# Question
Title: To what extent is control over when a substance is used relevant to addiction?
For example, let's say someone uses X amount of heroin a week, and no more than Y a day. If somehow their arm is connected to a device that randomly (unpredictably, but within their "waking leisure hours") administers heroin at no more than Y a day and X per week, would users feel as addicted or dependent on the substance? Or would the loss of control, not even necessarily being able to look forward to using the substance every day or at a certain time or after certain events or feelings, make it not nearly as satisfying or addictive?

# Answer
> 3 votes
This is a tough question to answer definitively. I won't address heroin specifically but rather drugs of abuse more generally since a lot of the addictive patterns are the same and heroin is less often studied in the lab.

I am not aware of studies that specifically use the protocol you are describing in human subjects; although you might be able to make some inference based on drug seeking behavior after hospital administration of opiates, for example.

However, in animal studies, drug sensitization protocols have been used where animals are given injections of some drug, and later are allowed to self-administer the drug. Typically, animals who were previously given injections of the drug are quick to develop self-administration habits compared to unexposed animals. It's hard to ask an animal what they "feel" and this may not be the same as "feeling addicted/dependent" but at least when they have an opportunity to self-administer they are more prone to take the opportunity.

This effect is sensitive to the particulars of the experiment, though: Higher self-administration doses don't show the effect (because undosed animals also quickly develop a habit). Limited exposure tends to create less or absent sensitization. Sensitization effects tend to be easier to detect when animals have to work harder for subsequent doses in a progressive ratio paradigm; on a fixed ratio paradigm the differences are minor or non-existent.

A great experiment to most directly address your question would be to dose one animal according to the self-administration patterns of another and compare them on addictive behaviors; however, one difficulty in such a comparison is that the animals that haven't been dosing themselves still need to learn *how* to dose themselves. I am not aware of a study that has done this but I hope if it has been done someone else can point it out!

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Ferrario, C. R., Gorny, G., Crombag, H. S., Li, Y., Kolb, B., & Robinson, T. E. (2005). Neural and behavioral plasticity associated with the transition from controlled to escalated cocaine use. Biological psychiatry, 58(9), 751-759.

Lett, B. T. (1989). Repeated exposures intensify rather than diminish the rewarding effects of amphetamine, morphine, and cocaine. Psychopharmacology, 98(3), 357-362.

Lorrain, D. S., Arnold, G. M., & Vezina, P. (2000). Previous exposure to amphetamine increases incentive to obtain the drug: long-lasting effects revealed by the progressive ratio schedule. Behavioural brain research, 107(1-2), 9-19.

Mendrek, A., Blaha, C. D., & Phillips, A. G. (1998). Pre-exposure of rats to amphetamine sensitizes self-administration of this drug under a progressive ratio schedule. Psychopharmacology, 135(4), 416-422.

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Tags: addiction, conditioning
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# Question
Title: Why are we the smartest species on the whole known universe?
Why?

One possible reason would be because intelligent give humans, and only humans, evolutionary edge compared to their peers. Gorilla, for example, are strong because strength give Gorilla evolutionary edge. For our species, that's intelligence. But how?

What evolutionary advantage does having high "intelligence" does to humans?

My friend told me that the greatest benefit of intelligence is that we "deceive" others betters.

Is that the main use of intelligent?

Deceiving others? Many of my mensa friends are honest. If anything I hate lies in any form except for jokes. Also we don't seem to have more children than normies.

How does having, say, high IQ help a person reproduce?

# Answer
> 3 votes
I just finished a special issue on 'Humans - Why we're unlike any other species on the planet' (*Sci Am*, September 2018).

In this issue, Kevin Laland has a paper (How we became a different kind of animal) and he nicely abstracts the answer to your question in your question title: *Why are we the smartest species on the whole known universe?*, namely:

> * Human accomplishments derive from **our ability to acquire knowledge from others** and to use that communal store of experience to devise novel solutions to life's challenges.
> * Other species innovate, too. Chimps open nuts with stone hammers. Dolphins use a tool to flush out hidden prey.
> * Our uniqueness has to do with a **capacity to teach skills to others over the generations** with enough precision for building skyscrapers or going to the moon.

Now, relating to your question body's focus, *What \[is the\] evolutionary advantage \[of\] having \[a\] high "intelligence" \[for\] humans?*

In that same special issue, Chet C. Sherwood explains this question in his contribution *'Are we wired differently?* by saying:

> Modern human brains are about threefold larger than those of our closest hominin acestors \[\]. \[T\]he parts of the cerebral cortex involved in higher-order cognitive functions, such as creativity and abstract thinking, have become especially enlarged. These \[...\] association regions \[...\] are loci for language, toolmaking and imitation.

Now, that last sentence couples the two papers nicely - we need that bigger brain to allow us to use language and imitation to be able to teach and learn, respectively.

Your next question, regarding that *My friend told me that the greatest benefit of intelligence is that we "deceive" others betters* \- Now that is exactly what is *not* the consensus as of now.

Thomas Suddendorf, again in that same special issue explains in his paper *'Two key features created the human mind'*:

> Why are we, and not gorillas, running the zoos? \[...\]. Research has revealed two distinct human features: complex scenario building and exchanging thoughts with others.Together these traits underlie critical human capacities such as language, culture., \[and\] **morality** \[...\].

Michael Tomasello, \[yes, again that same issue\], explains in his paper *The Origins of Human Morality - How we learned to put our fate in one another’s hands*:

> \[...\] \[S\]ituations of reciprocity can arise in which I scratch your back and you scratch mine and we both benefit in the long run.

While chimps may hunt together, when the bounty has been found and captured, the feeding is an individual matter. In contrast, humans have the tendency to take care for the group, and share food. Taking care of the group eventually pays itself of, as the group will take care of you. This is enhanced by the sense of morality, in which you will do no harm to others. If you do, you will be excluded from the group, and no one will scratch your back.

> Seeds of human morality were planted some 400,000 years ago, when individuals began to collaborate in hunting-and-gathering exploits.

<sub>**Reference**
**-** Special issue of *Sci Am*, September 2018</sub>

# Answer
> 3 votes
The evolution of higher intelligence in hominids is an empirically difficult enough evolutionary question that (a) it might be better for biology.se and (b) any answer needs to be taken with a pinch of salt, but I'll give you a feel for it. By that I mean, "watch the way multiple accidents of evolutionary history made evolution more favourable among our ancestors than most animals".

The 2003 documentary Walking with Cavemen discussed one model of what happened to early hominids: a decline in African rainforest coverage c. 8 Mya led to arboreal primates evolving bipedalism for more efficient locomotion, and this meant hands no longer compromised between movement and tool usage. Hand-brain co-evolution would have involved a positive feedback, which may (or may not - always bear that in mind) be part of the reason for rapid brain growth among Australopithecines. The same documentary also discussed how subsequent climate change in Africa changed the ecosystem enough to provide new nutrition opportunities for early *Homo* species, and how the move from North Africa to West Asia led to bamboo tools.

There are many models for what encouraged the evolution of higher intelligence in our ancestors, at various points in the past 5 Mya or so. The reason a trait is more favoured in one species than another comes down to unique cost-benefit analyses. Large brains are expensive, but the shift from a mostly herbivorous diet to one more reliant on meat, especially bone marrow (which only hominid tools could access), is part of why they were "worth it" in our genus.

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Tags: intelligence, evolution, evolutionary-psychology, anthropology
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# Question
Title: What is the term for doing things or behaviors that contrast to what you really feel?
For instance a person who is racist wanting to hire black people because they want to project an image that they aren't racist. Or if they doesn't like obese people but still interacts with them to make it look like they actually like them.

Is there a term for that?

# Answer
> Is there a term for that?

The closest term I can think of relevant to psychology is the Freudian concept of ***reaction formation*** the classic example being the gay homophobe
> 3 votes

# Answer
What you describes may refer to bad faith:

> * Some examples of bad faith include: a company representative who negotiates with union workers while having no intent of compromising; a prosecutor who argues a legal position that he knows to be false; an insurer who uses language and reasoning which are deliberately misleading in order to deny a claim.
> * In his book Being and Nothingness, the philosopher Jean-Paul Sartre defined bad faith (French: mauvaise foi) as hiding the truth from oneself. The fundamental question about bad faith self-deception is how it is possible. In order for a liar to successfully lie to the victim of the lie, the liar must know that what is being said is false. In order to be successful at lying, the victim must believe the lie to be true. When a person is in bad faith self-deception, the person is both the liar and the victim of the lie. So at the same time the liar, as liar, believes the lie to be false, and as victim believes it to be true. So there is a contradiction in that a person in bad faith self-deception believes something to be true and false at the same time.

Finally, that person can also have implicit attitude, passive-aggressive and microaggression.
> 1 votes

# Answer
This is not really a scientific term, but it instantly reminds me of **keeping up appearances**:

> To pretend that everything is good, for example with your marriage or your financial situation, even though you are having problems.
>
> *Their marriage was over, but they wanted to keep up appearances for the children.*
> 1 votes

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Tags: social-psychology, terminology, self-control
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# Question
Title: Would non-neural physiological insights be considered to be in the field of neuroscience?
For example, would e.g. SCR (skin conductance response) or hormone level be considered to be "neuroscientific measures" according to general definition of neuroscience?

# Answer
> 2 votes
There is increasing scientific evidence to incorporate other organ systems when considering the whole function of the nervous system. Neuroendocrinology, neurogastroenterology, and neuroimmunology are burgeoning fields of research.

If for instance, you were interested in the effects of stress on neurodevelopment, you would likely want to be measuring cortisol levels in your animal model.

If you were performing a study on human fear response, you might want to record SCR in addition to other measures (EEG, fMRI, etc.).

The definition of neuroscience is intentionally broad. There are many biochemists, for instance, who are interested primarily in cell structure, stability, and the transport mechanisms within who study neural tissue specifically because neurons happen to be interesting cases (axons can be very long, how do nutrients and proteins get to where they need to be?).

