# Question
Title: Why is it only positive charge that gets injected into a neuron when we inject a current into it?
Learning about the basics of theoretical neuroscience from the youtube lectures from Michale Fee's introduction to neural computation course.

We're considering a very simplified model of a neuron, where it's just a spherical shell (no ion channels) and the only way to inject current into it is via an electrode that takes charges from a saline solution and pumps them into the neuron.

This simplified model corresponds to the neuon being a capacitor.

It's then said that "As positive charges build up on the inside of the membrane, they repel positive charges away from the outside of the membrane"

My question: why is it that only positive charges are pumped into the neuron from the saline solution? Why aren't any negative charges pumped in?

# Answer
> 1 votes
Both positive and negative charges are pumped in; in fact, you can't really do one without doing the other, it just happens in different places. When you "pump in positive" charge you are making the electrode contiguous with the inside of the cell more positive while making a ground electrode in your bath more negative. If you "pump in negative" then the opposite happens.

Here's an example of an experiment I've done myself:

Here's a similar example from a paper by someone else, *Blanton, M. G., Turco, J. J. L., & Kriegstein, A. R. (1989). Whole cell recording from neurons in slices of reptilian and mammalian cerebral cortex. Journal of neuroscience methods, 30(3), 203-210.*

In a current-clamp experiment, you measure voltage while injecting current to a cell. In these experiments, there is 0 current at the start, then either a positive or negative current is applied for a couple hundred milliseconds, and then the current returns to zero. If you inject a positive current, the cell depolarizes (voltage becomes less negative), and sufficient current will lead to action potentials ("spikes") if you had a biological neuron or if you implemented voltage-gated channels in your circuit. If you inject a negative current, the cell hyperpolarizes (voltage becomes more negative).

In the second image, you see both the voltage responses (top) and the injected current (bottom); you'll see the injected currents on the bottom are in both positive and negative directions.

So, it is not the case that "only positive charge gets injected into a neuron"; the current is chosen by the experimenter, so that only happens if that's all the experimenter chooses to do. When the author you reference writes "*As positive charges build up on the inside of the membrane, they repel positive charges away from the outside of the membrane*" they're just giving an example of what happens when positive charge is injected, not saying that negative charge is not injected.

# Answer
> -2 votes
In equilibrium there are more positive ions on the outside of the cell as on the inside. This is where the potential is set to zero. Now you can use both types of ions. Positive as well as negative. When you pump in negative ions the potetial difference will grow. But then no signal will run along the neuron's axon. When the small channels are opened only positive ions will flow. The constant potential difference is kept up by Vm. If the channels in the real neurons are opened when the cell body has given a signal for this, the positive ions flow to the inside and this gives a change in potential. This ingoing of ions propagates through the axon. The potential Vm is for a short while reduced to zero and the channels open. The positive ions flow in, causing a flowing in in the direction of signal propagation. This short inflow propagation *is* the signal. Shortly after the initial ions have flown in the are pulled out again by Vm and the stationary potential difference is established again. Like the potential difference in a battery (which works with ions too, but instead there are electrons flowing between the + and - terminals, instead of the positive ions in the neuron). So a short in and outflow finds place when a signal (a potential spikewhich is essentially a zero potential spike but because we set the equilibrium potential to zero this is a potential spike).

Why does your pictured model say that a positive current flows inside? Well, in the zero potential state (which is a atate with more positive ions on the outside of the membrane than on the inside) there is no current flowing. This unevenly distribution is caused by an electric potential due to negative charges. The channels are closed to maintain this difference. The positive ions are drawn from the inside through a one way door so to speak. The moment they are drawn to the outside (by an electric field) the door is shut behind their back so they can't go back to the inside. Only when the channels are opened the ions can flow back. When the channels are open they can be pulled back to the outside again when the channels are still open. This happens shortly after ions have flown in. The net result is a pitential peak. The Vm in your model is the driving force of the positive ion movement. But why are no negative ions involved in the flow between the two sides of the membrane? Why are only positive ions flowing in and pulled out? Because they are needed to pull the ions out of the inside of the cell. They constitute the Vm and in your model only the positive charges flowing in are considered. This is not how it goes though. The positive ions flow in (positive current) because the membrane has opened for them (channels are opened). But then they fast flow back again ( negative current) to contribute to a new potential difference. This is also caused by Vm and I don't see this in the model you give. Now what constitutes Vm in reality? Something to think about!

The answer is: Because this happens in a true neuron. Only positive ions rush in (this momentary rush-in gives the spike potential, a short time in which the potential goes from the rest potential to zero) during a signal traveling. The in-rush of positive ions travels down the axon to inform another neuron. The non-zero rest potential is the restored shortly after the rush-in by other means, so not by ions passing through the channels back again. That's why it takes a short while before a new spike can be sent.

I am not sure if I get the pictured model completely. The Vm pictured resembles the rest potential. The circle resembes the cell body. But the capacitor is misleading. It might rsesemble both sides of the membrane (which indeed have the capacity to store charge) but drawing it outside the cell and connected to the cell is misleading. The cell itself is a capacitor. The circle, that is. You can't separate the capacitor and the body (circle). The is a non-zero rest potential. A loaded capacitor so to speak. Then the plates of the capacitor are connected (which in the model happens via the circle but in reality finds place in the circle). Then the plates are recharged again. Again via the circle. It is Vm that recharges the capacitor, but remember it is the circle itself that is the capacitor (it would have been clearer if the cell was drawn as two concentric circles). A new rest potential is installed. Of course some positive ions have to flow out the neuron too. It would get pretty crowde if the always rush in when a signal travels. So there will be also ions outward, that is a negative current will be seen alsi (if inward if plus).

More information: https://elifesciences.org/articles/22152

For your information:

How Are Electrical Signals Propagated?

> A two-part schematic shows a comparison between two different types of membrane receptors as they respond to an extracellular signal. In panel A, an extracellular ligand binds to a G-protein-coupled receptor and initiates a relatively slow activation sequence. In panel B, an extracellular ligand binds to an ion channel receptor and initiates a much more rapid electrical response. In both illustrations, each protein receptor is shown embedded in a simplified cell membrane, and the cell membrane is represented as a strip of parallel, vertical grey lines. The area above the membrane represents the extracellular environment, and the area below the membrane represents the intracellular environment, or the area contained inside the cell. The G-protein-coupled receptor and the ion channel receptor both span the cell membrane multiple times and have extracellular and intracellular regions. Figure 2: Comparing the activation of an ion channel receptor with that of a G-protein-coupled receptor Activation of both a G-protein-coupled receptor (a) and an ion channel receptor (b) cause a conformational change in the receptor protein. G protein activation can lead to multiple intracellular events through a variety of intracellular proteins, and this signaling can take seconds to minutes. When a G protein activates transcription, this can take up to 20 minutes. In contrast, ion channel receptors open pores in the cell membrane, causing the formation of electrical current. This receptor activation therefore causes a much faster response within the cell, on the order of milliseconds. © 2008 Nature Publishing Group Moreau, C. J. et al. Coupling ion channels to receptors for biomolecule sensing. Nature Nanotechnology 3, 620-625 (2008) doi:10.1038/nnano.2008.242. All rights reserved. View Terms of Use Figure DetailThe opening of ion channels alters the charge distribution across the plasma membrane. Recall that the ionic composition of the cytoplasm is quite different from that of the extracellular environment. For instance, the concentration of sodium ions in the cytoplasm is far lower than that in the cell's exterior environment. Conversely, potassium ions exist at higher concentrations within a cell than outside it. Such differences create a so-called electrochemical gradient, which is a combination of a chemical gradient and a charge gradient. The opening of ion channels permits the ions on either side of the plasma membrane to flow down this dual gradient. The exact direction of flow varies by ion type, and it depends on both the concentration difference and the voltage difference for each variety of ion. This ion flow results in the production of an electrical signal. The actual number of ions required to change the voltage across the membrane is quite small. During the short times that an ion channel is open, the concentration of a particular ion in the cytoplasm as a whole does not change significantly, only the concentration in the immediate vicinity of the channel. In excitable cells, the electrical signal initiated by ion channel receptor activity travels rapidly over the surface of the cell due to the opening of other ion channels that are sensitive to the voltage change caused by the initial channel opening. Electrical signals travel much more rapidly than chemical signals, which depend on the process of molecular diffusion. As a consequence, excitable cells respond to signals much more rapidly than cells that rely solely on chemical signals (Figure 2). In fact, an electrical signal can traverse the entire length of a human nerve cell — a distance of as much as one meter — within only milliseconds. How Do Different Types of Excitable Cells Work? Neurons, muscle cells, and touch receptor cells are all excitable cells — which means they all have the capacity to transmit electrical signals. Each of these cells also has ion channel receptors clustered on a particular part of its surface. For example, the receptors that respond to chemical signals are generally located at synapses — or points of near contact between adjacent cells.

> Of the various types of excitable cells that respond to chemical signals, neurons are perhaps the most familiar. When electrical signals reach the end of neurons, they trigger the release of chemical messengers called neurotransmitters. Each neurotransmitter then diffuses from its point of release on one side of the synapse to the cell on the other side of the synapse. If the neurotransmitter binds to an ion channel receptor on the target cell, the related ion channel opens, and an electrical signal propagates itself along the length of the target cell.

> Neurons have ion channel receptors specific to many kinds of neurotransmitters. Some of these neurotransmitters act in an excitatory capacity, bringing their target cells ever closer to signal propagation. Other neurotransmitters exert an inhibitory effect, counteracting any excitatory input and lessening the chance that the target cell will fire.

> Skeletal muscle cells also rely on chemical signals in order to generate electrical signals. These cells have synapses that are packed with receptors for acetylcholine, which is the primary neurotransmitter released by motor neurons. When acetylcholine binds to the receptors on a skeletal muscle cell, ion channels in that cell open, and this launches a sequence of events that results in contraction of the cell.

