# Question
Title: Why do people who stutter have less difficulty singing than speaking?
From what I have read, stutterers tend to have much less trouble singing than speaking. Do we know why this is the case?

# Answer
> 13 votes
**Short answer**
Singing increases the duration of voiced intervals in stutterers.

**Background**
Singing is an example of one of the most effective methods to decrease stuttering* (Stager, 2003). It is a so-called *fluency-increasing (FI) condition* in stutterers and reduces stuttering by more than 90%. Some of the few, subtle acoustic differences between song and speech are the more isochronous rhythm and greater fundamental frequency stability within each syllable in songs (Tierney *et al*., 2012). Other effective fluency-evoking conditions are speech pacing (e.g., with a metronome), chorus speaking, speech slowing, and whispering (Andrews *et al*., 1982).

The main effects of FI conditions (including singing) are an increase in **phonation duration** and **speech slowing**. The reduction of stuttering seems most directly related to phonation. Phonation is the production of vocal sounds, i.e., vowels. Specifically, the frequency of very short (in the range of 30–150 ms) phonated intervals is decreased, and the longer duration phonated intervals are increased when stutterers are singing. Indeed, it has been suggested that the most effective FI conditions, and perhaps therefore the most effective treatments for stuttering, might share the common property of reducing the number or proportion of short intervals of phonation, or of quick transitions between phonated and nonphonated speech production, and/or might be associated with an increased number or proportion of longer, slower, or more consistent phonation. Among the best supported treatment approaches for stuttering are those that emphasize increased, prolonged, or continuous phonation and/or slower initiation of speech (referred to as prolonged speech treatment programs) (Ingham, 2012).

Most fluency-evoking conditions, however, have only temporary effects. Moreover, normal fluency has been defined for stuttering in terms of four variables or characteristics: the absence of stuttering events, speech rate within a normal range, normal overall naturalness of speech, and normal levels of physical and cognitive effort on the part of the speaker. Of the various methods used, only chorus speaking meets these four demands (Ingham, 2012).

**References**
**-** Andrews *et al*., *J Speech Hear Res* (1982); **25**(2): 208-16
**-** Ingham *et al*., *J Comm Disorders* (2012); **45**: 198–211
**-** Stager *et al*., *J Fluency Disorders* (2003); **28**: 319–36
**-** Tierney *et al*., *Cereb Cortex* (2012); **23**(2):249-54

**Note**
* Being a stotterer myself, I wish to emphasize that when the speech therapist at primary school instructed me to *sing* my presentation to my class mates to reduce my stuttering I chose the less embarrassing alternative, namely stammering unintelligibly for half an hour about the planets in the solar system instead of singing about them. One can quickly envision the utter ***non-practicality*** of the singing approach in everyday life. The effect of FI conditions is scientifically interesting, and they are useful tools for speech therapists, but they are not practical treatments, unfortunately.

# Answer
> 1 votes
Another explanation for this is that the centers for speech and singing, respectively, are located in different parts of the brain. People with speech impediments, and even severe brain damage from trauma such as Aphasia or Tourette Syndrome, tend to exhibit damage in the speech areas of the left hemisphere of the brain. The parts of the brain that are responsible for singing are located in the right hemisphere, however.

Both sides of the brain can vocalize. But for very severe cases of brain damage, the ability to sing where speech is impossible is somewhat reliant on committing a song to memory before the left side of the brain is damaged...

> It’s because the melody and the long-ago memorized words to those songs are housed in the right hemisphere of the brain, so they’re accessible to people with damaged left hemispheres, who do still struggle with putting new, original thoughts into words.

Furthermore, scientists at the Max Planck Institute in Germany discovered that speech can be successfully processed in the right hemisphere of the brain when words are simply spoken rhythmically, without melody. This would also support AliceD's answer but, the article also states:

> The level of familiarity with the song lyrics and whether the texts contained formulaic phrases was found to be even more important. Daily expressions like ‘How are you?’ are highly automatized at the motor level, and common song lyrics can be recalled from long-term memory.

That said, people who stutter do not generally have trouble forming new thoughts to put into words... they simply have trouble putting those words into clear, concise sentences. So, that sort of speech impediment should also not prevent them from being able to commit songs to memory... thereby enabling them to recall songs from the right hemisphere of their brain and sing them immaculately. There are also studies that show vocal training as a method to temporarily, and sometimes in the longer-term, improve fluency in those living with various speech-related neurological impairments.

---
Tags: cognitive-neuroscience, clinical-psychology, language, speech, language-processing
---


# Question
Title: Does putting something on a scale of left-to-right bias people in one direction?
I'd like to know what research has found about whether talking about politics on a scale of left to right biases people in any way. Perhaps to answer questions such as if the scale were to be inverted, would it have any difference?

# Answer
> 2 votes
Yes. In fact, it has been demonstrated in experiments that you can get people to assert they believe the opposite of what they previously said if you can successfully frame the idea with its political polarity inverted.

I can't remember the experiments off the top of my head, but I think this podcast episode touches on it. https://youarenotsosmart.com/2019/03/01/yanss-146-tribal-psychology-rebroadcast/

It has been established that people who hold ideologies, or just very strong political beliefs, are motivated by the perception of whether something is left or right. Objective facts, even reproducibility, are less important.

---
Tags: statistics
---


# Question
Title: What is the brain doing when someone tries to solve a physics or math problem that they can’t make any progress on?
Is their brain actually working or is it day dreaming and not functioning if they’re staring at a physics problem and not capable of making any progress on it?

When a student who can’t come up with any ideas to write longer essays is trying to come up with sentences to write about, what is their brain doing if they’re not making any progress for a long time? Is it actually working or does it refuse to fire neurons to come up with ideas?

Is the reason some people can’t do physics because their brains can’t fire electricity at a high enough amplitude?

# Answer
> 1 votes
To survive, the brain has evolved to solve problems it faces at the best it can, from the problems of escaping a stalking tiger, finding food, competing for the fit mate in the ancient time to solving physics/math problems, trying to make ends meet, and planning for a secure future in the present time.

But the ability for a particular brain to solve any problem depends on both *the hard-wiring* of the involved neural circuits of the cognitive areas and *the informatio*n, both declarative (the memory that you’re conscious of) and non-declarative (the skills, the experiences you’ve learned), that the brain has. The hard-wiring is mostly genetically-determined, which is different among individuals, but *is* and *can b*e modified by practicing, aging, and diseases. The information the brain has is determined by what the brain has accrued from previous encounters, which are obviously vastly different among individuals. So, the ability to solve problems among different brain are different.

That’s why some people are genius, some are average, and some are handicapped. But no matter of what type they are, in the normal conditions, their brains always try to do it best to solve problems because it is inherent in the nature of the brain to do so. Of course, in some situations such as when the brain is bored from repeated stimuli, fatigued from prolonged working, in a sleepy stage, or in a pathological stage (i.e., having a cerebral concussion, an encephalopathy, or an encephalitis), it might not try to solve the problems as usual. But those are abnormal conditions.

So, when a student who can’t come up with any ideas to write longer essays is trying to come up with sentences to write about, the brain is still working and does not refuse to fire neurons to come up with ideas. And the ability to solve problems is not about firing electricity in the brain at a high enough amplitude but is about firing signals in the correct ways in the capable and knowledgeable neural circuits, which depend on the hard-wiring and the information as mentioned above.

Accordingly, to be better at solving problems, one has to practice solving problems (this will modify the hard-wiring of the involved neural circuits) and learn more and more (this will help increase the information that may be useful in solving problems).

You may find more information about the brain function on the net. The fairly good and not-very to understand one is Neuroscience (Purves D, Augustine GJ, David Fitzpatrick D, Hall WC, Lamantia AS, McNamara JO, Williams SM, editors. Neuroscience. 3rd ed. Sunderland, Massachusetts: Sinauer Associates Inc; 2004. ISBN-13: 9780878937257 ISBN-10: 0878937250.) in *Unit IV The Changing Brain* and *Unit V Complex Brain Functions*.

---
Tags: neuroscience, neuroimaging
---


# Question
Title: Does the informational content of the mind determine its structure?
I have been thinking for several years that maybe the mind could be described as a space, in the mathematical sense, of information and that similarly to the relativistic case of the spacetime whose geometry is determined by its content in mass-energy, the informational content of the mind could determine its structure. This would be a generalization of the Sapir-Whorf hypothesis with general informational content and not only language shaping the topology/ geometry of the "informational space" I think the mind must be.

Have similar considerations been published in psychology literature so far?

# Answer
I don’t think the question of ***whether the informational content of the mind determines its structure*** can be answered definitely by referring to current standard psychology or neuroscience references because there is still no consensus on what the mind is, and likewise for its structure. I’ll try to to give the answer based on current knowledge in physics and neuroscience, though.

First, let’s clarify what you mean by the phrase “***determine its structure***”. You give an analogy in your comment above: in general relativity, the distribution of mass-energy determines the space-time geometry (of that region). So, “determine its structure” here means “***determine the topology/geometry of the structure***”, not “***determine the basic structure, per se***”. That is, the mass-energy distribution does not determine the basic structure of the space-time – the basic-structure of space-time is still a 4-dimensional differentiable manifold, with three space coordinates and one time coordinate, coupled with the metric tensor g and governed by the Einstein Field Equation. \[1,2\] Each different space-time region with different mass-energy distribution just has different topology/geometry of space-time.

