. 2009.

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Tags: theoretical-neuroscience, encoding, behavioural-neuroscience
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# Question
Title: Cognitive bias believing you are good at the things you are bad at, as successes are more vivid?
What is the name for this cognitive bias?

## Scenario

I am bad at socializing with people. For 95% of the time I talked to people, I was very awkward. Yet, mostly only 5% of the opposite time stuck to my memory. Therefore I think that I'm a very social person. Although, overwhelmingly, I'm bad.

My mind is biased. I'm blind to all the times I failed, but can recount the outliers (successes) more vividly as if they were the norm.

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Replace "socializing with people" with anything else.

PS: found and highlighted in this video: https://www.youtube.com/watch?v=17LuaKpCoDw starting around 1:25

# Answer
> 0 votes
The self serving bias is the most likely bias at play. It affects what information we remember and how we interpret events. It ca be used to explain the dunning Krueger effect, which is the effect you are describing.

# Answer
> 1 votes
It could be described as quite a few cognitive biases. See https://en.m.wikipedia.org/wiki/List\_of\_cognitive\_biases.

For example, confirmation bias, illusory superiority or choice-supportive bias could be at work here in your description.

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# Question
Title: Publicly accessible database for the Autistic brain under MRI and/or fMRI
American neuroscientist James H. Fallon released many of the images of MRIs from diagnosed psychopaths and was able to identify a pattern when compared to the average individual. Is there a database for Autism that can be used in a similar way? If anyone can find a study specifically comparing autism and another type of brain that will be fine, as I seek to compare autistics, neurotypicals, and other different types of neurological disorders identifiable through brain imaging.

# Answer
> 1 votes
I'm not personally familiar with this project (outside my area of research), but a quick search brought me to the Autism Brain Imaging Data Exchange (ABIDE):

http://fcon\_1000.projects.nitrc.org/indi/abide/

Based on citation counts for the primary articles, it seems popular. If you want to compare to other types of brains you will probably need to use multiple data sets and combine them.

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Di Martino, A., Yan, C. G., Li, Q., Denio, E., Castellanos, F. X., Alaerts, K., ... & Deen, B. (2014). The autism brain imaging data exchange: towards a large-scale evaluation of the intrinsic brain architecture in autism. Molecular psychiatry, 19(6), 659. doi: 10.1038/mp.2013.78.

Di Martino, A., O’connor, D., Chen, B., Alaerts, K., Anderson, J. S., Assaf, M., ... & Blanken, L. M. (2017). Enhancing studies of the connectome in autism using the autism brain imaging data exchange II. Scientific data, 4, 170010. doi: 10.1038/sdata.2017.10.

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Tags: neuroscience, psychology, neuroimaging
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# Question
Title: Can the neurological damage done by alcohol be reversed?
I read online that heavy alcohol consumption can lead to neurological damage, specifically in areas that affect your cognitive performance and memory but what I couldn’t find is if the damage can be reversed.

https://www.verywellmind.com/alcohol-damages-day-to-day-memory-function-62982

https://www.addictioncampuses.com/blog/alcohol-abuse-cause-brain-damage/

# Answer
> 6 votes
Most of the acute neurological effects of ethanol alcohol, such as slurred speech, ataxia, and confusion/sedation, are reversible, and the symptoms will disappear after the blood alcohol level gets down to below the intoxication level. However, in very high dose, alcohol can cause stupor or even coma, with irreversible neurological damages from associated hypoglycemia (from the hypoglycemic effect of alcohol and from concomitantly inadequate food intake) or hypoxemia (from the respiratory depression effect of alcohol). Also, there can be indirect permanent brain damage from falls, car accidents, regurgitation with aspirations, drowning, etc.

Most of the chronic neurological effects of ethanol alcohol, such as Wernicke-Kosakoff syndrome, alcoholic cerebellar degeneration, and alcoholic dementia are irreversible, and at present, there are no effective treatments to reverse neurological damage in these conditions. However, further progression can be halted by quit drinking alcohol. And, in the case of Wernicke’s encephalopathy, if adequate dose of thiamine is given in time, neurological injuries can be reversed and permanent neurological damage may not occur.

