Cultural brain hypothesis and gene-culture co-evolution Recently, Joseph Henrich of UBC has been promoting his cultural brain hypothesis. The goal is to explain a selection pressure behind the development of the human brain and general intelligence. The basic premise is that our brains evolved to be better and better at accurately replicating cultural information (or memes) between generations. A secondary part of his hypothesis is that there was a tight co-evolution between culture and the genes that shape us.

This seems contrary to the more orthodox thinking of that genes shaped the base of humans largely without large-scale culture (when we were small hunter-gatherer tribes and thus culture was minimal), and then recently (on an evolutionary time scale) large-scale culture 'turned on' and there has not been a sufficient time for this to produce large genetic differences. In simplest terms, the co-evolution was minimal and instead we should think of the key players being gene evolution followed by cultural evolution (on different timescales).

To confuse things further, some scientists (like Satoshi Kanazawa of LSE) view most of what we associated with the 'perks' of human brain (such as general intelligence) as mal-adaptive on the individual level. Thus there seems to be a large distinction between the 3 general threads, which raises the question:

What is the key evidence for the cultural brain hypothesis and gene-culture co-evolution?

The only evidence I know of potential recent co-evolution of culture and genes is Dediu & Ladd's (2007) suggestion that the split between tonal and atonal languages is related to a recent (~6k years ago) mutation in the ASPM gene. Is there other evidence of recent co-evolution between genes and large-scale culture?

Related questions

Do atonal languages have a tonal ancestor?
Is religiousness a genetically heritable feature?

"evidence of recent co-evolution between genes and large-scale culture

This 2018 PLOS Computation Biology simulation study - The Cultural Brain Hypothesis examined the data from animals and humans. It found a relationship between brain size, adaptive knowledge, social learning, group size, and lifespan across the animal kingdom.

  relationships between brain size, group size, innovation, social learning, mating structures, and the length of the juvenile period that are supported by the existing empirical literature.

The study found evidence of cumulative cultural evolution explaining the brain human sizes.


Alcoholic behavior at a bar without having any alcohol? I am a recovering alcoholic sober 11 month.  I do not crave alcohol, or need it anymore. I have adapted skills that I am no longer depressed. but enjoying life again.fun, happy, with good social skills.  I have treated myself to a month in Mexico were I have vacationed over 20 years drunk at beachside bars.  This first week, I headed to the first bar with a big party crowd.  I have met 15+ people of what I used to be like.  After 3 day same time they are all drunk and acting crazy.  By the time I left all 3 days I could swear I was drunk, lost all inhabitions, over talkative Without any alcohol. Any still no craving.???

See the placebo effect, it's been known to work in situations right up to double blind studies on dogs. Very weird.

Also, I would guess you would consider yourself a people pleaser? I forget the name of it but there's a phenomenon whereby individuals begin to imitate their cohort (mirroring?, Stockholm effect?)


Do you need to pay an extra $300 to be able to retrieve data from the Emotiv Epoc via the python-emotiv library? In the Emotiv website, they offer to pay an extra $300 to access "raw EEG data". If I don't pay that, will I still be able to retrieve the EEG data with the python-emotiv library?

For the non-eeg emotiv Epoc, the SDK only offers to retrieve the actions and their values detected from the device. But no raw data.


What does "non-linear processing" mean, exactly? In the following sentence from "How does the brain solve visual object recognition?" by DiCarlo et al.:

  In sum, our view is that the “output” of the ventral stream is
  reflexively expressed in neuronal firing rates across a short interval
  of time (~50 ms), is an “explicit” object representation (i.e., object
  identity is easily decodable), and the rapid production of this
  representation is consistent with a largely feedforward, non-linear
  processing of the visual input.

I'm familiar with "feed-forward" but not with the meaning of "non-linear processing" in a neuroscience context. What does "non-linear processing" mean, exactly?

The idea of linear/non-linear in neuroscience is the same as in mathematics. A process $f(x)$ is linear if $f(\alpha x) = \alpha f(x)$ and $f(x+y) = f(x)+f(y)$ for all $x$, $y$, and $\alpha$.


Does female attractiveness correlate with age progression? I'm interested in Evolutionary Psychology and the male perception of female beauty. One of the ideas I'm trying to investigate is the correlation between female fertility and her attractiveness. A figure I heard several times is that at around age 25 females are the most fertile and thus most attractive.

I'm trying to verify this experimentally. It seems to me like a simple experiment would be to present an observer with a lineup of photos of the same woman at different ages. Everyone has photos at different ages, but I'm looking for the one where the posture and facial expressions are controlled, as to reduce variation due to factors other than age.

My question is - Are there posture controlled lineups of the photos of age progression from 15 to 50 that I can use for such experiment?

This image is from a video of a woman aging, but it has no age indication. I'm looking for something with shorter age gaps (15-16-17-18-...50). It seems one of the relevant search terms is "age progression" are there others?

In my opinion, things that I find attractive change with circumstances.  My age plays a role, how well you know someone or the more things you enjoy about them as you get to know them and then how those same things can bother you down the road or on certain days or when in certain groups.

Other factors like past experience, upbringing, things you find attractive might be qualities, or physical characteristics that a carer or influence of yours had: family members, teachers, movie stars, musicians, etc.

Ex girlfriends can change what you find attractive in future relationships.  If you have a strong distaste for an ex then you might find qualities that she had unattractive if similar qualities are found in a new interest.  Where as if you miss that person and hold them in high esteem, you may go looking for a kind of replica or replacement to satisfy the feeling you got when those qualities are present.  But you may also resent those qualities because they remind you of that other person and this might contribute to lessening the attractiveness in them.

There is no answer to attractiveness.  Some of us find it attractive to need someone to boost them up.  Physical appearance doesn't necessarily matter, e.g. if someone who had an okay home life but had a mother, aunt, or other care giver that they really cared about who never seemed to obtain any satisfaction in life and was always unhappy but still got up and did it all in hopes that the child would have a better life, and maybe did it with a fake smile just for them, now this child may find other under-appreciated women attractive and try to give them that extra spice in life that the other people they care about never seemed to see, not necessarily sexual either, though it seems to be man's MO to believe he is a gift from god to bestow upon women.  It's not as though a person has an attraction to "mother figures" or their own mother, I've never really read Freud, but it seems people who hate or fear Freud fear themselves and their own perverse minds thanks to the rash, cruel judgments of others, or their, or their parents' religion makes them feel shameful about it.  Nobody wants to be run out of town, or labeled something they are not due to something the brain automatically does due to conditioned responses. (mind you, I don't believe in free will; I'm more of an "interacting processing" guy; ref. Robert Anton Wilson 'Maybe Logic'.)

I realize this is not exactly what you were asking for, but I think any study you can conduct will have no true control, especially without an extensive psychological study done on each individual subject and possibly even pictures of the women from their lives.  Even if it is solely on physical appearance, the reasons I might like a certain kind of eyes more than the majority is perhaps I spent many crucial points of my life with someone who had eyes like that, or a "double chin and a plastic smile."


Cognitive bias believing you are good at the things you are bad at, as successes are more vivid? What is the name for this cognitive bias?

Scenario

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

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

Replace "socializing with people" with anything else.

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

It could be described as quite a few cognitive biases.  See https://en.m.wikipedia.org/wiki/List_of_cognitive_biases.

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


Is the oscillatory power inversely proportional to the frequency? I'm trying to understand neuronal synchronization/desynchronization and oscillation, as well as the psychedelic state. The following sentence confused me a bit.

Psilocybin reduced spontaneous cortical oscillatory power from 1 to 50 Hz in posterior association cortices, and from 8 to 100 Hz in frontal association cortices.

