# Question
Title: What's the difference between a general psychiatric evaluation and a clinical psychiatric evaluation?
I've seen a few references (e.g. at VeryWellMind) to the fact that there are three kinds of psychiatric evaluations: General, Clinical, and Emergency.

The nature of an Emergency evaluation almost goes without saying. These are the kinds of evaluations that happen in emergency departments and urgent care clinics when someone is experiencing an acute crisis and may need immediate stabilization and/or hospitalization in order to prevent them from harming themself or others. I'm having a much more difficult time understanding the critical differences between a General and a Clinical evaluation. Both of them seem to happen when there is no acute crisis, but there are concerns that a patient may have a mental disorder that could benefit from psychiatric treatment.

What's the difference between a general and a clinical psychiatric evaluation? For example, is one of them more in-depth than the other? Is one more focused on getting a bare diagnostic label and the other more focused on deciding a treatment plan? Is a general evaluation done outside the clinical context (e.g. forensic psychiatry)?

I did find the Practice Guideline for the Psychiatric Evaluation of Adults (2nd ed) which indicates (p 11) that a Clinical evaluation is specifically done on a referral basis. This would imply that a General evaluation is *not* done on a referral basis but rather happens when a patient shows up at a psychiatrist's office without a referral in a non-emergency scenario, but the guide's writeup on the General evaluation (p 9) does not discuss the presence or absence of a referral as an essential element of the evaluation.

# Answer
When you asked

> is one of them more in-depth than the other? Is one more focused on getting a bare diagnostic label and the other more focused on deciding a treatment plan?

you were almost there.

As indicated by the UK's NHS page on Psychiatry, there will be an initial evaluation which will be a general assessment on the mental health and sometimes a little physical health of the patient. This can sometimes be referred to as a general evaluation.

Among other considerations, such as suicidality and any risks to others, the initial assessment will generate a general diagnosis of the problem presented, what therapy may be required, an assessment of urgency, the patient's support network (friends, family groups they can, and do, call upon), and whether any medication may be required before and/or during clinical appointments.

The clinical evaluations occur during the therapy sessions. During therapy, the initial diagnosis may be more refined into a more detailed diagnosis, and as things progress, the therapy sessions, timings, etc. along with any medication can be adjusted.

General evaluations look at the surrounding areas of the issue, such as external support availability and what, if any, are being employed. Clinical evaluations narrow in on the finer details of the issue, although that is not to say that clinical evaluations ignore the general issues. Everything is taken into consideration during a clinical evaluation.
> 1 votes

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Tags: psychiatry, diagnosis
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# Question
Title: Replication or conceptual replication of card trick in Mind Field Ep 8?
In Mind Field S1 E8 Michael Stevens presents a magician performing a trick with participants. Each participant is shown pairs of photographs of people and are given the forced choice of which one they preferred to work with. After being presented with all of the options, the magician performs a sleight of hand to sneak cards from the "no" pile into the "yes" pile while the participant is filling out a form. Then the participant is shown cards from the file that they believe are purely those that they said "yes" to, and asked to explain why they said "yes". When presented with cards that the participants said "no" to they appear to have made up rationalizations.

Are there studies that replicate this effect?

# Answer
Great question.

This paradigm is called "choice blindness":

> Subjects saw two photographs of people and were asked which they found more attractive. They were given a closer look at their "chosen" photograph and asked to verbally explain their choice. However, in some trials, the experimenter had slipped them the other photograph rather than the one they had chosen, using sleight of hand.

It has indeed been successfully replicated both by the original authors (Johansson et al), and some independent labs. From Book, 2020:

> Many studies have provided evidence that this experimental effect is robust and has been replicated across a variety of domains, such as financial decisions (McLaughlin & Somerville, 2013), speech intention (Lind et al., 2014), taste and smell preferences (Hall et al., 2010), moral attitudes (Hall et al., 2012), and voting intentions (Hall et al., 2013).

For a more extensive review with additional studies, see Mouratidou, 2020 (pp. 18-23). However, note that what conclusions can be drawn from the results has been questioned, and remains under investigation.
> 2 votes

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Tags: social-psychology, memory, decision-making, metacognition, rationality
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title: How can one induce psychogenic death?

text:
# Question
Title: How can one induce psychogenic death?
I saw something about psychogenic death. I am wondering if it can be induced by a desire. I think that it can by a person being lazy and not caring about the world. It is said to happen with prisoners of war. The article says that it is not suicide but I don't know if it is true. It cannot happen all at once, it just happens because the person does not care.

There is an article here: https://www.eurekalert.org/pub\_releases/2018-09/uop-pcd092018.php

Reference to the original research is: Leach, J. (2018). ‘Give-up-itis’ revisited: Neuropathology of extremis. Medical hypotheses, 120, 14-21. https://doi.org/10.1016/j.mehy.2018.08.009

# Answer
> 4 votes
> I am wondering if it can be induced by desire.

Psychogenic death refers to death triggered by psychic stimuli. The individual finds himself in a situation where external forces have lead to a restriction of his world and in addition, believes that this situation is unalterable.

Freud called this the death-drive. Except no person of his own volition would drive himself to death. This is obvious. The force of life is strong in every kind of being. The key here is the external 'psychic stimuli' that triggers this so called death-drive as well as the external factors that brings about this confluence of psychic factors. Thus to think of this as a 'desire' is to misunderstand the psychology of the situation as well as to misunderstand what is meant by desire. So no.

> I think it can by \[sic\] a person being lazy and not caring about the world. It is said to happen with prisoners of war.

One situation which demonstrates this is carceral solitary confinement with little or no meaningful contact. There has been a great deal of legal argument as to whether this constitutes torture and/or cruel and unusual punishment. For this reason International law discourages its use within penal institutions, and prohibits it entirely for juveniles whereas the US actively encourages it. Anna Conley writes:

> One of the most serious human rights violations is occurring today throughout the US. In US jails and prisons, individuals are held in solitary confinement for weeks, months and even years. Solitary confinement can cause significant psychological damage, including cognitive delays, increased suspicion and paranoia, increased anxiety, fear, aggression and hostility, heightened feelings of helplessness and depression, and increased thoughts and attempts at self-mutilation and suicide. Many individuals held in this severe form isolation are juveniles or individuals with serious mental illnesses, to whom it is particularly damaging.

> Although solitary confinement is common in the rest of the world, nowhere is it more prevalent as a long-term prisoner management tool than the US.

> US courts have found solitary confinement is a violation of the 8th Amendment of the US Constitution in certain cases, yet the practise persists.

Refs:

* Conley, A. (2013). Torture in US jails and prisons: An analysis of solitary confinement under International Law. *ICL Journal, 7*(4), 415-453. https://doi.org/10.1515/icl-2013-0402 \[Free PDF\]
* Stumpfe K. D. (1979). Der psychogene Tod des Herrn J. Ein Fallbeispiel \[The psychogenic death of Mr. J. A case report\]. *Zeitschrift fur Psychosomatische Medizin und Psychoanalyse, 25*(3), 263–273. https://pubmed.ncbi.nlm.nih.gov/494838/

# Answer
> 2 votes
Leach's hypothesis is based upon case reports of prisoners of war subject to the most severe forms of incarceration and profound deprivation. A minority of prisoners reportedly completely withdrew and ceased any form of goal directed behaviour (eating, drinking etc.). Presumably, the prisoner's 'giving up' was in response to their self-evaluation that survival was impossible in the circumstances.

Leach, J. (2018). ‘Give-up-itis’ revisited: Neuropathology of extremis. Medical hypotheses, 120, 14-21. https://doi.org/10.1016/j.mehy.2018.08.009

# Answer
> 1 votes
> It cannot happen all at once..

im not so sure this is true. according to:
*\[The psychogenic death of Mr. J. A case report\]*

psychogenic death occurs when:

> *The individual finds himself in a situation where external forces have lead to a restriction of his world and, in addition, is subjectively sensing of the inalterability of his situation. Decisive to the perception of the environment is the subjective emotional view of things which can greatly diverge reality.*

it *seems* like this process should take some time to complete, with reports ranging from anywhere between three to five days, to as long as a month.

however, according to the case of mr. j:

> *The patient suffered from a painful herniation of intervetebral disk. After the operation of the disk he still had backache. He thought that the operation had been unsuccessful.* ***The following day the patient showed the symptoms of the psychogenic death and died within one day.***

while this isnt *technically* the same as “all at once”, considering durations reported in other cases, mr. j achieved resolution relatively quickly.

one might argue this wasnt exactly an authentic case, as the definition of 'psychogenic' is: *“having a psychological origin or cause rather than a physical one”*, and the impetus for the case of mr. j was an overwhelming despair brought on by persistent physical pain causing him to believe a prior surgery was unsuccessful.

so basically, little column a, little column b.

also, the entire process may have technically taken longer than the article made it sound, since due to the fact we dont *really* have any information regarding mr. j's state of mind prior to undergoing the procedure he subsequently deemed “unsuccessful”, we have no idea when he began to *sense his world had become inalterably restricted*.

i just felt like it was an interesting observation as far as the answers to this post are concerned.

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Tags: motivation, personality-disorder, death
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# Question
Title: Is a desire for a certain food related to the nutritional need for that food?
It appears that, from time to time, everybody has a strong desire for some specific food.

I want to know whether this is the feedback of the body needing certain nutrients or whether it's purely related other influences such as emotions.

* **Q:** To what extent are such cravings influenced by current nutrient levels1 in the body?

**1**: When you're dying of thirst you'll definitely want some water. I'm rather talking about "Damn, I really want an orange." (lack of citric acid and vitamin C).

# Answer
> 5 votes
I think this question may be better asked at biology.SE. I have to cite popular science press here, but nevertheless, clearly the answer seems to be: **no.**

Scientific American:

> Peter Pressman of the Cedars Sinai Medical Center in Beverly Hills, Calif. and Roger Clemens of the University of Southern California School of Pharmacy explain. Food craving, defined as an intense desire to eat a specific foodstuff, is a common occurrence across all cultures and societies. These yearnings (...) are not linked to any obvious nutrient insufficiency.