> In contrast to neurons and skeletal muscle cells, some excitable cells have ion channels that open in response to mechanical stimuli rather than chemical signals. These the hair cells of the mammalian inner ear and the touch receptor cells of both human finger pads and Venus fly traps. Cells that respond to touch have their ion channel receptors clustered at the position where contact usually occurs.

> Conclusion Excitable cells, such as fast-acting neurons and muscle cells, have specialized channels that open in response to a signal and permit rapid ion movement across the cell membrane. The opening of just a single ion channel alters the electrical charge on both sides of the membrane. The resulting charge differential then causes adjacent voltage-sensitive channels to open in chain-reaction fashion, creating a self-propagating electrical signal that travels down the entire length of the cell. Sometimes, this sequence of events is triggered when a chemical signal — such as a neurotransmitter — binds to an ion channel receptor on cell's surface. Other times, a cell's ion channels open in response to mechanical (rather than chemical) stimuli.

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Tags: neuroscience, theoretical-neuroscience, electrophysiology
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# Question
Title: What is it called when the brain creates an alternative reality?
I recently heard of a phycological phenomenon where someone's brain can create its own ongoing reality. someone can go through a traumatic situation and their brain creates a whole new life without the person realizing it. You could basically be in a coma or locked in a basement right now and wouldn't know because you are in a made-up world.

Example: A dude who got into a fight and got knocked out for a few minutes. In those few minutes, he lived 10 years of his life before one day waking up on the ground with paramedics around him and being told none of that was real.

I want to write a book about this but I can't figure out what this is called!!! I just need a name for it or some theory behind why it happens.

# Answer
You seem to be referring to two different phenomena to me.

The first is where the brain creates an alternative reality while awake, and the second is where you see/hear something going on different to actual fact while in a coma.

## While awake

This phenomenon is referred to as hallucinations. They can be auditory, visual, olfactory, gustatory or tactile. They can also be a combination of two or more of these types.

Hallucinations are

> **where someone sees, hears, smells, tastes or feels things that don't exist outside their mind.** They're common in people with schizophrenia, and are usually experienced as hearing voices. Hallucinations can be frightening, but there's usually an identifiable cause. For example, they can occur as a result of:

**Not all hallucinations are caused by major illness**.

One example would be that gustatory hallucinations (where you taste something not there) can be caused by physical illness. The common cold, just like covid, has been known to make you lose your sense of taste but it can also change the taste of food.

Auditory hallucinations can be caused by tinnitus.

## While in a coma

There have been anecdotal reports of people recovering from comas reporting of hearing people around them. The fact that although they don't respond, they **may** actually be able to hear, smell feel and taste, and that means that they may in actual fact build up a picture in their mind of what is going on while not being able to see it, and that picture may be different to actual fact. Either because what they are feeling/tasting/hearing is different to what they should, or they hear accurately, but because they cannot see it, they build up the wrong idea of how bad things are.

Science Focus suggests:

> Patients in a coma appear unconscious. They do not respond to touch, sound or pain, and cannot be awakened. Their brains often show no signs of the normal sleep-wakefulness cycle, which means they are unlikely to be dreaming. Yet many people who have recovered from comas report dreams into which something of the outside world penetrated. Others recall nightmares that seemed to go on and on.
>
> Whether they dream or not probably depends on the cause of the coma. If the visual cortex is badly damaged, visual dreams will be lost; if the auditory cortex is destroyed, then they will be unable to hear dreamed voices.
> 1 votes

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Tags: terminology, theory-of-mind
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# Question
Title: Is there a study that supports the claim that sexual deprivation leads to sexual deviancy?
Can anyone give studies that, if they exist, prove that sexual deprivation leads to sexual deviancy in later stages of life?

# Answer
*Personality Theories* Seidman and colleagues(1994) examined loneliness/intimacy problems regarding sexual offenders which suggested lack of social skills created intimacy problems

Bowlby (1988) which suggested people may take part in forms of sexual abuse as a result of loneliness/isolation which sexual deprivation is a by-product of

*Cognitive Theories* (Scott & Lyman, 1968; Scully, 1990; Sykes & Matza, 1957)

Note: personality theory(Sigmund Freud) tend to lack empirical evidence as pointed out by (Stinson, Sales & Becker, 2008)

further reading/source:https://smart.ojp.gov/somapi/chapter-2-etiology-adult-sexual-offending

"Hope this helps"
> 1 votes

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Tags: sexuality
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# Question
Title: What is the difference between the processing of visual information and auditory information?
We can read:

> The visual cortex is located in the occipital lobe of the brain and is primarily responsible for interpreting and processing visual information received from the eyes. The amount of visual information received and processed by the visual cortex is truly massive. Nearly half of the brain is in some way dedicated to vision—either direct communication pathways from the retina of the eyes to the occipital lobe, or to indirect visual processing and visual skills. The visual cortex is divided into six critical areas depending on the structure and function of the area. These are often referred to as V1, V2, V3, V4, V5, and the inferotemporal cortex. The primary visual cortex (V1) is the first stop for visual information in the occipital lobe.

We can read:

> The primary auditory cortex is the first region of cerebral cortex to receive auditory input.

> Perception of sound is associated with the left posterior superior temporal gyrus (STG). The superior temporal gyrus contains several important structures of the brain, including Brodmann areas 41 and 42, marking the location of the primary auditory cortex, the cortical region responsible for the sensation of basic characteristics of sound such as pitch and rhythm. We know from research in nonhuman primates that the primary auditory cortex can probably be divided further into functionally differentiable subregions.\[36\]\[37\]\[38\]\[39\]\[40\]\[41\]\[42\] The neurons of the primary auditory cortex can be considered to have receptive fields covering a range of auditory frequencies and have selective responses to harmonic pitches.\[43\] Neurons integrating information from the two ears have receptive fields covering a particular region of auditory space.

> The primary auditory cortex is surrounded by secondary auditory cortex, and interconnects with it. These secondary areas interconnect with further processing areas in the superior temporal gyrus, in the dorsal bank of the superior temporal sulcus, and in the frontal lobe. In humans, connections of these regions with the middle temporal gyrus are probably important for speech perception. The frontotemporal system underlying auditory perception allows us to distinguish sounds as speech, music, or noise.

On top of that it is known that the structure of the neurons in the cortex is the same where ever you look (though the division of the visual system is structure-based as can be read above). The information processing is just different in both (the neurons have different connection strengths).

How do the two processes, though implemented on the same structure, differ from one another? Is the process of hearing more a serial parallel process due to the serial character of sound? How are the connection strengths between neurons involved? Wat makes sound different from vision?

# Answer
> 1 votes
Visual and auditory senses are processed completely independently, up to a point. Obviously, they rely on different physical quantities (air pressure for sounds, photons for vision), are sensed by different organs (cochlea for sounds, retina for vision). Finally they reach the brain in different areas (mostly, but not exclusively, V1 for vision and A1 for audition). We are pretty sure they are processed completely independently up to this point. Then it becomes less clear.

Psychologically there are known interactions between the visual and auditory senses (the ventriloquist effect or the McGurk effect for examples). Physiologically there are areas that respond to both and demonstrated effects of one modality on the other in most areas, including by the way V1 at least in rodents. Although it is still unclear what these interactions are and whether they exists in all species.

For the rest, these questions are way too broad to be answered without providing a complete lecture on the state of knowledge in the field. But basically because these senses are processed independently at early stages, there is good evidence that they are processed quite differently. But as they obviously interact in the cortex they must be converted into some sort of common framework at some point. This "common framework" is most likely modality-specific (spatial localization, time perception, language etc.) because of the functional specialty of cortical areas.

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Tags: neuroscience, brain
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# Question
Title: How to interpret a BBC news article on the effect of race on intelligence?
> In spring 1998, Robert Plomin claimed to have discovered a gene linked with intelligence. **More recently, the Human Genome Project was cautious when approaching areas implying racial differences since research actually shows greater genetic differences within races than between races.** However, not all individuals are endowed with the same intelligence and many believe this must have something to do with our genes and the way they interact with the environment. Identical twins are more likely to obtain the same score in an IQ test than twins from two separate eggs that have a different genetic make- up.
>
> It is important to remember that genes work by interacting with the environment, so social factors will also infl uence intelligence. Intelligence tests may be more of an assessment of social factors, such as your educational background. **Black children adopted into white middle-class families score signifi cantly higher on average than those in working-class families – implying a cultural slant to tests.**

My classmate thinks that this article suggests that race is suggested as determining intelligence, because race is mentioned several times in the article as being linked to intelligence, whether genetically or through social factors. I want to check this before confronting her, but I think not. Who's right?

In my view, the first bolded sentence dismisses race as a determinant, because there are 'greater genetic differences within' each race than between different races.

The second bolded sentence also rejects race, because it only shows a cultural slant to tests and the first sentence of the last para states 'social factors will also infl uence intelligence.'

Source: ‘Are you born brainy?’, 17 November 2004, from BBC News at www.bbcnews.com

# Answer
> 4 votes
The relationships between race and IQ is a sensitive topic for many good reasons. It also raises a lot of deep questions about how to assess the role of genetics and environment.

A good summary of the literature on Intelligence with a discussion of racial differences can be found in the article "Intelligence: Knowns and Unknowns" (FREE PDF).

### Within-group versus between-group variance

You write:

> In my view, the first bolded sentence dismisses race as a determinant, because there are \> 'greater genetic differences within' each race than between different races.