It is taken from this article on how Broadband Cortical Desynchronization Underlies the Human Psychedelic State, featured in the Abstract section.
Now, as far as I've understood, the "power" of an oscillation is the square of its amplitude. In the quoted sentence, they say that the oscillatory "power" decreased with the increase of Hertz. Judging by that sentence, it would seem that an increase in the amplitude of a neuronal oscillation means a decrease in the oscillation's frequency. Is this correct, incorrect or perhaps imprecise?

This is sort of sloppy writing about their results, and statistical significance.
In the paper, they're analyzing data in bands 1-4Hz, 4-8Hz, 8-13Hz, 13-30Hz, 30-50Hz, and 50-100Hz.

Psilocybin reduced spontaneous cortical oscillatory power from 1 to 50 Hz in posterior association cortices

means "we saw significant reductions in all of the bands except 50-100Hz".

and from 8 to 100 Hz in frontal association cortices

means "we saw significant reductions in all of the bands except 1-4Hz and 4-8Hz".
They're not saying anything in those sentences about the magnitude of the changes, only about the locations in space and in the frequency domain where they saw changes. And it doesn't really mean they don't see changes in the other bands, just that any changes there did not meet their criteria for significance. They're also sort of mixing a quantitative and qualitative assessment of the data. The sentence in the abstract refers to Figure 3 of the paper, where you can see that the magnitude and extent of the changes is far more frequency dependent than that short sentence conveys.


What neurobiological changes are associated with the end of the critical period in children? Developing children are in a critical period during which they are much better at learning certain tasks like speaking a language. After the critical period ends, children have a qualitatively more difficult time learning these tasks.

What specific changes in a child's brain are responsible for the drastic difference in learning during and after the critical period? Are these changes just to the plasticity and rate of neuorogenesis?

Notes

The best understood critical period is phoneme recognition and production; I am fine with answers that are specialized to this task.
It is important to explain how the neurobiological changes produce a change in learning that seems so qualitatively different and sudden compared to the gradual decreases in learning at other times.

Related questions

How is a young child able to learn language so easily?

Why does neuroplasticity decrease in adults?

Computational models of early learning in children

The truth is, we don't fully know. There are likely a number of factors. One of them seems to be the Brain Derived Neurotrophic Factor (BDNF). This molecule seems to be involved with maintaining and encouraging neuron growth. In Rats with a transgenically accelerated rise in BDNF levels, the critical period began earlier, and finished earlier as well (Huang et al., 1999). This doesn't exactly get at the heart of the question, because clearly there is some interaction between experience and expression of this gene. It's a good starting point, however.
References
Huang, Z.J., Kirkwood, A., Pizzorusso, T., Porciatti, V., Morales, B., Bear, M.F., Maffei, L., & Tonegawa, S. (1999) "BDNF Regulates the Maturation of Inhibition and the Critical Period of Plasticity in Mouse Visual Cortex", Cell 98(6): 739-755. doi:10.1016/S0092-8674(00)81509-3


What percentage of the population have the brain anomaly associated with the inability to exhibit empathy? According to an article on livescience.com, "Narcissists' Lack of Empathy Detected in Brain Scans", research seems to indicate that a low volume of grey matter in the left anterior insula is associated with an inability to exhibit empathy.

  Researchers used magnetic resonance imaging to scan the brains of 34 people, including 17 individuals who suffer from narcissistic personality disorder, and found that pathological narcissists have less gray matter in a part of the cerebral cortex called the left anterior insula.

What percentage of the population have this particular condition?

In short, the question cannot be answered as-is.  I will explain why, and then answer a broader question that you may find useful instead.

Reverse Inference:

As background, consider the common problem of reverse inference: Suppose we identify subjects with relatively low grey-matter volumes (GMV) in the left anterior insula (LAI).  Can we conclude that these subjects have low empathy?  Well, the source paper for the referenced article already says ... not really:

  GM volume of the left anterior  insula  was  marginally,  positively
  correlated  with emotional empathy (... p<.10 ...).

What about NPD, can we conclude that they have NPD?  Well, subjects with low LAI GMV might have NPD, or they might just be good singers!  Or maybe they are just good at learning new languages!  In fact, low LAI GMV is associated with some cognitive advantages, as well as many mental disorders.  See, one of the problems with reverse inference is that psychological constructs simply do not line up well with gross neuroanatomical features - that is, brain regions do multiple things.

Anatomical Abnormality:

A second issue is with the concept of an abnormality.  Although the source paper discusses "structural abnormalities in fronto-paralimbic brain regions of patients with NPD," it does not define this abnormality.  Consider this figure from the paper:

Here, the vertical (Y) axis represents LAI GMV.  It does appear that NPD patients (green) have lower LAI GMV than healthy controls (yellow).  However, where is the abnormality?  What volume difference constitutes an identifiable condition?

Normal Distribution:

Technically, we should also be concerned with the low power of this paper (only 17 subjects in each group).  For example, an earlier study (with 11 subjects in each group) found differences in the right anterior insula rather than the left.  Hmmm...  Replication crisis anyone?  But let's put that aside for a minute, and consider the question at hand.

Suppose for a minute that low LAI GMV did indicate something about empathy (though it probably does not), and that there was a definable abnormality of LAI GMV (though there probably is not), what percentage of the general population would have such an abnormality?

Well, it's reasonable to use a normal distribution to estimate this.  For this, we need average and standard deviation values for LAI GMV.  I am not aware of a meta-analysis looking at this, but some individual studies report such values.  For example, this study of 39 subjects reports LAI GMV (corrected for total brain size) mean = 2209mm3 and std = 214.2mm3.  Supposing that this is representative of the general population (I wouldn't assume that, but it's a start), a normal distribution might look like this:

For this example, I just went with the cut-off being the mean for clinical patients in the study (2124mm3), resulting in about 35% of the population below the cut-off, but you can construct your own graph with whatever cut-off you deem useful for your purposes.


What causes people to betray each other when facing the prisoner's dilemma? When confronted with the Prisoner's Dilemma, people often refuse to cooperate. Instead, they choose to betray other people, even when cooperation yields a more favorable outcome.

Why do people behave in that way? Is it a genealogical feature which is embedded during evolution?

'Short' answer
The way people respond to the prisoner's dilemma strongly depends on how the experiment is set up. In a repeated game, where the same 'prisoners' meet each other multiple times, the tit-for-tat strategy seems to be favored. This, because contenders learn the other's behavior and start anticipating the choice from their opponent to manipulate the outcome. It is not so that people by default betray their opponent. The betrayal (confession) is the selfish option and is favorable when you have no idea what the other will do, as it will always work in favor of yourself. The cooperation (keeping silent) is the most risky one and you only do that when you like to take big risks (unlikely, most people don't), or when you have a fairly good idea what your opponent will do.

Background
The prisoners’ dilemma is about cooperation and competition and applies to social settings, business and politics. In the traditional version of the game, the police have arrested two suspects A and B. Both were involved in he same crime and they are interrogated separately. The police offers A and B to confess and by doing so giving away the accomplice, or to keep silent (source: Library of Economics & Liberty).

When A will confess and gives away B, A will be granted a shorter sentence as A has confessed and has aided the cops in sentencing B, and vice versa when B confesses. If A so confesses, but B holds silent (not knowing he has been given away), B will face an exceptionally harsh sentence because of refusing to admit his crimes (say 5 years in jail).

When both confess they will both face reduced sentences because they are helping the police as a witness (say 2 year in jail).

When both keep silent they can only be sentenced on minor charges because of a lack of proof (say a sentence of just 1 year).

The “dilemma” faced by the prisoners is that, whatever the other does, each is better off confessing than remaining silent. But the outcome obtained when both confess is worse for each than the outcome they would have obtained had both remained silent.