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Clin Psychopharmacol Neurosci 2013; 11(3): 107-117 https://doi.org/10.9758/cpn.2013.11.3.107

Ann Clin Biochem. 2017 May;54(3):308-322. doi: 10.1177/0004563216687335. Epub 2017 Mar 16

J Del Signore, Steven & Rodal, Avital. (2016). The membrane strikes back: phosphoinositide binding regulates Skywalker function. Nature Structural & Molecular Biology. 23. 956-957. 10.1038/nsmb.3313.

J. Herzog, Josiah & Deshpande, Mugdha & Shapiro, Leah & Rodal, Avital & Paradis, Suzanne. (2017). TDP-43 misexpression causes defects in dendritic growth. Scientific Reports. 7. 10.1038/s41598-017-15914-4.

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Tags: neuroscience, physiology
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# Question
Title: Sex With Ghosts - Possible Clinical Diagnoses
Spectrophilia, is described by Wikipedia as the sexual attraction to ghosts or sexual arousal from images in mirrors, as well as the phenomenon of sexual encounters between ghosts and humans.

A quick and easy search shows us that many people claim to have had these encounters, and seem completely convinced of their experiences.

**Question:**

If someone walked into a psychiatrists office with these claims, (assuming they are seemingly normal otherwise, and have no history of mental illness), what would they most likely be diagnosed with? And what medicine might they be prescribed?

> Things we're assuming to be true:
>
> Ghosts aren't real.

# Answer
> 2 votes
Sleep paralysis can sometimes result in hallucinations corollary to the paralysis experience. Similarly, bipolar I and other psychotic disorders (viz. the schizophrenia spectrum) could produce vivid enough hallucinations and delusions, though in general, vivid visual hallucinations are quite rare.

It is highly unlikely that someone who is describing these experiences is not experiencing any other symptoms.

Standard treatment would depend primarily on what other issues the patient might be experiencing.

If the patient is experiencing dissociation and misinterpreting this as sex with ghosts for some reason, cognitive or dialectical behavior therapy would be the indicated treatment.

If the patient were agitated, or disoriented to time, place, or person, the psychiatrist would likely prescribe psychotherapy and an atypical antipsychotic (e.g. risperidone, brexipiprazole).

--

Sharpless, Brian A., et al., Journal of Clinical Psychology, 2010; vol 66: pp 1292-1306.

Bell, CC, et al., " American J Psychiatry, 1986; vol 143: p 1484.

Ranier Biobehavioral Institute: "Sleep Paralysis."

Mayo Clinic. "Dissociative Disorders."

# Answer
> 1 votes
It is very much unlikely that someone would have this kind of delusion but be completely normal otherwise.

People suffering from Delusional Disorder (F22.0), the only disorder with isolated delusions, usually have "realistic" delusions such as pathological jealousy, not hallucinations such as intercourse with a ghost.

All disorders which could cause delusions such as sexual hallucinations usually cause other symptoms as well and these people are not usually otherwise "normal" at all.

In short, what you describe is not a psychological disorder that has been encountered as yet.

Historically, the belief in succubi and the conviction that one has been the victim of one are not a psychological disorder but an interpretation of real events (e.g. sleep paralysis) within the context of superstition.

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Tags: abnormal-psychology, psychiatry, schizophrenia
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# Question
Title: What tools exist to measure work meaningfulness?
Do you know of methods/tools/criteria used (in sociology, social psychology or occupational science) in order to evaluate how meaningful some particular work can be for a particular person?

I am not asking what (in general) could make work meaningful, but whether some models/tools/lists of questions exist that can be used to measure someone's perception of his own work's meaningfulness.

I've come across a few tools such as the "Meaningful Activity Wants and Needs Assessment" (regarding life balance, more than occupational meaningfulness), "WAMI Work and Meaning Inventory", and a few other tools aimed at assessing job satisfaction, work motivation, etc.

I wonder if other formal models/tools could be suggested.

# Answer
There are a bunch of them! For a great review of many definitions and measures of meaningfulness, see if you can get a copy of A Narrative Evidence Synthesis of Meaningful Work: Progress and Research Agenda. The authors are pretty responsive in my experience and will send you a copy.

One thing to keep in mind, though, is that there are a bunch of different definitions of work meaningfulness. Everybody has their own approach, some are better than others (i.e., more likely to actually measure meaningfulness and not something related like engagement or intrinsic motivation), and there isn't really a consensus yet. The WAMI you mentioned is built by highly-regarded meaningfulness researchers, is very commonly used in studies of meaningfulness, and I think it's a great "safe bet" measure for getting overall work meaningfulness.

However, if you're looking to zoom-in a little and look at *sources* of meaning (is it the challenge of your work that you find meaningful, or bonding with coworkers?) like those described in On the meaning of work: A theoretical integration and review, then you might want to check out the Comprehensive Meaningful Work Scale.

Hope that helps!
> 6 votes

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Tags: social-psychology, io-psychology
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# Question
Title: If the optic nerve transmits to both hemispheres, how do split-brain experiments work?
From what I understand, the optic nerve of each eye transmits information to both hemispheres of the brain. This is unlike other sensory and motor information, where (for example) the right hand is controlled by the left and vice versa.

Most sources I read skip over this information or don't explain it clearly, but I found it stated this way in this Introduction to Psychology ebook and this blog post (quotes pasted below; scroll for it).

However, I also read about split-brain experiments (such as those by Sperry and Gazzaniga) performed on patients who had undergone corpus calloscotomy, where the link between the two hemispheres of their brain was broken. Many of these experiments are vision-based, showing different visual stimuli to each eye and observing reactions in the corresponding hemisphere. But **this assumes that the right eye transmits information only to the left, and vice versa**, which, according to the other two sources, does not seem to be the case.

Taking it further, this Psychology Today article mentions studies on hemispheric transfer, which showed that subjects could read text more efficiently when fed directly to the right-eye (∵ contralateral control), rather than going to the left eye and then having to be transferred to the left hemisphere for processing—again implying that vision follows the contralateral principle.

# Relevant quotes

To avoid forcing people to follow through links, I've pasted the relevant quotes here. Feel free to skip past to my main question below.

**The *Introduction to Psychology* ebook:**

> Although the principle of contralateral control might lead you to expect that the left eye would send information to the right brain hemisphere and vice versa, nature is smarter than that. In fact, the left and right eyes each send information to both the left and the right hemisphere, and the visual cortex processes each of the cues separately and in parallel. This is an adaptational advantage to an organism that loses sight in one eye, because even if only one eye is functional, both hemispheres will still receive input from it.

**The blog post, titled *A dominant preference: Eye or hand?***

> One of my previous blog posts contained data confirming that a person’s preferred hand and foot often are aligned on the same side of the body. This is the case for both left- and right-handers.¹
>
> The neural wiring from eye to brain is more complex. Optic nerve fibers from one eye travel to both the right and the left hemispheres.

**The *Psychology Today* article:**

> A team of researchers from UC Santa Barbara, led by Gazzaniga, recently tested information transfer using MEG. Language is processed in areas of the temporal lobe on the left side of the head. When you read with your left eye, the information first ends up in the right hemisphere and must be transferred to the left hemisphere via the corpus callosum to be processed. To test the efficiency of the hemispheric transfer the researchers showed a randomized list of words and nonsense words to the left or right eye of a number of research participants. They then measured how effectively the subjects would be able to distinguish words from nonsense words. The study showed that subjects were significantly more efficient in determining the nature of the string of letters when the information was fed directly to the left hemisphere via the right eye. Apparently the brain has difficulties processing information that has had to travel long distances.

# My question

Assuming my first information is accurate, here's one explanation I can think of: each eye *usually* sends information only to the opposite eye, but the optic nerve fibres travel to both hemispheres *in case* one eye stops functioning, in which case the remaining eye begins transmitting to both hemispheres. That seems a bit of a stretch, though.

**So, here's my question:** How do vision-based split-brain experiments account for the fact that the optic nerve reaches both hemispheres? Are there other properties of transmission that I'm not aware of (such as my hypothesis above)? Or is the assertion that the optic nerve transmits to both hemispheres simply false?

# Answer
> 9 votes
Some of those pop science articles might be simplifying a bit by saying the stimuli are provided to the *left or right eyes*. In fact, they are actually presented to the *left or right visual field* which is an important distinction. The left *visual field*, from both eyes, goes to the right hemisphere, and vice versa.

The experimental paradigm is illustrated in Gazzaniga 1995:

Gazzaniga, M. S. (1995). Principles of human brain organization derived from split-brain studies. Neuron, 14(2), 217-228.

You will see that they go to great lengths to make sure the image stays in one visual field, tracking the eye movements and moving the image accordingly to prevent any "peeking."

So no, these experiments don't depend on remodeling of the connections from the eyes to the different hemispheres, and you are correct that each eye sends some information to each hemisphere. However, that information is not complete: it is separated by visual field. Your Intro to Psychology eBook shows this in Figure 4.2:

The "red" axons from each eye are on the right side of each retina, collect light from the left visual field, and travel to the right hemisphere. Vice versa for blue.

# Answer
> 3 votes
**Short answer**
Split brain subjects do not (necessarily) have to have an ablated *optic chiasm*.

**Background**
You have to realize that the site where the right and left visual hemi-fields are split occurs in the *optic chiasm*. This structure is situated anatomically at a different location than the major highway between both hemispheres, namely the *corpus callosum* (Fig. 1). Hence, your question...

> How do vision-based split-brain experiments account for the fact that the optic nerve reaches both hemispheres? Are there other properties of transmission that I'm not aware of (such as my hypothesis above)? Or is the assertion that the optic nerve transmits to both hemispheres simply false?

...can be answered with the fact that split-brain subjects don't (necessarily) have their optic chiasm severed. And optic nerves do transmit to both cortices for sure (Fig. 2); each hemifield is projected to the same cortical region. This feature allows us to see depth, using binocular vision through a process referred to as **binocular disparity**.

Fig. 1. Mid-saggital section through the brain. source: Studoku

Fig. 2. Visual pathway. source: The Brain Recovery Project

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Tags: neuroscience, vision
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# Question
Title: Meditation for patients with neuroleptic induced tension
Patients taking antipsychotic (neuroleptic) drugs often suffer from some kind of discomfort or tension. This can manifest as a neuroleptic induced dysphoria, akathisia, or some kind of anxiety.