From a more comprehensive take on this from the WSJ:

> For decades, researchers surmised that food cravings were the body's subconscious effort to correct nutritional deficiencies. Longing for steak could indicate a need for protein or iron, according to this theory. Chocoholics might be low on magnesium or other mood-altering chemicals that chocolate contains, including phenylethylamine, a compound humans produce when they're in love. But a growing body of research casts doubt on the nutritional-deficiency notion. After all, few people crave vitamin-rich green leafy vegetables and many other foods contain more phenylalanine than chocolate—including salami and cheddar cheese.

So the more cogsci.SE related questions might be about the complex cultural, affective, cognitive and neuropsychological factors (such as stress and social norms) that foster cravings for certain foods.

# Answer
> 3 votes
Short answer is YES, at least for rats, who do have chemosensors in their brain and alter their liking of salty foods and foods containing certain amino acids. See this question and question on Biology.SE:

Do humans have chemosensors for nutrients or chemicals?

Do omnivore mammals vary food preferences based on dietary needs?

# Answer
> 1 votes
Adding to the current answers, there can be many reasons for food cravings and avoidance.

Orloff & Hormes (2014) points out that the main hypotheses discussed in research receive little support, with the notable exception of a postulated role of cultural and psychosocial factors.

They also point out interesting links with eating disorders. For example, they point to research on food cravings that have been identified not only as reliable predictors of subsequent consumption of the desired food, but also as potential triggers for episodes of binge eating, especially in bulimic and overweight individuals.

Cravings during pregnancy seem to be different. While Miller (2011) points out that

> It’s a common misbelief that food cravings are a signal from the body that it’s missing some nutrient

Caitlyn Placek (2017) states that

> The onset of cravings for items not typically desired is often considered a hallmark of pregnancy. Given the ubiquity of cravings, this phenomenon remains surprisingly understudied.

Fetal nutritional needs maybe are small early in pregnancy compared to later (Tierson, et al. 1985), but nevertheless, there are specific fetal nutritional needs which are hopefully fulfilled. Anecdotally, my wife craved for lots of liver, and after birth it was found the baby had next to no thyroid gland. Severe iodine deficiency causes hypothyroidism that results in impaired somatic growth and motor development in children (Chung, 2014) and according to WebMD

> There are few foods that are as nutritionally dense as beef liver. A three-ounce serving of liver can provide 14 mcg of iodine along with the many other vitamins and nutrients it contains.

Quoting from Orloff & Hormes (previously mentioned);

> Women experience an increase in food cravings at two specific times during their life — when perimenstrual and when prenatal Orloff & Hormes, 2014\]). The prevalence of excess gestational weight gain (GWG) is a growing concern due to its association with adverse health outcomes in both mothers and children. To the extent that prenatal food cravings may be a determinant of energy intake in pregnancy, a better understanding of craving etiology could be crucial in addressing the issue of excessive GWG. This paper reviews the available literature to corroborate and/or dispute some of the most commonly accepted hypotheses regarding the causes of food cravings during pregnancy, including a role of (1) hormonal changes, (2) nutritional deficits, (3) pharmacologically active ingredients in the desired foods, and (4) cultural and psychosocial factors.
>
> \[...\]
>
> Various psychosocial factors appear to correlate with excess GWG, including the presence of restrained eating. Findings strongly suggest that more research be conducted in this area.

They also pointed out with references that the most common trajectory of food cravings across gestation shows a peak in frequency and intensity during the second trimester, followed by a subsequent decline as the pregnancy progresses to term.

> Research has also consistently documented a significant drop in cravings following delivery (Worthington-Roberts et al., 1989; Belzer et al., 2010).

## References

Belzer, L. M., Smulian, J. C., Lu, S. E., and Tepper, B. J. (2010). Food cravings and intake of sweet foods in healthy pregnancy and mild gestational diabetes mellitus. A prospective study. *Appetite 55*, 609–615. https://doi.org/10.1016/j.appet.2010.09.014

Chung, H. R. (2014). Iodine and thyroid function. *Annals of Pediatric Endocrinology and Metabolism 19*(1), 8-12. https://doi.org/10.6065/apem.2014.19.1.8

Miller, R. S. (2011). Nutritional needs during pregnancy. *Nursing made Incredibly Easy, 9*(5), 21-24. https://doi.org/10.1097/01.NME.0000403193.68168.d0

Orloff, N. C., & Hormes, J. M. (2014). Pickles and ice cream! Food cravings in pregnancy: hypotheses, preliminary evidence, and directions for future research. *Frontiers in psychology, 5*, 1076. https://doi.org/10.3389/fpsyg.2014.01076

Placek, C. (2017). A test of four evolutionary hypotheses of pregnancy food cravings: Evidence for the social bargaining model. *Royal Society open science, 4*(10), 170243. https://doi.org/10.1098/rsos.170243

Tierson, F. D., Olsen, C. L., & Hook, E. B. (1985). Influence of cravings and aversions on diet in pregnancy. *Ecology of Food and Nutrition, 17*(2), 117-129. https://doi.org/10.1080/03670244.1985.9990886

Worthington-Roberts, B., Little, R. E., Lambert, M. D., and Wu, R. (1989). Dietary cravings and aversions in the postpartum period. *Journal of the American Dietetic Association, 89*(5), 647-651. https://doi.org/10.1016/S0002-8223(21)02220-3

# Answer
> 0 votes
The answer to that question is Yes, but...

There is whole new science of psychofisics which is trying (and succeding) in makeing food more palatable... So you have combination of sugar, salt and fat which can be choosen over missing nutritiens.

Look for key words satiation, palatable, salt crawing, bliss point and psychophisics of taste in your search.

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Tags: cognitive-psychology, motivation, feeding
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# Question
Title: How do young children (toddlers) experience social pressure, such as apparent "embarrassment"?
I have a child who just turned two. When dropping them off at daycare, I said something to them in front of a small number of their peers (asked them about a song they like singing at home) which I could tell embarrassed them - they froze up, gave me a stern/mean sideways look, and went back to their activity. The teacher saw it and interpreted the look the same way I did, as embarrassment.

I would have thought a 24 month old was too young to feel embarrassed (if that is what it was), but I know my kid pretty well, I spend a lot of time with them, and I'm sure their face and body language was telling me "drop it and go away please." I've never seen that facial expression on them before.

Does research show how children might feel internally in that moment, or how complex their inner cognition is at that age? I'm not sure if toddlers can feel "embarrassment" the same way a teen/adult might, or if they didn't like feeling singled out/being the center of attention, or if they have any concept of being "juvenile" vs "cool", etc.

# Answer
Yes, toddlers do already feel embarrassment, and it appears that this feeling starts during the second year of life, following the development of self-awareness. In the past, it has for instance been investigated by studying blushing in young children.

Embarrassment is quite closely related to shyness, feeling self-conscious, and anxiety. In the case of your child, it is not strange to think they might feel put on the spot or shy about their singing. Specifically, this can be called exposure embarrassment, when a child feels put on the spot, and/or feels like they are observed by others. They can also feel like this when they are asked to perform in front of an audience, looking into a mirror while other people look at them, and when they receive many compliments. In a study on 22-month-old children, they showed overt signs of embarrassment in these situations.

The feelings of embarrassment of your child are different than those of older children and adults. The feeling of embarrassment with toddlers is much more fleeting and bound to a specific event. When children develop a theory of mind (the ability to understand and take into account another individual's mental state), this changes their shyness and embarrassment. Research shows that generally when children are around 7, they start feeling worried about how they are perceived by others, and can fear they look foolish. So in the case of your kid, it was probably just the momentary embarrassment of being put on the spot, but not because they might feel juvenile or cool.

A little later on, children also develop second-hand embarrassment, like when they feel embarrassed by their parents. This starts when children are about 9. And from my experience as an educator: no matter how cool you are, your kid will most likely be embarrassed of you at some point. I taught pupils who parents were very seen as cool people by practically everyone, and still their kids were embarrassed.

If you would like to read more about it, this chapter is an interesting read, and I could find it almost in full on Google Books

Crozier, W. R. (2010). Shyness and the development of embarrassment and the self-conscious emotions. In K. H. Rubin & R. J. Coplan (Eds.), *The development of shyness and social withdrawal.* (pp. 42-63) Guilford Press.
> 5 votes

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Tags: developmental-psychology, social-cognition
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# Question
Title: Which unit should be used to compare perceived spatial frequency of 2 different sized image? Cycle per image or cycle per degree?
I am interested in the topic of spatial frequency and its impact on face processing. I have been reading about previous studies that have used different spatial filtering thresholds for their stimuli. Some studies used frequencies below 8 cycles per image for Low Spatial Frequency (LSF) and above 32 cycles per image for High Spatial Frequency (HSF) stimuli.

However, I noticed that the size of the stimuli used in these studies varied, which could affect the degree of visual angle at which the stimuli were presented. For example, if one study used 250x250 pixel stimuli presented at 4 degrees of visual angle, and another study used 700x700 pixel stimuli presented at 12 degrees of visual angle (with the same 8 and 32 cycle per image values for LSF and HSF respectively), the cycle per degree values would be different in each study for both LSF and HSF conditions(8/4 = 2 **vs** 8/12 = 0,66 for LSF; 32/4 = 8 **vs** 32/12 = 2.66 for HSF). Does this mean that the participants in these studies perceived different spatial frequencies than those in other studies that used different stimuli sizes?

Should we scale the cycle per degree values to the total degrees of visual angle when we consider the perceived frequencies of participants and compare it with different studies? Or is there another approach that should be taken to address this issue?

# Answer
> 3 votes
It's common practice to express size and related matters, such as visual acuity measures, in terms of **angles** (minutes of arc) (Stronks & Dagnelie, 2014). E.g., grating visual acuity tests don't make sense when disregarding distance, because *any* size measure inherently changes when the distance changes to the eye, as you explain in your question. Using **angular subtense** instead of distance measures is therefore crucial (Fig. 1). Angular subtense can be expressed in minutes of arc.