The prisoner's dilemma can be viewed at as a puzzle, illustrating the conflict between individual and group rationality. A group whose members pursue rational self-interest may all end up worse off than a group whose members act contrary to rational self-interest. More generally, if the payoffs are not assumed to represent self-interest, a group whose members rationally pursue any goals may all meet less success than if they had not rationally pursued their goals individually (source: Stanford University).

A slightly different interpretation takes the game to represent a choice between selfish behavior and socially desirable altruism (behavior of an individual that benefits another at its own expense). The move corresponding to confession benefits the actor, no matter what the other does (selfish), while the move corresponding to silence benefits the other player no matter what that other player does (altruism). Benefiting oneself is not always wrong, of course, and benefiting others at the expense of oneself is not always morally required, but in the prisoner's dilemma game both players prefer the outcome with the altruistic moves to that with the selfish moves. This observation has led David Gauthier and others to take the Prisoner's Dilemma to say something important about the nature of morality (source: Stanford University).

Now - to come to your question - you talk about 'betrayal' (which is probably referring to 'confessing') and cooperation (probably referring to 'holding silent'). You have to realize that keeping silent means you have to know that the other person will (likely) do that too. In a one-shot situation you cannot know. However, it is only when the game is repeatedly performed, and when the subjects can learn the behavior of their 'accomplice' that subjects start to make educated guesses. A particularly fruitful strategy, surprisingly, in a repeated game is the 'tit-for-tat' approach, an almost childish approach to the dilemma, where people cooperate with their partner on the first round, then adjust their behavior to match your partner’s, as in, you do to them what they just did to you. If your partner cooperated (stayed silent) the last time, you also choose to cooperate (stay silent too) this time; if they defected (confessed) last time, you respond in kind by retaliating (confessing) against them (source: Seltzer in Psychology Today, 2016).


Thinking with organs/systems other than the brain Neurohormones are produced in many different bodily systems other than the brain--skin, intestines, stomach, etc. Has there been any research suggesting whether or not some people might actually perform cognitive functions normally associated only with the brain (like processing sensory input to make complex decisions) with parts of their body other than their brain?

For example, crows have demonstrated they are capable of complex problem solving, even though they do not have a cerebral cortex. Scientists now believe crows use their telencephalon to perform complex reasoning tasks.

Thus, crows use a part of their physiology not previously associated with complex reasoning for complex reasoning.

So, to extend the idea even further, could humans also be using organs or systems to handle processes usually presumed to be handled only by the brain?

Since so many bodily systems produce neurohormones, they seem like likely possible candidates.

Has any research been done to test this proposition?

To answer your question – no. It is the brain that ‘thinks’ and does complex cognitive reasoning. And actually, it depends what you mean by ‘thinking’. I have studied Neuroscience for a long time and there is no evidence to suggest that the type of complex reasoning you are talking about is performed by any organ other than the brain (in any animal).

It is true that other organs than the brain produce neurohormones, but it doesn’t mean these organs are the site of action of these neurohormones.

As for the specific parts of the brain involved – I don’t know – there is still a lot of research on this going on. The telencephalon is part of the brain, and includes both the cerebral cortex and sub-cortical regions. There is strong evidence to suggest the prefrontal cortex (cortex) and hippocampus (sub-cortical) are highly-involved in complex reasoning. And many other parts of the brain are also involved in conscious and unconscious cognitive processes.

Yes, we also have a brainstem, a spinal cord and an enteric nervous system, which perform complex neural computations – but they do not ‘think’ the way we commonly think about thinking. As for non-neural parts of an organism – there is no evidence that those ‘think’.

I hope this help. I'd be interested in what others have to say on this.

Regards

HM

BSc (Biomedical Sciences – Neuroscience) (UCL)

#

Here are some references that I studied from last year:

These University-level textbooks:
--- "Anatomy and Physiology" by Tortora et al;
--- "Neuroscience" by Purves et al;
--- "Principles of Neural Science" by Kandel et al;

Also:
The Making of Memory by Steven Rose;
The Human Brain by Susan Greenfield;

From Neuron to Cognition via Computational Neuroscience
.https://mitpress.mit.edu/neuron-cognition

Cerebral cortex – Scholarpedia article
www.scholarpedia.org/article/Cerebral_cortex

An integrative theory of prefrontal cortex function,
Miller & Cohen 2001, Annual review of neuroscience

The hippocampal system mediates logical reasoning about familiar spatial environments, Goel et al 2004 - Journal of Cognitive Neuroscience, MIT Press

Role of the hippocampus in imagination and future thinking
Maguire & D Hassabis - 2011 - PNAS

Think Twice: How the Gut's "Second Brain" Influences Mood and Well ...
www.scientificamerican.com/article/gut-second-brain/

may be useful:
.http://engineering.mit.edu/ask/how-does-random-group-molecules-form-thinking-breathing-human ;;;;;
.https://www.theguardian.com/science/neurophilosophy/2013/aug/09/a-new-way-of-thinking-about-how-the-brain-works

As for evidence that anything else than networks of neurons can enable cognitive processes – eg. skin in your leg or bone in your arm – I have never seen. Although computer transistor circuits are a possible (non-biological) candidate.


Taking Control of Your Dream I experienced a weird situation a while back wherein I was dreaming hut was pretty sure I was in a dream and could control it to my wishes. I even had a break in my sleep and immediately went back to sleep and was again in the same situation. Can someone try to go in this state by planning or is it purely random?

The term for this phenomenon is "lucid dreaming". It is common to have some lucid dreaming experiences, but different people have different occurrence rates of lucid vs non-lucid dreams, and the level of "control" varies as well.

A previous SE Q&A addresses some of the possible influences on lucid dreaming including the potential to learn to have more lucid dreams as a skill.


Cognitive Behavioral Therapy 101 Let's say that I'm completely green about psychology and CBT (like I really know nothing, apart from that CBT exists). Is there a good introduction/ seminal work, but with relatively low barrier of entry and not too massive (something that could be learned/ studied in several evenings)?
I'm aware of this question, but what I'm looking for specifically is a book or a more involved/ in-depth resource.

I think that you should look at one of the more well rated books on CBT.

Aaron beck is the father of CBT so maybe start with his book if you can't make a decision.


How do our emotions toward a subject affect our brain activity within similar activities? I'll bring an example: there are people who love to dance and could do it for hours. Yet, if you'd make them run a long distance they would get tired really soon just because they don't like running not because they wouldn't have the stamina. On the other hand there are people who love long distance running and could run for hours yet if they are forced to dance they get easily tired.

Both activities are physical so while doing either of them, our brain releases endorphins, which make us feel good. However it seems that just our emotion toward the activity we are doing defines whether we actually feel good.

So my question is:
Is there any difference in brain activity while doing something you love or doing something similar you don't like?

If our emotions do affect our brain activity significantly, would it be possible to psychologically train ourselves to like/dislike a certain activity we want to do more/less?

Ok, so since it has been two years and no-one has answered, and this is indeed a very interesting question, here is my attempt to shed some light on it.

  Is there any difference in brain activity while doing something you love or doing something similar you don't like?

Yes, without getting too deep into specifics - there certainly difference. Primarily these are that doing something that you love will produce more dopamine than doing something you dislike [e.g., 1]. Dopamine is linked to motivation to act and energy hence why it is easy to do more of the things that you enjoy [1].

  If our emotions do affect our brain activity significantly, would it
  be possible to psychologically train ourselves to like/dislike a
  certain activity we want to do more/less?

Yes, I think this can be done by managing the rewards involved. Think about the dopamine production - how do you maximise this, while minimising other detrimental factors (e.g., stress/cortisol).