What is the basic structure of the mind? Certainly, there is no standard answer for this yet. However, currently, there are several theories \[3-5\] that assert that the mind is composed of information and information processing, which is the concept similar to the concept of your question. But none of these theories propose that the basic structure of the mind is determined by its informational content although the topology/geometry of the mind or what the individual mind is actually like is determined by its informational content. For example, in the Integrated Information Theory, the mind is invariably the integrated information, and in the Basic Theory of the Mind, the mind is invariably the composite of information processes – no matter what the informational content of the mind is. But, like the case of topology/geometry of space-time above, what the mind is actually like in each individual case is determined by its informational content.

Another obvious analogy is us. Each of us has different physical and mental compositions, which determine who each of us individually is (or determine the topology/geometry, if you will, of each of us). But the basic structure of us are all the same – the basic structure of homo sapiens.

To recap, the informational content of the mind determines the topology/geometry of the mind but does not determine the basic structure of the mind. This is what I can logically conclude from the current scientific knowledge.

References:

1.Wikipedia. Space Time.

2.Wikipedia. General Relativity Theory.

3. Doyle B. Mind-body Identity Theory The Information Philosopher.
4. Tononi G. Integrated Information Theory of consciousness: An updated account. Arch Ital Biol. 2012 Jun-Sep;150(2-3):56-90.
5. Ukachoke C. The Basic Theory of the Mind. 1st ed, 2018. Charansanitwong Printing Co.: Bangkok, Thailand.
> 1 votes

---
Tags: philosophy-of-mind, nature-nurture
---


# Question
Title: Does monism imply that computers can have consciousness?
According to The Basic Theory of the Mind, the mind is not a different entity from the brain, but an emergent property of the brain. Based on this assertion, can it be concluded that computers and any other information processors have or can have consciousness and mind?

# Answer
Note: While "The Basic Theory of the Mind" may potentially be well researched and possibly accurate, it is (as far as I know) a self-published discourse by a non-researcher, that is not peer-reviewed. As such, I will not address it specifically.

Monism, the view that the brain and mind are one entity, is often associated with a family of philosophy of mind viewpoints called functionalism \- the idea that mental states are defined solely by their functional role. A related approach is computationalism \- the idea that mental states are defined by their information processing function.

Thus, computationalism's answer to the hard problem of consciousness (the question of how the brain gives rise to the mind under monism), is that the mind is an emergent phenomenon due to information processing in the brain. A well-known theory that supports this particular view with evidence is Integrated Information Theory (IIT). While this is a popular view, it is not the only one, and hence **it is not fair to say that monism implies computationalism**.

A list of monistic alternatives to computationalism can be found on Wikipedia. A couple of interesting examples:

Physicalism: The physical properties of the brain also matter (ie, not just its information processing properties). This implies that a brain made of silicon, performing the exact same information processing as a brain made of carbon, may not share the same conscious experience, because they are physically different.

Eliminative materialism: Conscious experience does not exist. That is, people's common-sense understanding of the mind is incorrect, and the mind is essentially reducible to the biological properties of the brain.

Wikipedia also mentions functionalism, behaviourism, type physicalism, and emergentism. Other alternatives worth mentioning:

Representationalism: The mind is an internal representation of the brain - ie, not a physical phenomenon, but an interpretation of physical phenomena.

Philosophical zombies: The conceivability of a zombie, physically indistinguishable from a human being, but having no conscious experience (no mind), suggests that computationalism is incorrect.

Idealism: We are making a mistake trying to determine how the mind arises from the brain, because it is the other way around - the mind is the fundamental reality from which all else arises.

Cognitive Closure: We simply lack the intellectual capacity to understand the brain-mind relationship.
> 5 votes

---
Tags: theoretical-neuroscience, consciousness, philosophy-of-mind, qualia
---


# Question
Title: why we failed to convince our own mind by reasoning and rational arguments over mental illness like depression, anxiety, phobia?
For example, one of my friend has fear of heights, even if there is a strong glass window and no reason for him to fall off. He is even aware and admits his fear is irrational.

Many may say it’s in subconscious mind or neurologically left brain, in that case, can you let me know experiments(better if I can do it myself) , research paper and scientific resources that explains this phenomenon in details.

Is there no way to communicate to this part of brain? Does it not follow rationality?

Does philosophical perspective helps? As some of spiritual/non-spiritual thinker may claim?

**Edit**: Reference: https://acmelab.yale.edu/sites/default/files/our\_unconscious\_mind.pdf ”Research has recently brought to light just how profoundly our unconscious mind shapes our day-to-day interactions“

# Answer
> 1 votes
Some scientists will say that a fear of heights (and spiders, snakes, and the dark) are innate, i.e. that we are born with them because they confer an evolutionary advantage. In other words, a fear of heights tends to prevent falls, and a fear of snakes tends to prevent snake bites. We tend to have little control regarding when these fears arise.

However, the *amount* of fear/anxiety we feel for any given thing or situation can be modulated. For example, many therapists use a strategy called "exposure therapy," exposing the patient to the feared thing or situation repeatedly, in a safe manner, which typically results in a reduction in the intensity of the anxiety response. Another example: when people do regular physical exercise, many studies show that their mood rises and they react less strongly to negative events. They even feel less physical pain when injured (compared to sedentary adults). There are many other strategies one can use to modulate painful feelings, which can be found in the book of Sudism (sudism.org). EDIT (Dec 14 2019): Sudism is a philosophy, not a science, owing to the fact that it is not currently possible to precisely measure positive and negative affect (i.e. our feelings of pleasure and pain). Take care.

EDIT (Dec 14 2019) -- Here are some supporting references that illustrate that (A) exposure therapy is beneficial for reducing anxiety, that (B) physical exercise is beneficial for reducing physical pain, and that (C) certain fears are innate:

---
Tags: depression, philosophy-of-mind, anxiety, theory-of-mind, mental-illness
---


title: How to assess a comorbidity?

text:
# Question
Title: How to assess a comorbidity?
By what criteria can a comorbidity be determined in a diagnosis? Is it pretty much educated guess-work?

I'm casually studying the DSM-5... by what standards can one be confident that a disorder is accompanied by a comorbidity? Is it common to misdiagnose a disorder due to a concurrent comorbidity?

# Answer
> 1 votes
If we consider the field of psychiatry, usually a comorbidity is understood as the simultaneous occurrence of two or more mental disorders in the same person. But attention can also treat physical comorbidity, when there is coexistence of physical and mental pathologies for example. But that does not clarify your question. Sometimes DSM can help and sometimes cause confusion. What needs to be highlighted is the crucial role of clinical evaluation. It is through the evaluation process that we can understand the course of the disease development, its predisposing factors, current difficulties and the symptomatological evolution. A good assessment can see if and when there is a major disease and which diseases can act secondarily. Some symptoms may work together, some clinical conditions of comorbidity have a temporally defined course of action. Although the experience of the clinician counts a lot, we cannot ignore the remarkable role played by exams, tests and other diagnostic instruments. In the case of psychological assessment, which is my background, we can often see from the evidence that new insights are made into each case and from there, build a more effective intervention plan. Hope this helps. Good luck.Here you can find some more.

---
Tags: diagnosis
---


# Question
Title: How would I know if I've been brainwashed?
Thinking about the "re-education" camps in parts of the world. They attempt to replace one idiology in you head with another and is considered brainwashing.

On the other hand, the first idiology got in their head by their parents. So is that not also brainwashing of a sort?

How would I know if I have been brainwashed to believe things that aren't necessarily true? How can I prevent being brainwashed by the media?

For example I believe that we can find out how the world works through science and experiment but maybe I've just been brainwashed to believe that and really the only way to find out about how the world works is by divine revelations by angels.

So how can I tell?

# Answer
> 2 votes
I'll go about this question focusing on the definitions, rather than jumping onto the answer proper. Clarifying definitions may already help you a step closer to an answer.

> * On the other hand, the first id\[e\]ology \[of children\] got in their head by their parents. So is that not also brainwashing of a sort?

the definition of **Brainwashing**...:

> a forcible indoctrination to induce someone to give up basic political, social, or religious beliefs and attitudes and to accept contrasting regimented ideas

...readily answers this Q, namely a kid's brain is a clean slate, virtually devoid of "political, social, or religious beliefs". So no, this is not brainwashing.

> * How would I know if I have been brainwashed...\[?\]

Brainwashing was coined by journalist **Edward Hunter** in September 1950 described how Mao Zedong’s Red Army used terrifying ancient hypnotic techniques to turn the Chinese people into mindless, Communist automatons. "Brainwashing” was a word-for-word translation from xi-nao, the Mandarin words for wash (xi) and brain (nao). In the Korean war later in the '50s, thousands of American soldiers, including high-ranked officers, petitioned to end the war, made false claims of war atrocities by the Us and even refused to re-enter the army after they were freed. The US jumped on it and said these people were brainwashed. However, when the media hype was over, scientific research revealed what truly made these soldiers following the ideas of the "communists"; they were tortured (source: Smithsonian Magazine).