The only way of directly comparing HSF and LSF stimuli with different contrasts, different sizes, and different distances (i.e., visual angles) is, hence, to look at their visual subtense, including images with spatial filters such as gratings.

Alternatively, you can project them onto a common reference, such as retinotopic coordinates and express the stimulus characteristics as distance measures occupied on the retinal surface (Stronks & Dagnelie, 2014).

**References**
**-** Paudel *et al*. *IET Optoelectron* (2013); **7**(1): 1–8
**-** Stronks & Dagnelie, *Expert Rev Med Devices* (2014); **11**(1): 23–30

source: Paudel *et al*. (2012)

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Tags: cognitive-neuroscience, experimental-psychology, vision, psychophysics, experiment-design
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# Question
Title: What are the evolutionary advantages of displaying fear?
The advice to not show fear is often given, and for good reason. Displaying fear will make one appear weaker, increase the likelihood of others attacking, and cause self-doubt to spread. However, it is peculiar that evolution has integrated not only the feeling of fear in the body, but also its outward display. In situations of fear, we not only fight against the fear itself, which(fear) is sometimes unhelpful, but also against the outward display of fear, which is always harmful.

# Answer
I'd turn the question on its head: it's not necessary that there are evolutionary advantages to *displaying* fear, it's that there are evolutionary advantages to *being afraid*, and to some extent for *detecting* fear.

Fear responses in humans are demonstrations of the fight-or-flight response. Accelerated breathing, increased muscle tension, piloerection, etc, are all part of getting ready to respond to a threat. Masking these behaviors may be beneficial, but being utterly unprepared to act can be costlier than letting someone else know you are afraid. For a predator or aggressor, knowing you are ready to fight back can be more of a deterrent than communicating that you have not detected them and are unprepared for them to strike.

At the same time, there may be social benefits to letting others know you are afraid: it's a signal to others in your social group that they should also be afraid and be prepared to react to an attack by an eagle or tiger, for example. Children need to learn from their parents what situations are dangerous.

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Debiec, J., & Olsson, A. (2017). Social fear learning: from animal models to human function. Trends in cognitive sciences, 21(7), 546-555.

Öhman, A., & Wiens, S. (2003). On the automaticity of autonomic responses in emotion: An evolutionary perspective.

Olsson, A., & Phelps, E. A. (2007). Social learning of fear. Nature neuroscience, 10(9), 1095-1102.

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*for a broader perspective on "Why didn't/did X evolve", see this Biology.SE Q&A: https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont*
> 5 votes

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Tags: neuroscience, social-psychology, evolutionary-psychology
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# Question
Title: Which function to use for fitting learning curves?
**Background**
I am fitting learning curves for cochlear implant (CI) users. These folks get a CI, and then need to start learning to understand speech again. They keep on improving for years. Along the way, speech recognition is tested frequently. The outcome measure of speech tests is a simple word or phoneme correct score. The %correct score runs from a minimum of 0%, to a maximum of 100%. No rocket science thus far.

Typically, these learning curves start at a value around 25% and end at 80% (barred the rock stars, CI users never reach 100%). In the beginning they learn quick, and this levels off as to what seems a maximum (Fig. 1).

**Question premise**
Now I seek to fit a function to these data, because I want to know how *fast* they learn. I did this using regression analysis using the least-squares method in MATLAB. The function I used I found in another software package called GraphPad Prism. While the latter package was not used to analyze the data, I did use it as an inspiration to find a proper model. The function I fitted through the data (red line in Fig. 1) GraphPad calls a 'one-phase association function'

Y = Y0 + (Plateau-Y0).(1-exp(-Kx)), which translates to Y = Y0 + (Plateau-Y0).(1-e(-Kx)) if I am not mistaken (I don't understand the fancy formula make up, hope this'll do...) (Fig. 2). The link explains the backgrounds, but in a nut shell, it is based on a biochemical process, namely the interaction between an enzyme and a substrate. My purpose is a totally different one, namely a psychophysical one to model a learning process.

I chose the 'one-phase association' function, because the main parameters in the model follow my needs very well: it has a start value Y0 that reflects the baseline score when people get their CI, and there is a maximum (Plateau). In addition, it has the K value, which in (psycho-)physics would be called tau, which describes the slope. And this slope is what we need, as we want to know how *fast* these people learn.

**Specific questions**

1. Is the 'one-phase association' a proper way to fit a learning curve? It is a function I only know from Biochemistry;
2. A colleague over in the USA used a 'logit' function for this purpose. Afaik, a logit function does not have a slope parameter and hence, from my pov, it would be less fitting for my purposes (pun not intended). Is a logit function the best way to fit a learning curve?\*

* **EDIT**: after a literature search I found that the logit function is a sigmoid function, and, hence, it does have a slope parameter

Fig. 1. Learning curve obtained in quiet at 65 dB speech level. Blue crosses: raw experimental data. Red line: fitted logarithmic function. Diamonds: derived fitting features irrelevant to the question proper. source: own work

Fig. 2. One-phase association Y=Y0 + (Plateau-Y0)*(1-exp(-K*x)). source: GraphPad

# Answer
Sigmoids are more general and probably better for modeling learning than a simple exponential. Your exponential fits decently, but it probably doesn't describe the actual underlying process very well.

Importantly, learning is often not fastest at the start, there is often some level of "aha!" moment later on. Sigmoids can capture this.

There are a variety of sigmoidal functions, but they are all differentiable and have a central peak in the first derivative. The *time to peak* and *slope at peak* are both parameters you can use to measure learning rate, though they measure somewhat different things. Which one is more applicable will depend on how learning in your paradigm varies across subjects and conditions. Looking at the data you posted, the peak slope (peak of the first derivative) is probably a decent choice, although I'm not sure you really have enough data points in the first month to get a good measure.

Exponential fits are likely to be more unstable, and in the data you've posted it looks like your fit is overfitting the beginning and end of the learning process, so you're missing the most important part for determining the actual "speed", which is between your first 3 data points; none of these are fit well. With an exponential fit, you are supposing that *the most learning occurs at the point of the first trial*. In most tasks without substantial prior instruction, you need at least a couple of trials to even figure out what is going on, and can't start to improve until then. If that first "trial" is a whole block then maybe this is not a terrible assumption, but that's mainly because you've already passed the peak slope of the sigmoidal function early on; if you used the entire data then a sigmoid would still fit better.

See also https://en.wikipedia.org/wiki/Learning\_curve and:

Culler, E., & Girden, E. (1951). The learning curve in relation to other psychometric functions. The American journal of psychology, 64(3), 327-349.

Gallistel, C. R., Fairhurst, S., & Balsam, P. (2004). The learning curve: implications of a quantitative analysis. Proceedings of the National Academy of Sciences, 101(36), 13124-13131.

Daller, M., Turlik, J., & Weir, I. (2013). Vocabulary acquisition and the learning curve. Vocabulary Knowledge: Human ratings and automated measures, 47, 185.
> 3 votes

# Answer
This equation $Y\_0 + (Y\_{max}-Y\_0)\left\[1-e^{-\kappa x}\right\]$ is simply an exponential approach, that is the solution to a first order differential equation. It is the most widespread equation in physics describing a process where the rate of change of a system is related to the state of the process. In the context of learning, it tells you that the better you are, the slower you keep improving. For that reason it is considered, as far as I know, the principled way to model learning.

As you figured out $Y\_0$ is your starting point, $Y\_{max}$ your asymptote, $\kappa$ the rate of change and $x$ your variable, usually time $t$. You'll often rather see this equation as $e^{-\frac{t}{\tau}}$, where $\tau$ is called the time constant and has the same unit as $t$ (obviously $\tau=\frac{1}{\kappa}$ and doesn't change anything about the meaning of the equation). It tells you, in the context of a resistor-capacitor circuit for example, the time it takes for the capacitor to discharge its energy through the resistor (in facts only about 1 third its energy, and is considered fully discharged after $3\tau$ because it has less than 5% its original energy remaining). So for learning this parameter has a clear meaning as well (learning time), and you can interpret it the same way people do in physics.

A logit function has a slope value as well. It is the natural way to model anything related to odd-ratios but I would argue it is not meaningful in the context of learning. If all you want is a descriptive model to compare the speed of learning it doesn't really matter what model you use as long as it fits data well. But I don't see the point of using a less principled and more complicated model when a simple exponential works.

A last point is that you could use a binomial distribution and Maximum likelihood estimation to fit your curve, instead of mean squares. It's just slightly nicer mathematically as mean squares kind of assumes that you could have a ratio correct \>100%. But that's just a detail, both techniques will give you good results.
> 1 votes

# Answer
You could use something like Desmos to rapidly try out different functions and see how well they fit the different datasets you have.

The site allows you to vary different function parameters using sliders and see how the shape changes in response.

For example, here's a plot using Demos that reproduces the shape of the curve used to fit the data in Fig 1 quite well.

The above plot and sliders can be seen here: https://www.desmos.com/calculator/w0ye3ynpia

You can imagine the various curve fitting packages as essentially varying the parameter sliders to find the curve with minimum deviation from the data points.
> 1 votes

# Answer
**Short answer**
Learning curves can be fitted well with standard psychometric curves, like the Weibull function.

**Background**
I decided to also post an answer here myself, as I've been working on the data after the answers came in. I accepted Bryan's answer as they rightfully suggested that these data should not be fitted with a simple exponential, but with a psychomteric (sigmoid) curve. I chose the Weibull and went on from there.

A general form of the psychometric curve has two horizontal asymptotes, corresponding to minimum (guess rate) and maximal performance (1-lapse rate). They are often denoted as gamma and lambda, respectively (eq. 1).

Eq. 1. General psychometric curve (Strasburger, 2001)

A generalized psychometric curve is shown in Fig. 1.  Fig. 1. Psychometric curve (Strasburger, 2001)

The Weibull function is a popular used sigmoid for psychometric fitting purposes. Its function is shown in eq. 2. Note that gamma, or lapse rate, is omitted here, but can be simply added back in the first factor.