Group differences can be quantified. They are often quantified in psychology in terms of cohen's d (i.e., the size of group differences in terms of the standard deviation). You sometimes hear the claim that within group differences are larger than between group differences. This point is often highlights that just because a group on average is higher on a variable, there is a large proportion of people in the lower group than are higher than people in the higher group. The claim is often made to remind people not to stereotype. However, from a scientific perspective, we are often quite interested in the size of the difference between group means and the causes of such differences.

Importantly, group differences need to be very large before between-group variance is larger than within group variance. A grouping variable can have an effect of an outcome variable without needing to achieve this degree of group difference.

The size of the group differences says very little about whether the effect is causal.

### Race as cultural slant

> The second bolded sentence also rejects race, because it only shows a cultural slant to tests and the first sentence of the last para states 'social factors will also influence intelligence.'

I don't think the second bolded sentence entirely rejects race. However, the wording "cultural slant" does go some way towards this argument.

However, I'd challenge the "cultural slant" argument. In particular, if some environments lead to higher IQ, I would be more inclined to interpret that as an effect of environment on IQ rather than saying that IQ tests have a cultural bias. You might argue that the kind of intellectual functioning represented by IQ tests is more valued by some cultures, but that's quite different. Once you operationalise IQ in terms of a general factor that emerges from a wide range of cognitive ability measures, then it makes sense to proceed with this. This is the variable that has been validated (i.e., predicts educational attainment; entry into prestigious professions; job performance particularly in cognitively demanding job; future income; etc.)

Also, to show that environment influences IQ is interesting, but it does not refute the role of genetics. Researchers in this space (e.g., looking at twin studies) often aim to estimate the proportion of variance in IQ due to environment and genetics. To show an effect of $A$ does not mean that there is not an effect of $B$.

# Answer
> 0 votes
## Simple minds

> We believe the burden of proof must shift to those who argue for a 100% culture-only position... they need to address why, if important minority-specific developmental processes such as stereotype threat (Steele, 1997) and racial stigma (Loury, 2002) exert such a powerful influence on school achievement, the correlation matrices representing developmental processes can be so similar across ethnic and racial groups (Section 5). They need to explain why, if gene–environment interactions are as widespread and difficult to disen- tangle as often claimed (e.g., Block, 1995), identical twins reared apart grow to be so similar (Bouchard, 1996; Bouchard & Loehlin, 2001). Some culture-only hypotheses are too ambiguous to be tested.

These strike me as quite simplistic and ad hoc arguments. Bouchard is adding further empirical twin data about personality and "special mental abilities", rather than IQ. Neither are "developmental processes" the same thing as IQ. And yet he thinks the IQ gap is a real - unitary - difference in intelligence. Why?

A lot of researchers (this is a highly cited article) seem to have invested a lot in IQ tests being an inherently fair, and complete, measurement of G. When in reality these very same arguments can be used to support the claim that the IQ gap is *not* representative of intelligence.

Such is 'psychology'. If personality and so on is not much of a cultural artefact, culture and genetics are really pretty distinct here, then are the effects of a racist culture mediated by the genetics of a person? If different ethnicities only differ in IQ and not pace of development, do IQ scores reflect a norm or definition of G which is valid for all groups?

These are only "too ambiguous to be tested" if we believe IQ tests are the gold standard which cannot be added to, even interpreted. IMHO it's from a false need for simplicity: one score with the best correlations. Sadly, social and individual psychology surely doesn't work like that

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# Question
Title: ANOVA or Multiple Regression for Big 5 predicting criteria instead of SEM
I am working on a project where I am studying the relationship between personality and certain economic outcomes. Direct measures for the economics outcome is available, while for personality I am using a Big Five Inventory from here In many studies, I have seen SEM being used when such questions are asked, but there we need an a-priori structure. But I have no such apriori structure in mind. I wish to find if the economic outcome is different for different people based on their personalities.

I want to ask if alternative strategies can be used such as one way ANOVA or multiple linear regression.

1. **Is it possible to use ANOVA** for example, dividing people into extraverted vs non-extraverted, neurotic vs non-neurotic etc. by first calculating for each person the score for each factor by taking the arithmetic mean and then dividing the sample into two groups by median? So for example, each person would be in a category like Open-Conscientious-Non Extravert-Agreeable-Non Neurotic or Non Open-Conscientious-Extravert-Agreeable-Non Neurotic etc. And then use 2x2x2x2x2 ANOVA to see if there are statistically significant differences. Is it possible? Are there examples in the literature where psychometric scales like the Big 5 have been used in this manner?
2. **Or can multiple linear regression be used** by deriving the scores of each factor by simple arithmetic mean? I understand SEM also includes path analysis which is based on regression, but I am talking about the usual Multiple Regression, such as $Y = \beta\_0 + \beta\_1 Openness + \beta\_2 Conscientiousness + .... + \beta\_5 Neuroticism$.

# Answer
You should not do median splits on continuous measures of the Big Five. Personality traits are continuous variables and generally approximately normally distributed. If you convert into categorical variables, you will throw out a lot of meaningful information and reduce your ability to predict criteria of interest. So in short, you should not adopt the "ANOVA" approach.

It is quite normal to estimate bivariate correlations with the criteria and combine this with a regression model with the Big Five as predictors of your criteria.

Of course, you could also do SEM and this is basically equivalent to multiple regression albeit it involves specifying a measurement model for the Big Five and it seeks to give you regression coefficients and variance explained of the underlying latent variables. Regarding your point about a priori structure, you do have that: the scoring key for the Big five specifies which items should load on which factors.

I generally prefer multiple regression, because it rests on fewer assumptions than SEM, and is in some senses more reproducible.
> 2 votes

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Tags: big-five, regression
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# Question
Title: Is Rotter's Interpersonal Trust Scale fixed?
I am new to psychology and recently have been looking for a metric of trust. I found that Rotter's Interpersonal Trust Scale (IST) is widely used, so I checked the original paper published by Rotter in 1967. But I didn't found the scale per se, and instead, I only found the constituents of the scale, which is 25 items plus 15 filler items.

Is the complete version published later in Rotter's other papers? Or the scale itself is intentionally left semi-designed and should be finalized on use?

# Answer
Is this what you are looking for?

Chun K-T, Campbell JB. Dimensionality of the Rotter Interpersonal Trust Scale. Psychol Rep. 1974;35: 1059–1070. doi:10.2466/pr0.1974.35.3.1059
> 1 votes

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# Question
Title: What fraction of the population has secure attachment style?
Attachment theory suggests that we divide attachment styles into secure attachment style vs insecure attachment styles.

What fraction of the population would be classified as having a secure attachment style, and what fraction as having an insecure attachment style? Is there are any data?

If there is any data on the breakdown between different types of insecure attachment style, that would also be interesting. I am most interested in the US or Western cultures, if it is culturely-dependent, but I would be interested in any references.

I found a reference that describes Mary Ainsworth's initial study of infants from middle-class Baltimore families as having the following proportions: 66% secure attachment (type B), 20% insecure-avoidant (type A), 12% insecure-ambivalent (type C). I found a reference to a 1992 study from Fonagy et al. that seemed to suggest a split of about 57% secure attachment, and 42% insecure attachment. Another website reports the proportions as 70%, 15%, 15%. That's a fair bit of variation among numbers.

# Answer
> 1 votes
I'm not sure why the numbers would need to remain exactly the same; don't attachment style proportions vary across populations? There is some evidence for large variations between socioeconomic statuses, for example. Attachment styles are mostly caused by parent-child interactions, after all, and the prevalence of the secure attachment style is because of the prevalence of secure parent-child interactions rather than some mathematical golden rule. Also, differences in how attachment style is assessed can be significant, since the child's reaction is only loosely quantifiable.

Why do you need the exact percentages, especially since you acknowledge that cultural differences exist? The purpose/problem will determine the method of attack. The main idea that secure attachments predominate because this many parents are generally responsive isn't challenged by any of those statistics.

# Answer
> 0 votes
Welcome to Psychology.SE. The answer to your question is not that straight forward. You could have a strong attachment style amongst work colleagues but have an insecure attachment style with superiors or parents.

For different types of attachment (insecure/secure) I would suggest reading the works of John Bowlby who pioneered the theory of attachment.

For further reading there is also a book called *Understanding Disorganized Attachment: Theory and Practice for Working with Children and Adults* by David and Yvonne Shemmings

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Tags: social-psychology, developmental-psychology
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# Question
Title: Psychologist with different language and culture
Is it better to find a psychologist who is from the same culture, same language, same country .., so he/she will easily understand the problems we'll be speaking about ?

I'm Algerian, living in France, I speak French well, should I find an Algerian psychologist ?

Is it the right place to ask this question ??

# Answer
> 1 votes
Normally speaking, this would be deemed a personal advice question and such questions are off-topic, but it is a common question asked within therapy.

I cannot provide sources of information regarding who specifically to see as that is very personal and my advice regarding that could be incorrect for you personally.

What I can tell you is that there are many people from different backgrounds who are very aware of the different cultures around them. If you are Muslim for example, whether you need to see a Muslim therapist is down to who is available in your area and whether that is exactly what you need.

In order for the right person to be chosen, I recommend looking at who you would trust to speak about your issues. **If it is important**, are they aware of the culture you were brought up in and what that entails?

Whether you see a therapist from your culture or not, you may find your first choice is not quite right for you. That is unfortunately common but doesn't mean they were not qualified for the task. It can just be a matter of rapport. You either click with each other or you don't.

Only you can answer this question really and I wish you luck.

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# Question
Title: Is there a term/name for the feeling you get when trying to pat your head and rub your tummy?
I often hear the phrase "It's like patting your head and rubbing your tummy/belly" when referring to trying to perform two seemingly simple actions that inexplicably conflict with each other, preventing one or even both of the actions from being performed well.

Another popular example involves swinging your right foot in a clockwise motion while trying to draw the number 6.

It kind of reminds me of "cognitive dissonance", the uncomfortable feeling you get when holding two contradictory beliefs.