Your question seems also to radiate the mystical origins of the word brainwashing, namely that the media can somehow hypnotize you and change your thoughts mysteriously. Those are false believes. Of course the media affects your thinking, but it cannot "brainwash" you.

> * I believe that we can find out how the world works through science and experiment but maybe I've just been brainwashed to believe that and really the only way to find out about how the world works is by divine revelations by angels.

Some people believe God created the earth and all its life on it. Others choose evolution to be key to life, and the big bang for the creation of the universe instead. It's a choice you can make. Many scientists are also believers. In other words, you don't have to choose, and support both views. Nothing brainwashy about either side.

---
Tags: cognitive-psychology, social-psychology, thought
---


# Question
Title: How can I determine which of Brainwave is dominant as one state by EEG data?
I am a student working on EEGs.

I have a EEG data of Brainwave in 4 emotional states, namely anger, sorrow, joy and pleasure. Is there any method for determining the difference between these emotional states by analyzing the 5 Brainwaves (gamma to delta)? And how can I detect which brainwaves are dominant?

# Answer
Each "brainwave" is a range of frequencies that make up the signal, usually called a frequency band (ie. "the gamma frequency band"). To determine differences between bands, you would generally look at the power spectral density (PSD) of the signal. For instance, you may want to compare the average power in each frequency band.

In practice the PSD is estimated by calculating a periodogram.
> 1 votes

---
Tags: methodology, eeg, brain-waves
---


title: Are IQ tests "beatable"?

text:
# Question
Title: Are IQ tests "beatable"?
I have been watching a lot of Jordan Peterson's videos on YouTube recently. One of his themes is, that IQ is among the best studied metrics, with high predictability, validity and is generally believed to be a very real thing in psychology. He also mentions, that IQ can not be improved or trained.

My question is, whether I could improve my IQ (by that I mean the test score, not general intelligence), by simply studying for it, trying to learn about the different types of questions and how they are generally solved and by simply doing a bunch of tests and memorizing how to solve questions.

I have done a few IQ tests online and at the beginning, I was very confused about everything, like from which direction to read the boxes and stuff like that. After doing a couple and seeing how it is done and reading explanations about the different questions I feel, that I am doing a lot better now.

Similar to that, I was on a job interview once, where they asked riddles, presumably in order to assess IQ, without doing an IQ test.

I knew some of the riddles and simply answered some of them by sheer memory.

Isn't it possible to increase your test score of an IQ test by simply studying? And if you can, what makes the tests really valid? And finally, if IQ was such a high predictor of intelligence, wouldn't most job interviews be geared towards assessing your IQ in a legal manner?

# Answer
> 5 votes
Short answer:
**Yes, but it does not matter**

Long answer:
Each question has some *inner mechanism* that you either know or you don't. Usually you should know *how to do it*, but you don't know, that you *should do it that way*. Once you know the right method, next puzzle you would solve much faster - most IQ tests are like this. If you don't know the mechanism, it could be very hard to solve - IQ tests *should* be like this.
For example this one \- once you know, that there are 4 squares all the time, next puzzle of this kind will be much easier. Most puzzles use *Subtraction* and *Addition* \- once you try this two things, you will solve lots of IQ tests. You are expected to know this methods, and that it will be used in test.
Problem with IQ tests is *insufficient number of respondents* \- since it needs lots of people to create norm.
For example I created test with possible score 0-100, and 50% of people reached 80 points. When you take the test and had 80 score, your IQ should be 100. But when (because of better education for example) most scores begin to be above 80, norm will change and for 100IQ you would have to score 82 or more.

So yes, you can *study* for it, but when more and more people do it (and knows about using subtraction, 4 squares all the time and so), norm will change and tests would be harder for everyone anyway, since there will be always exactly 50% of people that could reach at least 100IQ. ( = take some online tests, since most people do it, otherwise it would put you into disadvantage.)

Sources:
Flynn effect \- raise in IQ due to education and also health (notice not genes).
More about norm
Tests commonly used \- in it you can hide math operations without using numbers.

---
Tags: iq
---


# Question
Title: Does sexual orientation influence gender bias?
Let's take three people: Alice, Bob, and Carol. Suppose Alice is heterosexual. That should imply that Alice finds Bob attractive at some level, but not Carol. Does this mean Alice is more likely to be biased in favor of Bob (and the reverse if Alice is homosexual)?

I've not found anything directly analyzing this. Closest was this paper, *The Influence of Sexual Orientation on the Perceived Fit of Male Applicants for Both Male- and Female-Typed Jobs*, but it dealt with whether the sexual orientation of the applicant affected whether the applicant was perceived by the hiring manager as suitable, i.e. it's not the sexual orientation of the hiring manager that's being investigated.

Presumably if the answer to the title question is "yes", then it would be advisable to appoint asexual people to e.g. settle sexual harassment complaints.

# Answer
The issue around attraction needs to be clarified and assumptions challenged and proven.

To imply that sexual orientation is solely and wholly responsible for attraction is a severe and gross oversimplification verging on stereotyping and discrimination. As Wiki argues physical attractiveness is distinct from sexual attraction. Just because someone is physically attractive and also falls within one's sexual orientation, that person may also not be attracted to the person. The person may already be in a fulfilling relationship or the other person has a wedding ring, to imply that humans are animalistic and therefore their desires translate into behaviour without much other consideration is quite improper and unscientific. You should not draw a specific scenario like studies on hiring interviews to imply that the evidence is not present. There are enough studies on attraction and behaviour in other fields to disprove the specific example of hiring interviewers. I am sure you would not like your race, age or any other stereotyping physical attribute to be the sole determinant for how people and the public assess you? Would you?

On that note, there has been research on attractiveness according to sexual orientation. If attraction is the basis of hiring decision-making process, this study disproves this. However, if you are implying sexual orientation goes through a different mechanism to affect the decision-making process at the hiring interview, then I would be keen to hear it. This 1992 study of 52 subjects (four groups of 13) found minimal or no difference between heterosexuals and homosexuals on the assessment of attractiveness. Both heterosexual and homosexual men rated younger sex subjects higher than older subjects. Your question implies that homosexual men should rate women lower than men as they are not sexually attracted to them. If there are no differences between attractiveness depending on sexual orientation, it seems hard to argue that asexual people should be used on hiring interview panels.

**References:**

Jankowiak, W.R., Hill, E.M., Donovan, J.M., (1992). The effects of sex and sexual orientation on attractiveness judgments: An evolutionary interpretation. *Ethology and Sociobiology*. Volume 13, Issue 2, Pages 73-85.
> 1 votes

# Answer
Partial answer: it's apparently the case that being physically attractive affects the hiring manager positively, assuming the hiring manager is of the opposite sex. The reverse is true if the hiring manager is of the same sex - the effect on the hiring manager is negative.

> Previous studies of organizational decision making demonstrate an abundance of positive biases directed toward highly attractive individuals. The current research, in contrast, suggests that when the person being evaluated is of the same sex as the evaluator, attractiveness hurts, rather than helps.

The authors speculate that the reason for same-sex negative feedback is the perception of self-threat.

This study does not examine sexual orientation, but given the fact that most (\>90%) of people are heterosexual, it's a possible confounding variable.
> 0 votes

---
Tags: bias, sexuality
---


# Question
Title: Does belief in an afterlife play a role in suicide rates?
Religious beliefs, in particular views on the afterlife, could plausibly influence suicide.

Is there some study which tries to look at how belief systems play a role in the number of suicides in some country or in the world?

# Answer
I think, from a statistical point of view, this question will be impossible to answer, because belief in an afterlife is almost always tied to powerful confounding factors, such as participation in a community of fellow believers, marital status, age, etc. I imagine that religious affiliation probably can have a strong protective effect regarding suicide - though I don't have any statistics to back that up - but I can't envisage how you would separate out the various components of religious affiliation and prove which component(s) made the crucial difference.

You might have heard of Émile Durkheim's famous book *Suicide*. (Forgive me if I'm assuming either too little or too much knowledge on your part.) Durkheim looked specifically at the effect of religious affiliation on suicide: he found that Jews in late nineteenth century France had the lowest rate of suicide, Protestants the highest, and Roman Catholics somewhere in the middle. Durkheim, however, attributed these findings to the fact that Jews tended to form very tight-knit communities, and that Protestants tended to be much more individualistic, than to any doctrinal difference.

On a more personal note, as a believer who has been through two episodes of severe depression, I think that, broadly speaking, belief in an afterlife probably does have a protective effect with regard to suicide - although there are plenty of factors whose effect is more potent. I have no background in academic psychology, so my advice is probably both unwelcome and unsound, but, if this is part of a formal research project, a good place to start would be to interview believers who had gone through, or were going through, an episode of severe depression. Also, John Donne's *Biathanatos* provides a very left-field exploration of Christian attitudes to suicide.
> 3 votes

---
Tags: depression, religion
---


# Question
Title: Why would someone state that "self-esteem doesn't exist"?
In the video "Self-esteem Doesn't Exist, the author Jordan Peterson clearly seems to argue he doesn't believe in self-esteem, given the title of the talk. However, I do not notice him mentioning anything in relation to this and therefore I do not understand what he means exactly (maybe because I am not an English speaker).