Eq. 2. Weibull. Note that lapse rate lambda has been omitted (Strasburger, 2001)

The Weibull function has been used before for learning curves, as shown by the paper cited by Bryan above (Gallistel *et al*., 2004). The logit function in the question is a variant on the Weibull.

Now, the speed of learning (beta') can be elegantly estimated by the maximum of the first derivative, as pointed out by Bryan in the accepted answer, *i.e.*, the point where the second derivative equals zero, according to

Eq. 3. maximal slope of the Weibull function. Note that lapse rate lambda has been omitted (Strasburger, 2001)

In my specific case, I had to use a derived version because of the 2log axis in my data as pointed out above in the question.

I recommend the Strasburger (2001) paper for further details.

For comparison, I plotted the same sample data as above in the question using a Weibull fit in Fig. 2. The fit is still not great, as it has difficulty finding the lower aymptote, because of the lack of data here. This was the reason I chose the simple exponential earlier, as I was worried about this. Note that I expanded the left-hand side of the x-axis here to better show the course of the lower asymptote.

Fig. 2. Sample data with Weibull fit using the same data as in the question. source: own work

A more convincing fit is shown in Fig. 3, where the data is quite obviously a sigmoid. For this reason, a weibull fit is better. Further, (Gallistel *et al*., 2004) also successfully fitted data that lacked data points around the lower asymptote (their Figs. 1 & 7).

Fig. 3. Sample data with Weibul fit using other data than in the question. source: own work

**References**
**-** Gallistel *et al*., *PNAS* (2004); **101**(36): 13124-31
**-** Strasburger, *Percept Psychophys* (2001); **63**(8), 1348-55
> 1 votes

# Answer
The Weibull function is a much used psychometric curve, and has also appeared in the literature to model learning curves (Horsfall *et al*., 2022). The graphed Weibull function in the quoted Strassburger 2001 paper looks correct. However, Eq. 2 mentioned by AliceD above from that same paper (Eq. 5 in Strassburger's 2001 paper) seems to have the minus at the wrong position. This was likely just a typo, yet a typo of the serious kind because it changes the character of the function fundamentally. Strassburger's starting equation, 1 - exp(-exp(log(x/a)\*b)), (Eq. 2) is correct and can be simplified to
1 - exp(-(x/a)^b) while he had 1 - exp((x/a)^(-b)) (Eq. 5).

Anyway, thanks a lot for calling my attention to the paper by Strassburger, it provides a useful summary.

**References**
**-** Horsfall *et al*., *Front Surg* (2022); **9**
**-** Strasburger, *Percept Psychophys* (2001); **63**(8), 1348-55
> 1 votes

# Answer
Is your objective to model:

* the decline in incremental daily learning over time, or
* the total cumulative learning,

My feeling is that this problem is better modelled by thinking of the problem as modelling the decline in incremental daily learning over time.

There are two reasons for my assertion:

1. The decline in daily learning accords more with reality, and
2. there are far more distributions to model deline, such as: exponential, Weibull, log-normal, gamma.

My gut feel tells me that modelling the incremental with a log-normal would be a great starting point.

Said another way, I think you should be modelling the probability density function (pdf) rather than the cumulative density function (cdf). In statistics, we start by modelling the pdf. The cdf is an outcome.
> 0 votes

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Tags: learning, methodology, cognitive-modeling, psychophysics
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# Question
Title: Is general intelligence meant to underlie all intelligence?
Is general intelligence, supposedly measured by IQ, meant to underlie all intelligence, be the thing that accounts for all intelligence / ability, or does all intelligence account for general intelligence? Who claims the former, that g is more basic, and why do they claim that?

I think the question matters a little, because, if it doesn't, then IQ scores are a product of learning and teaching successes, rather than vice versa -- given that ability in any sphere \[mathematics e.g.\] is not innate.

# Answer
This is an interesting question. Before I even attempt a broad answer, I want to note that we do not have professional consensus on the details here. However, I will cite some research that you can maybe check out and see what you think.

**Is general intelligence meant to underlie all intelligence?**

To answer this, we first have to define what general intelligence is. A good working definition is the following: *g* denotes the shared variance in a set of intercorrelated cognitive tasks.

So, when you look at people's scores in a number of cognitive tasks such as arithmetic, vocabulary-based tasks, etc, you find that this performance is highly correlated. Using factor-analysis, we can load these performances onto a general intelligence factor.

We are basically claiming that this high degree of correlation is the result of some underlying factor. (Spearman, 1927; Flanagan, 2014).

Now, it's important to note here that *we can't directly test for g*. We can only test for other cognitive factors that load onto g.

**Test scores as a product of learning and not internal ability**

So, you suggested that IQ could be a result of teaching success and that's a problem. I think IQ *is* a result, at least partly, of teaching success. The IQ test isn't designed to differentiate between biological tendencies and learned abilities.

g is also not necessarily purely biological or learned, it's usually seen as an factor that combines these together. In fact, most cutting edge models suggest that both innate ability to learn and ability that is gained in life load onto g. (Flanagan, 2014).

**IQ Scores and g**

Now, IQ isn't supposed to be a measure of g. It is rather a measure of a more limited kind of intelligence that combines reasoning, working memory, and a couple other cognitive abilities. (McGill et al., 2018)

It's got its uses, though these are limited and we are probably paying too much attention to it at the moment. IQ test scores are highly sensitive to test-taking conditions, internal and external. (motivation (Duckworth et al., 2011), attention, environmental conditions, etc).

So, while there is a credible theory for general intelligence, IQ probably isn't measuring it. It probably loads onto it, so it *may* reflect some aspect of g, but it's not directly measuring our general intelligence.

**Other Theories and Literature**

So, as far as I understand it, the idea of a general intelligence is widely accepted in the literature right now. However, there are detractors, famously Gardner (1983) who proposed that there are different types of intelligence that can't be loaded onto the same one.

While there is some support for this (Visser et al., 2006), I find that the evidence is largely unconvincing at the moment. There is evidence to suggest that these "different" intelligences just load onto g, they are second-stratum. MacCann (2014) does this for emotional intelligence and there's others abound for the rest. (The exception is possibly kinaesthetic intelligence? I don't have that much research on this).

(I would be remiss if I didn't mention that Gardner himself suggests that multiple intelligences can't really be tested empirically since they are only exhibited properly in naturalistic settings. I wouldn't want to hold a position on this matter that isn't empirically supported so I can't defend him.)

***Summary***

So, long answer short.

1. There is (probably) a general intelligence factor
2. This general intelligence factors includes stuff that was learned and stuff that's biological, so it does include teaching success
3. IQ tests are not testing for the general intelligence factor, it is testing for a subset of cognitive abilities
4. In fact, we probably can't test for the general intelligence factor with a single overarching test anyway
5. I'd recommend looking into CHC intelligence models for a cutting-edge cognitive model of how intelligence works
> 2 votes

# Answer
> Is general intelligence meant to underlie all intelligence?

I don't know what you are trying to ask. Are you trying to ask if general intelligence is the basis of all other intelligence? If this is what you are indeed asking, the answer is no. Long ago, scientists thought of g, general intelligence to be a number that encapsulates the sum of all of one's different intellectual abilities. (I know. It sounds vague and doesn't sound very scientific.) I don't think they intended to mean that g was like some precursor to each type of intellectual process and thus, the best indicator of a person's intelligence.

> Is g, measured by IQ, the basis of a person's intellectual abilities or does a person's overall intelligence lead to a number, g? Who claims the former and why?

I reworded this person's question because it wasn't very clear as written. I also think the question is almost exactly the same as the first question, except the person also asks who believes in g as the basis of intelligence.

There was once a time that most scientists and other experts in the field of intelligence believed in the concept of g, a number that encapsulates all the intellectual abilities of that person into one simple score.

As it still happens frequently today, in the early 1990's, there was a remarkable discrepancy in what most scientists believed intelligence was and what popular news articles and media such as movies believed. (This is a topic for a different question but it amazes me sometimes the huge difference between what scientists believe and what the public believes. I personally don't think this vast difference just happens by accident. The information conveyed to the public is usually distorted intentionally.)

Anyway, going back. In 1994, scientists in the field of intelligence were shocked by the public's completely backward notions of what intelligence was. The media was apparently butchering what scientists were saying. As a result, some 50 leading scientists and experts in the intelligence community signed a list of statements that was published in the Wall Street Journal, expressing dismay at the media's incorrect depiction of intelligence. This public statement was titled "Mainstream Science on Intelligence". It stated facts that were widely accepted by scientists and experts in the study of intelligence. Some of these statements were:

* IQ can be measured well and IQ tests are very accurate.
* There are different types of intelligence tests but there is only one type of intelligence.
* Intelligence tests are not culturally biased.

Such outrage by the scientific community! What a shock! Why would the media intentionally distort what the real science was?

Well, all these questions became moot because something really ironic occurred. It was determined that most of the claims made by Mainstream Science on Intelligence were wrong! It's ironic but no reputable scientist or expert in intelligence *today* would ever sign that statement that they had once so confidently signed and published in the Wall Street Journal. Studies made during and after the 1990's, actually disproved most of the statements in Mainstream Science on Intelligence. Scientists did a complete 180-degree turn. The lying media turned out to be right!

What's more ironic is that there are now laypeople who believe in the statements made by Mainstream Science on Intelligence. Not scientists but laypeople who haven't been keeping up with the science. They are accepting the statements made in the Mainstream Science on Intelligence as true. They believe things like IQ is an accurate and precise measure of general intelligence, g. Or, g actually is a great indicator of how smart a person generally is. Funny, no?

Anyway, the original question had asked **who** claims that general intelligence underlies all intelligence. I don't think anyone believes this. I never heard of anyone who believes that there are some group of genes (aka g) that has an effect on all our intellectual abilities and is the factor that mainly accounts for a person's intelligence. Next question...