Here are some ways to do this:

Break down the task so that you get a dopamine boost everytime you get one part done [e.g., 1]
Manage your expectations - much of reward is about expectations. If you want to be better than before when doing something, as opposed to be the best, then you are much more likely to find something.
Listen to music - in some cases this can raise dopamine levels to ensure that you have sufficient motivation to work [2]
Consume substances that will increase dopamine, like st johns wort, or its precursors, like Tyrosine.
This article [3] provides a set of potentially useful approaches that may be of use. However, before adopting them I would investigate the literature cited.

[1] Hoebel, B. G., Rada, P. V., Mark, G. P. and Pothos, E. N. (1999) 'Neural systems for reinforcement and inhibition of behavior: Relevance to eating, addiction, and depression'.

[2] Salimpoor, V. N., Benovoy, M., Larcher, K., Dagher, A. and Zatorre, R. J. (2011) 'Anatomically distinct dopamine release during anticipation and experience of peak emotion to music', Nat Neurosci, 14(2), 257-262.

[3] https://www.psychologytoday.com/blog/the-athletes-way/201112/the-neuroscience-perseverance

I am happy to clarify or expand on any part of this answer if you want, so just let me know.


'Model-free' learning in humans In reinforcement learning, there is a stark distinction between model-based and model-free learning algorithms, where model-free methods don't make use any explicit information about the dynamics of the environment.

It seems like this distinction would have some analog in human learning, but I'm having a very hard time finding any mention of it. Perhaps it would conditioning versus more cognitive forms of learning? I'd be overjoyed if someone could find an article using the term 'model-free' to refer to some aspect of human learning, or just reassure me of the term's correct human analog.

Does research on human learning featuring a model-free/model-based distinction exist?

As per the comments to the question, human research observing this distinction does exist. CHCH possibly alludes to an article by Gläscher, Daw, Dayan and O'Doherty (2010) which concisely defines the difference between model-free learning and model-based learning:

  Reinforcement learning (RL) uses sequential experience with situations (“states”) and outcomes to assess actions. Whereas model-free RL uses this experience directly, in the form of a reward prediction error (RPE), model-based RL uses it indirectly, building a model of the state transition and outcome structure of the environment, and evaluating actions by searching this model.

Gläscher et al. (2010) report fMRI evidence for neural activity consistent with model-based learning in the human intraparietal sulcus and lateral prefrontal cortex, and for model-free learning in the ventral striatum. They conclude:

  This finding supports the existence of two unique forms of learning signal in humans, which may form the basis of distinct computational strategies for guiding behavior.

References

Gläscher, J., Daw, N., Dayan, P., & O'Doherty, J. P. (2010). States versus rewards: dissociable neural prediction error signals underlying model-based and model-free reinforcement learning. Neuron, 66(4), 585-595.


Dopamine dysregulation syndrome in non-Parkison's subjects? I realize that giving L-dopa or similar drugs to people who don't need it would be unethical owing to their side effects*, but given that L-dopa is abused by some Parkinson's disease patients, are there perhaps some reports of similar side-effects/syndrome in non-Parkison's individuals who might abuse L-dopa? I basically want to know whether the drug-induced dopamine dysregulation syndrome can show up in more or less "healthy" (not counting the abuse itself) individuals. I'm aware of course that stimulants (amphetamine, cocaine etc.) can also produce some of the same effects, but these are drugs with a more complex pharmacology.

*Actually, after writing the above, I found out it was given in a fairly recent 2012 study which found no mood effects. It also mentions nothing like dysregulation syndrome being observed in these healthy volunteers. Furthermore, it says that testing higher doses "will be difficult, though, since higher doses of all currently available drugs that selectively augment DA neurotransmission are limited by side effects such as nausea, vomiting, dizziness and drowsiness." So I'm guessing abuse potential in healthy people is nearly nil because of this. Nevertheless, perhaps some accidental poisioning or other odball report exists.

Not quite the features of dopamine dysregulation I was looking for, but plain psychosis (persecutory delusions and auditory hallucinations) was discovered in a case of conversion disorder who imagined had Parkinson's and self-medicated. Of note is history family of schizophrenia, but psychosis subsided

Also in not quite healthy subjects, there's a 1971 study of L-dopa in depressed patients. Mood elevation was reported in this study (unlike in the one on healthy volunteers) and some sobjects developed hypomania, but practically all who did had mania before (so they were bipolar). But there's not much detail on the hypomanic features developed on L-dopa. The dosage was higher in this old study, mood effects were not noted until dosage exceeded 300mg, which above the one used in the 2012 study on healthy volunteers.


Why does speaking with rhythm help a subject get into a trance? Various hypnotism teachers tell you to speak with a relaxed voice with rhythm. You can see Derren Brown on this in The Experiment - The Assassin (from 4:48 to 5:40):

  Soft, rhythmical language, repeated phrases ...

Also here, in a paper from Robin Allott:

  A number of elements in successful oratory can be identified. Oratory uses some of the techniques also found in poetry: sound patterns (assonance, alliteration, repetition); strongly marked rhythmic patterns.

Why does rhythm help getting the subject in a trance?

This is not exactly my area, but I suspect it simply may not be anyone's area.
It is not clear from the research literature that speaking rhythmically does help get into a trance, mostly because it is not currently clear that "trance" is distinct from other forms of dissociation (though dissociation is often confusingly described as "trance-like" or variations thereof). The closest recent paper I could find (Becker-Blease, 2004), simply reports on subjectively reported associations between certain kinds of music and the experience of a "trance" state, but this does not answer the questions of why or whether speaking rhythmically induces dissociative states.
A non-paywalled review of dissociation and dissociative states in a clinical context can be found in a Review of Psychiatry chapter by Putnam, 1991. Putnam employs the following definition of dissociation:

Dissociation is a process that produces a discernible alteration in a person's thoughts, feelings or actions so that for a period of time certain information is not associated or integrated with other information as it normally or logically would be.

Unfortunately, while subsequent literature in the same line of research has tentatively described a difference between clinical and nonclinical dissociative experiences (Waller, Putnam and Carlson, 1996), this was only descriptive, and did not attempt to investigate ways of inducing dissociative states. The focus appears to have remained on clinical dissociation.
In conclusion, the literature and evidence currently does not seem to distinguish between the two possibilities that nonclinical dissociation either can or cannot be induced by rhythmic speech, and there does not seem to be any meaningful consensus or even particularly influential views on the cognitive processes underlying nonclinical dissociation. It simply does not seem to be an active area of psychological research.
References

Becker-Blease, K. A. (2004). Dissociative states through new age and electronic trance music. Journal of trauma & dissociation, 5(2), 89-100.
Putnam, F. W. (1991). Dissociative phenomena. Review of psychiatry, 10, 145-160.
Waller, N., Putnam, F. W., & Carlson, E. B. (1996). Types of dissociation and dissociative types: A taxometric analysis of dissociative experiences. Psychological Methods, 1(3), 300.