Could you clarify why exactly he claims self-esteem does not exist, or what he is referring to?

# Answer
In the video, he states:

> What is self-esteem? It is a word (actually it is two words). It is sort of something you think you might have or not have. **But, that's a figure of speech. That's not an empirical phenomenon.**

Thus, by stating "self-esteem does not exist", he is implying it cannot be empirically observed, i.e., it is not something that can be observed reliably and systematically.

From there on out, he starts arguing why this is so. Some key points:

* Reported self-esteem measures are pretty appalling.
* You can already model the concept of self-esteem with the Big 5. I presume he is implying here the concept is superfluous and implications of 'low or high self-esteem' are modeled better using Big 5.
* The introduction of the concept has lead to undesirable consequence of advocating for self-esteem. But, there is no reason to believe that increasing your self-esteem is a good idea. "It is not at haste that you should have a good opinion of yourself in every bloody situation."

He continues to give examples for these points, e.g., "self-esteem might become disconnected from the actual accomplishment", but I believe this is outside of scope what you are asking for here.
> 2 votes

# Answer
I assume the title is designed to be a bit provocative. But I think he makes a few claims:

1. Big Five personality (especially neuroticism and extraversion) explains self-esteem well.
2. It's very difficult to change a person's fundamental level of neuroticism.
3. Interventions that focus directly on increasing self-esteem in a way that are detached from reality may be counterproductive.
4. Beyond not being depressed, higher-levels of self-esteem may not necessarily be good or functional, especially if they are not grounded in intersubjective reality or lead to narcissism.
> 1 votes

---
Tags: learning, personality, analysis, self
---


# Question
Title: Laughing as a psychological defense when nervous
Say a persons experienced a scarring event in their life (ptsd), and so their mind has developed defense in which they laugh uncontrollably whenever their nervous. This is similar to Joker 2019, whenever Arthur was stressed or depressed he would break out in a laughing episode. However, I began to think otherwise, because later in the film Arthur was physically abused as a child (even being tied to a radiator), which may contributed to this being a physical disorder, but I'm looking for a psychological disorder.

What is the name/term for this condition.

I've thought of psuedobulbar affect (PBA), but after doing research, it is a physical disorder, not purely psychological.

# Answer
I haven’t seen the movie Joker (2019) ... yet ... but I have observed what is often referred to as *nervous laughter* occurring with many people, including those involved in the controversial *Milgram Experiment* (Milgram, 1963) as you can see in this YouTube video at 5 mins 40 secs for example.

There isn’t necessarily any psychological disorder which will cause nervous laughter, but it is a physical reaction to stress, tension, confusion, or anxiety.

Neuroscientist Vilayanur S. Ramachandran states (Ramachandran, 2004):

> We have nervous laughter because we want to make ourselves think what horrible thing we encountered isn't really as horrible as it appears, something we want to believe.

and also suggests that laughter is used as a defense mechanism used to guard against overwhelming anxiety. Laughter often diminishes the suffering associated with a traumatic event.

Psychologist and neuroscientist Robert Provine, from the University of Maryland, studied over 1,200 "laughter episodes" and determined that more than 80% of laughter isn't a response to anything he described as “resembling a formal effort at humour” (Provine, 1996).

## References

Milgram, S. (1963). Behavioral study of obedience. *Journal of Abnormal and Social Psychology, 67*(4), 371-378. doi: 10.1037/h0040525 Free PDF: https://pdfs.semanticscholar.org/29e4/8c1365346fc67137423a016096622ac6a215.pdf

Provine, R. R. (1996). Laughter. *American Scientist, 84*(1), 38-47. Retrieved from: https://www.webcitation.org/67VExLQDj

Ramachandran, V. S. (2004). *A brief tour of human consciousness: From impostor poodles to purple numbers*. New York, NY: Pi Press.
> 1 votes

---
Tags: abnormal-psychology, clinical-psychology
---


title: Emotions VS Maslow pyramid

text:
# Question
Title: Emotions VS Maslow pyramid
Where are the emotions in the Maslow pyramid?

When we go from inside of basic emotions outside like this:

in which direction at the Maslow pyramid we would move?

***Update:***

Based on ***@ArnonWeinberg*** Comment i need to mention these information about my prose of asking this question:

> I like to have one theory about this relations between the Psychology emotional growing and the Maslow pyramid levels, so i asked this kind, but could be another Emotional diagram which is more Updated

new Update:

i found this paper which is saying about computational mode of Emotions:

The Relationship Between Emotion Models and Artificial Intelligence

and this power-point:

Thanks for your attention.

# Answer
The 2 concepts you are referring to are Maslow’s hierarchy of needs (Maslow, 1943) and Plutchik’s general psychoevolutionary theory of emotion (Plutchik, 1980). **They are totally separate concepts**, but can be **linked only to a small degree**.

As someone progress within Maslow’s hierarchy of needs, the person can experience a variety of different emotions, depending on their experiences leading up to and upon achieving that level of attainment.

For example, someone who has met all their safety needs may experience a sense of optimism and trust in their environment. When meeting their love and relationship needs there will probably be experiences of love, but also there may be joy and serenity.

If for some reason the person loses an aspect or more of their safety needs, for example, there could be apprehension, worry, fear, annoyance, pensiveness...

## References

Maslow, A. H. (1943). A theory of human motivation. *Psychological review, 50*(4), 370-396. doi: 10.1037/h0054346 Free PDF: https://scottbarrykaufman.com/wp-content/uploads/2015/01/Maslow-1943.pdf

Plutchik, R. (1980). A general psychoevolutionary theory of emotion. In *Theories of emotion* (pp. 3-33). Academic press. doi: 10.1016/B978-0-12-558701-3.50007-7 Google Books: https://books.google.co.uk/books?hl=en&lr=&id=Ie1GBQAAQBAJ&oi=fnd&pg=PA3
> 3 votes

---
Tags: emotion
---


# Question
Title: Unable to run AxoGraph v1.7.6 on macOS 10.15 Catalina
After a recent MacOS update, I am no longer able to run the (latest) AxoGraph software for electrophysiology data analysis on my computer, as I get the following error message:

```
"AxoGraph.app" needs to be updated.

The developer of this app needs to update it to work
with this version of macOS. Contact the developer for
more information.

```

Screenshot:

I understand that this is because AxoGraph is a **32-bit application**, which is not supported by macOS Catalina. I have already contacted the support of the application for advice. In the meantime, **is there any good solution besides switching to a different software?**

# Answer
> 1 votes
# Response from AxoGraph Support

I received an answer from John of AxoGraph suggesting to follow the steps outlined in this tutorial to set up a virtual machine (VM) on my computer with an earlier version of macOS using the **Parallels** software ($79.99/year).

He also discouraged using **VirtualBox**, the free VM manager, as "there's more work involved, and it’s not so smoothly integrated with Catalina." In his reply, John also promised "to finish the new completely re-written 64-bit version of AxoGraph," which "is not far from completion," first releasing a new data-acquisition-only version, subsequently followed by an update with data analysis features. It sounded like all of this would take at least several months, though.

---

# My Solution

After some digging, setting up a virtual machine (VM) with an earlier version of macOS indeed did seem to be the best option for me at this point. What I was after, however, was a **free solution** \- and eventually, I managed to get a **Mojave VM** to work on my Catalina using **VirtualBox**. Getting through the whole process was a patchwork of several different sources (mostly following this tutorial and its comments), so I decided to re-write the **detailed steps I took below** (some steps may be adjustable but I used these specific settings with success):

### 1. Download macOS Mojave Installer:

1. Go to this link: https://support.apple.com/en-us/HT210190
2. Click on *Get macOS Mojave* in step 4, and open in **App Store**.
3. Click on *GET* \- that will open the updater, which will download the installer (if you already have Catalina installed, the "update" will stall after the download automatically)
4. Find it in your **Applications** folder as *Install macOS Mojave.app*

### 2. Create an ISO installation media using Terminal:

1. Create a temporary disk image from the install file & make a bootable installer using Terminal:

```
hdiutil create -o /tmp/Mojave.cdr -size 7000m -layout SPUD -fs HFS+J

```
2. Attach that file, with Terminal command:

```
hdiutil attach /tmp/Mojave.cdr.dmg -noverify -mountpoint /Volumes/install_build

```
3. Build it, with command:

```
sudo /Applications/Install\ macOS\ Mojave.app/Contents/Resources/createinstallmedia --volume /Volumes/install_build

```
4. Move it to your mac’s Desktop:

```
mv /tmp/Mojave.cdr.dmg ~/Desktop/InstallSystem.dmg

```
5. Unmount the file:

```
hdiutil detach /Volumes/Install\ macOS\ Mojave

```
6. Convert it to ISO:

```
hdiutil convert ~/Desktop/InstallSystem.dmg -format UDTO -o ~/Desktop/Mojave.iso

```
7. Rename it to remove the CDR extension:

```
mv ~/Desktop/Mojave.iso.cdr ~/Desktop/Mojave.iso