So is there a word for this sensation? "Operational dissonance" perhaps? I'd love to read more about it, but I've no idea what to search for.

# Answer
> 2 votes
Given the ridiculously inaccessible language that some authors in this field use, it is no wonder that useful terms are hard to come by - like, who came up with this catchy title for a paper?

> Bilateral phase entrainment by movement-elicited afference contributes equally to the stability of in-phase and antiphase coordination

Ugh.

Anyway, Franz, Zelaznik, & McCabe (1991), in their equally catchily titled paper "Spatial topological constraints in a bimanual task", came up with a much easier term to remember for the rubbing tummy / patting head phenomenon: The "spatial magnet effect".

This effect is a type of rhythmic or phase "entrainment" (as suggested by the cryptic title above), which is presumably the skill that allows dancers and musicians to coordinate their limb movements so well, at the expense of not being good at performing uncoordinated movements.

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Tags: terminology, cognitive-dissonance, coordination
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# Question
Title: What's the exact definition of a cognitive mechanism?
I've been trying to get to a specific definition of a cognitive mechanism, but googling it surprisingly didn't give me anything. The only things I've found out are :

1. How to know if something can be considered a cognitive mechanism : https://ajp.psychiatryonline.org/doi/full/10.1176/ajp.155.12.1677
2. I've come across examples like dissociation, planning fallacy(wrt entrepreneurship) etc.

They sounded more like cognitive processes, but I'd like a clearer definition of it. I also wanted to know when do we think about cognitive mechanisms vs behavioural mechanisms.

Would really appreciate the clarity!

Edit : I first found the term in the paper mentioned in point 1.

# Answer
Cognitive mechanisms involve **ways people receive information**, and **the way people think about, interpret, evaluate and therefore act upon that information received**.

From Heinström (2010):

> The way a message is presented, and particularly how it is emotionally framed, influences the way people interpret, evaluate and act upon it. This cognitive mechanism is utilized in things like advertising and political campaigns.

The paper is saying that advertising and political campaigns aim use these mechanisms to their benefit.

Sometimes, there can be more than one cognitive mechanism in play. It is not necessarily just a way information is presented, which is one mechanism, but it can apply to **information gained from experience (another mechanism) and/or elsewhere such as school or therapy (other mechanisms)**.

Cognitive mechanism of the brain during the decision making and learning process — Source: Zhou, et al. (2020).

During political campaigns, potential election candidates may use leverage techniques. For example, they may use collective and/or individual viewpoints and interpretations of past events gleaned from lobby groups etc. to get their message across.

Before, and during the campaign, the lobby groups may use the same sort of cognitive mechanism in similar formats to their advantage.

The information received during cognitive mechanisms can be via messages in marketing campaigns, from news reports, experience of certain situations etc.

Experience (or even lack of experience) of certain groups of people can influence behaviour toward those particular groups, especially when hearing negative and disparaging remarks about them.

On top of that, with information gained through experience (e.g. traumatic experiences), these mechanisms can be congruent or incongruent with the reality of the situation.

These and more are what are studied when looking at, say, cognitive mechanisms of treatment in depression (Roiser, et al. 2012) and cognitive mechanisms underlying the creative process (Gabora, 2002) as examples.

You said

> They sounded more like cognitive processes

**A mechanism is part of a process** just as any dictionary would define as, for example,

> In a machine or piece of equipment, a mechanism is a part, often consisting of a set of smaller parts, which performs a particular function.

When you take all the cognitive mechanisms together, you will then be able to form the cognitive process(es) involved in forming memories, thoughts and ideas.

## References

Gabora, L. (2002). Cognitive mechanisms underlying the creative process. In *Proceedings of the 4th conference on Creativity & cognition* (pp. 126-133). https://doi.org/10.1145/581710.581730

Heinström, J. (2010). Negative affectivity—The emotional dimension. In *From Fear to Flow: Personality and Information Interaction*; Chandos: Amsterdam, The Netherlands, 75-103.

Roiser, J. P., Elliott, R., & Sahakian, B. J. (2012). Cognitive mechanisms of treatment in depression. *Neuropsychopharmacology, 37*(1), 117-136. https://doi.org/10.1038/npp.2011.183

Zhou, K., Wei, R., Zhang, Q., & Xu, Z. (2020). Learning system for air combat decision inspired by cognitive mechanisms of the Brain. *IEEE Access, 8*, 8129-8144. https://doi.org/10.1109/ACCESS.2020.2964031
> 1 votes

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Tags: cognitive-psychology, neuroscience, cognition, behavioural-neuroscience
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# Question
Title: Can you get 1.5 mm DIN connectors for EEG in the USA If you're not affiliated with a hospital?
I'm trying to find 1.5 mm DIN touchless connectors that would plugin to an EEG like this one (https://neuro.natus.com/products-services/xltek-brain-monitor-eeg-amplifier). I just want the connector that I can solder my own wire onto. I found one website that I think had what I was looking for, but when I tried to create an account to order them they told me I had to be affiliated with a hospital. Is there something special about these connectors? If not, anyone know where I can find them?

# Answer
> 0 votes
Medical devices are regulated, and typically only sold through clinical channels. That doesn't mean all the components are necessarily regulated or that they can't be sold to individuals, but I suspect *you are trying to contact a clinical supplier*. They're used to dealing with institutional clients, they aren't a retail outfit, and it's probably not worth their time to make a special case for you. They probably aren't even too excited to sell the connectors you're looking for; they're looking to sell whole systems and to provide supporting materials and replacement parts only as needed to maintain their main customer base.

I'd recommend looking for other suppliers, but you may need to build your own or work with a shop that can do it for you.

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Tags: eeg
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title: Symptoms of increase leptin receptor

text:
# Question
Title: Symptoms of increase leptin receptor
A genetic mutation that increases leptin receptor number. Does that lead to increase appetite or weight gain?

I found online that a decrease in the leptin receptor number could produce a feeling of fullness. So it's reasonable to assume that the increase would lead to an increase in appetite and weight gain. But I am not sure of it.

> Congenital leptin deficiency is a condition that causes severe obesity beginning in the first few months of life. Affected individuals are of normal weight at birth, but they are constantly hungry and quickly gain weight. Without treatment, the extreme hunger continues and leads to chronic excessive eating (hyperphagia) and obesity.

# Answer
Leptin, a 160-kDa hormone produced and secreted by the adipose tissue in direct relation to the amount of body fat, has been called the "obesity hormone" or "fat hormone" and also the "starvation hormone". When scientists discovered leptin in 1994 (Zhang, et al. 1994), excitement arose about its potential as a blockbuster weight loss treatment.

Izquierdo, et al. (2019) points out that

> Leptin, a hormone that is capable of effectively reducing food intake and body weight, was initially considered for use in the treatment of obesity. However, obese subjects have since been found to have high levels of circulating leptin and to be insensitive to the exogenous administration of leptin. The inability of leptin to exert its anorexigenic effects in obese individuals, and therefore, the lack of clinical utility of leptin in obesity, is defined as leptin resistance.

You spoke of leptin receptors saying

> a decrease in the leptin receptor number could produce a feeling of fullness.

There is only one leptin receptor. The leptin receptor, also known as ObR, is a single membrane-spanning receptor belonging to the class I cytokine receptor family (Wauman, et al. 2017) and it is either efficient in detecting leptin levels or it is not. A decrease in leptin, or the condition of leptin resistance as discussed by Izquierdo, et al. (2019), would increase appetite and therefore increase hunger levels. Continuous low leptin levels or leptin resistance will lead to an increase in body weight to the point of obesity.

An increase in leptin, or high leptin receptor activity, would suppress appetite due to an induced feeling of fullness. Continuous high levels will lead to starvation and weight loss.

It is a balancing act.

Under normal conditions, the balance between leptin and the leptin receptor (ObR) regulates body weight by balancing food intake and energy expenditure (Wauman, et al. 2017).

Everyone has their individual leptin level threshold.

WebMD explains this as follows, quoting Robert H. Lustig, MD, professor of pediatrics at the University of California, San Francisco:

> "Leptin tells your brain that you have enough energy stored in your fat cells to engage in normal, relatively expensive metabolic processes," he says. "In other words, when leptin levels are at a certain threshold — for each person, it's probably genetically set — when your leptin level is above that threshold, your brain senses that you have energy sufficiency, which means you can burn energy at a normal rate, eat food at a normal amount, engage in exercise at a normal rate, and you can engage in expensive processes, like puberty and pregnancy".
>
> But when people diet, they eat less and their fat cells lose some fat, which then decreases the amount of leptin produced.
>
> "Let's say you starve, let's say you have decreased energy intake, let's say you lose weight," Lustig says. "Now your leptin level goes below your personal leptin threshold. When it does that, your brain senses starvation. That can occur at any leptin level, depending on what your leptin threshold is."
>
> "Your brain senses that and says, ‘Hey, I don't have the energy onboard that I used to. I am now in a starvation state,'" Lustig says.
>
> Then several processes begin within the body to drive leptin levels back up. One includes stimulation of the vagus nerve, which runs between the brain and the abdomen.
>
> "The vagus nerve is your energy storage nerve," Lustig says. "Now the vagus nerve is turned on, so you get hungrier. Every single thing the vagus nerve does…\[is\] designed to make you take up extra energy and store it in your fat. Why? To generate more leptin so that your leptin can re-establish its personal leptin threshold... It causes you to eat and it causes you to get your leptin back to where it belongs."