Is serotonin conclusively linked to depression? Some highlights from the article "The Depressing News about Anti-Depressants":

ever since a seminal study in 1998, whose findings were reinforced by landmark research in The Journal of the American Medical Association last month, that evidence has come with a big asterisk. Yes, the drugs are effective, in that they lift depression in most patients. But that benefit is hardly more than what patients get when they, unknowingly and as part of a study, take a dummy pill—a placebo. As more and more scientists who study depression and the drugs that treat it are concluding, that suggests that antidepressants are basically expensive Tic Tacs.
One team of researchers wondered if antidepressants were "a triumph of marketing over science." Even defenders of antidepressants agreed that the drugs have "relatively small" effects. "Many have long been unimpressed by the magnitude of the differences observed between treatments and controls," psychology researcher Steven Hollon of Vanderbilt University and colleagues wrote—"what some of our colleagues refer to as 'the dirty little secret.' "In Britain, the agency that assesses which treatments are effective enough for the government to pay for stopped recommending antidepressants as a first-line treatment, especially for mild or moderate depression.
But if experts know that antidepressants are hardly better than placebos, few patients or doctors do. Some doctors have changed their prescribing habits, says Kirsch, but more "reacted with anger and incredulity."
Doctors see with their own eyes, and feel with their hearts, that the drugs lift the black cloud from many of their depressed patients. But since doctors are not exactly in the habit of prescribing dummy pills, they have no experience comparing how their patients do on them, and therefore never see that a placebo would be almost as effective as a $4 pill. "When they prescribe a treatment and it works," says Kirsch, "their natural tendency is to attribute the cure to the treatment." Hence the widespread "antidepressants work" refrain that persists to this day.
Right about here, people scowl and ask how anti-depressants—especially those that raise the brain's levels of serotonin—can possibly have no direct chemical effect on the brain. Surely raising serotonin levels should right the synapses' "chemical imbalance" and lift depression. Unfortunately, the serotonin-deficit theory of depression is built on a foundation of tissue paper. How that came to be is a story in itself, but the basics are that in the 1950s scientists discovered, serendipitously, that a drug called iproniazid seemed to help some people with depression. Iproniazid increases brain levels of serotonin and norepinephrine. Ergo, low levels of those neurotransmitters must cause depression. More than 50 years on, the presumed effectiveness of antidepressants that act this way remains the chief support for the chemical-imbalance theory of depression. Absent that effectiveness, the theory hasn't a leg to stand on. Direct evidence doesn't exist. Lowering people's serotonin levels does not change their mood. And a new drug, tianeptine, which is sold in France and some other countries (but not the U.S.), turns out to be as effective as Prozac-like antidepressants that keep the synapses well supplied with serotonin. The mechanism of the new drug? It lowers brain levels of serotonin. "If depression can be equally affected by drugs that increase serotonin and by drugs that decrease it," says Kirsch, "it's hard to imagine how the benefits can be due to their chemical activity."

Is this article true?  What evidence is there that serotonin is linked to depression?

It's all about the receptors, really.  There are 7 families of serotonin receptors that perform different functions within the brain, and according to Wikipedia 14 different subtypes have been discovered.

The article assumes that a blanket level of serotonin would be sufficient to "perk" up the brain, wherein it is much more complicated.  Serotonin serves to modulate the level of excitation or inhibition depending on the circumstances.  Most of the "effect" from today's antidepressants is related to modulating projections from the dorsal raphe in the brainstem to dopaminergic neurons in the frontal cortex, but some of the serotonergic neurons in the basal ganglia can be hyperactive in situations where there is mild psychosis.  So, depending on the etiology of the depression, suppressing those neurons local to that portion of the anatomy can actually be helpful.

So, it's less to do with the transmitter that is being discussed, and everything to do with which subtypes of receptors are being agonized or antagonized.  While we have learned a tremendous amount about the relationships between neurotransmitters at different nuclei, we still have a lifetime or more of research to go.


What are the major changes in the APA Publication Manual from 5th to 6th editions? A lot of journals use APA style for journal article submissions. In 2009 APA released the 6th edition with several changes to the 5th edition.

What's a good summary of the important changes in the 6th edition?
Or, alternatively, what is a good online resource listing these changes?

If you're going to be submitting articles to APA journals you should have access to the APA Publication Manual 6th edition. And it is useful to use a template (see here for discussion of 6th edition LaTeX packages) and a citation system that supports the rules.

There are changes that permit new things (e.g., longer abstracts, bullet lists, and keywords are permitted, single-spaced tables) and there are new suggestions (e.g., stronger encouragement to report confidence intervals; you can say "subjects" if you want; "I" and "we" are recommended over "the researchers").
However, if you already know the 5th edition, then  changes of particular interest are those  where compliance with the 5th edition would actually lead to violation of 6th edition rules.

Changes that stood out to me:

Provide two spaces at the end of sentences (but this doesn't make much sense if you use LaTeX)
Formatting of headings have changed and are simplified so that five-heading papers have the same first four headings as four-heading papers
Figure captions are now placed on the same page as the figure below the figure.
Tables and figures now appear before appendices
Footnotes are now placed on the same page that they are referenced.
Report p-values to two or three decimal places exactly and those less than .001 as p<.001.

References changes that stood out to me:

Include city and state for book publishers even if city is well known
Provide DOI with any references that have a DOI

General summaries of changes from 5th to 6th edition

Of course there are lots of little changes, check out some of these references for some other reviews of changes and resources:

John Dugan has a good summary of the changes in the 6th edition: mentions changes to end of sentence spacing, running head, headings, bias, repeated citation of same source in same paragraph, recording publisher location, references with 6+ authors, and DOIs.
Ace-editor provides an overview of changes
The APA has a tutorial on the 6th edition. My preference was to mute the voice over and just read the text.
Sample papers in 6th edition: one experiment paper from APA and a two experiment paper from APA, another example with commentary
The official APA style blog has a few posts on 6th edition changes.
Fairly extensive set of notes listing changes
Jody Davis lists changes
Hughes (2010) et al provide an academic review of the changes.
General set of guidelines on APA 6th edition from Indiana Wesleyan University

References

Hughes, G., Onwuegbuzie, A., Daniel, L., and Slate, J. (2010).
Editorial: Apa publication manual changes: Impacts on research reporting
in the social sciences. Research in the Schools, 17(1). PDF


What are the considerations for using wide-reaching messages and training over individual-focused efforts for changing behavior? In most places that I've worked, when some sort of problem arose or corrective action needs to be taken, one of the first responses is to send mass emails at an organization or team level and set up mandatory group training sessions. Sometimes, this is in place of an effort to correct individual actions that led to the problem on a personal level.

Does the use of broad messages (email, group training, individual training mandated for all individuals) have an impact on behavior that is equal to or greater than the use of individually-focused efforts?

I realize that in some cases, the occurrence of a problem could indicate a lack of training that does need to be addressed at a larger level to minimize future occurrences. I also realize that that some incidents might be accidental - the person realized that they did or didn't do something and personally took corrective action to prevent it in the future. However, I'm especially interested in cases where an individual performed some type of action (or inaction) that led to the occurrence of a problem and did not take corrective action on their own and if group-oriented messages have a chance of changing their behavior.

The first thing that comes to mind when reading this is diffusion of responsibility. Because responsibility has not been explicitly assigned, as it would be in a one-on-one meeting, people tend to feel like they do not need to do anything.


Is "Schizophrenic" considered to be a derogatory or offensive term? In US English, "Schizoid" is considered a derogatory term, while "patient/person with Schizoid Personality Disorder" is the "politically correct" term (and more accurate).

For this reason I wanted to be sure, is calling someone "Schizophrenic" (assuming the diagnosis is correct) considered offensive in any way? Is is more "correct" to use the full "patient/person with schizophrenia"?

You never know what's gonna offend someone...That being said, "hallucinations in people with schizophrenia" does seem the safer option, but "schizophrenics" (not capitalized) is used plenty often. Here's an interesting Google result:

  Schizophrenics Anonymous (SA) is a self-help group for persons who have schizophrenia or a schizophrenia-related illness.

I don't see them using "schizophrenics" outside of the title though, which further supports the use of "persons / people with schizophrenia". This follows a general guideline: one should avoid defining people by their afflictions and emphasize their personhood foremost. It might seem trivial with occasional use, but conflating a condition with an object category (person) might affect perception of those people, including their self-perceptions / identities, since these are largely matters of emphasis already.
(This is armchair theorizing without references...or any arms on the chair...Please edit or comment with any support or disagreement.)