```
8. Exit Terminal via Terminal command:

```
exit

```

### 3. Create a new virtual machine (VM) in VirtualBox:

1. Download **Oracle's VM VirtualBox Manager** (https://www.virtualbox.org) & install it on your Mac
2. Open **VirtualBox**
3. Click on **New**
4. Select *Type: Mac OS X* and *Version: Mac OS X (64-bit)*
5. Memory size: *8192 MB* (at least 3 GB)
6. Hard disk: *Create a virtual hard disk now*
7. Hard disk file type: *VDI*
8. Storage on physical hard disk: *Fixed size*
9. File location and size: *32.00 GB*

### 4. Tweak the VM before installation:

1. With your newly created VM selected in VirtualBox, go to *Settings***Storage**:
    1. Click on *Empty* → Remove \[*square with a red cross at the bottom*\]
    2. Click on *Controller: SATA* → Add optical drive \[*CD with a green plus sign*\] → *Add* → Find the .iso file you created and click *Choose*
2. *Settings**Display*: **Video Memory** \- at least *128 MB*
3. *Settings**System*: **Processor(s)** \- at least *2*

### 5. Install the macOS on your VM:

1. With your VM selected in VirtualBox, click *Start*
2. Wait until the *Language* selection appears; select your preferred language and continue
3. *macOS Utilities*: **Disk Utility** → Continue
4. Select *VBOX HARDDISK Media* → click on **Erase** in the toolbar
5. Name the drive as you wish and keep the default selections: *Format: Mac OS Extended (Journaled)* and *Scheme: GUID Partition Map*; click *Erase*
6. *Quit* Disk Utility when done
7. Select **Install macOS**, *Continue*, and *Agree* to the license
8. Select the hard drive you just erased and **Install**
9. MacOS starts installing; wait and **be patient**! (It took about half an hour for me. The VM may restart at least once in the process.)
10. Go through the **MacOS setup** (select your Country, keyboard, etc.)
    * It is recommended that you do not log in with your Apple ID at this time and click *Set up later* instead
    * I also did not allow *Location Services*, nor *data collection* from Apple
    * Once installed, you can eject the installation disc from within the VM
    * It also might be a good idea to go to *System Preferences...**Software Update**Advanced...* → uncheck *Check for updates*

### 6. Install the latest version of AxoGraph on your VM:

1. Open **Safari** within your VM
2. Go to https://axograph.com/download
3. Click on **Mac OS X 10.4 and up\***
4. **Install** AxoGraph

> # Voilà!
>
> ***Now you can run AxoGraph, as well as other 32-bit applications, on your MacOS Catalina!***

* You should be able to turn off the VM from within, as you usually would shut down your Mac
* It is booted again by selecting your VM in VirtualBox and clicking *Start*

---
Tags: data, software, electrophysiology, analysis
---


# Question
Title: Believing only one thing matters, when in reality, it was a chain reaction. What's the bias called?
Assume I had a business. That business would've been very close to be sold to a bigger company, **if only I didn't mess up some of my papers.** Thing is though, I didn't really only mess these papers. The issues started years ago when I thought I'd be smart and not fully fill out all the forms and so on. In time, it all added up, but given that it was some precise papers at the end that got me, I'm prone to say "ah, if only this \[most recent evil\] didn't happen!".

What bias am I guilty of?

# Answer
The described scenario is about *ascribing the problem to a single mistake, while the real problem was long-term wrong behaviour.* From the list of cognitive biases or fallacies, this is the closest what I could find:

**Fallacy of the single cause:**

> The fallacy of the single cause, also known as complex cause, causal oversimplification, causal reductionism, and reduction fallacy, is a fallacy of questionable cause that occurs when it is assumed that there is a single, simple cause of an outcome when in reality it may have been caused by a number of only jointly sufficient causes. It can be logically reduced to: " X caused Y; therefore, X was the only cause of Y" (although A,B,C...etc. also contributed to Y.) (Wikipedia)

The terms bias and fallacy are used to describe how being *unaware* of deceptive logic or prejudice results in wrong conclusions. In the scenario in the question, one is *consciously* trying to interpret the situation in attempt to avoid the full truth, which can be described with the terms, such as:

* **Minimisation** \- a type of deception involving denial coupled with rationalisation in situations where complete denial is implausible (Wikipedia).
* **Belittling** \- regarding or portraying as less impressive or important than appearances indicate (Dictionary.com).
> 1 votes

---
Tags: bias
---


# Question
Title: What predicts the severity of rejection pain?
A number of studies show that social rejection causes actual pain. Is there a study that focuses on finding the personality dimensions that predict the amount of such pain? For example, is there a correlation between extroversion and the severity of rejection pain?

An answer nearby suggests that there is some kind of *"sensitivity"* to a person, but I am so far unable to determine what exactly this *"sensitivity*" means.

<sub> References:
K. D. Williams and allies — "Ostracism: Consequences and Coping"
Naomi I. Eisenberger and allies — "Does Rejection Hurt? An fMRI Study of Social Exclusion" </sub>

# Answer
> 2 votes
I have found 2 papers that may be relevant to your question -

This paper probably answers your question the most - I have only schemed through it, and it seems that the results were insignificant. You can check out the paper in more detail, hopefully it will get you to more resources that can help with your research.

I have also found this paper which does not entirely answer your question, but I think will help with your insight.

Also keep in mind that some neuroimaging research on social exclusion in causing activation in regions (e.g. dACC) associated with physical pain employs reverse inference method. This does not mean the results are entirely unworthy of considering - just something to keep in mind when looking at neuroimaging result interpretations.

References

McDonald, Melissa & Donnellan, M.. (2012). Is ostracism a strong situation? The influence of personality in reactions to rejection. *Journal of Research in Personality. 46*. 614–618. doi: 10.1016/j.jrp.2012.05.008.

Park, M., Lee, K.H., Sohn, S., Eom, J., & Sohn, J. (2014). Degree of extraversion and physiological responses to physical pain and sadness. *Scandinavian journal of psychology, 55*(5), 483-8. doi: 10.1111/sjop.12144

Poldrack R. A. (2011). Inferring mental states from neuroimaging data: from reverse inference to large-scale decoding. *Neuron, 72*(5), 692–697. doi: 10.1016/j.neuron.2011.11.001

---
Tags: social-psychology, personality, pain
---


title: Why do we find things fun?

text:
# Question
Title: Why do we find things fun?
One may cause to argue that Fun activities are solely based off psychological and physical identification with certain activities, but surely there is a deeper analysis on why we find things fun.

Furthermore, what is the relationship of personal experience to what an individual finds fun. Some argue that what we find fun is solely defined by personal experiences, but what about activities that many individuals find fun- regardless of personal experiences.

# Answer
> 4 votes
I would argue that a positive emotional experience is something that evolved for conscious organisms in order for consciousness to function in a way that supports survival and reproduction (thus, sex and eating are pleasurable experiences).

Once having this system, an organism can then find other ways to trigger it that may not lead to better survival or reproduction, but still don't compromise survival and reproduction. Often, this may be through human invention. For example, our love of sugar evolved in a world where sugar indicated health (high energy foods that help you survive). Now, we're able to produce the sugar by itself with technology; it no longer occurs only in the context of nutritional food.

Thus, humans are able to exploit their reward systems and "fun" need not pertain to healthy activities, but may have roots in the evolutionary purpose of pleasure.

# Answer
> 1 votes
I think that a person finds something fun if it is challenging (it makes you learn something new, grow, etc.), yet he/she has a talent for it so he/she is doing well at it. Isn't that fun. On the other hand if you do something and it's hard and you're just not getting it, it's not fun and you'll probably consider exploring something else.

# Answer
> 0 votes
I think that some things are fun because our brain knows that the activity can make you happy and release dopamine.

For example, say you're going to play a game that you've never seen or played before. At first you probably won't be that in interested in it. But when you start playing it, you start to like the game. Then your brain documents it as fun, So when you see that game or think of it and start playing it, you will experience fun.

The reason why your brain probably thought of it as fun is because it's a game, and games are triggers for dopamine release when you win, advance in the game, get more points, etc. This is all due to primitive behaviors relating to triggers of dopamine.

Now say you're a kid and you're playing around with your friend. I think the reason that playing around with someone makes you happy and is fun is because that particular person makes you happy. So doing things with them such games will let you have fun.

---
Tags: personality, motivation
---


# Question
Title: Is there research into why people use piercings or tattoos for personal reasons?
I am interested in reasons why people engage in body modifications, such as piercings or tattoos. I am aware of some religious reasons, and some religions forbidding such activity, but I am interested in personal reasons in particular.

For example, I don't see how piercings and tattoos communicate fitness or fertility, help with symmetry, or improve sexual attractiveness. Perhaps there are other emotional or linguistic meanings involved?

Is there research into why people use piercings or tattoos for personal reasons?