## References

Izquierdo, A. G., Crujeiras, A. B., Casanueva, F. F., & Carreira, M. C. (2019). Leptin, Obesity, and Leptin Resistance: Where Are We 25 Years Later?. *Nutrients, 11*(11), 2704. https://doi.org/10.3390/nu11112704

Wauman, J., Zabeau, L., & Tavernier, J. (2017). The leptin receptor complex: heavier than expected?. *Frontiers in endocrinology, 8*, 30. https://doi.org/10.3389/fendo.2017.00030

Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L., & Friedman, J. M. (1994). Positional cloning of the mouse obese gene and its human homologue. *Nature, 372*(6505), 425–432. https://doi.org/10.1038/372425a0
> 0 votes

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Tags: genetics
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# Question
Title: Slope of psychometric function too steep?
I am in a project where we are preparing a visual decision making experiment which requires participants to detect vertical grating in a patch of dynamic noise (the noise pattern is updated on every frame; the experiment design is partly a replication of a published paper). We need to find signal contrast level that would result in 75% accuracy rate, and after multiple attempts with QUEST and the method of constants, finding this level seems impossible — the thresholds estimated by those two methods result in either close to 100% accuracy, or chance performance. The experiment is implemented in PsychoPy.

What could be the reason for these difficulties finding the "right" contrast level for the grating? The image below is an attempt to fit a psychometric function to the experimental data -- the slope is almost vertical. The horizontal orange line is the 0.75 level, the vertical axis shows the proportion of "yes" responses, and the values on the horizontal axis are contrast levels.

# Answer
> 1 votes
Regardless of what the chance level exactly was, as alluded to in the comments, the scores leaps from 0.1 to 0.8. This results in nearly vertical slopes that are prone to convergence errors and hence lead to suboptimal threshold estimates in terms of accuracy. MATLAB always warns me when that happens. I have no experience with *PsychoPy* unfortunately.

If you wish to achieve better accuracies of your threshold estimates of grating contrast levels between 0.035 and 0.04, you simply need more measurements in that range. Above 0.04 there are about 10 redundant points all basically centered at 100% correct. These measurements should be redistributed to the relevant region around threshold instead.

A convenient way of designing such a threshold experiment is using a dynamic procedure that reduces step size along the way, like a staircase procedure (Levitt, 1971). Staircase procedures may be less suitable if you wish to generate psychometric curves. If this is the case, using a stair case to swiftly determine thresholds and then choosing a number of fixed gratings below and above the approximate threshold to generate a psychometric curve can help a lot.

<sub>**Reference**
**-** Levitt, *JASA* (1971); **49** 467-77</sub>

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Tags: methodology, vision, psychophysics, signal-detection, task-analysis
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# Question
Title: Why are flat line EEG recordings not perfectly zero microvolt?
I just look at several flat line EEG brain waves and all of them are not exactly at zero microvolt, in the sense there seems to be always a small signal or irregularities to be seen, as well as baseline offsets. Is it possible for flat line EEG brain wave to be 100% zero microvolt?

These are some examples to be found of non-flat EEGs in the literature, e.g., here and here and here.

# Answer
Every electronic device generates internal noise (e.g., Stronks *et al*., 2019), including EEG machines. Further, environmental factors, most notably electrical devices and circuitry, may also impose noise on the EEG signal, think clinical equipment in hospitals, mobile phones *etc*. So even 'flat EEG's', *i.e.*, isoelectric EEGs obtained in 'brain dead' organisms, aren't perfectly flat. Such EEGs are devoid of physiological (cortical) electrical activity, yet environmental and internal electronic noise still show up in the EEG recording.

<sub>**Reference**
**-** Stronks *et al*., *Ear Hear* (2019); **40**(6): 1457–66</sub>
> 2 votes

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Tags: measurement, eeg, electrophysiology
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title: How does our brain remember reminders?

text:
# Question
Title: How does our brain remember reminders?
I was wondering about a rather remarkable phenomenon regarding how we recollect reminders. I've read stories where people keep a pillow, or even figures and dolls, near their door to make them remember specific tasks. And they do, upon seeing that object. How does our brain remember those reminders?

I searched online about this and found a lot of tips (like the above - dolls, pillows, etc) rather than explanations. I'm not sure if it *has* to do with memory (or how it even works) which is why I'm asking here. Thanks!

# Answer
> 2 votes
How does the mechanism behind a pillow set up at a door as a reminder differs from remembering that the pillow is called a pillow? In other words, as far as I can see, this question basically asks how memory works. That question can fill libraries and would be out of scope here.

Why the example stated in the question helps remembering stuff is, imho, simply because it is just that a **salient** (a pillow belongs in bed, so it catches the eye) visual reminder (people are **visually oriented** creatures) positioned at a place that you are certain to pass in the morning (the door) will help you remember to do something you planned to do. Importantly, a salient object will grab ones attention during highly **automated behaviors** (wake up - eat - brush teeth - grab bicycle - go to work... - *huh? What's that pillow... oh yeah!*). This all doesn't seem to be such a remarkable phenomenon at all?

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Tags: memory, brain
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# Question
Title: How to interpret genetic variance of IQ?
I am a layperson currently reading "The Bell Curve" and its various rebuttals such as "The Intelligence and How to get it". I do not want to go into controversies of the topics per se and those are irrelevant to my question.

To quote from Wikipedia:

*"Heritability" is defined as the proportion of variance in a trait which is attributable to genetic variation within a defined population in a specific environment. Heritability takes a value ranging from 0 to 1; a heritability of 1 indicates that all variation in the trait in question is genetic in origin and a heritability of 0 indicates that none of the variation is genetic.*

If for the sake of this question, if I were to assume heritability is 0.5, then is it right to understand that there is a 50% chance that I could have inherited my intelligence (as measured using standardised IQ test) and another 50% chance that my intelligence is not inherited? I also read that genes set the upper limit of intelligence, in which case is it right to assume that if a person did not inherit her intelligence because she falls into the latter group, are her limits of intelligence determined entirely by environment and education (or do genes still play a smaller role?).

I appreciate that the extent of heritability is scientifically debated among experts, but I am interested to know what is the debate really about and how to interpret the arguments related to nature vs. nurture. To explain my confusion further - a person who is only 170 cm likely inherited his height from his parents who are only 165 cm. A bit of extra height may have come from better nutrition (than a generation ago) which is an environmental factor. What would be a similar example when it comes to IQ?

# Answer
> 2 votes
As noted, heritability is calculated at a *population* level. It says nothing about inheritance at an *individual* level. For example, given parents with certain known IQs, can we use heritability to calculate the range of possible IQs of their children or how much of their children's IQ is attributable to genetics? No. As Wikipedia puts it:

> Heritability measures the proportion of variation in a trait that can be attributed to genes, and not the proportion of a trait caused by genes.

It seems to me that this value is practically useless for anything other than general comparisons between other heritability values! (See my question on Cross Validated (stats.SE) asking to confirm this.)

Put simply: **A trait with high heritability indicates that on average, children closely resemble their parents (and twins closely resemble each other) in that trait; conversely, a trait with low heritability suggests that children can have a wide variety of outcomes in that trait.** For example, if the heritability of height is high, then I would expect most children of tall parents to be relatively tall; whereas if the heritability of height were low, then tall parents could have children of virtually any height. Stated technically, a heritability of 50% means that half of the variance seen within a population can be accounted for by corresponding variation in genes:

> It measures how much of the variation of a trait can be attributed to variation of genetic factors, as opposed to variation of environmental factors.

Environmental factors known to affect IQ include nutrition, toxins, prenatal, perinatal, and family environments.

The reason that the question about the heritability of IQ remains open, is because as long as there are both genetic *and* environmental differences between populations, then it is a challenge to convincingly tease out which factors (including measurement error and random chance) cause the differences observed between those populations.

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Tags: intelligence
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# Question
Title: Do animals look for new ways to keep themselves motivated?
Humans tend to find ways to keep themselves motivated and happy. What about animals? Do they feel down and look for new ways to motivate themselves?

# Answer
**I’m not an expert on this subject** but, if we take the term of **prediction errors** and apply it to the animals (at least most of them) that may make sense.

The key element is probably "foraging" in this case. The brain itself drives (with the reward system of course) to animals for finding new ways for gathering food. In their *umwelt*, food sources are dispersed, unreliable in terms of availability, unreliable in terms of quality and quantity, and all too often snatched up by a faster-moving organism in terms of competition.

So animal needs to *update* its *predictions* to getting food. Predictions that are updated can lead to more successful interactions between the animal and its ever-changing environment.

As a result, understanding new perceptual aspects of an unexpected stimulus and assessing whether the surprise was better or worse than predicted may be critical for directing future behaviors. And of course, dopaminergic pathways in the brain support this process. Schultz, 2010; Bromberg-Martin et al, 2010. Moreover, the same neurons change their firing rates in different directions to express the presence of an unexpected reward and the absence of an expected reward. Hyde et al, 2015
> 1 votes

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Tags: animal-cognition
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# Question
Title: Why is deltaE not used as a measure of error?
I've recently read a few articles pertaining to visual memory. Most of them (e.g. Bays *et al*., 2009 use the continuous color recall task where they ask participants to recall the color of an object by clicking on a color wheel. They use as measure of error the angular distance between the participant's response and the actual angle on the color wheel of the object's color.

Why use this dependent variable? In the industry, people use deltaE to determine the color difference between a product and a prototype.

Wouldn't it make more sense to also use deltaE as dependent variable in psychology? From what I've read, deltaE tries to be accurate for human color perception.

# Answer
> 1 votes
**Short answer**
To me, it seems perfectly feasible to use **deltaE** both as dependent and independent variable of **color difference**.

**Background**
DeltaE (Fig. 1) can be used to generate the target stimuli by pre-selecting a set of different color pairs to use in the recall task (method-of-constant stimuli, MOC), or alternatively, by using different step sizes of deltaE along the color matching test (in case of an adaptive staircase procedure for instance). It will depend on the study setup what specific method one wishes to use (MOC or an adaptive test).