What cognitive bias prevents you from discarding stuff? Let's say person is moving homes and has lots of kids toys, suits, shirts, ties and other stuff that he seldom uses.

He is am planning to sell it all in a car boot sale even if he knows that it's counter productive. He would have to use ~30£ on entry fees and fuel, without even accounting for Sunday lost.

Logical solution would be just drive to the nearest skip or charity shop, and yet he can't make himself to do it, which of cognitive bias is at play here?

I don't think this is 'sunk cost' because he is loosing that stuff anyway, it's just that loosing it and knowing that someone else will be able to use it somehow makes ones loss more acceptable, which is sub-optimal and suggests a bias.

One possible explanation for the scenario you are describing is Endowment effect.

  In psychology and behavioral economics, the endowment effect is the
  hypothesis that people ascribe more value to things merely because
  they own them.

One of the theories that explain the phenomenon is based on loss
aversion :

  It was proposed by Kahneman and his colleagues that the
  endowment effect is, in part, due to the fact that once a person owns
  an item, forgoing it feels like a loss, and humans are loss-averse.


Does learning one discipline improve performance in another discipline? I have come across a lot of articles that suggest learning across disciplines would improve cognitive abilities. This is more often referred to as Integrative Learning. Also, nowadayas a lot of emphasis seems to be placed on Interdisciplinarity and cross-disciplinary research.

Thus (putting it plainly) if a economist learns psychology, his brain can draw inferences from psychology that could help his cognitive abilities in dealing with economics.

Is this true and supported by facts?
If this is true, does the brain automatically interrelates concepts or we need to train the brain in a particular manner?
Does this depend on age?

The answer to this question will depend on how you construe 'cognitive abilities.'  For instance, for certain formulations the answer is trivially yes: an economist who learns psychology may come away with psychological knowledge that could help his economics, like how to space out his studying to maximally improve retention; or how to deal with the cognitive dissonance of causing widespread financial collapse.  Demonstrations of transfer in the other direction -- from economics to psychology -- are even easier to demonstrate.  Our department, for example, has in recent years seen an influx of psychology graduate students whose backgrounds are in much more mathematically sophisticated disciplines.  These students are able to leverage their mathematical skills to great advantage in what has, in past years, sometimes been a field with excessively 'fluffy' methodology.  But in both these instances -- psych --> economics and economics --> psych -- we're talking not so much about 'transfer' of knowledge as of literal re-use.  If you buy paper plates for a picnic, can you also use them inside your house?  Of course you can.

The question gets harder when we zoom in further.  If we accept as given that the techniques of economics would be useful in the field of psychology, what about the atomic cognitive units which collectively constitute the edifice of economics knowledge?  Does the way of viewing the world one adopts when one has knowledge of economics, or the process of abstract thinking and symbolic manipulation one must acquire in the course of it, help with other disciplines in ways that do not directly relate to full-blown techniques one learns in economics?

The short answer is that nobody knows, so far as I'm aware.  Which doesn't mean that people don't have strongly held beliefs.  For many years students spent years learning Latin because it was thought to have various beneficial effects, though these have never been demonstrated to my knowledge.  Coming back to the economics example, the issue is that nobody seems to know what it even means to know economics.  Aside from the specific ability to solve economics problems, what kind of cognitive capacity can an economics expert demonstrate?  We have only begun to be able to answer this question with regards to mathematics (c.f. Ansari et al, 2005.) or to much of anything else.  Our sense of what mental representations are -- of what knowledge is built from -- is extraordinarily primitive.

However, there are substantive reasons to continue to believe in the possibility of non-trivial transfer.  The most compelling of these is the study of metaphor, for which the canonical work is probably Lakoff & Johnson's (1980) phenomenal and very readable book (see also Bowdle & Gentner, 2005; Holyoak & Thagard 1997 for more technical treatments.)  The idea is that knowledge structures representing one thing can sometimes be mapped onto knowledge structures representing another thing.  When such a mapping can be found, one is able to make additional inferences on the second thing that correspond to inferences based on the first thing.  According to these theorists, the ability to make inferences about the world that flow from these kinds of metaphorical transfer account for a large part of our intellectual ability.

An example might be useful.  A prominant metaphor, according to Lakoff and Johnson, is "An argument is a war."  According to this metaphor, we might understand a destination domain (argument) in terms of a source domain (war.)  This mapping between the two domains allows us to structure the former in terms of the latter.  Wars have winners and losers, for instance; wars end when one side surrenders or is destroyed; one succeeds in war by hurting one's enemy; and so on.  By extension, then, an argument has a winner and loser; an argument ends in surrender or destruction; and in an argument the goal is to hurt your opponent.

This construction of what it means to have argument, and of how one should conduct onself in the course of an argument, would lead to very different results than, say, the metaphor "An argument is a dance."  It's clear, from this formulation, how consequential is the choice of metaphor in constructing one's attitude to and behaviors during an argument.  Metaphors are not simply colorful language (the argument goes) they are instructions for how we might leverage certain knowledge structures and behaviors (those involving war, in this case) for application in a completely unrelated domain (an argument, in this case.)

The most powerful idea latent in this metaphorical construction of cognition is that metaphorical extension is not only (or even mostly) about language -- any knowledge representation can potentially be aligned with another, and the tools and circumstances governing the use of the former could (potentially) be used to gain 'experience' in the latter automatically, for free. (See Durso et al., (1994) for a nice example of how this might culminate in an 'insight' experience.)  And in fact, DARPA has been very interested in this kind of 'bootstrap learning' looking for ways where experience in a relatively cheap (in dollars or risk) domain might be leveraged to benefit a more expensive domain, although the results of this work have not yet lit the world on fire.

Concerning the automaticity of this process, the answer seems to be both yes and no.  Insofar as people do use some kind of metaphorical extension to understand the world, and to apply knowledge across situations, then the process occurs automatically, at least to some extent.  (Note that the details of this process are still very much in question.)  But even if it is automatic, Chrysikou (2006) showed that the cross-pollination between disparate types of knowledge can be improved by conscious effort.  In her study, subjects who spent ten minutes performing the "creative uses" task (in which they generated novel and unusual applications for various objects; for example, a creative use for a toothpick might be as a javelin for a grasshopper) solved significantly more insight problems than subjects who did not perform the CUT beforehand.  One theory for these results is that the process of coming up with creative uses energized the machinery used to create ad hoc categories (see Barsalou 1983), and that the ability to blend disparate forms of knowledge in these dynamic bundles is an important component in  problem-solving.

This seems relevant to the original question in that whatever benefit is automatically gained simply by possessing a varied store of cross-discipline knowledge, seems to be enhanced by purposeful engagement and cross-linkage between these cognitive components, an enhancement that manifests concretely in increased problem-solving performance.

All that being said, in my opinion the extent and mechanisms of cross-domain transfer are still largely undetermined.  Despite the considerable theoretical literature in support of it, at this point the proponents of deep transfer are running on faith as much as anything.

EDIT: Note that an earlier question on this site explores some of these same ideas.

References:

Ansari, D., Garcia, N., Lucas, E., Hamon, K., & Dhital, B. (2005). Neural correlates of symbolic number processing in children and adults. NeuroReport, 16(16), 1769.

Barsalou, L. W. (1983). Ad hoc categories. Memory & Cognition, 11(3), 211–227.

Bowdle, B. F., & Gentner, D. (2005). The career of metaphor. Psychological Review, 112(1), 193–216.