# Answer
> 4 votes
This question is far too broad for this forum. In fact, entire books have been written on this topic. An extensive review by Wohlrab, Stahl, & Kappeler (2006) "Motivations for getting tattooed and pierced" divides the literature into 10 broad categories of reasons:

* Beauty, art and fashion
* Individuality
* Personal narrative
* Physical endurance
* Group afﬁliations and commitment
* Resistance
* Spirituality and cultural tradition
* Addiction
* Sexual motivation
* No speciﬁc reason

To keep this answer's length sane, I'll just focus on the areas that you seem most concerned with.

**Sexual attraction:**

There are probably a few different ways that tattoos and piercings can increase sexual attractiveness. For example, tattoos can be used to camouflage scars.

Human sexual preference is highly affected by environmental (ie, psychological, social, cultural, rather than genetic or evolutionary) factors. For example, sexual attraction can be susceptible to conditioning and imprinting, leading to an extensive list of fetishes and paraphilias, including stigmatophilia \- "sexual arousal from body modifications such as piercings and tattoos".

Related to this, tattoos and piercings may provide exploitability signals \- tattoos on women are associated with promiscuity for example, which is attractive to some:

> Results suggest that sexual attraction to exploitability cues functions to motivate men to employ exploitative strategies towards accessible targets ...

And in much the same way as humans are prone to decorate spaces around them, so they decorate themselves as well - with fashion, accoutrements, and as it so happens, tattoos and piercings. Just as art and ornaments might decorate a room in your house, so they might decorate human bodies.

**Fitness and fertility:**

A common explanation for body modification from an evolutionary perspective is as a signal of fitness. This is called the handicap principle:

> ... reliable signals must be costly to the signaler, costing the signaler something that could not be afforded by an individual with less of a particular trait. ... Receivers know that the signal indicates quality because inferior quality signalers cannot afford to produce such wastefully extravagant signals.

Essentially, this is like saying "I am so fit / masculine / feminine that I can afford to mutilate my body without substantially affecting my attractiveness." For more details, see research by Carmen, Guitar, & Dillon (2012); Wohlrab et al (2008); and Koziel, Kretschmer, & Pawlowski (2010).

---
Tags: motivation, sexuality, physical-attraction, preferences, body-language
---


# Question
Title: Predicting the individual effects of psychotropic drugs
https://www.ncbi.nlm.nih.gov/m/pubmed/23796468/

I have searched the national library of medicine but I could not find any papers about predicting both the therapeutic and adverse effects on the specific patient (individual) in front of us.

People work on/ have an extremely similar chemistry (all cells do that was the phenomenon that the theory of evolution explained) but it is not identical (absolutely) across individuals otherwise we should predict drugs would have absolutely the same effects on all individuals.

As drugs do have different effects across individuals the expectation of the effects should be different too. Because we now know that they have a similar but slightly non-homogeneous chemistry.

How can we earnestly predict the effects, both therapeutic and adverse, of psychotropic drugs on the specific patient in front of us?

# Answer
> 3 votes
Predicting individual side effects is generally not feasible in current clinical practice, although in the purview of "personalized medicine", mostly as a research goal/topic. For psychotropic medications, this is largely envisaged to work through pharmacogenomics:

> In pharmacogenomics, genomic information is used to study individual responses to drugs. When a gene variant is associated with a particular drug response in a patient, there is the potential for making clinical decisions based on genetics by adjusting the dosage or choosing a different drug, for example. Scientists assess gene variants affecting an individual's drug response the same way they assess gene variants associated with diseases: by identifying genetic loci associated with known drug responses, and then testing individuals whose response is unknown. \[...\]
>
> Scientists believe many idiosyncratic effects result from individual variation that is encoded in the genome. Thus, genetic variation in genes for drug-metabolizing enzymes, drug receptors, and drug transporters have been associated with individual variability in the efficacy and toxicity of drugs. Genetics also underlies hypersensitivity reactions in patients who are allergic to certain drugs, such as penicillin, wherein the body mounts a rapid, aggressive immune response that can cause not only a rash, but can also hinder breathing and cause edema to the point of cardiovascular collapse.
>
> Predicting serious ADRs \[adverse drug reactions\] is a priority for pharmacogenomic research. For example, the enzyme CYP2D6, one of a class of drug-metabolizing enzymes found in the liver, breaks down and terminates the action of certain antidepressant, antiarrhythmic, and antipsychotic drugs. Molecular cloning and characterization studies of the gene that codes for this enzyme have described more than 70 variant alleles (Meyer, 2000). These alleles contain one or more point mutations, only some of which affect enzyme activity; however, some of these alleles involve gene deletions and duplications that can lead to increased enzyme activity. Individuals who are homozygous or heterozygous for the wild-type or normal activity enzymes (75%–85% of the population) are called extensive metabolizers; intermediate (10%–15%) or poor (5%–10%) metabolizers are carriers of two alleles that decrease enzyme activity (Ingelman-Sundberg, 1999); and ultrarapid metabolizers (1%–10%) are carriers of duplicated genes. The most common alleles can be detected by DNA chip microarrays, allowing most patients to be assigned to a particular phenotype group. \[...\]
>
> With the completion of the Human Genome Project, anticipation was high that genetic information would radically improve medicine, that side effects would be more predictable, and that patients could be screened for likely drug responses. But thus far, progress has been much slower than what the initial excitement suggested.
>
> A great deal of this delay relates to the fact that an individual's response to drugs is multifactorial, resulting from multiple gene and environmental interactions (Haga & Burke, 2004). Scientists also recognize that even as the knowledge base continues to expand, the clinical translation of that knowledge still requires empirical evidence, generated for a particular disease and drug combination, before treatment can be customized to a patient's genotype. Thus, much work remains to be done before personalized medicine can reach its fullest potential.

Last year the FDA has issued a warning against improper/premature use of pharmacogenomics to select antidepressants. An excerpt...

> For example, the FDA is aware of genetic tests that claim results can be used to help physicians identify which antidepressant medication would have increased effectiveness or side effects compared to other antidepressant medications. However, the relationship between DNA variations and the effectiveness of antidepressant medication has never been established. The FDA is aware that health care providers may have made inappropriate changes to a patient's medication based on the results from genetic tests that claim to provide information on the personalized dosage or treatment regimens for some antidepressants. \[...\]
>
> There are a limited number of cases for which at least some evidence does exist to support a correlation between a genetic variant and drug levels within the body, and this is described in the labeling of FDA cleared or approved genetic tests and FDA approved medications.

As noted in a review of last year there are now several guidelines trying to put together the available knowledge:

> There are multiple guidelines in various stages of development during the past 5 years including those by the Clinical Pharmacogenetics Implementation Consortium (CPIC), a registered service mark of the US Department of Health and Human Services and other authoritative scientific consortia \[(e.g., Dutch Pharmacogenetic Working Group (DPWG)\] for cytochrome P450 and drug therapy including for psychiatry.

CPIC has a database page roughly ordered by the drug in question, e.g. "CYP2D6, CYP2C19 and Selective Serotonin Reuptake Inhibitors". The DPWG guidelines currently seem to be one large (book-sized) pdf document, not restricted to psychotropic drugs. Various papers, e.g. Lunenburg et al. describe how their methodology (and thus sometimes conclusions) differs from CPIC etc. The latter consortium also publishes journal papers on their individual drug guidelines, e.g. they have one on "Genotypes and Dosing of Tricyclic Antidepressants".

# Answer
> 2 votes
> How can we earnestly predict the effects, both therapeutic and adverse, of psychotropic drugs on the specific patient in front of us?

The basic answer is that you cannot necessarily predict accurately how any medication will affect any individual person.

Medications **can** in general, carry risks of side effects. The risk levels of each side effect will also be different. Anyone who is licensed to prescribe medications have access to enough literature to assess the level of risk based on risk factors known to the medical profession.

As an example, here in the UK, we have the British National Formulary (BNF), which provides guidance on prescribing in general, as well as guidance on prescribing for children and those who are pregnant etc.

Detailed information is also given as to the drug indications and dose, contra-indications, known side effects and risk factors among other things to consider.

An example side effects list etc. for Paroxetine (a Selective Serotonin Reputable Inhibitor) can be viewed at https://bnf.nice.org.uk/drug/paroxetine.html (NOTE: I have been advised that this may be restricted to UK website visitors only). An alternative example from the US is from drugs.com

# Answer
> 2 votes
Therapeutic effects and adverse reactions of psychoneuro-pharmaceutical drugs are tested using the same gold standard as usd for more conventional drugs, namely in **randomized controlled trials**.

* Phase I trials focus on side effects and dosages in a small group of healthy subjects.
* Phase II testings assess efficacy and side effects in a medium-sized population of patients.
* Phase III testing assesses efficacy, effectiveness and safety in large numbers of patients. The outcome will tell you whether the drug works, how well it works and what side effects are to be expected and how often they occur.

These data do not allow to predict effects and side effects in a specific patient; they only allow you to estimate the chances that a drug will work and what side effects can be expected based on population testing.

Because of the renewed interest in psychoactive compounds to treat depression and addiction, there is currently an increasing trend to conduct RCTs on compounds like psilocybin (Lewis, 2019).