> I think the question matters a little, because, if it doesn't, then IQ scores are a product of learning and teaching successes, rather than vice versa -- given that ability in any sphere \[mathematics e.g.\] is not innate.

I didn't understand this question. How did you logically conclude "IQ scores \[are\] a product of learning and teaching successes" since "IQ scores \[are\] incorrect representation of intelligence"? It happens to be true but how did you conclude that from anything you said before or after? And, what do you mean by vice-versa? It doesn't make sense.

To set the record straight, there is no such thing as a g that represents the general intelligence of a person. Just because you are good at one thing, it's been determined that you might not be necessarily good at other intellectual pursuits. I strongly believe this to be true. Research has proven it. And, you personally see instances of this in real life.

Let me also state that an IQ test is also a very inaccurate method to measure intelligence, especially at the tail-end of the distribution on the right side. Furthermore, please keep in mind that the scientific field of intelligence is actually still in its infancy. Many basic concepts are still unproven to be true or not. We are still learning about ourselves. Current studies include determining what types of events appear in what part of the brain. It's all so very new.
> -2 votes

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Tags: intelligence
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# Question
Title: Does this recent twin study contradict Anders Erricson's view on the hereditary basis of talent?
The Swedish Psychologist K. Anders Ericsson has published many reports stating that talent is "made and not born". In his book 'The Cambridge Handbook of Expertise and Expert Performance', he has stated that "Consistently and overwhelmingly, the evidence showed that experts are always made, not born."

On the other hand, a recent twin study has stated that on average, a human's ability is 50% influenced by genetic factors, and 50% influenced by environmental factors. This seems to contradict Ericsson's experiment, as he has asserted that genetic factors influence a person's abilities by less than 1%.

Does the twin study contradict Ericsson's assertions, and if so, why would there be such a large contradiction? What factors could have caused these large differences in findings?

# Answer
While both Ericsson's work and the twin study feed into the nature-nurture debate, the twin study **does not** contradict Ericsson's assertions.

The misconception is in the following quote:

> a recent twin study has stated that on average, a human's ability is 50% influenced by genetic factors, and 50% influenced by environmental factors. This seems to contradict Ericsson's experiment, as he has asserted that genetic factors influence a person's abilities by less than 1%.

The results from Polderman et al. (2015) and the assertions made by Ericsson are not this simple. Polderman et al. (2015) is a massive meta-analysis that looked at 28 general domains of performance, including things as broad as "psychiatric" and "cognitive". They analysed close to 3000 studies to do this.

Ericsson's claims on the other hand are specifically about expert ability. This means that his assertions are limited to specific domains of performance, such as expert musical ability, which the twin study does not look at. His assertions are also limited to studies that actually have experts in them. The vast majority of twin studies in the meta-analysis do not have experts involved in them.

Ericsson and Harwell (2019) discusses objections based on studies like Polderman et al. (2015) in a section of the paper titled, "Inferring Genetic Limits for the Effects of Practice on Attained Performance".

In addition, the ACE model the meta-analysis uses has limited power when talking about gene x environment interactions. This is important because Ericsson's models often incorporate the idea that genetic factors exist but are less important than practise for experts. This is less important than the points mentioned above, but still relevant when critically evaluating the paper.

Thus, the twin study only shows that for most people, if we look broadly at general abilities, they can be explained (nearly 50%) by heritable genetic factors. However, Ericsson claims that for experts, if we look at domain-specific abilities, they are best explained by practice and not genetic factors. They are talking about slightly different things and thus one does not contradict the other.
> 2 votes

# Answer
Ericsson’s studies have repeatedly ignored the genetics of performance in any field. His favourite study of expert performance - the London taxi driver experiment \- also failed to control for prior genetic attributes that may have led these taxi drivers into their professions in the first place. A good place to start perhaps

## Reference

Macnamara, B. N., Hambrick, D. Z., & Oswald, F. L. (2014). Deliberate practice and performance in music, games, sports, education, and professions: A meta-analysis. *Psychological science, 25*(8), 1608-1618. https://doi.org/10.1177/0956797614535810
> -1 votes

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Tags: cognitive-psychology, validation, cognitive-development, twin-study
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# Question
Title: What is the link between descriptive norm & informational social influence? When the descriptive norm doesn't appear to be "correct"?
I'm a first-year psychology student and this week I'm learning (from a crappy lecturer) about social norms, specifically injunctive vs descriptive norms, and normative vs informational social influence.

I came across the following excerpt from my textbook:

> People conform to injunctive norms to gain social approval or to avoid social sanctions. \[...\] Conforming to descriptive norms typically has a different motivation, namely the desire to be correct. In many instances, following the group will lead to a correct outcome. For example,×following the crowd after arriving by train to an unfamiliar station will likely lead you to the exit. Deutsch and Gerard (1955) termed this type of motivation informational social influence.
> (Steg, L., Berg, A., & de Groot, J. (2019). Environmental psychology - An Introduction (2nd ed.). BPS Blackwell.)

My question is, what if the group action is obviously wrong from the start? For instance, smoking, littering, or vandalism. Is the descriptive norm in this case still motivated by *informational* social influence? Or is the association between these two concepts not always applicable?

# Answer
> 1 votes
In theory, a descriptive norm influences an individual by changing the individual's judgement of *what* is right. It is based on the idea that individuals use information from groups to make judgements about reality itself. (Deutsch and Gerard, 1955)

One way of conceptualising this in the train situation is social proof. You follow the people around you (i.e. are informationally influenced by them) because their actions are evidence supporting movement in a specific direction. You are assuming that members of the group know something you don't and are therefore following them. (Cialdini 1983)

**Informational Influence on Smoking**

If there was informational influence based on smoking, littering, vandalism, etc, then the action would stop being "obviously wrong". The informational influence would change the beliefs of the person who is being influenced, they would have to genuinely stop believing that smoking was "wrong".

So, for example, if I believed that smoking was bad because it caused cancer. Then, I hung out with people who smoked a lot, and I changed by beliefs to something like, "Oh, smoking can't be causing cancer. These people wouldn't smoke if it caused cancer", then that would be informational influence.

**Spreading Disorder and Broken Windows**

Now, what you might be getting at here is the somewhat debated "spreading disorder theory". This is a theory about the normative influence of littering and vandalism that combines descriptive and injunctive norms. (Keizer et al., 2008)

This model suggests the following mechanism:

1. People don't engage in things like vandalism and littering because they are "wrong".
2. People think vandalism and littering are "wrong" because there are injunctive norms against them. E.g. littering is convenient, but people are afraid of the social punishment that they might face if they littered, so they refrain from littering.
3. When people see an environment with littering, they are informationally influenced and their judgement of the existing social pressures changes. Essentially, where they previously believed "Littering leads to social punishment", now they believe "Littering does not lead to social punishment".
4. This leads to a weakening or disappearance of injunctive norms in general. So, "Littering does not lead to social punishment" is accompanied by the belief that, "There are fewer social punishments in this environment" (I.e. I can violate injunctive norms here OR there are fewer injunctive norms here).
5. So, individuals are more likely to violate injunctive norms against littering and vandalism because they judge injunctive norms to be weaker/less present in their environment.

This is similar to Broken Windows Theory (Kelling and Wilson, 1982), which is also worth looking into and will have similar implications for your question.

So, in this model, there is an informational influence from littering, but it's indirect. It influences judgements of descriptive norms which then, in turn, influences behaviour.

**An Empirical Note**

Now, the studies I have cited will have some experimental evidence, but it's important to note that this is a somewhat debated area of social psychology. There are criticisms of these models, both on specific points of design and more broadly about conclusions. O'Brien et al. (2019) published an interesting meta-analysis that discusses some of this and might be a good starting point for empirical considerations.

So, the answer to your question is:

1. If the group is "obviously wrong", there can't be direct informational influence unless it changes the individuals' belief about whether the group *is wrong*.
2. There are models that suggest an indirect informational influence with things like littering. Here, the informational influence erodes the normative influence that would otherwise prevent things like vandalism and littering.
3. The empirical evidence for this model is still somewhat debated.

# Answer
> 0 votes
You are correct in linking descriptive norms to informational influence. Whereas subjective norms, and injuctive norms are linked to normative influence. Put simply this is following the group so they will like you, as opposed to following the group because you think they are right (have more information than you).

It seems a better example that is akin to following a group to an exit in a train station, is if you followed the group and you were led the wrong way. To answer your question, yes the association is still motivated by informational social influence.

Smoking is related to normative social influence, rather than informational social influence, if you are curious about social group influence, such as peer pressure. Vandalism seems to be more related to the individual, than social influence.

There is some grey area here, if you consider other approaches to group psychology such as LeBon's contagion theory. This approach commonly highlights the spread of extreme ideas in groups.

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Tags: social-psychology, motivation, norms
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title: Network Architecture Diagram

text:
# Question
Title: Network Architecture Diagram
I am trying to teach myself some computational neuroscience and am reading through the following textbook: https://www.oxcns.org/b6\_text.html.

I'm finding this diagram confusing in particular c). My understanding is that the vertical bar is the cell membrane and the perpendicular connections to it are the connecting axon/synapse. This makes it look like the cell membrane has a connection coming out of it and connecting back to it. This can't be right, or is it?

# Answer
From Wikipedia submitted by Fabuio here's a tracing of a pyramidal neuron, a type found in neocortex:

Red is a tracing of the dendrites of the cell, blue is the axon. Generally, cells get input on their dendrites and send outputs via the axon.

The "cell membrane" isn't really shown here or in your diagram, but each of these lines represents a roughly cylindrical structure where the outside is comprised of a ring of membrane with the inside of the cell in the center.

Your network diagrams have simplified the "red" input-receiving part to be just a single vertical line, yes. The architecture in (c) includes self-connections, yes: it depicts 4 "cells" that receive external input and input from themselves and each of the other 3 cells, and additionally have output going someplace else. Words used for this type of self-connection include "autapse" for the physical connection, and "recurrent" for the cyclical pattern, though recurrent connections need not be direct (e.g., A to B to C to A is also a recurrent pathway from the perspective of A).