Is there a way these patients can overcome this unpleasant feeling with some kind of mind work, i.e. meditation concentrating on breathing, visualization, watching coming thoughts or something else?

Is there some research on this topic telling what kind of meditation could be helpful in relieving the discomfort? Is it even good to work with mind under these chemicals?

# Answer
> 2 votes
Akathisia is very difficult to handle. Sometimes akathisia responds to anxiolytic drugs such as benzodiazepines, propranolol, and even red wine. Amantadine, benztropine (for Parkinsonism) might also help. Mostly these are off-label prescriptions.

Meditation, exercise, and de-stressing measures are certainly helpful on general principle, though the best way to eliminate akathisia (if it is drug-induced) is to taper down the dosage or take a different medication. Finding a medication that treats the symptoms and provides a quality of life improvement despite side-effects is the job of the physician. You can think of it as quality of life improvement from reduction of symptoms plus quality of life improvement from minimization of side-effects, of which akathisia is one of the most common and unpleasant.

https://www.mdedge.com/psychiatry/article/89620/somatic-disorders/akathisia-restlessness-primary-condition-or-adverse-drug

King DJ, Burke M, Lucas RA. Antipsychotic drug-induced dysphoria. Br J Psychiatry 1995; 167:480–482.

Healy D, Farquhar G. Immediate effects of droperidol. Hum Psychopharm 1998; 13:113–120.

Jones-Edwards G. An eye-opener. OpenMind 1998; September:12,13,19.

Jones-Edwards G. On the receiving end. New Therapist 2000; 7:40–43.

Belmaker RH, Wald D. Haloperidol in normals. Br J Psychiatry 1977; 131:222–223.

Kendler KS. A medical student’s experience with akathisia. Am J Psychiatry 1976; 133:454.

Healy D, Savage M (1998) Reserpine exhumed. Brit J Psychiatry 172: 376–378.

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Tags: reference-request, abnormal-psychology, consciousness, psychiatry, meditation
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# Question
Title: How, other than pharmacotherapy, can those diagnosed with thought disorders be treated?
In general, major depressive disorder is treated with pharmacotherapy, and talk therapy, as well as other little things written below:

People know what the little things you can do if you're depressed are:

* exercise often
* make sure your eating is sufficient/not excessive
* make sure your sleep is sufficient/not excessive
* don't engage in "depressive" behaviors such as isolation, rumination etc.
* get involved more socially
* separate yourself from stressful situations

But, I can't think of any of the little things associated with thought disorders, like schizophrenia...

For some reason the only thing I can think of is Cognitive Remedial Therapy...

What are the corresponding little things that are the counterpart of the list shown above for thought disorders?

# Answer
Research by Josef Parnas and others has resulted in the Examination of Anomalous Experience, a philosophical structure for examining cognitive disorders. The research, between philosophers, neuroscientists, and psychiatrists indicates commonalities of disordered thought, especially anomalous self-experience. The EASE is designed to be used as a treatment aid for educating psychiatrists on how to recognize and respond to patients attempting to explain their thought disorder symptoms.

http://easenet.dk/

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Handest P, Parnas J. Clinical characteristics of first-admitted patients with ICD-10 schizotypal disorder. British J Psychiatry, 2005; 187 (Suppl. 48): 49-54.

Moller P, Husby R. 2000, The initial prodrome in schizophrenia: searching for naturalistic core dimensions of experience and behavior, Schizophr Bull, vol. 26, no. 1, pp. 217-32.

Parnas J, Jansson L, Sass LA, Handest P. Self-experience in the prodromal phases of schizophrenia: A pilot study of first admissions. Neurology, Psychiatry and Brain Research. 1998; 6: 97-106.

Sass L, Parnas J. Self, consciousness, and schizophrenia. Schizophrenia Bulletin, 2003; 29/3: 427-444.

Parnas J, Handest P, Sæbye D, Jansson L. Anomalies of subjective experience in schizophrenia and psychotic bipolar illness. Acta Psychiatrica Scandinavica. 2003, 108:126-133.

Parnas J, Handest P. Phenomenology of anomalous self-experience in early schizophrenia

Comprehensive Psychiatry. 2003: 44 (2); 121-34.

Parnas J, Bovet P, Licht D. (2005) Cluster A personality disorders: A review. In M. Maj, H. Aksiskal, JE Mezzich, A Okasha (eds.) Personality Disorders. WPA Series: Evidence and Experience in Psychiatry. Chichester, John Wiley & Sons.

Parnas J, Handest P. Troubles de la conscience de soi: importance pathogénique et clinique dans la schizophrénie debutante. Psychiatrie, Sciences Humaines, Neuroscience. 2005: 3 (suppl. 1) ; 17-29.

Parnas J, Handest P, Jansson L, Sæbye D. Anomalies of Subjective Experience among First-admitted Schizophrenia Spectrum Patients: Empirical Investigation. Psychopathology. 2005: 38; 259-267.

Skodlar B, Tomori M, Parnas J. Subjective experience and suicidal ideation in schizophrenia.Comprehensive Psychiatry. 2008, in press, avaiable online.

Vollmer-Larsen A, Handest P, Parnas J. Reliability of measuring anomalous experience: the Bonn Scale for the Assessment of Basic Symptoms (BSABS). Psychopathology, 2007, 40; 345-348.
> 0 votes

# Answer
Dialectical Behavior Therapy (DBT) is a unique skills training that consists of four modules: core mindfulness, distress tolerance, emotion regulation, and interpersonal effectiveness. Originally, this set of therapeutic skills were developed as treatment for the extremely unmanageable Borderline Personality Disorder. However, after immense success, the treatment group expanded vastly.

The modules were carefully and specifically designed to help individuals manage their behaviors, emotions, and thoughts. Each module includes a number of 'little things' intended to assist the afflicted in their area of need.

For example, the core mindfulness module teaches individuals to (with practice) slow their thoughts, bring themselves into the present moment, how to regain control of their thoughts by training the mind to focus on only one thing--on the one moment. This particular training is typically introduced in the form of deep breathing exercises where the focus of the exercise is to think of only the breath entering and leaving the lungs/body.

The other modules offer similar skillful training techniques specific to both the individual as well as the given module. I imagine that you will find the answers you seek by delving into the curriculum, techniques, and purposes that lay just beneath the surface of the DBT modules.
> 2 votes

# Answer
For a long time now I wanted to write a book on the subject of states of mind. Here are my findings:

People are normally prone to experience different states of mind throughout the day. From love to anxiety to anger to creativity. Each one distinctly colors Cognition and affects the outlook on past, present and future. For a certain time only. The state of mind affects the kind of action people are likely to take.

For example, romantic love is a state of motivation towards a specific individual. It is characterized by perceiving over-idealized image of a that person, desire to talk and be close to that person. Fantasies and thinking of that person. In case of love, there is clear, irrational thinking pattern of "putting that special person on the pedestal". The state of love would affect the lovers outlook on marriage and children.

Each state has a certain onset time and duration. In your question you mentioned avoiding reminiscences, as they are likely to pull the person into some of the more negative states of mind.

Same kind of definitions can be obtained for other cognitive states of mind that can "pull wool over ones eyes"- anxiety, fear, creativity, happiness, etc. **The little thing that can be done is remembering what different states feel like, what kind of actions they prompt and how they affect the outlook on the past, present and future.** This removes the fear of unknown.

The most important thing to remember is that each state is temporary, but yet it feels so seamless, that it is common to think this is how things would be forever.

Of course persistent cognitive disorders like schizophrenia can produce much more intense and bizzare states than an ordinary person would experience, but the mechanism of onset-experience-change should still be the same.
> 1 votes

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Tags: abnormal-psychology, depression, schizophrenia
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# Question
Title: How to test people's compatibility for friendship
I'd like to have a test that would predict whether two people will get along (enjoy conversation and possibly become friends) if they try? The idea is simple: many people pass the test and then, by looking at results, we can find matches for potential friendship. However, I feel that it's not easy to implement if at all possible.

It's obvious how to find shared interests, but I doubt it would be enough to find a match. So, the test should explore some personality characteristics. *The question is what should we test for and how to find matches based on results?*

I don't have education in psychology or something similar, and I couldn't find any relevant information. There are many articles regarding compatibility for romantic relationship, but that's not the same thing.

# Answer
> 1 votes
I spent a short period studying and developing conflict and cooperation models, the resulting research was proprietary so I was hesitant to actually respond to this question as there is nothing I can think of to reference directly except maybe some of the implications of the robbers cave experiment (the utility of this experiment is disputed). That being said, I don't believe I ever found a "test" that would predict the likelihood that any two participants would be friends. However, our previously mentioned research found that one of the most important *indicators*, not a test, but indicators, of potential friendship was not common interest, but common enemies or disagreements. though this answer may not be accepted as it does not meet standard requirements for acceptance, I felt that it was reasonable enough to mention if it helped point your search in the right direction.

# Answer
> -1 votes
There is no such thing as a test for compatibility in a friendship. There are measures for amity (that is, how much we feel someone *is* our friend), but no tests that predict whether two people would *become* good friends.

There are tests that aim to test for compatibility in romantic relationships. These are based on theories about what makes romantic relationships work, and some of them are employed on certain online dating platforms. Some of these platforms (e.g. Parship.de and Edarling.de), conduct studies to test their "scientific dating" principles and publish them. What is interesting in this context is that while there are clear indications for what makes a majority of romantic relationships work, but psychologists have as yet been unable to predict what makes people *fall in love*. So we know what would make them happy in the long term, but we don't know how to get them together. People fall in love for reasons that are very individual and cannot be systematized, yet.

In friendships, there are of course similar predictors as in romantic relationships, but since friendships are often much looser, friends spend very much less time with each other, and therefore don't need the same level of compatibility (because much incompatibility is compensated by less expectations and more time without each other), it is often enough for friends to share the same hobby, the same job, or live in the same neighborhood.

If you think of friendship as very intimate relationships with much sharing of emotions and thoughts, that is, of close "best" friends, then tests for romantic relationships would very likely cover aspects of these friendships as well.