<sub>**Reference**
**-** Lewis, *Sci Am*, January issue (2020)</sub>

---
Tags: neuroscience, cognitive-neuroscience, theoretical-neuroscience, cognitive-modeling, psychopharmacology
---


# Question
Title: Is it possible for someone to have anorexia without body image issues?
I've been reading about anorexia and as I understand it, it's an eating disorder where someone severely restricts their intake of food because of an intense fear of gaining weight, a distorted perception of weight, equating weight with self-worth, and things like that.

I was wondering, is it possible for someone to have anorexia without weight and body esteem issues? In other words, they severely restrict their food intake but not because of a fear of gaining weight or body esteem issues. I came across this Quora question, but the only answer there is an anecdotal one.

Or perhaps is there some eating disorder other than anorexia that matches this description? I came across this article, Does Everyone With an ED Have Body Dysmorphia?, but it didn't really help.

# Answer
> 6 votes
It is possible for someone to have an eating disorder without weight and body esteem issues (Sarkar, et al. 2013), but not Anorexia.

Fear of becoming fat or gaining weight and having a distorted view of themselves and of their condition are criteria required in the Diagnostics and Statistical Manual which is used for diagnosing mental health problems. Therefore, Anorexia would not be diagnosed without these criteria being present.

An eating disorder without body image issues would be diagnosed as EDNOS (Eating Disorder Not Otherwise Specified) under the 4th Edition, but as the 5th edition merged the former categories of *Eating Disorders* and *Feeding Disorder in Infancy or Early Childhood* and formed the new category, *Feeding and Eating Disorders*, the diagnosis under the 5th edition would be OSFED (Other Specified Feeding or Eating Disorder).

> OSFED is every bit as serious as anorexia, bulimia, or binge eating disorder, and people suffering from OSFED are every bit as deserving and in need of treatment – their eating disorder is just presenting in a different way. It is common for symptoms to not fit with the exact diagnostic criteria for anorexia, bulimia, or binge eating disorder – OSFED accounts for a large percentage of eating disorders (Beat Eating Disorders, 2017).

## References

Beat Eating Disorders (2017). *Other Specified Feeding or Eating Disorder (OSFED)*. Retrieved from: https://www.beateatingdisorders.org.uk/types/osfed

Sarkar, S., Padhy, S. K., Rao, P., & Gupta, S. (2013). Transient eating problems in an adolescent without body image disturbances: a diagnostic quandary. *Indian journal of psychological medicine, 35*(4), 410. doi: 10.4103/0253-7176.122244 PubMed Central: PMC3868099

# Answer
> 4 votes
That's a question of definition. Anorexia can be either a mental health issue or a symptom.

If by anorexia you mean anorexia nervosa, then per definition it's an eating disorder, that among other things, implies body image issues.

Notice however, that anorexia can also simply mean the symptom, which is a pathological lack of appetite. In this case, it's a symptom of another illness, and not an illness per se. The underlying cause can well be cancer, AIDS, for example. For example, as it is used by Ezeoke and Morley (2015).

Wikipedia even has two separate pages for the illness: https://en.wikipedia.org/wiki/Anorexia\_nervosa

and for the symptom: https://en.wikipedia.org/wiki/Anorexia\_(symptom)

<sub> Ezeoke, C. C., & Morley, J. E. (2015). Pathophysiology of anorexia in the cancer cachexia syndrome. Journal of cachexia, sarcopenia and muscle, 6(4), 287-302. </sub>

# Answer
> 3 votes
This could be ARFID or OFSED.

ARFID

> Avoidant Restrictive Food Intake Disorder (ARFID) is a new diagnosis in the DSM-5, and was previously referred to as “Selective Eating Disorder.” ARFID is similar to anorexia in that both disorders involve limitations in the amount and/or types of food consumed, but unlike anorexia, ARFID does not involve any distress about body shape or size, or fears of fatness.....a person with ARFID does not consume enough calories to grow and develop properly and, in adults, to maintain basic body function. In children, this results in stalled weight gain and vertical growth; in adults, this results in weight loss. ARFID can also result in problems at school or work, due to difficulties eating with others and extended times needed to eat.

OFSED (formerly EDNOS) refers to an eating or feeding disorder that does not meet the full diagnostic criteria of another eating disorder.

---
Tags: eating-disorders
---


title: Neurotransmitters by neuron types

text:
# Question
Title: Neurotransmitters by neuron types
I'm looking for a concise overview table of all types of neurons (whose number is at least in the hundreds) indicating which neurotransmitters they use pre- and post-synaptically (of which there are over 100 different ones).

If a type of neuron releases (or receives) more than one neurotransmitter the relative amounts would be interesting.

Furthermore: For each neurotransmitter there seem to be more than one receptor, so the table should include also the receptor (per neuron type and received neurotransmitter).

Ideally, to each pair of neuron type and released neurotransmitter the neuron types should be listed that receive this transmitter from this type of neuron. (It might turn out that "anything goes".)

# Answer
> 1 votes
Wikipedia has a comprehensive list of neurotransmitters, categorized as (a short list):

* Amino acids: glutamate, aspartate, D-serine, γ-aminobutyric acid (GABA), glycine
* Gasotransmitters: nitric oxide (NO), carbon monoxide (CO), hydrogen sulfide (H2S)
* Monoamines: dopamine (DA), norepinephrine (noradrenaline; NE, NA), epinephrine (adrenaline), histamine, serotonin (SER, 5-HT)
* Trace amines: phenethylamine, N-methylphenethylamine, tyramine, 3-iodothyronamine, octopamine, tryptamine, etc.
* Peptides: oxytocin, somatostatin, substance P, cocaine and amphetamine regulated transcript, opioid peptides
* Purines: adenosine triphosphate (ATP), adenosine
* Catecholamines: dopamine, norepinephrine (noradrenaline), epinephrine (adrenaline)
* Others: acetylcholine (ACh), anandamide, etc.

They then specifically present about 100 transmitters and the respected receptors in the tables and most of both are additionally presented in separate articles. They mention specific actions of main transmitters and they further categorize them by systems: noradrenaline, dopamine, serotonin, histamine and acetylcholine system.

What can be interesting to focus on:

* Which neurotransmitters/receptors are excitatory or inhibitory
* Which neurotransmitters are antagonistic or synergistic
* Which neurotransmitters/receptors are related with specific diseases
* Drugs that act on specific receptors

---
Tags: neuroscience, reference-request, neurophysiology, neuro-transmitters
---


# Question
Title: Neural correlates of pleasantness and unpleasantness
There are some basic cases of stimuli that are typically experienced either as pleasant or unpleasant, e.g. the major third as opposed to the tritone.

Assuming that there are different processes going on in my brain while listening to these two intervals, I'd like to know: What are the qualitative differences between these processes that would allow to understand that the first is experienced as pleasant and the other is experienced as unpleasant.

Just by thinking about it, there seem to be three possibilities:

1. The same regions/areals/neuron groups are active but in different characteristic modes, exhibiting different spatio-temporal patterns of neural activity.
2. Different regions are active in different modes.
3. Different regions are active but in somehow similar modes.

Assuming that the difference is mainly due to different activity modes (cases 1 and 2), I would like to know which characteristics might correlate with the pleasantness and unpleasantness of the expericence, e.g. some kind of "harmony".

# Answer
> 1 votes
Simply put, pleasant/unpleasant sensations are associated with the activation of certain **brain regions:**

> Many affective stimuli are hedonically complex mixtures containing both pleasant and unpleasant components. To investigate whether the brain represents the overall affective value of such complex stimuli, or the affective value of the different components simultaneously, we used functional magnetic resonance imaging to measure brain activations to a pleasant odor (jasmine), an unpleasant odor (indole), and a mixture of the two that was pleasant. In brain regions that represented the pleasantness of the odors such as the **medial orbitofrontal cortex** (as shown by activations that correlated with the pleasantness ratings), the mixture produced activations of similar magnitude to the pleasant jasmine, but very different from the unpleasant indole. These regions thus emphasize the pleasant aspects of the mixture. In contrast, in regions representing the unpleasantness of odors such as the **dorsal anterior cingulate and midorbitofrontal cortex** the mixture produced activations that were relatively further from the pleasant component jasmine and closer to the indole. (The Journal of Neuro Science)

---
Tags: neuroscience, consciousness, music
---


title: Functional vs. synaptic connectivity

text:
# Question
Title: Functional vs. synaptic connectivity
I used to believe that connectivity is nothing but synaptic connectivity and thus a long-term concept: synapses grow and synaptic strengths change on rather large time scales. But recently I found that connectivity sometimes is used as a short-term concept, e.g. in statements like this:

> *»\[C\]ortical connectivity will reflect clear changes when transitioning into states of reduced consciousness.«*

Assuming that transitioning into a state of reduced consciousness takes place in some seconds or minutes, also connectivity would have to change on this time scale. But what kind of connectivity would this be?

The authors of the paper cited above call it "functional connectivity" and measure it by the so-called "weighted phase lag index".

How is functional connectivity defined or explained (understandable to a non-specialist) and how does it relate to synaptic connectivity (which can easily be understood by non-specialists)?

# Answer
That one looks a bit familiar to me!

**Short, simple answer**

*(extracted from the longer answer below...)*

Measures of functional connectivity are *just correlations* (correlation here referring broadly to statistical relationships, not a specific statistic): they do not say anything about the causes of those correlations including whether they are direct or indirect. The "connectivity" is *functional* in that it is measured only by the *function* at the measured nodes.