On the other hand, deltaE can very well be used during data analysis to determine the difference between the presented color and the subject's response to that color. The advantage of using a single number (deltaE) over, *e.g.,* RGB values is that deltaE is a single number (*i.e.* an angle) and can hence be straightforwardly used as an outcome measure, whereas RGB values would have to be recoded along three axes and somehow transformed into a single number representing response error.

Fig. 1. Color wheel. source: Nguyen *et al*. (2018)

**Reference**
**-** Nguyen *et al*., *BioResources* (2018); **13**(3), 6250-64

# Answer
> 0 votes
Delta E is used extensively in vision research, however the study you sited only tested hue recall (all samples and test responses were designed to vary in hue and minimally in luminance and saturation).

This is one possible criticism of the studies. One of the major improvements in Delta E 2000 is a hue dependent rotation. We are more or less sensitive to certain hue regions. While this is one source of criticism, they are generally relying on large color differences to differentiate successful trials vs. unsuccessful trials and Delta E does not have any meaning for large color differences.

A more accurate reinterpretation might be to say that they aren't calculating color differences at all but rather the variation of the response distribution and the underlying probability density functions. The variation analysis is not dependent on individual color difference calculations.

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Tags: measurement, methodology, vision, psychophysics, color
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# Question
Title: What is the cochlear frequency response by number of hair cells?
I am trying to recreate the cochlea/basilar membrane response to sound and want to know how the hair cells are bucketed or binned by frequency, so an ideal list would be something like 10 kHz - 12 kHz: 2,000 hair cells and this across the frequency range of human hearing. I think there's overlap in the frequency response so an average would work.

# Answer
The basilar membrane of the cochlea has a logarithmic frequency distribution, at least for the better part, **such that an equal space is occupied per octave from 1 kHz and onwards** (Fig. 1). This means that an octave at low frequencies is represented by more hair cells than an area of basilar membrane spanning an octave at high frequencies. The density of inner hair cells is similar across the basilar membrane, at least in normal-hearing folks. When we grow older, basal hair cells (*i.e.*, those encoding high acoustic frequencies) degenerate first, leading to decreased densities in those regions. In normal hearing folks, there are about **100 hair cells per mm** (Fig. 2).

Given the total length of the basilar membrane of **36 mm** (Keen, 1940 and the two figures below you should be able to divide the basilar membrane into any number of frequency bands and convert those to distances along the cochlea using the Greenwood function of the human cochlea (Fig. 1). Then you can determine how many inner hair cells are devoted to each band using Fig.2 (about 100 HCs per mm). You can check the resulting model after you have applied it by comparing the cumulative number of modeled hair cells across the full frequency range of the human cochlea (~20 Hz - ~20 kHz, give or take) with the total number of inner hair cells present in the human cochlea (3,500).

Fig. 1. Greenwood map of the human cochlea. source: Greenwood (1961)

Fig. 2. Hair cell densities in man along the basilar membrane. source: Wright *et al.* (1987)

**References**
**-** Greenwood, *J Acoust Soc Am* (1961); **33**(484): 1344-56
**-** Keen, *J Anat* (1940); **74**(4): 524–7
**-** Wright *et al*., *Acta Otolaryngol (Stockh)* (1987); **436**: S15-24
> 2 votes

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Tags: neuroscience, neurophysiology, neuroanatomy, hearing
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# Question
Title: Why are there so few women in math and science Olympiads?
Why are there so few women in math olympics (IMO and etc)? If this is also related to the low participation of women in the Olympics compared to men, I would like to know.

Why Are There Still Only Few Women in Science An interesting article you can find on Nytimes about why low number of women in science

I also found some studies that try to explain why women's participation in math olympics is low. They have shown that many women also believe the stereotype that women are bad at math. Women who hold this belief may be reluctant to compete in math competitions, so it probably makes up for this effect.

Women and Mathematics: Stereotypes, Identity, and Achievement Both Genders Think Women Are Bad at Basic Math

I sent some studies that I read and found relevant.

# Answer
This is my first answer here, so bear with me. Suggestions on how to make this answer better are welcome.

There are several studies that indicate that men are more interested in things and women are more interested in people.

In Scandinavia where genders are the most equal there is a bigger gap between men and women in the STEM fields. Which suggests that the interest in people or things is biological and not perse social or cultural.

To compete in the math olympics you need to be really good in what you do. Or for the sake of argument to be a high level engineer or any other high level position in the STEM field.

You will have more men than women. Because there are less women to begin with.

Plus women excel in verbal skills. So they have more options outside STEM fields only.
> 2 votes

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Tags: mathematical-ability, social-desirability
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# Question
Title: What is the neurological mechanism responsible for losing one's temper?
I'd imagine that losing one's temper is quite normal, I can not think of anyone who has not experienced it. For me, it is rare, but does happen, I find that there can be 3 broad stages occur (*note: this is **not** a self help question, but just an example*), a generalized example would be:

1. "The calm before the storm" - I actually feel calm just after the object of frustration occurs and before the next stage - this step is usually very short.
2. "The storm" - it feels like the anger/rage comes from within and erupts, for me, it is in shouting, for some it is violence, for others, it is both. The length of this stage varies.
3. "Sunshine again" - not all sunshine and lollipops, but calmer with rationality kicking in.

My question is what neurological triggers initiate each step?

# Answer
*I have addressed your three points in three parts.*

---

* *The calm before the storm.*

I would dispute the calm before the storm. I would suggest this would depend on the trigger. Sometimes people can experience a feeling of shock at what they are processing, before they become angry.

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* *The storm.*

The sympathetic nervous system is the part of the autonomic nervous system that is responsible for our fight and flight response.

What causes people to get angry?

> You might have many things to feel threatened about — from financial crises and peer pressure to drug addiction and war — and some people respond in a negative way. Still, most people don't walk around feeling mad all the time. When someone explodes with anger, there's usually a triggering event — such as a disagreement at work or being stuck in traffic — that brings a mix of simmering emotions to the boiling point.

What happens when we get angry?

> When we get angry, the heart rate, arterial tension and testosterone production increases, cortisol (the stress hormone) decreases, and the left hemisphere of the brain becomes more stimulated.

Increased heart rate and arterial tension primes the body for fight or flight.

Testosterone is linked with aggression.

> Cortisol is released in response to stress, sparing available glucose for the brain, generating new energy from stored reserves, and diverting energy from low-priority activities (such as the immune system) in order to survive immediate threats or prepare for the exertion of rising to a new day.

The left side of the brain is responsible for;

> Dopamine \[II\] is the neurotransmitter that is not only responsible for modulating a lot of our physical movement, but also sex, aggression, motivational drive, and, counter-intuitively, long-term planning and restraint or impulse control. In nearly all right-handed and most left-handed humans who are left-brain dominant, dopamine rules the left side of the brain.

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* Calm after the storm

The parasympathetic nervous system is the part of the autonomic nervous system responsible for the more restful activities and will restore the autonomic nervous system's balance.

> The body takes about 20 minutes to return to normal after a full fight/flight response. ..//...
>
> ...//... Angry people will not completely comprehend any explanations, solutions, or problem solving options until their body returns to normal again. \[III\]

What happens when we get angry? Hormonal, cardiovascular and asymmetrical brain responses
Neus Herrero, Marien Gadea, Gabriel Rodríguez-Alarcón, Raúl Espert, Alicia Salvador. Hormones and Behavior, 2010; 57 (3): 276 DOI: 10.1016/j.yhbeh.2009.12.008

How dopamine may influence gender differences in psychiatric disorders \[II\]
Published on May 17, 2011 by Emily Deans, M.D. in Evolutionary Psychiatry

Controlling Angry People \[III} What would you do if you came face-to-face with an angry person?
Published on January 5, 2011
Jack Schafer, Ph.D.
Let Their Words Do the Talking
> 7 votes

# Answer
Anger can demonstrate itself outwardly in an argument form with another person. A voice can be raised. One can yell. You can positively express anger through sport.

Firstly there's some muscle tension presumably it increases the focus on dealing with the negative subject matter at hand. The body's chemical messengers release a burst of energy. Your breathing rate increases. You can not pay attention to anything else but the negative subject matter. You have extra mental sharpness and focus. Blood moves out from the gut towards the muscles in order to prepare for exertion. The body temperature rises. The skin perspires. The stress hormone cortisol is released. Adrenaline and noradrenaline releases create the 'fight' state of arousal.

The prefrontal cortex is located just behind your forehead it's a region in the mammalian brain which deals with judgement. It receives signals from other regions in the brain it can switch off your emotions. Learning new things like new skills by understanding and piecing together information helps to improve your prefrontal cortex.

By improving your prefrontal cortex you can better regulate your emotions. The prefrontal cortex is connected to another part of the brain, the amygdala. It interacts with the prefrontal cortex.

The prefrontal cortex's connection with the amygdala is important. An expression of an intention to inflict damage to you can be identified by the amygdala. The prefrontal cortex can then decide to intervene if it wants to. The arousal's adrenaline sometimes lasts for days therefore it increases the chances of further moments of anger.

Websites used:

1. https://www.betterhealth.vic.gov.au/health/healthyliving/anger-how-it-affects-people#expressing-anger-in-healthy-ways
2. https://www.mentalhelp.net/anger/physiology/
3. https://www.masterclass.com/articles/prefrontal-cortex-explained#what-are-the-parts-of-the-prefrontal-cortex
4. https://www.nature.com/articles/s41467-020-15920-7
> 0 votes

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Tags: neuroscience, emotion, cognitive-neuroscience
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# Question
Title: Psychometric information on IPIP representation of NEO facets
The IPIP (International Personality Item Pool) website provides a copy of the IPIP representation of the NEO 30 facet form.