Chrysikou, E. G. (2006). When Shoes Become Hammers: Goal-Derived Categorization Training Enhances Problem-Solving Performance. Journal of Experimental Psychology: Learning, Memory, and Cognition, 32(4), 935–942.

Durso, F. T., Rea, C. B., & Dayton, T. (1994). Graph-Theoretic Confirmation of Restructuring during Insight. Psychological science, 5(2), 94–98. Association for Psychological Science.

Holyoak, K. J., & Thagard, P. (1997). The analogical mind. The American psychologist, 52(1), 35–44.

Lakoff, G., & Johnson, M. (1980). Metaphors We Live By. The University of Chicago Press.


How to calculate IQ from bhatia battery test? How to find out IQ from bhatia battery test? Suppose time for each of the 5 subtests is noted down. What are the steps to reach at an IQ value from here?

I hadn't heard of the Bhatia measure before. A little research (see page 42 of Sharma and Sharma) explains that it is a performance based measure of ability for children in India. In general, you should obtain the test manual to learn about the recommended scoring procedure. A quick Google suggests it might be available from here: http://www.npcindia.com/

Reference

Experimental Psychology  By Ram Nath Sharma, Rachana Sharma


Perceptual flicker when rotating my face Informal Experiment:

I look up at a wooden beam on the ceiling, or I look at the office door; both the door and the ceiling are about 2 meters from my face.
I rotate my face 90 degrees left or right at a rate of about 90 degrees per second. (You may have to adjust this rate to experience the flicker. Too fast or too slow, and you won't experience the flicker.)

Results:

My visual perception (of the edge of the door or ceiling) flickers rather than being smooth and continuous.
I typically perceive 4 (but sometimes 5 or 6) images during the rotation, which translates to 1/3 second between images or one image per 30 degrees of rotation.

Notes:

Ensure that ambient illumination doesn't flicker. Sunlight is suitable. Most electrical light that runs on AC is not.
I understand that not everyone who tries this experiment will experience this phenomenon.
This phenomenon also occurs when viewing a sheet of paper held at arm's length and pressed against a contrasting wall (e.g., white paper on brown wall). Rotating the paper instead of your face does not generate the phenomenon.
The intention of the linked YouTube video is only to show which plane to rotate.
I recorded a video of my face during the experiment. Reviewing the video, I see no eye movement.

Question:

Is there any research on this phenomenon? (I have been unable to find anything on it, perhaps because I don't know the proper terminology.)

I'm guessing that you are experiencing the interplay of two mechanisms: When you start to turn your head, the "vestibulo-ocular reflex" tries to hold the visual scene steady by counteracting your head movement. But as you continue to turn your head (apparently at about 30 deg. intervals), a "saccade" kicks in to restore your gaze to a point straight in front of your face.

A similar effect can be observed when the visual scene moves, as when you look out a train window, but in this case, rather than the vestibulo-ocular reflex, it would be "smooth pursuit eye movement" that tries to hold the visual scene steady. (Wikipedia has good articles for all three of the quoted terms.)

An interesting way to check this hypothesis would be to videotape your face as you perform the experiment and observe your eye movements in the video. I'm looking forward to a YouTube posting...


Why do some people react verbally to intrusive thoughts and/or embarrassing memories? It seems to me that there are two kinds of intrusive thoughts. The first consists of those thoughts that didn't actually occur in real life, but are nonetheless intrusive and embarrassing and disturbing to the individual (i.e. thoughts of harming someone else, or unwanted sexual thoughts directed towards individuals). The seconds consists of past memories of embarrassing moments, particularly from childhood.

I've noticed that many people will respond to these thoughts in some way. I've had many friends tell me that if I hear them 'talking gibberish' or 'making strange noises', it is because they are having a bad thought. I myself have noticed now that I will talk out loud when I remember an embarrassing thought -- but I won't speak of the thought, I will say random things, like "Okay, okay, okay" or "I love you". Usually, I will repeat a phrase over and over under my breath, until I catch myself doing it.

I've also noticed certain individuals will use verbal gestures to show that they are thinking of something negative. My father will scratch his head and blow out of his mouth for several minutes at a time when he is having intrusive thoughts, or 'conversations'.

Is there an explanation for this phenomena? Why is it that externalizing our thoughts seems to 'rid' our head of them?

It might be a way of distracting ourselves, to change the subject and deviate the focus from thoughts we don't like to anything our mind makes up.

  When anxiety becomes overwhelming, it is the ego's place to protect the person by employing defence mechanisms. Guilt, embarrassment and shame often accompany anxiety.
  https://en.wikipedia.org/wiki/Defence_mechanisms

It is also possible that some of us use this as a way to acknowledge their feelings of shame. we can see this when laughing (when its a honest laughter), as it effectively relax the athmosphere.

But in any case, we can't "get rid" of a thought. It is only discarded from the present moment and may be intrusive again at another inopportune moment; until we address the issue.


What is the scientific term for the expectation, that a personal experience positively deviates from what first- or second-hand experience suggests? What is the scientific term for the tendency of people to believe, that their expected experience positively deviates from what their first- or second-hand experience suggests?
An example for this effect would be an older European Lady dating a young African man and - despite knowing that many such relationships are dominated by asymmetric economical and romantical interests - believes, that her own relationship will be different.
Another example are people who are educated and experienced enough to know how cults work, yet fail to identify the cult they themselves are currently involved in.
Generally, I would say it is a form of self-delusion, or hope, if you want to give it a positive spin - but I am looking for a more specific term for this particular type of self-delusion.

Are you referring to the optimism bias from a social psychology perspective?

Your brain has a built-in optimism bias. The phenomenon is also often
referred to as "the illusion of invulnerability," "unrealistic
optimism," and a "personal fable."
This bias leads us to believe that we are less likely to suffer from
misfortune and more likely to attain success than reality would
suggest.2 We believe that we will live longer than the average, that
our children will be smarter than the average, and that we will be
more successful in life than the average. But by definition, we can't
all be above average.

Source: VeryWellMind


Do only humans spend a lot of time daydreaming (or having "stimulus-independent thoughts")? A paper
Killingsworth et al., A Wandering Mind Is an Unhappy Mind, Science 12 November 2010: 932 (or a free pdf) starts with the following statement:

  Unlike other animals, human beings spend
  a lot  of  time  thinking about  what  is  not
  going on around them, contemplating
  events that happened in the past, might happen
  in the future, or will never happen at all. Indeed,
  “stimulus-independent thought” or “mind wandering” appears to be the brain’s default  mode
  of operation (1-3).

While the claim is supported for humans by the cited papers and their finding:

  Mind wandering
  occurred in 46.9% of the samples and in at least
  30% of the samples taken during every activity
  except making love.

I couldn't find a strong evidence that for all other animals it is not true. Even if it, arguably, may sound plausible for domestic animals, it seems less convincing for primates, elephants or dolphins (without a proper experimental support).

Are there any research on "wandering mind" for other animals? If so, do they support or refute the "unlike other animals" line?

It seems that it is still a matter of debate whether animals are capable of mind wandering. For instance, there are a lot of publications about foresight, a future directed instance of mind wandering. Much of it comes from one group, e.g.,

  Suddendorf T, Corballis MC. (2007) The evolution of foresight: What is
  mental time travel, and is it unique to humans? Behav Brain Sci.
  30(3):299-313; discussion 313-51.

  Suddendorf T, Corballis MC. (2010) Behavioural evidence for mental
  time travel in nonhuman animals. Behav Brain Res. 215(2):292-8.

But, for a review see:

  Cheke Lucy G., Clayton Nicola S.. Mental time travel in animals. WIREs
  Cogn Sci 2010, 1: 915-930.