I don't know why the author used a different diagram structure for these pseudo-pyramidal in panels a-d; perhaps it's because they originate in different sources, but the "open triangle with an upward stick" in (a), "closed triangle with upward stick" in (b), and "almost a triangle with a fat stick" in (c) and (d) are all representing the same thing, the important differences in the different architectures only involve what is connected to what.
> 0 votes

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Tags: neuroscience, cognitive-neuroscience, theoretical-neuroscience
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# Question
Title: What are good resources to learn about the mechanisms of motivation
Thanks for taking the effort to read this post! As not being a psychologist or neuroscientist, but an engineer I want to study the mechanisms of (human) motivation. The goal is to be more able to identify what the drivers of motivation are of myself and other people in order to be more effective and better able to understand the actions of other people.

The best source would probably a book, ideally a source that starts with first principles. In terms of difficulty I would prefer a book not much more challenging than "Thinking Fast and Slow", since I am not well trained in processing literature in this field. However, if there is a possible very good but difficult source, I'm up for a challenge.

Some personal situations that made me question motivation mechanisms

* Why I sometimes have no motivation to do the dishes and sometimes is goes easy while the task stayed constant.
* Why my motivation is not impacted to go for a run when it's raining, but it severly is when I need to buy groceries

Question:

* What are usefull authors/titles to study the mechanisms of (human) motivation?

# Answer
Mihaly Csikszentmihalyi is considered to be the father of the field of Positive Psychology, and introduced the notion of "Flow" when studying happiness and motivation.

While Mihaly focused on studying happiness, the concept of flow is highly related to motivation, and how to reach it. I was about to copy paste some excerpts from the Wikipedia page about Flow, but you better read it directly from the source: it is very well explained there!

Mihaly's 1990 book Flow: The Psychology of Optimal Experience is quite well written and accessible to non professionals. \[Note that I did not find his TED talk very representative of his work, should you be thinking about watching it instead of reading the book.\]

Hope it helps!
> 1 votes

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Tags: motivation
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# Question
Title: Why are there receptors inside neural cells?
Reading a recent article which argues on why psychedelic substances are more effective than the naturally occurring neurotransmitters in the brain:

*Breakthrough study discovers that psychedelics breach our neurons

Now, I am just an undergrad researcher in chemistry so my knowledge is rather limited in drug design. Yet this has sparked my curiosity. I had never heard of receptors being located solely inskde a neuronal cell. This makes me ponder and is my question, what role do they traditionally serve ignoring this specific case? Why are they inside if the role of receptors is communication between cells?

# Answer
> Why are they inside if the role of receptors is communication between cells?

'Receptors' are ubiquitous in biology and not just for communication between cells: they carry signals within cells, too.

Additionally, even for communication between cells, receptors don't need to be outside the cell, because some molecules like steroid hormones freely cross membranes. In that case, the reason the receptors are inside the cells is so that they are located where they are going to have their effects on transcription.

Also remember that biology isn't necessarily "designed for" exogenous ligands that might be presented: just because there is a receptor that some drug binds to doesn't mean the thing binding is the thing that is "supposed to" bind.

I'm not aware of a known signaling role for intracellular 5HT2a receptors *specifically within mammalian neurons*; they are also found in other species and other cell types. Certainly it's common for receptors (including 5HT2a) to be trafficked between the cell membrane and internal membranes as an important regulatory mechanism, so that's another reason you'd find them inside cells. Internalization can be caused by both agonist and antagonist binding (Raote et al 2007).

---

Raote, I., Bhattacharya, A., & Panicker, M. M. (2007). Serotonin 2A (5-HT2A) receptor function: ligand-dependent mechanisms and pathways. Serotonin receptors in neurobiology, 105-132.
> 5 votes

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Tags: neuroscience, neurophysiology, neuroanatomy
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# Question
Title: are there any critiques of the concept of "minimisation" in offender treatment?
Minimisation is when an offender believes their punishment is or was disproportionate. this is often said to be a counterproductive mentality because it lessens the responsibility from offenders. is this really true ? and does minimisation always lead to counterproductive outcomes and increased risk of re offending ?

## Resource:

Marshall, W. L. (1994). Treatment effects on denial and minimization in incarcerated sex offenders. *Behaviour Research and Therapy, 32*(5), 559-564. https://doi.org/10.1016/0005-7967(94)90145-7

## Abstract

> Although much has been written about the fact that many sex offenders either deny they committed an offense or minimize their offense in some way (Murphy, 1990), very little research has focused on changing these stances despite the fact that treatment of other issues cannot proceed until denial is overcome and minimization has at least been significantly changed. Two studies have described the nature of excuses provided by sex offenders (Pollack & Hashmall, 1991; Scuily & Marolla, I984), and it is clear that these excuses represent a form of minimization, generally by shifting responsibility to factors or persons outside the offender. However, in these studies no suggestions were offered about how to eliminate such justifications.
>
> Murphy (1990) outlined several approaches to the modification of the more general category of cognitive distortions and some of these procedures seem relevant to dealing effectively with denial and minimization. The only study, however, which has specifically targeted these problems, is reported by Barbaree (1991). Barbaree found that among 26 incarcerated rapists, 54% denied they had committed an offense and a further 42% minimized either their responsibility for the offense, or the harm they had done or the extent of their offending (frequency, forcefulness or degree of sexual intrusiveness). Barbaree’s incarcerated child molesters showed similar patterns (66% denied and 33% minimized). Treatment reduced the number of deniers who remained in therapy for the full program, from 22 to 3, but 15 of those deniers who admitted to having offended, were still minimizing at the end of treatment. Of the 15 who initially admitted but minimized their offense(s), only 3 gave up all evidence of minimizing as a result of treatment.
>
> Overall, these results are impressive, although the number of offenders who continued to minimize is perhaps less encouraging. However, Barbaree did provide pre- and post-treatment evaluations using the Multiphasic Sex Inventory (Nichols & Molinder, 1984), which gives some indication of the degree of change in minimizing, albeit indirectly. He found significant reductions on 5 of the 6 subscales of the MS1 with the most salient being reductions in Justifications. So although many of Barbaree’s treated offenders continued to minimize, it may be that their degree of minimization was reduced.
>
> Many clinicians, unfortunately, take the simple course of excluding deniers from their treatment programs, while others accept only those who are said to be motivated to change. In the latter cases, it is quite probable that most who are judged to be poorly motivated are also either denying or minimi~ng their offending. Excluding such potential patients seems likely to markedly reduce the number of sex offenders eligible for treatment and may very well eliminate from treatment some of the most dangerous offenders. In our treatment programs (Marshall, 1973; Marshall & Barbaree, 1988; Marshall, Eccles & Barbaree, 1991; Marshall & McKnight, 1975; Marshall & Williams, 1975) we have never refused treatment to deniers, because we expect most sex offenders to initially deny or minimize their ofIenses and because we assume it is our responsibility to facilitate their full admissions. The present report represents our first attempt to both describe our procedures for overcoming denial and reducing or eliminating minimization, and to report the effectiveness of these procedures.

# Answer
> 1 votes
#### Yes

Diederik F. Janssen, MD, in his article "Paraphilia": Acultural or Anti-Anthropological? \[Sexual Offender Treatment, Volume 9 (2014), Issue 2\], made an argument that cognitive distortions in general (not just minimization) as it relates to persons convicted of sexual offenses may represent cultural conflicts rather than psychopathology.

> There have long been calls for culture-sensitive approaches in sex offender treatment (S.O.T.) literature (e.g. Lewis, 1999). This relates in the first instance to the most basic of legal and medical definitions. Authoritative definitions of "sexual abuse" adapted at the WHO level are dubiously drafted to include all sexual liaisons that can be said to "violate the laws or social taboos of society" (WHO, 1999, p. 15). The International Association for the Treatment of Sexual Offenders takes note of "great discrepancy throughout the world as to what constitutes a sexual offense"...(Coleman et al., 2000, pp. 13-14).
>
> Yet it is easy to find contemporary S.O.T. handbooks that have little to say about the dimension of culture beyond single-sentence complaints that available literature is "almost exclusively focused on mainstream western societies" (Jackie Craissati, in Beech, Craig & Browne, eds., 2009, p. 14)....
>
> How notions of culture are factored in or out of this scene of expert knowledge-making thus itself makes for a central anthropological question. Thinking about culture happens to touch upon basic elements of the post-DSM-III conceptual toolkit of S.O.T. A seminal paper on "cognitive distortions" in child sex offenders argued that if an account of such offences does not honor "accepted standards" obtaining in their society, it is "simply a cognitive distortion" (Abel et al., 1984, p. 100). In many subsequent psychometric approaches to such alleged distortions, references to "other cultures" in forensic contexts are specifically labeled instances of exculpatory "rationalizations" or as pillars of dysfunctional "implicit theories"....
>
> This frank but arguable equation between cultural "sync" and fact seems used to cut short and medicialize any contextualizing frame for sex offences that might be construed as contrary to S.O.T. objectives. Ethnographic observation here shrivels into "excuse": it becomes a symptom of the "disorder" said to "underlie" offenders’ deviation from culturally accepted truisms (for a critical review see Janssen, 2012).

What he is referring to here are "accounts" of crimes, given by convicted offenders, that perceive the underlying behavior in ways that the treating clinicians consider to be wrong (e.g. minimized). For example, if a person from a culture in which non-consensual sexual touching is considered either acceptable or only a petty offense travels to the West and gets caught committing such behaviors, they are *naturally* likely to perceive what they did as no big deal and the punishment inflicted to be grossly over-severe.

For a reversed example that might be easy to relate to, Western countries generally consider Blasphemy to either be not an offense or only a minor one, while some countries elsewhere in the world consider it not only a major felony but potentially a capital one. A non-believing person from a Western country who gets caught up in a foreign criminal justice system for expressing their frustration by blaspheming a local deity is likely to see what is happening to them as grossly unfair. Criminal justice officials from that foreign society, however, are likely to see these expressions as minimizations of what they perceive as gross transgressions against natural order and thus see the offender as psychopathological and in need of treatment.