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Tags: social-psychology, personality
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# Question
Title: How am I able to distinguish between Chinese and Japanese when I don't speak either language?
The only words in Chinese that I know are "Ni How" (hello) and "she she" (thank you). And the only words I know in Japanese are "Domo arigato Mr. Roboto" (thank you very much Mr. Roboto). Yet I am able to tell the difference between when a person is speaking Chinese and when a person is speaking Japanese.

How am I able to do this?

# Answer
> 1 votes
Japanese is not very tonal, is spoken very fast, and has relatively few phonemes. Consonants are often followed by a vowel. Chinese on the other hand is highly tonal and is spoken relatively slowly, as information is encoded extensively in tone. They are almost complete opposites. There are also various phonemes that occur more often in one language than the other, and emphasis is very rare in Japanese (e.g. it's "wa-ta-shi", never "wa-TA-shi"). It is also very regularly paced, with each syllable usually taking the same amount of time. Chinese varies the syllable lengths considerably.

Compare the following (romanized) Japanese

> mou ichido itte morae masu ka

with the equivalent (romanized) Mandarin Chinese

> qǐng zài shuō yíbiàn

It's clear that they are different languages, and that one is far more tonal than the other. These both mean the same things, asking the speaker to repeat what they had just said.

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Tags: language-processing
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# Question
Title: Fit a psychometric function when the maximum is not 100% (not because of lapse)
I found that currently the form of psychometric function assumes that the proportion correct lies between 0.5-1 given the range of stimulus level, but how to fit a psychometric function when the subject's performance never goes to 1 (and it is not because of lapse)?

An example of how this situation can happen: suppose I want to study how stimulus presentation time affect a small target's visibility in a given peripheral visual field location by a 2AFC task. The target's feature is fixed throughout the experiment. I can imagine that with longer stimulus presentation time (like 1 ms vs. 200 ms), subject can make more correct responses, but because of the limit of peripheral vision, the correct response rate can never go to 100% even if you present the stimulus for a very long time. How can I fit a psychometric function (proportion correct ~ stimulus presentation time) to data like this?

# Answer
> 2 votes
Yes. When you fit your psychometric function you try to maximize $p(X|\theta)$, with $X$ your observations and $\theta$ your parameters. When you assume 100% correct answers, you would typically assume that your psychometric function is $\Phi(s|\theta)$, $s$ being your stimulus value and $\Phi$ being a cumulative normal. More specifically $\Phi(s|\theta)=\frac{1}{\sigma\sqrt{2\pi}} e^{-\frac{(s-\mu)^2}{2\sigma^2}}$. Here $\theta$ is both the mean $\mu$ and the std $\sigma$. To have a psychometric function that does not go to 100% correct, you just need to add a third variable to $\theta$. It doesn't matter whether the observer's performance is limited by lapses or another factor, mathematically that's equivalent. Then you fit your data with $\Phi'(s|\theta)=\frac{\lambda}{2}+(1-\lambda)\Phi(s|\theta)$. With $\lambda$ your lapse rate, assuming this lapse rate is symmetrical. You could add a 4th parameter if you have a good reason to assume the lapse rate is different near 0 and near 1 (then $\theta=(\mu,\sigma,\lambda\_{low},\lambda\_{high})$). Also, you might run into issues because if you fit with $\lambda$ unconstrained, you could get values higher than 1 or lower than 0. So when fitting it is helpful either to use a constrained algorithm (e.g. a quasi-Newtonian gradient descent, in Matlab that would be fmincon), or better to transform your parameter using a function that is bounded like the cumulative normal function itself. In other words, use $\Phi'(s|\theta)=(\frac{\Phi(\lambda\_{low})}{2})+(1-\frac{\Phi(\lambda\_{high})}{2})\Phi(s|\theta)$.

It is in facts recommended to always allow for a lapse rate, as you could misestimate the slope of your psychometric function when you do not.

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Tags: measurement, methodology, vision
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# Question
Title: Why do we forget what we try to remember?
Almost everybody has had an experience where someone asks them what their favorite book is, and they immediately forget every single book they have ever read. This infuriating consequence of attempting to dig into memory is mysterious enough by itself. Why does this happen? Why do our memories suddenly disappear when provoked?

I have searched for this and this, but the results don't provide a direct and suitable enough answer.

# Answer
> 3 votes
What you are describing may be the tip of the tongue (TOT) phenomenon.

There are two major explanations for this: the direct-access view and the inferential view.

* The **direct-access view**: the memory strength is just not strong enough to recall the item, but strong enough to trigger the recall
* The **inferential view**:
> It claims that TOTs aren't completely based on inaccessible, yet activated targets; rather they arise when the rememberer tries to piece together different clues about the word. **Emotional-induced retrieval often causes more TOT experiences than an emotionally neutral retrieval**, such as asking where a famous icon was assassinated rather than simply asking the capital city of a state.

The second view is interesting, because frustration is an emotion by definition. So when you are frustrated for not remembering the word, your frustration by itself narrows down your ability to retrieve it. This loop goes on until you yell "fuck it. I quit".

So while emotion plays an important role in memorizing a piece of information, it also may hindrance you to recall it back. But if you can devote a lot of cognitive resource (thinking it hard) without being frustrated, then you can still retrieve it.

TOT is seemingly a very important topic in memory research.

Sources: Tip of the tongue, Recall (memory)

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Tags: memory, long-term-memory, semantic-memory
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# Question
Title: Volition v.s. Cognitive Control v.s. Motivational Salience
The concepts of volition, cognitive control, and motivational salience, seem quite similar. From the perspective of layman, they all seem to mean "the extent to which your goals influence your behaviors".

So, to psychologists, what is the difference? Or are they actually synonyms, even within psychology?

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What sparked the question was that it is almost as if multiple discovery has occurred, and different sets of scientists are studying the same thing without realizing it. I realize though that is rather implausible, since psychologists aren't dumb. Surely if they actually were the same thing, *someone* would have noticed that besides me. So my conclusion is that there actually is some difference that I don't understand, or that they actually are the same, and psychologists know that, but they just haven't effectively communicated that yet (and so the three wikipedia articles should be merged).

Just as an example, it appears that volition, self-control, and willpower are considered synonyms.

# Answer
I would argue that they are not the same, but you are correct that there could be some overlap. I think you will also find that people in different schools of thought might prefer a particular term for philosophical reasons in some situations, and in others the terms are more clearly distinct.

I would say that *volition* involves conscious decisions to do certain behaviors: that's it. In my experience, "volition" isn't often used in neuroscience and psychology, it comes up more often in philosophy. It may also be used in psychiatry but that is a field I am less familiar with. Similarly, self-control and willpower are not typically used in studies of the biological basis of behavior, except to relate to more colloquial discussions.

*Cognitive control* (see Miller, 2000 and Ridderinkhof et al., 2004) is similar but often involves *inhibition* of some unwanted behavior. It often comes up in the context of addiction as something that is absent/lacking, or in suppressing attention to an otherwise distracting stimulus. Cognitive control is also used to refer to error detection and behavioral correction, keeping focus towards some future goal. The neural correlates of cognitive control are usually identified in the prefrontal cortex.

*Motivational salience* (see Berridge & Robinson, 1998, Ventura et al., 2007, and Bromberg-Martin et al., 2010) is in many ways the opposite of cognitive control. Often, cognitive control is marshaled *against* other salient motivations. For example, in addiction, you could say that there is a high motivational salience towards the rewarding features of a drug: in someone with an addiction, those salient rewards motivate future use of the drug. Suppressing motivational salience in order to achieve some other goal (for example, sobriety) requires cognitive control. The neural correlates of motivational salience are usually identified in the ventral striatum or amygdala.

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Berridge, K. C., & Robinson, T. E. (1998). What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience?. Brain research reviews, 28(3), 309-369.

Bromberg-Martin, E. S., Matsumoto, M., & Hikosaka, O. (2010). Dopamine in motivational control: rewarding, aversive, and alerting. Neuron, 68(5), 815-834.

Miller, E. K. (2000). The prefontral cortex and cognitive control. Nature reviews neuroscience, 1(1), 59.

Ridderinkhof, K. R., Ullsperger, M., Crone, E. A., & Nieuwenhuis, S. (2004). The role of the medial frontal cortex in cognitive control. science, 306(5695), 443-447.

Ventura, R., Morrone, C., & Puglisi-Allegra, S. (2007). Prefrontal/accumbal catecholamine system determines motivational salience attribution to both reward-and aversion-related stimuli. Proceedings of the National Academy of Sciences, 104(12), 5181-5186.
> 1 votes

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Tags: cognitive-psychology, motivation, executive-function, free-will, willpower
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# Question
Title: How to control subject's response bias in 2-interval force choice task
I am using a two-interval force choice (2IFC) task to estimate detection threshold and choose an appropriate signal level for my following experiment, by estimating sensitivity ($d'$) for each signal level.

Since it is a 2IFC task with signal equally distributed on two intervals, I expect close-to-zero response bias and plan to estimate $d'$ directly from proportion correct. After running experiment on 3 subjects (one complete 2500 trials, two complete 1250 trials), two of them show slight response bias (ratio of response to interval 1 vs. 2 is 0.91 and 1.12), but one subject shows large response bias (ratio of response to interval 1 vs. 2 is 0.53).

Here is my question:

1. For the subject with large response bias, is it still valid to estimate $d'$ from proportion correct anymore? And is it still valid to estimate $d'$ directly from hit rate and false-alarm rate?
2. If I hope to let this subject to continue participating in this experiment, how should I let him/her to lower response bias? Directly telling him/her "You have pressed key #1 too often, press key #2 more when you are not sure"? Is it going to interfere the experiment?
3. For future naïve participants, should I let them know do not bias toward one response too much before the start of experiment, or should I tell them only when they have made too much bias? If the latter case, how much bias is considered to be "too much"?

# Answer
> For the subject with large response bias, is it still valid to estimate d′ from proportion correct anymore?

No. Within the signal detection theory framework, a 2I-2AFC paradigm is identical to a 1I-2AFC paradigm except that the decision variable Y in the 2I-2AFC paradigm is X2-X1 (difference between the observations on the first and second intervals). The effects of bias are the same and d' needs to account for any bias.

> And is it still valid to estimate d′ directly from hit rate and false-alarm rate?