**General References.**

Healthline. Alcohol-Related Neurologic Disease

Wikipedia. Alcohol intoxication

Wikipedia. Wernicke-Korsakoff syndrome

**Academic References.**

Arts NJM, Walvoort SJW, Kessels RPC. Korsakoff’s syndrome: a critical review. Neuropsychiatr Dis Treat. 2017; 13: 2875–2890. doi: 10.2147/NDT.S130078

Harper C. The Neuropathology of Alcohol-Related Brain Damage. Alcohol and Alcoholism. 2009 Mar-Apr; 44(2):136–140. https://doi.org/10.1093/alcalc/agn102

Ridley NJ, Draper B, Withall A.Alcohol-related dementia: an update of the evidence. Alzheimers Res Ther. 2013; 5(1): 3. doi:10.1186/alzrt157

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Tags: neuroscience, alcohol
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# Question
Title: Is homosexuality a psychological illness or a natural disposition of a person's sexual orientation?
Homosexuals are oft criticized for their sexuality to which they would say they are just not attracted to the member of the opposite sex and that it's the other way round.

So, is this attraction to member's of the same-sex a (by-birth) psychological illness (that could be treated), a natural disposition, or just voluntary choice?

Or maybe something else?

# Answer
> 5 votes
Freud (1905) believed that every human was innately bisexual, and that monosexuality (i.e. hetero- or homosexuality) is a result of internal and external influences during psychological maturation.

Currently, the question of a biological, e.g. genetic or uterine, cause of non-heterosexual sexual orientation is still a subject of research and has not yet led to any conclusive results. Until that question has been answered with some level of certainy, **we simply do not know** whether homosexuality is a natural variety of sexuality or a deviation from an inborn disposition through influences after birth. (Wikipedia summarizes the research well: http://en.wikipedia.org/wiki/Biology\_and\_sexual\_orientation)

What you must differentiate is *homosexual behavior*, which can appear in heterosexual individuals such as experimenting adolescents or prisoners, and *homosexuality*, which is a preference for same-sex partners, which might not show up in behavior at all. Historically, many homosexuals led heterosexual lives, marrying, mating with and procreating with opposite-sex partners, despite a contrary sexual preference.

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* Freud, S. (1905). Drei Abhandlungen zur Sexualtheorie. Leipzig: Deuticke.

# Answer
> 4 votes
It never should have been considered an illness. Homosexuality was at one time viewed as a psychological illness from DSM-I in 1952 to the 7th printing of DSM-II in 1974. Psychologist corrected themselves and it is no longer viewed as an illness.

Homosexuality can happen as a result of scarcity and sexual drive. (as such often happens in prisons) It can also happen as a single sexual desire; those having no desire to have sex with the opposite gender. Most of the time it is present from birth but things can happen in someones life to cause them to have homosexual desires.

All attempts to "treat" homosexuality have failed as conversion therapy works only for those who are extremely religiously motivated and causes harm to those individuals. Abstinence works for both homosexuals and hetrosexuals who find conflict with their sexuality but autonomic functions eventually force the body to be somewhat sexual.

# Answer
> 3 votes
Disclaimer, we're in the fuzzy zone of psychology where nothing is certain, only likely to be certain, and "likely" is not that close to 100%.

Is homosexuality ...

1. A psychological illness? No (although what's an "illness" is itself fuzzy, see female hysteria).
2. A natural disposition of a person? To some extent.
3. A voluntary choice? Probably not.
4. Something else? Partly.

See a recent paper published in *Science*. It studied 477,522 US & UK participants and is the largest study performed to date. Its conclusions are, homosexuality is caused by multiple genes *and* "something else", with the former accounting for less than a third of the effect. The "something else" remains to be explored, but the obvious candidate is environmental factors, such as cultural norms.

If the *Science* paper is too dense to be understood, there are various summaries in the popular media such as this one.

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# Question
Title: Can Transcendental meditation be used in lab setting via Digital instructor or do we need a practitioner for TM?
I am starting my thesis, and as I was doing research on types of meditations effect on self compassion. I am new to this research, so I had wanted to know from anyone with experience. Someone, who has carried a research regarding Transcendental meditation. I want to know if for using TM for my research, will I need a practitioner or I can use a certified youtube video, where the digital instructor will be enough to guide my participants for TM?

# Answer
As per the official site:

> The TM technique is not "one size fits all." It's taught one-on-one and is carefully personalized for you.
>
> Only certified TM teachers can instruct you in the authentic TM technique.

You could, obviously, perform some form of meditation that you consider equivalent to it. However, you won't be able to claim that you are testing the authentic TM, which is, in general quite secretive regarding the concrete process.

There are TM dropouts who claim to reveal the whole process, like this guideline. Performing upon these also carries the risk of being considered 'not the authentic TM.'
> 5 votes

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