### Resource:

> Janssen, D. F. (2014). "Paraphilia": Acultural or Anti-Anthropological?. Sexual Offender Treatment, 9(2).

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Tags: social-psychology, criminology
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# Question
Title: What's the difference between simultanagnosia and neurological extinction?
Both of these terms describe the inability to perceive more than one object at a time. I'm not too sure what the big difference is between them. Note that I'm referring to 'extinction' as used in *neurology* (wiki article), and not as used in *psychology*.

# Answer
In *extinction* the patient may be able to get attention to an object in the contralesional field if it is the only salient object. If there is a competition from another object the patient won't draw attention toward the contralesional field (opposite side of the lesion; generally right parietal lobe).

*Simultagnosia* is described as the inability to perceive more than one object at a time in each visual field. It is consequence of bilateral damage to the parietal lobe

**References**

E. Bruce Goldstein-Sensation and Perception-Wadsworth (2010)
> 1 votes

# Answer
extinction is when two stimuli are presented at once and the patient only identifies one of them but is able to identify each by itself. in simultaneous agnosia, the patient can't voluntarily switch between two stimuli and everything other than the one stimulus the patient focuses, on is "dark".
> -1 votes

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Tags: cognitive-neuroscience, terminology
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# Question
Title: Is digital notetaking a variation of hoarding disorder?
In recent years, note taking apps such as ever note, obsidian, and such have gained immense popularties. It has become a passion of many people to create the maximum number of notes, organize and interconnect them to the maximum degree.

However, if one looks at this from an outside prespective, then it seems as a form of hoarding. I had before asked this question on reddit with some help input, but I didn't feel I got a satisfactory input.

What does the science say?

related

# Answer
> 3 votes
> It has become a passion of many people to create the maximum number of notes, organize and interconnect them to the maximum degree.

Apart from the beginning, there is a key area within the NHS link you provided.

At the beginning, it states that:

> A hoarding disorder is where someone acquires an excessive number of items and stores them **in a chaotic manner, usually resulting in unmanageable amounts of clutter**.

You said the notes are arranged and interconnected.

The NHS page also says:

> ## What's the difference between hoarding and collecting?
>
> Many people collect items such as books or stamps, and this is not considered a problem. The difference between a "hoard" and a "collection" is how these items are organised.
>
> A collection is usually well ordered, and the items are easily accessible. A hoard is usually very disorganised, takes up a lot of room and the items are largely inaccessible.
>
> For example, someone who collects newspaper reviews may cut out the reviews they want and organise them in a catalogue or scrapbook. Someone who hoards may keep large stacks of newspapers that clutter their entire house and mean it's not actually possible to read any of the reviews they wanted to keep.

What you have described is a collection of notes, organised and linked up as much as possible. That is not hoarding as described by the NHS.

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Tags: cognitive-psychology
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# Question
Title: How to calculate absolute power for EEG from power spectra density?
For example, I have power spectrum density calculated by pwelch

```
f = EEG.data;
f = f(2, :);
N = EEG.pnts;
Fs = EEG.srate;
NFFT = 2^nextpow2(N);
NOVERLAP = 0;
WINDOW = 512;
[spectra, freqs] = pwelch(x, WINDOW, NOVERLAP, NFFT,Fs);
deltaIdx = find(freqs>1 & freqs<4);
deltaPower = mean(spectra(deltaIdx));

```

The code comes from EEGLab, and can be found here: https://sccn.ucsd.edu/pipermail/eeglablist/2014/008043.html

How should I calculate absolute power from it? What's the relationship between absolute power and power spectrum density?

# Answer
I had to do some searching to be able to answer this question. As a matter of fact, a similar questions was once asked on Signal Processing.

To make the explanation more laymen-like, I think the answer means the following:

With pwelch or an FFT analysis you can calculate the amplitude of sinusoids with particular frequencies (see this answer ). These amplitudes squared, result in the absolute power within these specific frequencies. The resulting power per frequency is the power spectral density (PSD). In neuroscience, people do not often work with individual frequencies but work with frequency bands, such as the alpha band (8-14 Hz). This can be calculated by taking the average or the integral.

The absolute power (W), you referred to, is the power of the entire signal. It thus does not make a distinction between the different frequencies. This can be calculated, by summing the power of each frequency (i.e. taking the integral of the signal). By summing, you have the total amount of power within the signal. The absolute power can be used to normalize the PSD, by dividing the PSD by the absolute power (as described in the answer on Signal Processing).

**Average vs integral**

It seems that it is possible to calculate either the average or the integral of a frequency band. But when would you take the integral and when would you take the average? The average is an easy way of calculating how high the power is in a specific frequency band. This way, it does not matter how large the range of a frequency band is. The alpha band average will not be more inflated then the delta band (0-4 Hz) because of a bigger range.

When you take the integral there will exist differences that are affected by the size of the frequency band, because you do not divide the sum by the amount of samples (i.e frequencies). However, it does allow you to normalize the PSD with the absolute power. Say, the integral of the alpha band results in `2W`, the integral of the delta band results in `1W`, and the absolute power of the entire spectrum equals `10W`. Then we know that the alpha band plays a 20% part and the delta band a 10% part in the total signal. With mere averaging, this would not be possible because we 'neglect' the size of the range.

I think it depends on what exactly you are after. I haven't work with the absolute power and am not familiar with it's user. Perhaps it has something to do with comparisons between exp. conditions (within frequency-bands, i.e. alpha vs alpha) or within exp. conditions (between frequency bands). *If an actual expert could elaborate on why one method is beneficial over the other, that would be great.*
> 4 votes

# Answer
I found this article very helpful https://raphaelvallat.com/bandpower.html, there are some good graphs for visual.

I am trying to learn this content myself, but my understanding is that pwelch outputs power *density* \[units^2/Hz\] then you can calculate an area under that power density plot (integrate) to get just power \[units^2\] aka absolute power.
(area = PSD\[units^2/Hz\]\*Freq\[Hz\] = Power\[units^2\]).
For example, integrate from 1-4Hz to get delta power. (there is a visual of this in the link above).

The last line of your code (deltaPower = mean(spectra(deltaIdx));) calculates the average of the power spectral *densities* within the defined range.

I believe when people say "band power" they are referring to the absolute power (integral of the PSD) across one of the bands (delta, theta, etc). I'm not sure if the PSD alone is commonly used with EEG, but I can't say.

Alternatively, pwelch has an input option spectrumtype='power' and it should output straight to power instead of PSD. (haven't tried it yet). Then I imagine you just sum the powers within your desired range.

Alternatively alternatively, you could also just do fft()^2 to get \[units^2\] which is power. I'm not sure the difference between that vs integrating a PSD. Just offering up ideas. Would also like an expert input!
> 1 votes

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Tags: methodology, eeg, analysis
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# Question
Title: Why is the same process responsible for both synaptic strengthening and excitotoxicity?
Here are two quotes from Wikipedia with their respective pages.

Synaptic Plasticity "Two molecular mechanisms for synaptic plasticity involve the NMDA and AMPA glutamate receptors. **Opening of NMDA channels (which relates to the level of cellular depolarization) leads to a rise in post-synaptic Ca2+ concentration and this has been linked to long-term potentiation, LTP** (as well as to protein kinase activation); strong depolarization of the post-synaptic cell completely displaces the magnesium ions that block NMDA ion channels and allows calcium ions to enter a cell – probably causing LTP, while weaker depolarization only partially displaces the Mg2+ ions, resulting in less Ca2+ entering the post-synaptic neuron and lower intracellular Ca2+ concentrations (which activate protein phosphatases and induce long-term depression, LTD)."

Excitotoxicity "For example, when glutamate receptors such as the **NMDA receptor or AMPA receptor encounter excessive levels of the excitatory neurotransmitter, glutamate, significant neuronal damage might ensue. Excess glutamate allows high levels of calcium ions (Ca2+) to enter the cell.** Ca2+ influx into cells activates a number of enzymes, including phospholipases, endonucleases, and proteases such as calpain. These enzymes go on to damage cell structures such as components of the cytoskeleton, membrane, and DNA."

This implies that the same process responsible for strengthening synapses can also lead to cell death, but it's unclear to me what mechanism mitigates this or even whether they're directly related. Is the quanta of neurotransmitter in the presynaptic vesicles increased at an exponentially smaller rate as it strengthens, making it exceedingly unlikely that it would lead to excitotoxicity? If so, is excitotoxicity at such sites triggered due to some unrelated malfunction, such as a nearby cell "leaking" neurotransmitter into the extracellular space? Are normally functioning cells capable of undergoing excitotoxicity solely due to synaptic strengthening via LTP?

# Answer
You may have heard the adage the dose makes the poison. Excitotoxicity is generally not a *good* thing or something that cells are built to do intentionally, it's a consequence of a malfunction. It's a bit like asking the question "why is speed both responsible for getting a car where it's going and also for leading to damage when a car strikes another object?" The whole reason the car is at threat for the latter is that the former is necessary for its purpose; if cars didn't need to move to be useful, they'd have lower risk of crashing. If neurons didn't need to communicate and change to be useful, they wouldn't experience excitotoxicity.

Calcium is the key player here: calcium is an important signaling molecule in cells. Time and intensity are both important for calcium: you can read on the synaptic plasticity Wikipedia page how calcium is involved in both long-term potentiation (strengthening synapses) and long-term depression (weakening synapses). In both cases it's driven by a calcium *increase*. The rough signaling logic is no calcium change = no synaptic change, small but long-lasting calcium change = synaptic depression, large and brief calcium change = synaptic potentiation.

Calcium is involved in lots of other processes in cells, too, and through ordinary neurotransmission these processes either aren't activated (perhaps because they're far from the synapses) or are affected weakly; with excitotoxicity, calcium is a bit out of control.