Maybe. If all of the assumptions from the 1I-2AFC paradigm still hold, then with appropriately defined hits and false alarms (e.g., a hit is when the subject responds "1" when the signal in the first interval) and you account for the $\sqrt(2)/2$ improvement from having two intervals, then yes you can still calculate d'. That said, with typical assumptions, the 2I-2AFC paradigm results in distributions that are symmetric about zero and therefore we don't expect a response bias. I would be worried that with a non-zero bias that the subject is not behaving as assumed. If that is the case, d' does not really mean anything.

> If I hope to let this subject to continue participating in this experiment, how should I let him/her to lower response bias? Directly telling him/her "You have pressed key #1 too often, press key #2 more when you are not sure"? Is it going to interfere the experiment?

Correct answer feedback sometimes works, but not always. The effect of influencing the preferred response bias of a subject depends on the subject and experiment.

> For future naïve participants, should I let them know do not bias toward one response too much before the start of experiment, or should I tell them only when they have made too much bias? If the latter case, how much bias is considered to be "too much"?

This comes down to the experimental design. If possible, I would exclude the subject from the analysis. If you are looking at population statistics, you need to include everyone. If instead, you are interested in the best subjects, a subject with an odd bias is probably not worth your time of dealing with.
> 1 votes

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Tags: methodology, psychophysics, signal-detection
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# Question
Title: Are there any significant alternatives to the theory that the mind exists?
Are there any psychological models which do not presuppose the existence of the mind?

In the same way that there are theories of physics which do not presuppose the existence of a luminiferous aether, is the sort of thing that I mean.

*Can* there be, or is it impossible by definition?

# Answer
> 1 votes
The denial of mind is called Eliminative Materialism or "Illusionism":

> Eliminative materialism is the claim that people's common-sense understanding of the mind (or folk psychology) is false and that certain classes of mental states that most people believe in do not exist. ... modern physicists are eliminativist about the existence of luminiferous aether. Eliminative materialism is the relatively new (1960s–1970s) idea that certain classes of mental entities that common sense takes for granted, such as beliefs, desires, and the subjective sensation of pain, do not exist.

Although not denying the mind, Methodological Behaviorism (or the Watson school), one of the more popular psychological approaches in the first half of the 20th century, rejects introspection as a useful methodology for studying it:

> Methodological behaviorism: Watson's behaviorism states that only public events (behaviors of an individual) can be objectively observed, and that therefore private events (thoughts and feelings) should be ignored.

The modern behavior analysis that emerged from this school of thought, and is still very active today, remains based on a logical behaviorism premise that the study of behavior should not reference the mind:

> Logical behaviorism is a theory of mind that mental concepts can be explained in terms of behavioral concepts.

# Answer
> 4 votes
Theory of mind doesn't really "presuppose" a mind. Theory of mind is just a name for a particular cognitive capacity: the ability to know that *you* have a mental state and to realize that *others* have a mental state, and that their mental state is not the same of yours. Calling this ability "theory of mind" might be a bit confusing because it sounds like it's a scientific theory, but it's not, it's just referring to an ability to theorize (make educated guesses) about the contents of other peoples' mental states. It could have been named something else (see Why is the theory of mind named as such? as well). Therefore, it doesn't really make any sense to think about "alternatives" to theory of mind, maybe just alternatives to the name of the ability.

Theory of mind is really important to human social interactions, and impairments in theory of mind are part of the spectrum of social difficulties in autism.

As one example of how theory of mind works day-to-day, very young children who have not yet developed theory of mind have difficulty understanding that knowledge *they* have is not *shared by everyone*. If they see you hide a candy under one of two cups, they would be confused why someone else who wasn't in the room to see where the candy was hidden doesn't know which cup the candy is under (Frith and Frith, 2005, tell a similar story to explain theory of mind).

The nature of the mental state is not actually a part of the definition of theory of mind. You might be thinking of philosophy of mind.

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Frith, C., & Frith, U. (2005). Theory of mind. Current Biology, 15(17), R644-R645.

# Answer
> 4 votes
Yes, depending on what "mind" means.

A common folk perception of the "mind" is that there is some sort of operator within the brain, a unified conscious homunculus. Instead, cognitive neuroscience informs us that the mind is a network of faculties — one of which is *consciousness*. Most other faculties, such as memory, perception, use of language, etc., aren't problematic, but consciousness is.

If I may, I'll rephrase your question to "Are there significant theories that deny the existence of consciousness", the answer is still, intriguingly, yes.

One is the attention schema theory, developed by Michael S.A. Graziano. Very, very, simply, Graziano posits that what we think of as consciousness is nothing more that our ability to pay attention to what we are paying attention to.

That's inevitably a gross oversimplification. The Wikipedia article on AST provides more depth, as does Graziano's essay in the New York Times: *Are We Really Conscious?*. His 2013 book, *Consciousness and the Social Brain*, is an engrossing treatise on the theory.

# Answer
> 2 votes
If “the mind” in your question means a non-material entity that exists in an animal and that can sense signals from the environment (see, hear, smell, etc.), operate the signals, resulting in various mental activities (thinking, solving problem, planning, remembering, recalling, etc.), and send signals to its effectors (hand, legs, lips, etc.) to respond to the environment, then the answer is yes. There is a physical theory (with scientific evidence and verifiable predictions) that proves that there is no need to presuppose the existence of something like a luminiferous ether or any other exotic entity to explain the mind and its existence – the mind is just the information-processing processes of the brain. The theory that proves this is “The Basic Theory of the Mind”.

This theory also proves that qualia (i.e., what the color red is like, what the happiness is like, what the thinking is like, etc.) and consciousness (i.e., the awareness and experiences of what the color red is like, of what the happiness is like, of what the thinking is like, etc.) are also physical phenomena that need no exotic entities to account for – they are just signaling patterns and signaling states of neural processes.

Other interesting concepts of this theory are as follows:

> 6. Because a neural process that performs a certain function without qualia occurring and a neural process that performs the same function with qualia occurring have different information in the processes, they require different signaling patterns. Therefore, they have different physical effects on other neural processes, at least from the different effects of different signaling patterns. Qualia thus have physical effects.
>
> In addition, because qualia induce the consciousness neural process to create conscious awareness and experiences of themselves and because the consciousness neural process is a physical process, qualia cause changes in a physical process and thus have physical effects.
>
> It can be proved similarly that consciousness (conscious awareness and experiences) has physical effects.
> 7. The fact that qualia and conscious awareness and experiences of them occur in only the final-stage sensory perception and the highest-level cognitive and executive neural processes, which are the latest-evolved neural processes, and never occur in more primitive neural processes, such as the brainstem, cerebellum, and basal ganglia, indicates that they are results of nervous system evolution.
> 8. The fact that it took more than two billion years after life had appeared on earth and hundreds of millions of years after the nervous system had developed before neural processes that were advanced enough to create qualia and consciousness could emerge into existence also means that qualia and consciousness came into existence because of no other cause than evolution.
> 9. The fact that qualia and consciousness still exist today indicates that they have been selected to remain in the evolutionary process. This means that they must have effects that help increase the chance of survival of animals that have them. Qualia and consciousness thus are the evolved functions to help increase the chance of survival of animals, including humans, that have them.
>
> ….

Thus, it concludes that we (our minds with qualia and consciousness) are evolved physical entities to help increase the chance of survival of ourselves and our species and that you (your mind with qualia and consciousness) are here to help increase the chance of your own survival and your species.

There are several other theories about consciousness and qualia but none directly answer your questions about the mind as this theory does. I list some of them here in case you are interested in reading more about this matter:

1. Block N. Comparing the major theories of consciousness. In: Gazzaniga MS, editor. The Cognitive Neurosciences (Chap 77). 4th ed., Cambridge, MA: MIT Press; 2009:1111–1122.
2. Kanai R, Tsuchiya N. Qualia. Current Biology. 2012 May;22(10):392–396.
3. Orpwood R. Neurobiological mechanisms underlying qualia. J Integr Neurosci. 2007 Dec;6(4):523-540.
4. Seager W. Theories of consciousness. An introduction and assessment. 2nd ed. New York, NY: Routledge; 2016. ISBN 978-0-415-83409-4.

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Tags: theory-of-mind
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title: Bounds on skew and kurtosis of IQ

text:
# Question
Title: Bounds on skew and kurtosis of IQ
The question of whether IQ is Normally distributed, or instead follows e.g. a Pearson type IV distribution, has been debated since at least the 1910s. The quotient- and deviation-based definitions give rise to very different eras in that debate, of course. (However, the distribution of an integer-valued IQ cannot be exactly Normal, even on a deviation-based definition.) A Normal distribution is uniquely characterised by its mean $\mu$ and standard deviation $\sigma$. Its next two moments are the skew $\gamma\_1=0$ and excess kurtosis $\kappa\_\text{excess}=0$. To disambiguate, I've defined

$$\gamma\_1=\mathbb{E}\bigg(\tfrac{X-\mu}{\sigma}\bigg)^3,\\,\kappa\_\text{excess}:=\mathbb{E}\bigg(\tfrac{X-\mu}{\sigma}\bigg)^4-3.$$

By contrast, a Pearson type IV distribution requires all four moments to be specified.

While we can't literally prove $\gamma\_1=\kappa\_\text{excess}=0$ empirically, we can constrain such quantities. Have any empirical studies provided either upper or lower bounds on these moments of the IQ distribution (or something analogous such as another quantification estimating psychometric $g$), on either the quotient or deviation definition? In the interests of keeping this question appropriate to the site, I don't care what method of defining or measuring IQ was assumed in a particular study, so there's no need to take a stance on that.

# Answer
> 2 votes
There are studies where higher order moments are analyzed. Just off the top of my head, see (Johnson, Carothers, Deary, 2008). The actual point of this study was to examine the Greater Male Variability Hypothesis (which the data was found to be strongly consistent with), however they also analyzed the distributions of ability more generally. They analyze the Scottish Mental Survey data, which tested essentially all children of Scotland of a given age. They find that the distribution is definitely unsymmetrical with more people below the mode. Here is the relevant part of the abstract:

> ... Clear analysis of the actual distribution of general intelligence based on large and appropriately population-representative samples is rare, however. Using two population-wide surveys of general intelligence in 11-year-olds in Scotland, **we showed that there were substantial departures from normality in the distribution, with less variability in the higher range than in the lower**. Despite mean IQ-scale scores of 100, modal scores were about 105... This is consistent with a model of the population distribution of general intelligence as a mixture of two essentially normal distributions, one reflecting normal variation in general intelligence and one reflecting normal variation in effects of genetic and environmental conditions involving mental retardation.