**Functional connectivity**

Functional connectivity refers to temporal correlations in some measure of nervous system activity. Both positive and negative functional connectivity is possible. The canonical example is correlation in the BOLD fMRI signal, which is often defined as the Pearson correlation in the resting state BOLD signal time series between remote voxels, or across blocks during some task.

For EEG, functional connectivity measures include coherence, amplitude correlations (such as the Pearson correlation of the signal envelope, typically band-pass filtered into named bands like delta/theta/alpha/beta/gamma), and measures of phase relationships such as the phase lag index and weighted phase lag index.

What these measures share in common is that they record some statistical non-independence in the activity measured in different areas of the brain. However, they differ greatly in temporal and spatial scale depending on the modality and subsequent signal processing.

Importantly, measures of functional connectivity are *just correlations* (correlation here referring broadly to statistical relationships, not a specific statistic): they do not say anything about the causes of those correlations including whether they are direct or indirect. The "connectivity" is *functional* in that it is measured only by the *function* at the measured nodes.

For example, consider a weighted directed graph of nodes A, B, and C. Even if there is no edge connecting A and B, if C drives both A and B then there will be functional connectivity between A and B.

You would even expect to observe functional connectivity *between the brains of different people* if they were, for example, watching the same video *(as an aside...I think someone actually did this experiment, leading to some bogus claims about universal consciousness or something like that...the real explanation is more like "when two people listen to the same audio track, in which sometimes there is speech and sometimes there is no speech, they both have more activity in their auditory cortex during speech" which is considerably less profound...)*.

A synaptic connection between nodes P and Q almost certainly implies there will be functional connectivity between P and Q (though it may not be measurable depending on the strength of that connection and the structure of the rest of the network), but the inverse is not true: functional connectivity is insufficient to claim a real synaptic connectivity.

Personally, I wish another term was used besides *connectivity* but this is the field standard terminology.

Functional connectivity can be distinguished from two other types of connectivity: effective and structural.

**Effective connectivity**

Effective connectivity refers to model-based measures of causal influence of some brain area on another. Examples include the use of dynamic causal modeling (see for example Friston 2009, which is also highly relevant to the rest of this answer) and multivariable autoregressive modeling (see for example Cheung et al 2010).

**Structural connectivity**

Structural connectivity refers to the physical axonal connections between brain areas. In neuroimaging, it is often measured using diffusion tensor imaging which takes advantage of the fact that water more freely diffuses along axon tracts rather than perpendicular to them. Structural connectivity can also be measured more directly using neuronal tracers (dyes).

The term *structural connectivity* is used both in the context of connection strengths between certain areas relative to other areas, as well as to overall white matter integrity which can be disrupted in disease.

Note that while structural connectivity is often expected to correlate with functional connectivity, it doesn't need to.

**Synaptic connectivity**

These other terms are mostly used in the broad areas of neuroimaging and EEG/MEG. Using these modalities, even effective and structural connectivity only loosely imply synaptic connectivity. Detecting true synaptic connectivity requires more invasive electrophysiological techniques such as paired patch clamp recordings, or via anatomical reconstructions using tracers or electron microscopy. Synaptic connectivity can also be observed in real time using live-cell imaging of dendritic spines after injection or genetic expression of a fluorescent marker.

---

Cheung, B. L. P., Riedner, B. A., Tononi, G., & Van Veen, B. D. (2010). Estimation of cortical connectivity from EEG using state-space models. IEEE Transactions on Biomedical engineering, 57(9), 2122-2134.

Friston, K. J. (1994). Functional and effective connectivity in neuroimaging: a synthesis. Human brain mapping, 2(1‐2), 56-78.

Friston, K. (2009). Causal modelling and brain connectivity in functional magnetic resonance imaging. PLoS biology, 7(2), e1000033.

Jones, D. K., Simmons, A., Williams, S. C., & Horsfield, M. A. (1999). Non‐invasive assessment of axonal fiber connectivity in the human brain via diffusion tensor MRI. Magnetic Resonance in Medicine: An Official Journal of the International Society for Magnetic Resonance in Medicine, 42(1), 37-41.

Nägerl, U. V., Willig, K. I., Hein, B., Hell, S. W., & Bonhoeffer, T. (2008). Live-cell imaging of dendritic spines by STED microscopy. Proceedings of the National Academy of Sciences, 105(48), 18982-18987.

Vinck, M., Oostenveld, R., Van Wingerden, M., Battaglia, F., & Pennartz, C. M. (2011). An improved index of phase-synchronization for electrophysiological data in the presence of volume-conduction, noise and sample-size bias. Neuroimage, 55(4), 1548-1565.
> 2 votes

---
Tags: neuroscience, neurophysiology, connectionism
---


# Question
Title: Does an electrical stimulation of a right claustrum leads to a temporary loss of consciousness?
In a study by Koubeissi et al. (2014) there was an experiment on a patient to find out which part of the brain caused her epilepsy. In this experiment they have found out that if they electrically stimulate her left claustrum, the person would lose consciousness.

My question is: If they have stimulated her right claustrum, would that caused her a loss of consciousness as well? In other words: Are both claustrums necessary for a conciousness to appear in an ordinary healthy human brain?

<sub> Koubeissi, M. Z., Bartolomei, F., Beltagy, A., & Picard, F. (2014). Electrical stimulation of a small brain area reversibly disrupts consciousness. Epilepsy & Behavior, 37, 32-35. </sub>

# Answer
It's probably a bit more complicated than that. Cortical areas tend to be highly connected with their contralateral counterparts, so it's not really fair to expect that the effects of stimulation on one side of the brain doesn't impact the contralateral side.

The claustrum is itself a small gray matter region, but it is surrounded by white matter as well. Koubeissi et al used a fairly strong stimulus when they saw effects on consciousness; I have a hard time believing this stimulation was *only* affecting the claustrum and not fibers of passage at that stimulation intensity.

---

A recent study of 5 epilepsy patients attempted to replicate the Koubeissi finding, stimulating the claustrum (bilaterally in 4/5) in epilepsy patients, but none of the patients lost consciousness despite experiencing other effects. The authors suggest that the results presented in the earlier case study could be based on the unique circumstances of that patient, which include their epilepsy history and prior resection, and that the stimulation location in that Koubeissi case was not really directly in the claustrum. Additionally, Bickel & Parvizi were unable to use a stimulus as strong as the prior case report because their patients experienced negative side effects like painful muscle responses that Koubeissi did not see.

*Bickel, S., & Parvizi, J. (2019). Electrical stimulation of the human claustrum. Epilepsy & Behavior.*

---

Damasio et al, 2013 is another case study, where the patient had bilateral damage to a substantial portion of the brain, including the claustrum bilaterally. This patient had quite a bit of impact to various functions due to this damage, but they were still conscious. Therefore the answer to "*Are both claustrums necessary for a conciousness*" seems to be "no"; in a *healthy brain* it's a bit harder to say, because it's not ethical to damage the claustrum in healthy brains.

*Damasio, A., Damasio, H. & Tranel, D. Persistence of feelings and sentience after bilateral damage of the insula. Cereb. Cortex 23, 833–846 (2013).*

---

There are also other papers showing suppression or recovery of consciousness through stimulation of other brain regions besides the claustrum.

*Redinbaugh, M. J., Phillips, J. M., Kambi, N. A., Mohanta, S., Andryk, S., Dooley, G. L., ... & Saalmann, Y. B. (2019). Central thalamus modulates consciousness by controlling layer-specific cortical interactions. bioRxiv, 776591.*

*Schiff, N. D., Giacino, J. T., Kalmar, K., Victor, J. D., Baker, K., Gerber, M., ... & Farris, S. (2007). Behavioural improvements with thalamic stimulation after severe traumatic brain injury. Nature, 448(7153), 600-603.*
> 2 votes

---
Tags: cognitive-neuroscience
---


# Question
Title: Can two neurons in the brain be connected more than once?
Can two given neurons in the human brain can be directly connected more than once, either mutually or in the same or direction? Also, can the same neuron have transitive connections to itself (in order to amplify itself for example)?

# Answer
> 4 votes
I guess the answer depends on what you mean with "connected more than once".

Initially, being connected is a strictly binary relation: either two neurons are connected or not. (The question may be: directly or not. Indirectly, each pair of neurons is connected, as I assume.)

If you consider "being connected more or less strongly" - which is not a binary relation anymore - you may consider the degree of connectedness as a natural number 1, 2, 3, ... and in this case, you might want to count synapses between two neurons. And surely, there can be more than one:

> »An important experimentally observed feature \[...\] is the distribution of the number of synapses from one neuron to another, which has been measured in several cortical layers. All of these distributions are bimodal with one peak at zero and a second one at a small number (3–8) of synapses.«

If you want to consider pathways between two neurons A and B - shortest sequences of connected neurons starting with A and ending with B - then the answer is "yes, of course" again:

> »\[Each neuron\] is within two or three connections of all the others via myriad potential routes.«

---
Tags: neuroscience, neuroanatomy, neurophysiology
---