Excitotoxicity occurs in extreme circumstances, like seizures (where the balance between excitation and inhibition is off in some way) or stroke (where there isn't energy available to keep up with ion concentration gradients. There is no healthy situation that would lead to excitotoxicity, there must be some pathology.
> 2 votes

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Tags: neuroscience, plasticity
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# Question
Title: Where exactly do Emotions and Feelings arise in the human body?
Traditionally, the heart region was always associated with emotions and feelings in humans. But in one recent philosophy lecture I watched on Youtube, the orator said that the right brain is, in fact, the origin of emotions and the heart is just for pumping the blood.

In Yoga and many other traditional Eastern disciplines, the Chakra Theory is quite prevalent and the *Anahata* or the Heart chakra/meridian is quite strongly associated with emotions.

What is the stance of modern medical science on this? Can the source of all emotions be explained completely in the right hemisphere of the brain through neuroscience? Or is there any scientific backing for the linkage of Heart to emotions? Or such a discovery might be possible in future?

# Answer
> 5 votes
As far as we know, all the "thinking parts" are in the brain/central nervous system. That includes emotions and feelings, which are labels for certain cognitive experiences. Definitely not the "right brain", though, that's some foolishness that seems to persist in pop science without any evidence. I wouldn't recommend learning about the brain from someone who repeats those myths.

Brain Right hemisphere is random and left hemisphere is linear? really?

About the left and right side of the brain

The closest thing to what you mention about the heart in modern psychology or neuroscience would be the somatic marker hypothesis which suggests there is a two-way interaction between brain and body for emotional experiences. For example, the brain causes an increased heart rate (among other things) when presented with threatening stimuli, and part of the experience of the emotion of anxiety includes feeling that faster heart rate. It isn't that the emotion is *generated in* the heart, though, it's still an emotion in the brain, but what leads to experiences of emotion can include influences of the body.

# Answer
> 1 votes
The part of the nervous systems that is associated with emotions, is the limbic system.
Via the amygdala, a little almond shaped part of your brain, this part of the nervous system can interact with the autonomous nervous system, which controls parasympathic as well as sympathic reactions. This affects heart rate as well as digestion.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917081/

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Tags: emotion, brain, neurology
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# Question
Title: Is there any recent review of the book "Scripts, Plans, Goals, and Understanding: An Inquiry Into Human Knowledge Structures"?
My advisor asked me to read this book. However, I wonder if there is some recent review of the book that integrates AI and cognitive findings in recent years. Just want to know if there's any view in the book that is outdated.

Thanks a lot!

# Answer
That's not really how scientific publishing works; people don't typically "review" old books.

They do cite them, though. You can search for a book or paper on Google Scholar and click the "cited by" link to see all the work that has cited that book. From there, you can see how different sources are using it: are there specific theories or conclusions that are referenced? Are they mostly criticizing it as outdated? Do they cite other, newer work alongside it that you might also read?

You can also search *within* the cited work; adding "review" to your search might find you recent reviews that have cited this book among others; you shouldn't expect any of them to cover that specific source in depth, but they might cover a similar topic (or they could be in an adjacent area).

All of this can be quite the undertaking, though that's what research is, so it would be helpful to start with some idea of what you're looking for. That might come from paging through the original book or from starting with considering why your advisor recommended this book.
> 2 votes

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Tags: cognitive-modeling, artificial-intelligence
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# Question
Title: How mental illness episode are taken into account in personality psychology?
**Issue:** Personality psychology investigates personality: its components, how it relates to life outcomes (job performance, income, longetivity, etc.), and also how personality evolves during life (the life-span, or some periods such as adolescence, or adulthood, etc.).

Personality psychology has found that some personality traits predict mental health outcomes: having high levels of neuroticism make people at higher risk of developing mental illness (anxiety disorder, depression, etc.) (Lahey, 2009).

Clinical psychology, on the other hand, has found that mental disorders are associated with behavioral changes. Depression can make people withdrawn socially, make them irritable, or abuse substances. Therefore, mental illness episodes can alter people's personality.

**Question:** For the study of personality evolution/development, how *long-term* (for months or for years, like 5 years of 10 years\*) mental illness episodes are taken into account in personality psychology? Are there some researchers in particular who took into account the appearance and disappearance of mental illness when studying personality change, and how is it done?

Below as examples, two actual research items on personality change by very influential personality psychology researchers, where there is no mention of mental illness:

Bleidorn, W., Hopwood, C. J., Back, M. D., Denissen, J. J., Hennecke, M., Hill, P. L., ... & Zimmermann, J. (2021). Personality trait stability and change. *Personality Science*, 2, 1-20. https://doi.org/10.5964/ps.6009 \[PDF\]

McAdams, D. P., & Olson, B. D. (2010). Personality development: Continuity and change over the life course. *Annual review of psychology*, 61, 517-542. https://doi.org/10.1146/annurev.psych.093008.100507 \[PDF\]

**Further illustration:** If a person became, say, more impulsive, withdrawn, immoderate (uncontrolled consumption of alcohol) as a result of suffering from a depression, this change in behavior will be simply attributed as **a change of personality**, rather than interpreted as **the experience of a mental illness episode**.

Conversingly, the personality change resulting for the curing of the depression (better sociability, better emotion regulation, lower immoderation, etc.) will again be simply attributed as a change of personality.

\*Although I have more in mind disorders such as depression or anxiety here, I recall a recent news reporting where people had been misdiagnosed for autism spectrum for 30 to 50 years.

**References:**

Lahey, B. B. (2009). Public health significance of neuroticism. *American Psychologist*, 64(4), 241. https://doi.org/10.1037/a0015309 \[PDF\]

# Answer
> 1 votes
The papers you cited points to potential motives and reasons for change in personality; and also looks at potentials within the genes vs environment debate within the whole field of psychology.

Personality refers to the **enduring** characteristics and behaviour (APA, n.d.). Mental health issues may spark differing behaviours such as impulsiveness, aggressiveness, timidity etc. but these behaviour changes typically change back to the regular behaviour patterns determined by the person's actual personality.

Findings from Shea, et al. (1996)

> suggest that self-reported personality traits do not change after a typical episode of major depression. Future studies are needed to determine whether such change occurs following more severe, chronic, or recurrent episodes of depression.

Christensen & Kessing (2006) tried to investigate whether personality traits predict onset of the first depressive or manic episode (the vulnerability hypothesis) and whether personality might be altered by the mood disorder (the scar hypothesis), and they suggested that, again, further investigation was needed.

In 2009 it was found that in medium-term follow-up, depressive episodes are unlikely to result in a personality scar persisting after recovery from an episode (Jylhä, et al. 2009).

## References

APA. (n.d.) *Personality* https://www.apa.org/topics/personality

Christensen, M. V., & Kessing, L. V. (2006). Do personality traits predict first onset in depressive and bipolar disorder?. *Nordic journal of psychiatry, 60*(2), 79–88. https://doi.org/10.1080/08039480600600300

Jylhä, P., Melartin, T., Rytsälä, H., & Isometsä, E. (2009). Neuroticism, introversion, and major depressive disorder--traits, states, or scars?. *Depression and anxiety, 26*(4), 325–334. https://doi.org/10.1002/da.20385

Shea, M. T., Leon, A. C., Mueller, T. I., Solomon, D. A., Warshaw, M. G., & Keller, M. B. (1996). Does major depression result in lasting personality change?. *The American journal of psychiatry, 153*(11), 1404–1410. https://doi.org/10.1176/ajp.153.11.1404

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Tags: personality, mental-illness
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# Question
Title: Why do men have greater variance than women in mental test scores?
Hedges and Nowell (1995) write that

> Sex differences in central tendency, variability, and numbers of high scores on mental tests have been extensively studied. Research has not always seemed to yield consistent results, partly because most studies have not used representative samples of national populations. An analysis of mental test scores from six studies that used national probability samples provided evidence that although average sex differences have been generally small and stable over time, the test scores of males consistently have larger variance. Except in tests of reading comprehension, perceptual speed, and associative memory, males typically outnumber females substantially among high-scoring individuals.

However, they don't really say anything about the reason for this aside from that "Our results shed little light on the origins of sex differences in \[...\] variability" (p45).

What theories are there of the reasons for this sex difference in variability on mental tests, and how strong is the evidence to support these theories?

# Answer
I've heard two theories related to genetics. Mental traits are massively polygenic (many genes with tiny effects). Men (XY) do not have a duplicate X chromosome like women (XX), which means that mutations to an X chromosome that disrupt typical gene expression can affect men more than women, driving variance in mental scores. The second theory is related to the fact that individual men are less likely to pass on their genes than individual women. Counter-intuitively, most of our ancestors are women. Men may have evolved a riskier genetic strategy that produces more high and low cognitive scores in phenotypes. Consider that men also take more risks. This is a behavioral outcome that may have emerged from the same selection pressure.

See also:

https://en.wikipedia.org/wiki/The\_Bell\_Curve

https://www.amazon.com/Intelligence-That-Matters-Stuart-Ritchie/dp/1444791877
> 4 votes

# Answer
Women are more selective in choosing mates than men and compete with one another for mates less than do men; most will be able to reproduce. Men, on the other hand, who deviate from the average in ways that matter will be more likely to reproduce than other men. This is one explanation for the hypothesis. An alternative explanation is that, because men can reproduce much more than can women, the benefits of having a highly divergent but successful offspring outweigh the drawbacks of having a well below average offspring. These hypotheses are discussed and a review of the research into the greater male variability hypothesis (one of many such reviews) is presented in Thöni, Christian, and Stefan Volk. "Converging evidence for greater male variability in time, risk, and social preferences." Proceedings of the National Academy of Sciences 118.23 (2021): e2026112118. Also of interest is a mathematical model claiming to support the hypothesis, Theodore P. Hill (2020) Modeling the evolution of differences in variability between sexes, Journal of Interdisciplinary Mathematics, 23:5, 1009-1031.
> 0 votes

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Tags: intelligence, test, sex-differences
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