See the study for further discussion around kurtosis and skewness. They also reference other studies you may find valuable.

# Answer
> -1 votes
One answer is that, since $g$ does not really exist as a unidimensional biological entity (rather, it is a near infinite-dimensional soup of inherited DNA and accumulated life experiences), the question of its univariate distribution is moot.

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Tags: measurement, intelligence, statistics, iq
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# Question
Title: Unilateral vision in split brain subjects
I am just beginning to learn psychology and came across concept of split brain. I was wondering if a person has only left eye working and has their corpus callosum cut, would they be effectively blind since the left brain won't receive any visual stimuli?

# Answer
> 2 votes
**Short answer**

* The *corpus callosum* is not necessary for low-level visual processing;
* Both eyes project to both hemispheres; the left visual hemifield of both eyes is projected to the left hemisphere, the right hemifield to the right.

**Background**
The site where the right and left visual hemifields are split occurs in the *optic chiasm*. This structure is different from the major highway between both hemispheres, namely the *corpus callosum* (Fig. 1). Hence, your question...

> \[I\]f a person has only \[functionality in the\] left eye\[,\] and \[..\]their *corpus callosum* \[is severed\], would they be effectively blind\[,\] since the left brain won't receive any visual stimuli?

...can be answered with ***no***, as both eyes will still transmit their input to the visual centers in the brain (Fig. 1). In fact, when one eye is not functional, the fieldof view will still be nearly complete, as both hemifields of the one remaining retina is projected to both cortices (Fig. 2).

The function that is effectively lost when there is only one eye left, is depth perception; the use of both eyes, and the fact that they are slightly offset, allows us to see depth, using binocular vision through a process referred to as **binocular disparity**.

Fig. 1. Mid-saggital section through the brain. source: Studoku

Fig. 2. Visual pathway. source: The Brain Recovery Project

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Tags: neuroscience, perception, vision, neurophysiology, neuroanatomy
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# Question
Title: What genetic polymorphisms are linked to aggression or violence?
Anecdotally, there are reports of varenicline causing agression, but larger studies tended towards the finding of no effect over controls.

This got me into thinking about possible genetic polymorphisms that are implicated in aggression. Varenicline acts as a partial agonist of α4β2-nicotinic receptors -- maybe if you did a study of a prison population, you'd find those some polymorphism in this receptor among those incarcerated for a violent crime? (There isn't).

**More broadly, are there any good candidate genes implicated in aggression/violence?**

# Answer
> -1 votes
I had a similar experience 8 years ago, I felt rage that I have never felt before. The day I nearly punched the wall, I understood my completely uncharacteristic behaviour was induced by the drug. Then I asked everyone close if they had noticed recent changes in me, they had. I talked to my doctor and I weaned off of it, my behaviour returned to normal and now at nearly 50 years of age, this was the only such brief period of episodal rage I have ever experienced. It was intense, I've often thought of the poor souls who have comitted suicide and their loved ones who hypothesize the drug is to blame. I would believe it, given my experience.

I am female, have the low MAOA activity gene (homozygous), I also possess 2 homozygous mutations in COMT genes, these affect (slow) degradation of neurotransmitters. I also possess mutations related to dopamine receptor inefficiency, decreased BH4 production (precursor to dopamine), and folate metabolism (precursor to BH4). I am naturally and consstently one of the most even tempered people I know, I have rarely even experienced PMS and my reproductive years will soon be over. Interestly, the MAOA mutation I have has been called the "happiness" gene for woman (not-so for men, infact it's the opposite). I have 2 copies, resulting in even more self-reported happiness in day to day life, which is true for me, but was not for my time on the drug when I had anger, aggression, and rage, like never before. Incidently, it did work for me in giving up the cigerettes.

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Tags: psychopharmacology, genetics, aggression, nicotine
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# Question
Title: What are some books about the effect of childhood experiences on adult life?
I would like to read some books about the effects of childhood experiences on the adult life. For an example, somewhere I read that adult males who had an aggressive father they are usually not aggressive (because they find it repulsive and inhumane), and also, they are not able to show anger in the proper dose when needed. The example may not be accurate but I hope I conveyed what I mean. I have a PhD (not in neuroscience or psychology) so I think I can manage even a bit more academic oriented books. However, it would be nice to have some books suitable to average layman person too. It would be nice someone could read such a book and by comparison to themselves realize that some trait of them is not actually normal and should be fixed.

# Answer
There are many books (both academic and non-academic) available on Adverse Childhood Experiences (ACEs), a growing area of research focused on how traumatic childhood experiences affect health and well-being in later life. A quick search for ACEs on Google or Amazon will yield many results.
> 2 votes

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Tags: social-psychology, reference-request
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# Question
Title: Is there any research about effect of unfamiliar environment on stress?
It seems intuitive to me that there is some kind of stress when one is put in an unfamiliar place (There's probably effect on cognitive abilities too). However, I can't find any paper in psychology which discusses that potential relationship.

# Answer
> 3 votes
I have found the following

Older people's cardiac responses as indicators of stress in familiar and unfamiliar environments (Lewis & Phillips, 2012)

I also found:

Padilla, A. M., Alvarez, M., & Lindholm, K. J. (1986). Generational status and personality factors as predictors of stress in students. *Hispanic Journal of Behavioral Sciences*, 8(3), 275-288.
DOI: 10.1002/dev.420220608

> stressful events center on loss of familial and cultural ties as well as on relative discomfort in an unfamiliar social environment

## References

Lewis M. J. & Phillips J. E. (2012). Older people's cardiac responses as indicators of stress in familiar and unfamiliar environments. *Psychophysiology*, 49(4): pp. 478-483
DOI: 10.1111/j.1469-8986.2011.01321.x PMID: 22176515

# Answer
> 2 votes
You may be interested in related research on how unfamiliar environments negatively affect sleep quality.

Tamaki, M., Bang, J. W., Watanabe, T., & Sasaki, Y. (2016). Night watch in one brain hemisphere during sleep associated with the first-night effect in humans. Current biology, 26(9), 1190-1194.

This research has also received substantial popular press coverage, for example from CNN and NPR.

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Tags: cognitive-psychology, social-psychology, psychology, stress
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# Question
Title: Can listening to sad songs lead to depression?
When we listen to a sad song, we may experience sadness ourselves. Can this sadness lead to depression?

# Answer
> 7 votes
If you are talking about clinical depression as an illness, the direct answer to your question is: I don't know.

There was a study of the effect of different genres of music on how people felt (https://www.ncbi.nlm.nih.gov/pubmed/27900748). Note the participants only listened to the music for 15 minutes and the study in general is not that powerful.

But if you are talking about making people feel sad or low then maybe. There have been studies that show that negative ruminations can lower people's mood. My thinking is that if the songs lead to negative ruminations then yes it can depress your mood.

There are also some other research suggesting that "sadness" as a feeling can be felt helpful or pleasurable by some people.

It is important to distinguish between sadness and depression. The latter is a clinical diagnosis made by a professional that is generally constant in a person's life, the former is a feeling or emotion that is fluid and can change from one moment to another.

Also an important question to think about is causation: is it really the songs leading to sadness or sadness leading to listening to these songs?

Reference: https://www.ncbi.nlm.nih.gov/pubmed/26257625

https://www.ncbi.nlm.nih.gov/pubmed/29094761

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Tags: emotion, abnormal-psychology, depression
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# Question
Title: What is the difference between principal neurons and pyramidal cells?
I am reading Kandel's "Principals of Neural Sciences". There the book sometimes refers to excitatory neurons as principal cells, and sometimes as pyramidal cells.

Can anyone tell me the difference? I mean, are there pyramidal neurons which are not projection neurons? And are there projection neurons which are not pyramidal?

# Answer
> 4 votes
**Short answer**
In the cortex, pyramidal cells and projection neurons can be used interchangeably, as both terms refer to the same cells.

**Background**
One way to classify neurons is based on their function. Two functionally distinctive types of neurons have been classified, namely

* Projection neurons, which send an axon out of the structure where their soma is located, and
* Intrinsic neurons, which make synapses only within the structure where their soma is located.

Hence, projection neurons cover some distance, whereas intrinsic neurons act more locally. Projection neurons are also called principal cells, and intrinsic neurons are also called interneurons (Masland, 2004).

In the cortex, **projection neurons are pyramidal neurons**, and account for approximately 80% of all cortical neurons Han & Šestan, 2013. They often send their axons for long distances, sometimes out of the brain altogether Beckers, 2011. They serve as both the sole output from and the largest input system to the cortex. Interneurons, in contrast, represent approximately 20% of all cortical neurons and form local synaptic connections (intrinsic) that play critical roles in shaping cortical network activity patterns Han & Šestan, 2013.

In the periphery, the term projection neuron is not used as far as I know. That doesn't mean there aren't neurons that cover great distances in the periphery; in fact, the longest axons in the human body are thought to be situated in the **sciatic nerve**, which runs from the base of the spinal cord to the big toe of each foot. However these cells are not referred to as projection neurons, but simply as spinal neurons.

<sub>**References**
**-** Beckers, *Curr Biol* (2011); **21**(24): PR975
**-** Han & Šestan, *Neuron* (2013), **80**(5): 1103–05
**-** Masland, *Curr Biol* (2004); **14**(13): R498</sub>

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Tags: neuroscience, terminology, neural-network, neurophysiology
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# Question
Title: How do I interpret an effect of electrode position in ERP research?
The example I have in my research is that both conditions show greater amplitude and latency in the parietal electrode sites than in the occipital ones.

I'm not sure how meaningful this is for my research question, which is primarily concerned with how processing of the two conditions potentially differs (spoiler: no effects of condition!). The effect of electrode sites does not interact with anything, so is just the case that there is greater activity in the parietal sites - can I argue something about the processing involved in both conditions based on this finding?