It also provides some information comparing IPIP NEO with official NEO. However, the information provided is incomplete for making an assessment of the psychometric properties of the test. For example, I'd like to know about: (a) how items were chosen; (b) what was the sample size and characteristics used to generate the comparative correlation information provided; and (c) what is the factor structure of the IPIP NEO.

Thus, my questions:

* Where can I find information on how the IPIP NEO (30 facet version) was developed?
* What studies have examined the psychometric properties of the IPIP NEO (30 facet version) both in absolute terms and relative to the official NEO?

# Answer
> 4 votes
The table found at your second link (comparing the IPIP NEO and official NEO) seems to have come from this paper by Goldberg (1999): http://projects.ori.org/lrg/PDFs\_papers/A%20broad-bandwidth%20inventory.pdf. This paper discusses the generation of the IPIP items as well as the sample it was originally administered in. A 2006 paper (also by Goldberg) provides additional information on IPIP development:

Unfortunately, I was unable to locate information on the factor structure of the IPIP NEO 30 facet form, only the IPIP 50-item FFM (Ehrhart, Roesch, Ehrhart, & Kilian, 2008), which seems to be a different measure (http://ipip.ori.org/newFinding\_Labeling\_IPIP\_Scales.htm).

Ehrhart, K. H., Roesch, S. C., Ehrhart, M. G., & Kilian, B. (2008). A test of the factor structure equivalence of the 50-Item IPIP Five-Factor Model Measure across gender and ethnic groups. *Journal of Personality Assessment, 90*(5), 507–516.

Goldberg, L. A., Johnson, J. A., Hogan, R. , Ashton, M. C., Cloninger, & Gough, H. G. (2006). The international personality item pool and the future of public-domain personality measures. *Journal of Research in Personality, 40*, 84–96.

# Answer
> 1 votes
I know that the question is old, but it is still relevant so I will attempt to answer.

In the meantime Johnson has developed a 120-item version of the IPIP-NEO. The development is described in detail here:

Johnson, J. A. (2014). Measuring thirty facets of the Five Factor Model with a 120-item public domain inventory: Development of the IPIP-NEO-120. Journal of Research in Personality, 51, 78–89. https://doi.org/10/bc99

And there is an additional validation study here:

Kajonius, P. J., & Johnson, J. A. (2019). Assessing the Structure of the Five Factor Model of Personality (IPIP-NEO-120) in the Public Domain. Europe’s Journal of Psychology, 15(2), 260–275. https://doi.org/10/gh8gk3

I can definitely recommend reading both papers. While the IPIP-NEO-120 has some psychometric problems, the NEO-PI-R is also far from perfect. I believe IPIP is the future due to its non-proprietary nature.

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Tags: reference-request, measurement, personality
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title: Condensed NEO-PI test

text:
# Question
Title: Condensed NEO-PI test
I'm looking for a condensed form of the NEO-PI test. Current short forms come in at 40-50 questions, I'm wondering if it's possible to achieve a very basic degree of accuracy with 20 items.

# Answer
> 3 votes
There is a very short 10 item questionaire. The BFI-10 (see Rammstedt & John, 2007). I have never used it on my own, but i just read through it quickly. Although it seems fairly acceptable. So, if you want to use it, you should definitely read the article carefully.

Regarding your question: I would answer a careful 'yes'. In some cases it is possible to achieve a very basic degree of accuracy with just using a few items. However, this highly depends on the way the test is constructed and the kind of construct you want to investigate. The broader your construct, the more items you will need in order to account for every facet appropriately (e.g. a very broad personality aspect like 'extraversion' vs. a specific facet like 'assertiveness'). Furthermore, the longer your test, the better the reliability will tend to be (see Spearman-Brown Formula).

To sum up: It depends on the situation whether or not a short questionnaire can be basically accurate. You should always check for it´s reliability and validity.

Rammstedt, B., & John, O. P. (2007). Measuring personality in one minute or less: A 10-item short version of the Big Five Inventory in English and German. Journal of research in Personality, 41(1), 203-212.

# Answer
> 2 votes
If your aim is to measure the Big 5 only, then perhaps 4 or 5 items per factor will give you a rough idea. If you're planning on publishing the research, then I'd strongly encourage you get at least 8 items per factor. The IPIP website has a range of options for measuring the Big 5 with different length inventories: http://ipip.ori.org/newMultipleconstructs.htm There are many other Big 5 instruments available including the BFI and BFI 2.

If you need full facet-level measurement (i.e., the 30 facets), then I'd encourage you to use the full length instrument.

# Answer
> 1 votes
If you want to use IPIP, better use the Mini-IPIP (20 items) instead of selecting items yourself:

Donnellan, M. B., Oswald, F. L., Baird, B. M., & Lucas, R. E. (2006). The Mini-IPIP Scales: Tiny-yet-effective measures of the Big Five Factors of Personality. Psychological Assessment, 18(2), 192–203. https://doi.org/10/d5649w

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Tags: personality
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# Question
Title: Which R packages have good collections of psychology datasets?
The open source statistical software R has a range of contributed packages. Some of them include datasets.

I teach research methods in psychology and I'm looking for interesting real-world dataset to use as the basis for tutorials. I've found a few in contributed R packages (e.g., AER, psych), but I'm not aware of a general resource listing R packages that supply multiple interesting, real-world, psychological datasets. In particular, some textbooks have an aligned R package containing many interesting datasets.

* **What R packages include multiple interesting, real-world, psychological datasets?**
* **For any package identified, it would be good to have a sense of the kinds of datasets contained**

# Answer
> 9 votes
Some extremely large personality data sets can be downloaded at http://personality-testing.info/\_rawdata/ in CSV format.

They are not packaged in R, but I post the link because you indicate in your reply to USER:what that you are having trouble finding any data sets what so ever.

# Answer
> 6 votes
680 datasets that were originally distributed alongside R and some of its add-on packages are collected on GitHub. An index lists the datasets and the packages they came from.

If you just want datasets and don't mind that they were not part of any R package, then there are many available for free on the web. For example, Quandl lists over 7 million datasets. Google turns up many other collections.

# Answer
> 6 votes
The languageR package contains several interesting real-world datasets relevant to psycholinguistics. These datasets are presumably also described in the accompanying textbook.

# Answer
> 1 votes
Not R packages, but:

Best psychological datasets I found on the internet was from the dataverse at Harvard: https://dataverse.harvard.edu

https://osf.io also has good data sets, but the search engine is mediocre. It is usually more convenient to search from google directly.

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Tags: statistics, data, teaching-of-psychology
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# Question
Title: Must researchers pay to use items (but not scoring) from standardized tests?
I would like to use the items from a standardized test in a research study. I would like to know whether I need to pay to use the items for this purpose? Or are the items alone potentially free, whereas one must pay to use specialized administration and/or scoring methods?

If it matters, the specific test I am interested in is the Woodcock-Johnson III Math Fluency subtest.

I often read papers in which researchers used the items from this test and report analyses using number or proportion correct answers, i.e., not norm-referenced scores. I am wondering whether they needed to pay to do so.

# Answer
If the test/questionnaire is proprietary, one way to use the items would be to pay. Another way would be to ask the authors for permission to use the items for your project free of charge (which they might actually give you).

Simply using the items without paying or asking is likely copyright infringement (for proprietary tests). It usually does not make a difference what you use the items for or how you analyze results.

Best way to handle proprietary tests/questionnaires is to not use them at all and look for free alternatives. If there are none, make your own, validate it and make it freely available :).
> 1 votes

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Tags: measurement, mathematical-ability
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# Question
Title: What is meant by "adaptive emotions" in this explanation of the TARGET model?
I was reading an article about TARGET, an approach to grounding emotional disregulation (*e.g.* from trauma). It introduces a mnemonic, FREEDOM, as follows:

> 1. Focusing: Concentrating on a single idea grounded in our core values and sense of authentic self
> 2. Recognizing: Paying attention to identifying what is triggering the alarm reaction, even small things which we ordinarily wouldn’t notice
> 3. Emotions: Differentiating alarm-driven emotions from main, **adaptive** emotions
>
> ...

I think I understand alarm-driven emotions. But *everything* feels alarm-driven in that state. What are examples of adaptive emotions I might have? I'm not sure what I'm supposed to distinguish here.

I can only seem to find research papers on this topic, no infographic or guide. Probably the model is meant for psychologists to utilize, not directly for patients / the layperson. But I'm looking for grounding techniques for trauma and would like to know.

# Answer
I found the publication the article was referring to. In the paper they are referred to as "main" emotions.

> The goal of this skill is to identify two types of emotions. The first are "alarm" or reactive emotions such as terror, rage, and guilt. A second type of emotion, "main" emotions, include positive feelings and feelings that represent positive strivings. By balancing both kinds of emotions a person can reflect and draw on his/her own values and hopes even when the alarm is activated.

It's more salient to me to relabel them **reactive** versus **goal-driven** emotions. (Maybe even **"intentional"** emotions.)
> 0 votes

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Tags: emotion, trauma
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# Question
Title: Is there any evidence for a link between religiosity and belief in conspiracy theories?
I've heard claims made that more religious individuals were more likely to fall for various conspiracy theories. I've personally been able to find studies linking religiosity to belief in qanon conspiracy theories, but since Qanon is a conservative conspiracy theory it makes sense more religious people, who tend to be more conservative, would be more prone to believing conservative leaning theories so I don't take that as proof of a link between religiosity and general belief in conspiracy theories.

Thus I'm asking, has there been any peer reviewed studies that look at religiosity and (general) belief in conspiracy theories, and if so was a link found between the two, and if so how large a link?

I'm a little more interested in the USA perspective, but since I suspect the trends are mostly the same in most 1st world countries I'd accept studies that look at any country that's generally '1st world'. I'd accept studies of religiosity for Christianity, or general religiosity regardless of specific religion practiced. I really just want to know if the claims that religious folks are more likely to fall for conspiracy theories has any basis on reality.