# Answer
The question is quite vague, as it is unclear what the sample size is and whether OP is talking about an anecdotal experiment or the outcome of a well-powered statistical analysis. Moreover, there is mention of two conditions, but I fail to see what the difference is between the two.

Assuming a normal sample size, I can say that the measured amplitudes of electrophysiological signals are often unreliable. This is due to a variety of factors.

* Impedances affect signal size, as high impedances reduce the measured potentials. Impedances can vary between subjects, but also between sessions within subjects, due to for example differences in the effectiveness of the scrubbing and whether enough conductive paste is used in case of EEG.
* Impedance differences between active and reference electrode affect noise level. Noise may vary from day to day and even within a session due to interfering background electric fields.

In contrast to amplitude, peak latencies are often far more reliable.

So it all depends on the power of your analysis. If there is truly a difference in amplitude, then you should look at the physiology involved in your task and see whether brain mechanisms can be involved.
> 1 votes

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Tags: cognitive-neuroscience, vision, eeg, event-related-potential
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# Question
Title: What makes words (entities) positive or negative?
I am conducting a lexicon study asking people to classify words as being positive, negative, or neutral. It seems to be a very natural ability for us to perform such classifications.

The next step is for me to understand what makes a word (or an entity behind it in general) positive. There could be a variety of reasons:

* *(usefulness)* highly effective, useful;
* *(budget)* reasonable price, discount;
* *(comfort)* cozy, comfortable shoes;
* *(joy)* tasty pie, pleasant sleep;
* *(emotion)* incredible adventure, happiness;
* ...

(Naturally some words could fall into more than one category.)

I am looking for some research on the topic to learn from. Please advise.

# Answer
> 4 votes
The classification of affect as positive (as in "good") or negative (as in "bad") is called valence.

There is a large body of research regarding word valence, owing to interest from corporate communications and public messages, for example as delivered through social media. To further address demand, Bradley & Lang (1999) developed a database of dictionary words and their valence scores, that is available for download. More recently, such databases have been developed for dozens of languages, and the English database has been greatly expanded as well. These databases often feature multiple dimensions of affect, but if you are not interested in them, then just look at valence and ignore the rest.

With such databases in hand, it is possible to test how different factors predict word valence. Many hypotheses have been tested, such as word length, conjugations, age of acquisition, etc. A comprehensive review by Warriner et al (2013) lists a few more examples of correlations with lexical properties, such as smell, color, and motion:

> Most correlations that emotional ratings show with other semantic properties are weak to moderate, with the exception of correlations with variables that directly tap into emotional states.

Of particular note, and extensively studied in this field, are concreteness, imageability, context availability, and familiarity. Familiarity for example, is a term that has to do with how well known and how common words are - common words tend to be rated more positively than uncommon ones. This has to do with the mere-exposure effect, and more generally, processing fluency (a.k.a. "cognitive ease"):

> Fluency and familiarity have been shown to lead to the mere exposure effect. Research has found that repetition of a stimulus can lead to fluent processing which leads to a feeling of liking. ... Later research observed that high perceptual fluency increases the experience of positive affect.

Another good list of databases and research on concreteness, imageability, context availability, and familiarity can be found in Riegel et al (2015). As I said, it's a big field, but hopefully this gets you started.

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Tags: emotion, reference-request, language
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# Question
Title: How to compare effectiveness of psychological treatment for psychological illness, versus medical treatment for medical illness?
I'm a college student. I read somewhere that people often assume that mental health issues do not get better, and that a person ends up seeing a psychiatrist forever. So I was wondering if there was a way to compare treatments for medical vs psychological issues.

Like let's say we pick 10 common physical illnesses and 10 common psychological illnesses. And then look at best treatments for each. For instance, assume sinus infections are the top physical illness and depression is the most common mental illness. Further assume that the best treatment for depression is CBT, and for sinus infection is nasal corticosteroids. How would I go about comparing the effectiveness of corticosteroids for sinus infections versus CBT for depression? Is there a particular number, some effect size, or something else that I can take from one research study and compare it to the other?

Thanks for help or clarification.

# Answer
You asked:

> Is there a way to compare treatments for medical vs psychological issues?

I would say **no** because we aren't looking to compare medical treatments to psychological treatments. It isn't possible to do so and there isn't any real world application for such a process, i.e., it doesn't tell us anything useful.

---

The question I think you're getting at is:

> Can we show that a treatment for a psychological disorder is effective at treating the psychological disorder, in the same way that we can see that a medication is effective in treating a physical disease/disorder?

The answer to that question is absolutely!

When we implement a treatment for a psychological disorder we are often hoping to reduce the **symptoms** of that disorder, rather than finding a cure. When we are looking at the effectiveness of psychological treatments we are looking for a statistically significant difference in measured behaviours from before treatment to after treatment. Researchers in the paper linked below used 4 treatment conditions to (1) determine if treatments for depression were effective and (2) to compare the effectiveness of the treatments against each other (Elkin et al., 1989).

The statistics can get very complicated when it comes to showing effectiveness of treatments.

I believe that it is extremely important to note that many psychological disorders are life long and many people can experience a wide range of symptoms that vary in intensity for their entire lives. So, to bring it back to your original question, psychological disorders don't have an easy 'cure' the way that some physical diseases/disorders do. Seeing a counsellor/therapist/psychologist for CBT Treatment does not have to mean having a life long relationship with a counsellor/therapist/psychologist. The treatment includes learning skills/tools to cope with your situation and if CBT is successful the person can end therapy whenever they have learned enough skills/tools to live a full and healthy life.

<sub> Elkin, I., Shea, M. T., Watkins, J. T., Imber, S. D., Sotsky, S. M., Collins, J. F., ... & Fiester, S. J. (1989). National Institute of Mental Health treatment of depression collaborative research program: General effectiveness of treatments. Archives of general psychiatry, 46(11), 971-982. </sub>
> 4 votes

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Tags: therapy
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title: Is autism caused by genetics?

text:
# Question
Title: Is autism caused by genetics?
Is autism and Asperger's syndrome caused by genetics or some other factor such as the environment?

I am aware about the Neanderthal Theory of autism, Asperger and ADHD, but am not interested in this due to it appearing too broad and to me seems based off of opinions like preferring the cold to the heat which is not always the case, a the term "lack of social life" seem's very broad and not clear nor specific in the aspects of socializing that they are not good with. The aspect of having big brains is also very broad and does not cover in any detail about what it means by that, however if it means intelligence then this is a development from back when we needed to hunt for food as we started to create things and fleeing particular pray on sight became instinct. The section about being meat eaters does not conclude anything as many autistic people are vegans the same as neurotypicals so does not lead us anywhere. The section about woman being more submissive sexually is also not conclusive as most autistic people are asexual so there is no real dominance by both genders as most do not even partake in sexual activities. The graphs included are also questionable as they all seem to be in favor for aspies as they score higher on everything which i would say for things like the chances of having OCD they would be very much correct as the chances of having this when on the spectrum is 40 times more likely. A lack of organization is mentioned which to me does not seem right i feel that we over plan and organize. These category's specified do not cover everyone on the spectrum so therefore is not conclusive.

# Answer
In light of a recent question in MedicalSciences.SE, I thought I would update this answer to include some information from my answer there.

Autism spectrum disorder (ASD) now affects one in 68 births in the United States and is the fastest growing neurodevelopmental disability worldwide (Edmiston, et al. 2017) *\[free access paper with links to cited papers\]*.

Alarmingly, for the majority of cases, the causes of ASD are largely unknown, but it is becoming increasingly accepted that ASD is no longer defined simply as a behavioral disorder, but rather as a highly complex and heterogeneous biological disorder (Edmiston, et al. 2017).

With information available, the genetic and environmental causes of Autism is open to speculation and interpretation.

The NHS webpage on Autism states (Emphasis mine)

> **Most researchers believe** that certain genes a child inherits from their parents could make them more vulnerable to developing ASD.
>
> **Cases of ASD have been known to run in families**. For example, younger siblings of children with ASD can also develop the condition, and it's common for identical twins to both develop ASD.
>
> **No specific genes linked to ASD have been identified**, but it may be a presenting feature of some rare genetic syndromes, including Fragile X syndrome, Williams syndrome and Angelman syndrome.

On environmental causes the NHS say that

> **Some researchers believe** that a person born with a genetic vulnerability to ASD only develops the condition if they're exposed to a specific environmental trigger.
>
> **Possible triggers** include being born prematurely (before 35 weeks of pregnancy), or being exposed in the womb to alcohol or to certain medication, such as sodium valproate (sometimes used to treat epilepsy during pregnancy).
>
> **No conclusive evidence has been found** linking pollution or maternal infections in pregnancy with an increased risk of ASD.

Research Autism has some referenced information on leading research into the causes of Autism from the Medical Research Council, National Autistic Society and the Autism Society of America; and the crux of the matter from what is said here is that the causes are still being investigated and

> There is no known single cause for autism, but it is generally accepted that it is caused by abnormalities in brain structure or function

The site also provides a list of publications on the **possible** causes of Autism

There has been research into autoimmune disorders causing ASD.