# Answer
> 5 votes
Conspiracy Theories and the Paranoid Style(s) of Mass Opinion

Alternate link

Replication data

This paper has some measurement of how much religiosity explains some intermediate views that may predict conspiratorial thinking. It shows how much those views predict conspiratorial thinking. It breaks down those views in various ways (Figure 3), but doesn't show the breakdown by religion. Some of the intermediate views are explicitly religious in nature, but that doesn't mean that all religion predicts conspiratorial thinking.

I think the paper is mostly talking about predicting conspiratorial thinking, so it's dealing with correlations, not causations.

# Answer
> 2 votes
Another paper that has some empirical results from Australia:

> The results showed that believers and non-believers did not differ in the belief in conspiracy theories. Unpacking this further though, we did find that the extent to which religious worldviews were endorsed predicted belief in conspiracy theories. Among believers, **the importance attached to their religious worldview was directly associated with higher belief in conspiracy theories and this link was partly mediated by higher anti-intellectualism.** \[...\] We find that it is not the self-categorization as religious, but the extent to which religious worldviews are endorsed that could predict people's beliefs in conspiracy theories.

The paper also somewhat predictably found that (in line with much other research) trust in political institutions was inversely correlated with belief in conspiracy theory. Besides the dry results, it also has this discussion bit as to how religiosity (and even belief in ideologies like Marxism) might share mechanisms with conspiratorial thinking:

> What then is the link between religiosity and the belief in conspiracy theories? It is clear that research evidence is not straightforward. On the one hand, there is indirect evidence that religiosity is positively correlated with the belief in conspiracy theories. Broader beliefs that support conspiracy theories in general are assumed to underpin the tendency to believe in conspiracy theories (van Prooijen & Douglas, 2018). Beliefs in God that have been connected with perceiving the world as a place where everything is planned and controlled (Laurin, Kay, & Moscovitch, 2008) might well serve this function. Indeed, previous research has linked religiosity to higher conformity and security values (Schwartz & Huismans, 1995), stronger conservatism and traditionalism (Norris & Inglehart, 2004), and higher political conservatism (Esmer & Pettersson, 2007). As there is no room for coincidence, random events are threatening and seen as a consequence of secret actions performed by a group of malevolent people (Imhoff & Bruder, 2014), and so religious individuals with high religious identification may be more inclined to endorse conspiracy beliefs than non-religious individuals.
>
> On the other hand, recent studies seem to suggest that both more conservative and religious and less conservative and non-religious individuals may adhere to conspiracy beliefs for different reasons (e.g., Farias, 2013). This notion represents the functional view on conspiracy beliefs and the so-called belief replacement hypothesis, according to which people are naturally predisposed to believe and that those who reject religion, intuitively choose something else to replace it with (e.g., Newheiser, Farias, & Tausch, 2011). Based on this view, atheists too, whether explicitly or implicitly, espouse various types of beliefs that are meaningful, help them to explain the world and, ultimately, can play a compensatory role in dealing with adverse circumstances. According to Newheiser et al. (2011), Existentialism, New Atheism, Humanism, and Marxism are examples of such beliefs systems endorsed by atheists, but also less clearly structured beliefs, like conspiracy theories, can appeal to atheists.

(Actually on this kind of theorizing angle, there are more publications; there's even a volume, but empirical ones are actually much scarcer on the link with religious aspects.)

If you're curious as to some methods details in this Australian study, anti-intellectualism was measured on an ad-hoc scale mostly dealing with questions regarding trust in experts and the value of (higher) education. Belief in conspiracy theories was fairly standard in asking about whether the official explanation for things like 9/11, the death of Lady Diana or the assassination of JFK (interestingly perhaps, no mention of global warming, even though that's sometimes centrally featured in contemporary US research on conspiracy theories.) The intensity of religious belief was measured with questions like how often the subject departed in everyday life from the prescriptions of their religion etc.

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I've not read the full paper in this case, but the above finding from Australia seems confirmed in another study:

> Belief in conspiracies is not restricted to the fringe dwellers of society. International research suggests that such beliefs are quite common and that conspiracy theories may serve three basic psychological motives (i.e., epistemic, existential, and relational) for individuals. Yet, little is known about conspiracy theory awareness or belief in Australasia. We report the first large systematic investigation of system-justifying motives using two nationally representative samples of Australians (n = 1011) and New Zealanders (n = 754). Our findings show that almost all are aware of local and international conspiracies, the majority endorse one or more, and that all three psychological motives consistently relate to conspiracy belief, but not to awareness. **In a series of hierarchical multiple regressions, we find that relational (i.e., increased anomie and disillusionment with the government) and existential motives (i.e., less trust in others and *increased religiosity*) are uniquely and relatively more important than epistemic needs (i.e., decreased analytic thinking) as predictors of increased local and international conspiracy belief.** Findings are discussed in terms of the importance of understanding conspiracy theories as an ideological belief system that may function to serve underlying psychological motives.

This one is probably more interesting/convincing as it used a nationally representative sample, not often done in psychology research. It also used a fairly "thick" index of 8 "international" conspiracy theories, ranging from 9/11, aliens, jfk, chemtrails, vaccines, to global warming, asked as separate question... plus seven "local" ones, like in the case of Australia, about the Port Arthur shooting, the death of PM Harold Holt etc. There's a preprint of this paper freely available at https://osf.io/4pnxy/)

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There's also a more limited study from Italy, which only inquired about a specific (Covid-19) conspiracy theory in relation to religion:

> Religion and conspiracy theories could show both similarities and dissimilarities. First, as alternative religiosity and conspiracy theories tend to spread knowledge stigmatized by the authorities, we expect that alternative religious beliefs are positively associated with conspiracy beliefs. Second, as religion and conspiracy theories explain events with the agency of invisible forces and detect patterns in nature, also conventional religious beliefs are supposed to be positively associated with conspiracy beliefs. Third, church attendance is hypothesized to discourage conspiracy beliefs, as exposure to religious authorities could deter the adhesion to unofficial narratives. By employing data coming from the Italian joint edition of the European Values Study–World Values Survey 2018, the paper tests the hypotheses by analysing the association between the multiple dimensions of individual religiosity and belief in a conspiracy theory on pharmaceutical companies. Results show that, **after controlling for confidence in political and religious institutions and attitudes towards science, only alternative religious beliefs, here measured by belief in the reincarnation, are positively associated with belief in the big pharma conspiracy theory**. Empirical evidence suggests taking caution when looking at similarities between conventional religiosity and conspiracy beliefs.

Given that the Catholic church has been pretty supportive of the official state messaging on Covid-19, including on vaccines, I'm not too surprised of this finding.

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Tags: cognitive-psychology, social-psychology, religion
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# Question
Title: Why actual happy experiences don't have some side effects like stimulant drugs?
Science says that the mental side effects of stimulant drugs, like depression, are caused due to the overload of dopaminergic activity in the brain, but when people experience actual great things the dopaminergic overload is basically the same, but without side effects; on the contrary. Seems like the hormonal overloads aren't the central problem at all.

So why kissing a loved one for the first time doesn't cause depression like using cocaine?

# Answer
For one, drugs work on a very specific neurotransmitter activating a specific pathway, and they also come in great doses. Whereas experiences are much more complex activating different pathways in different way and deactivating others simultaneously. Another point to take is that due to this large quantity of neurotransmitters being released at once, as in the example of cocaine, this will exhaust the synapses via both down regulation of post-synaptic receptors and also depletion of presynaptic neurotransmitters. Yet, this is an oversimplification of a hugely complex system like brain.
> 1 votes

# Answer
**To an extent, they do.**

Opponent process theory is a neurological concept that tries to explain a wide range of human perceptual phenomena. The general idea is that after some input stimulus, the body tends to infer an "opponent process" that results perceiving the opposite stimulus. This theory has been used to explain visual afterimages, which cause you to perceive a negative color image after staring at a positive color image for a little while. This theory has also been used to examine emotional states, with experiments suggesting that strong emotions tend to be closely followed by opposite ones. Colloquially, this has been referred to as a "happiness hangover", which describes a depressed emotional state that occurs after a highly positive one, such as after returning from a vacation or after everyone at your party has gone home.
> 0 votes

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Tags: neurology, dopamine
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title: How is greed different from compulsion?

text:
# Question
Title: How is greed different from compulsion?
I want to learn how is human **greed** different from **compulsion** in psychology? Which one is intentional and which one is unintentional? If it makes sense at all? One of the lecturers in our school mentioned that greed is more intentional, whereas compulsion is more an unintentional attribute of the mind. I appreciate any comments or helps in distinguishing these two. Thank you

According to the Cambridge dictionary:

**Greed**: a very strong **wish** to continuously get more of something, especially food or money

**Compulsion**: a very strong **feeling** of wanting to do something repeatedly that is difficult to control

But I don't know if it is technically sound or not?

# Answer
> 2 votes
Looking at the synonyms of the two words may be instructive. The synonyms can be visualised according to the Atlas of Personality, Emotion and Behaviour as:

Of note:

1. Greed is therefore a more dominant behaviour than compulsion.
2. Compulsion is more internal, whereas greed is more (anti)social.

# Answer
> -2 votes
Greed is the disordered desire for more than one deserves, not for the greater good but for one’s own selfish gain, and at the expense of others and society as a whole. Greed may be motivated by a variety of factors, including food, money, possessions, power, celebrity, prestige, attention, adoration, and sex. Whereas, compulsions are habitual, rule-bound behaviours that a person feels compelled to engage in in order to avoid painful situations. It is more like a strong “want” to do something over and over again that is difficult to control.

References from: "Is Greed Good?" by Neel Burton, M.D. on Psychology Today.

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Tags: definition
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