Edmiston, et al. (2017) stated (emphasis mine):

> **there are likely multiple, biologically defined subgroups within the ASD spectrum**(3–7). Specifically, there is growing evidence that supports maternal immune dysfunction **may** underlie the behavioral abnormalities observed **in a subset of children affected with the disorder**(8). Several immunologic risk factors have been described including: genetic associations with immune-related genes(9–16), family history of autoimmune disease(15, 17–21), maternal inflammation and infection during pregnancy(22–27), and altered immune responses in the children, and are associated with increased impairments in core and associated features of ASD(28). More specific to this review, maternal anti-brain autoantibodies, which are thought to access the fetal compartment during gestation, have been identified as one risk factor for developing ASD and are proposed to contribute to early neurodevelopmental perturbations in the developing fetus(29–31).
>
> References
>
> 3. Lord C, Risi S, Lambrecht L, Cook EH, Leventhal BL, DiLavore PC, et al. The autism diagnostic observation schedule-generic: a standard measure of social and communication deficits associated with the spectrum of autism. Journal of autism and developmental disorders. 2000;30:205–223.
> 4. Newschaffer CJ, Croen La, Daniels J, Giarelli E, Grether JK, Levy SE, et al. The epidemiology of autism spectrum disorders. Annual review of public health. 2007;28:235–258.
> 5. Snow AV, Lecavalier L, Houts C. The structure of the Autism Diagnostic Interview-Revised: diagnostic and phenotypic implications. Journal of child psychology and psychiatry, and allied disciplines. 2009;50:734–742.
> 6. Ousley O, Cermak T. Autism spectrum disorder: Defining dimensions and subgroups. Current Developmental Disorders Reports. 2013;1:20–28.
> 7. McDougle CJ, Landino SM, Vahabzadeh A, O’Rourke J, Zurcher NR, Finger BC, et al. Toward an immune-mediated subtype of autism spectrum disorder. Brain Research. 2015;1617:72–92.
> 8. Onore C, Careaga M, Ashwood P. The role of immune dysfunction in the pathophysiology of autism. Brain, Behavior, and Immunity. 2012;26:383–392.
> 9. Warren RP, Singh VK, Cole P, Odell JD, Pingree CB, Warren WL, et al. Increased frequency of the null allele at the complement C4b locus in autism. Clinical & Experimental Immunology. 1991;83:438–440.
> 10. Warren RP, Odell JD, Warren WL, Burger RA, Maciulis A, Daniels WW, et al. Strong association of the third hypervariable region of HLA-DRβ1 with autism. Journal of Neuroimmunology. 1996;67:97–102.
> 11. Torres AR, Sweeten TL, Cutler A, Bedke BJ, Fillmore M, Stubbs EG, et al. The association and linkage of the HLA-A2 class I allele with autism. Human immunology. 2006;67:346–351.
> 12. Campbell DB, Li C, Sutcliffe JS, Persico AM, Levitt P. Genetic evidence implicating multiple genes in the MET receptor tyrosine kinase pathway in autism spectrum disorder. Autism Research. 2008;1:159–168.
> 13. Thanseem I, Nakamura K, Miyachi T, Toyota T, Yamada S, Tsujii M, et al. Further evidence for the role of MET in autism susceptibility. Neuroscience Research. 2010;68:137–141.
> 14. Mostafa GA, Shehab AA. The link of C4B null allele to autism and to a family history of autoimmunity in Egyptian autistic children. Journal of Neuroimmunology. 2010;223:115–119.
> 15. Jung JY, Kohane IS, Wall DP. Identification of autoimmune gene signatures in autism. Translational psychiatry. 2011;1:e63–e63.
> 16. Torres AR, Westover JB, Gibbons C, Johnson RC, Ward DC. Activating killer-cell immunoglobulin-like receptors (KIR) and their cognate HLA ligands are significantly increased in autism. Brain, behavior, and immunity. 2012;26:1122–1127.
> 17. Comi AM, Zimmerman AW, Frye VH, Law PA, Peeden JN. Familial Clustering of Autoimmune Disorders and Evaluation of Medical Risk Factors in Autism. Journal of Child Neurology. 1999;14:388–394.
> 18. Atladóttir HO, Pedersen MG, Thorsen P, Mortensen PB, Deleuran B, Eaton WW, et al. Association of family history of autoimmune diseases and autism spectrum disorders. Pediatrics. 2009;124:687–694.
> 19. Vinet É, Pineau CA, Clarke AE, Scott S, Fombonne É, Joseph L, et al. Increased Risk of Autism Spectrum Disorders in Children Born to Women With Systemic Lupus Erythematosus: Results From a Large Population-Based Cohort. Arthritis & rheumatology (Hoboken, NJ) 2015;67:3201–3208.
> 20. Wu S, Ding Y, Wu F, Li R, Xie G, Hou J, et al. Family history of autoimmune diseases is associated with an increased risk of autism in children: A systematic review and meta-analysis. Neuroscience and biobehavioral reviews. 2015;55:322–332.
> 21. Chen S-W, Zhong X-S, Jiang L-N, Zheng X-Y, Xiong Y-Q, Ma S-J, et al. Maternal autoimmune diseases and the risk of autism spectrum disorders in offspring: A systematic review and meta-analysis. Behavioural brain research. 2016;296:61–69.
> 22. Chess S. Autism in children with congenital rubella. Journal of autism and childhood schizophrenia. 1971;1:33–47.
> 23. Meyer U, Nyffeler M, Engler A, Urwyler A, Schedlowski M, Knuesel I, et al. The time of prenatal immune challenge determines the specificity of inflammation-mediated brain and behavioral pathology. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2006;26:4752–4762.
> 24. Smith SEP, Li J, Garbett K, Mirnics K, Patterson PH. Maternal Immune Activation Alters Fetal Brain Development through Interleukin-6. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2007;27:10695–10702.
> 25. Atladóttir HÓ, Thorsen P, Østergaard L, Schendel DE, Lemcke S, Abdallah M, et al. Maternal Infection Requiring Hospitalization During Pregnancy and Autism Spectrum Disorders. Journal of Autism and Developmental Disorders. 2010;40:1423–1430.
> 26. Patterson PH. Maternal infection and immune involvement in autism. Trends in Molecular Medicine. 2011;17:389–394.
> 27. Garay PA, Hsiao EY, Patterson PH, McAllister AK. Brain, Behavior, and Immunity Maternal immune activation causes age- and region-specific changes in brain cytokines in offspring throughout development. 2012
> 28. Ashwood P, Van de Water J. Is autism an autoimmune disease? Autoimmunity reviews. 2004;3:557–562.
> 29. Braunschweig D, Van de Water J. Maternal autoantibodies in autism. Archives of neurology. 2012;69:693–699.
> 30. Fox E, Amaral D, Van de Water J. Maternal and fetal antibrain antibodies in development and disease. Developmental Neurobiology. 2012;72:1327–1334.
> 31. Fox-Edmiston E, Van De Water J. Maternal Anti-Fetal Brain IgG Autoantibodies and Autism Spectrum Disorder: Current Knowledge and its Implications for Potential Therapeutics. CNS Drugs. 2015;29:715–724.

In conclusion, they pointed out that Maternal autoantibody related (MAR) ASD:

> has been noted by numerous researchers describing the presence of maternal autoantibodies reactive to fetal brain proteins in a subset of mothers of children with ASD. Further, there is now an abundance of evidence supporting their deleterious role in neurodevelopment. For the most part, these studies have described similar experimental outcomes and, given the clinical and biological heterogeneity of ASD, there likely exists a complex relationship between the presence of maternal anti-fetal brain antibodies and developmental trajectory of exposed offspring. It is still unclear how and when these maternal autoantibodies arise, but studies currently underway may provide increased insight into their ontogeny.

## References

Edmiston, E., Ashwood, P., & Van de Water, J. (2017). Autoimmunity, autoantibodies, and autism spectrum disorder. *Biological psychiatry, 81*(5), 383-390. Pubmed Central: PMC5373490
> 6 votes

# Answer
Since the 1970s, researchers have found out and known that genes make a contribution to the pervasive developmental disorder or autism when two identical twins have shared a similar condition.

As the world progresses, scientists have found out the variety of genetic changes in the DNA that contribute to the autism spectrum. However, genetics cannot be solely accounted for the risks of developing signs for autism spectrum. There are various other factors involved as well,

* A child being born to older parents
* Low birth weight and premature infants
* Hormonal and metabolic imbalances
* Fetal exposures to the medications such as valproic acid or thalidomide
* Exposure to heavy metals and environmental toxins
* Fragile X syndrome and other inherited disorders
* Having an immediate family member with autism

Working with **Arizona Centers for Comprehensive Education and Life Skills**, I have realized children or adults with pervasive spectrum need distinctive care and affection.
> -1 votes

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Tags: abnormal-psychology, autism, aspergers
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# Question
Title: Are there some discussions about Buddhism in science?
Buddhists are masters in observing what occurs on their minds, i.e what we call subjective as feelings, thoughts and more first-person stuff.

They really seem to understand how inmaterial world works (it might be obvious to some of you), but they lack of a materialist point of view. For example, they can study feelings occurring on their minds and modify it, but do not have a clear idea regarding the brain-basis of those feelings.

Are there any reviews or essays discussing Buddhists' knowledge and how science can complement it?

# Answer
Some resources:
> 5 votes

# Answer
Another relevant book is *Why Buddhism is True: The Science and Philosophy of Meditation and Enlightenment* by the science journalist Robert Wright. The focus is on Vipassanā Buddhism, especially on meditation. His bibliography is extensive.
> 3 votes

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Tags: reference-request, cognitive-science-of-religion
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# Question
Title: Are there animals with only excitatory neurons?
Are there animals with only excitatory neurons?

I am not sure it is possible.

Also, maybe excitation/inhibition can become relative?

I however will be happy to read your opinion..

For example, are there animals with only glutamatergic neurons?

Thanks

# Answer
Not in any well-studied animal; for example, *C. elegans* certainly has both excitatory and inhibitory neurons. Even in animals with very simple and poorly understood nervous systems (for example, jellyfish) there are certainly inhibitory and excitatory neurotransmitters used, even though one could argue whether their nervous tissue cells are all that similar to neurons of more organized animals.

More broadly speaking, I think it is non-controversial to state that "excitatory" versus "inhibitory" communication between cells predates the development of nervous systems themselves.

Note that neurotransmitters used vary across species, so although glutamate is a common excitatory neurotransmitter in vertebrates, that does not mean glutamate is a common excitatory neurotransmitter in other animals.

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Bargmann, C. I. (1998). Neurobiology of the Caenorhabditis elegans genome. Science, 282(5396), 2028-2033.

Martin, S. M., & Spencer, A. N. (1983). Neurotransmitters in coelenterates. Comparative Biochemistry and Physiology Part C: Comparative Pharmacology, 74(1), 1-14.

Kass-Simon, G., & Pierobon, P. (2007). Cnidarian chemical neurotransmission, an updated overview. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 146(1), 9-25.
> 5 votes

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Tags: neuroscience, computational-modeling, neural-network, neurophysiology
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