Or for a quite current example, see:

  Osvath M, Karvonen E. (2012;7) Spontaneous innovation for future
  deception in a male chimpanzee. PLoS One (5):e36782.


How to run a multiple hierarchical regression with both categorical and scale predictors in SPSS? I'm currently carrying out research for my masters dissertation and i've run into a critical issue while trying to analyse my data. I'm a psychology student looking into predictors of male rape myth acceptance. My predictors are Sex, Age, Ethnicity, Estimated monthly income and Homophobia. My criterion variable and Homophobia predictor are both scale data, while Sex, Age, Ethnicity and Estimater monthly income are all categorical data.
I have successfully recoded Sex into a 0= female and 1= male binary variable and also dummy coded all of my other categorical variables. I've now come to do the analysis and I'm completely clueless on how I should enter the variables into the hierarchical model and then how to interpret the results after. I've only ever conducted a multiple regression using scale predictors before. I am also only familiar with dummy variables when they are entered into a model alone without any other variables as this is as far as our teaching went regarding them. If anyone can give me any help I'd appreciate it!

Basically, you've got three kinds of predictors:

Binary (e.g., gender sex coded female = 0, male = 1):  The coefficient is the degree to which males are higher than females on the outcome variable, holding all other variables constant.
Numeric (e.g., age in years): The coefficient is the effect of being one year older on the outcome variable holding all other variables equal
Nominal (3 or more categories; e.g., ethnicity). Here you create k - 1 dummy variables (where k is the number of categories). Each dummy category is the effect of being in that category relative to the reference category holding all other variables constant.

Once you understand how to interpret the coefficients, hierarchical regression really doesn't change anything. Hierarchical regression is really the same as running a set of regression models with different predictors (they just happen to involve incrementally adding predictors).


Why might a stutterer not stutter when talking to themselves, whispering, or singing? Background: I'm a stutterer myself and have always wondered what caused my stuttering. There have been reports of the effects of certain genes and environmental factors that causes stuttering. But there is nothing really concrete as far as I know. The main cause could be a multitude of factors that are up to debate.

From my own experience, I observe that I don't stutter/get a block when I talk to myself, whisper, and sing.  Otherwise I stutter, and even more frustratingly I sometime get a speech block and can't begin to say what I want until I change my wording.

The fact that I can speak normally in certain conditions means that I have the physical ability to speak normally.

Question

Based on the neural mechanisms of stuttering, why might a stutterer not stutter when talking to themselves, whispering, singing, etc.?

I'm not an expert in this field, but this seemed interesting enough I did some reading up on the topic. The two review papers I found quickly were Prasse & Kikano (2008) and Lawrence & Barclay (1998), both from the Journal of the American Academy of Family Physicians. I have no idea whether this is a reputable journal or not.

There appear to be three types of stuttering; developmental (acquired during youth, often leaves after age 4), neurogenic (acquired due to neurological trauma), and psychogenic (secondary symptom of latent psychiatric disorder) [1]. Interestingly, the articles disagree on whether psychogenic still exists (see Etiology discussion in [2]). While both articles suggested that the etiology of stuttering is largely unknown (see here, Etiology section), theories suggest that there's a neurologic dysfunction at play and/or physical causes relating to airflow. Specifically, the neurologic dysfunction suggests increased brain activity during speech in stutterers relative to non-stutterers. There's a lot of discussion about genetics and stuttering as well; read the articles for more.

Your situation as described seems to be in the "developmental" case, with a neurologic underpinning. Assuming no car crash or other blunt force trauma in your past, your stuttering comes and goes depending on the situation (i.e., if you're in public or private). As such, the symptoms you describe are likely related to stress, discussed in both articles above. It seems to be understood that stuttering as a disorder can be overcome with time and practice, and it seems that you have managed to do that to a small amount. However, stress is a large factor in stuttering, and can in fact exacerbate the problem tremendously. For what it's worth, I can also state anecdotally that stress is a large factor in stuttering, and for some people the severity of the stutter will increase as a factor of how stressful the situation may be.

I'm not sure that this addresses the singing aspect of your question. Hopefully someone else can address that.


Is there anything in Freudian psychoanalytic theory that is scientifically sound? I guess this question is quite context dependent, and here in Sweden there is a general movement for more evidence-based psychology. I think one of our biggest medical universities recently abandoned psychodynamics in favour of a more empirical approach to the field. In this general context it feels like it often happens that Freud and his work gets ridiculed and seen as pseudo-science by a lot of people.

I have only a basic knowledge and overview in the field, but I have to confess that I currently subscribe to the pseudo-science view of Freud's work as well. Is there anything he proposed or accomplished that actually has a sound scientific basis? Have there been any studies providing empirical support for freudian psychoanalytic concepts that I can use to form a critical view of his work which is more balanced and fact-dependent?

Freudian psychology (and it's derivatives) are indeed pseudoscience, by and large.  That said, Freud was arguably the first to systematically theorize and study human behavior and cognition, and in so doing laid the foundation for the scientific study of psychology.  It's generally useful for the purpose of such discussions to distinguish between Freudian psychoanalysis and Freudian psychodynamics.  The latter is generally sound though embryonic to the point of near-uselessness to contemporary students (except of course, from a historical perspective).  As such, there are concepts in Freud's work that have been scientifically validated.

The basic premise that we're unaware of the majority of our mental processes, for example, is perfectly valid.  More generally, the idea that behavior is the sum of concrete biological forces (what Freud called psychic energy) has been substantiated by quantitative evidence time and time again.  Once again, the problem is that it's very superficial and hand-wavy by modern standards, not to mention its propensity to be severely abused.

Modern attachment theory, that is, the idea that emotional bonds are an essential part of infant development, also very clearly originates with Freud.

Most interestingly, IMHO, is the concept of defense mechanisms.  Indeed the study of psychology and cognitive science has been impeded for years because of an over-reliance on subjective self-report.  Thanks to Freud, we recognize that people can be unaware of their own misrepresentations of fact.

It's actually quite difficult to find a nook of cognitive science that hasn't been positively influenced by Freudian psychology in some meaningful way.  Freud got many things right, but wasn't very concerned with establishing the validity of his claims.  In practical terms, this means that studying Freud from a historical perspective will be quite informative, but one will have a hard time applying his theories directly to modern research or therapy.  And of course, there are a significant number of Freudian claims that have been positively disproven in all but the most metaphorical sense (the general "death wish" comes readily to mind).

Another way to look at this is as a modeling problem.  Freudian psychology proposes a number of models of how the human psyche works, most notably the Id/Ego/Superego hierarchy.  At the time, this was a very useful model, but it has since been supplanted by better models that better predict behavior.  This having been said, Freud's groundwork is readily visible:  everybody agrees that automatic non-conscious processing occurs and that it influences conscious perception.  Similarly, it's well known that top-down influences of expectation, cultural bias or attention can affect conscious processing.  In this sense, the Id/Ego/Superego model is alive and well... it's just been refined a great deal.


Is it true that acting can affect one's behavior? Is it true that acting can affect one's behaviour?

For example, if someone plays a protagonist, can this affect them to be a good person? Is there any solid evidence for this?

This is true. Mot et al. (1994) published scientific research about it. Also there are a lot of actors that claim they feel that their personality has changed since they played a role.

Also a similair practice can be used for insecure people. If they act confident it has been proven that after some time, they feel more confident as well.

Edit:

Since I'm new to stackexchange I did not know how much detail is desired. Therefore, let me expand upon my original comment.

The article states the following hypotheses:

  (1) the actor chosen to play a given character would have personality characteristics similar to that of his or her corresponding character

  (2) the actor′s self-perceived personality profile would become more similar to the character′s during the rehearsal and production period.

Later on the article states that:

  Support emerged for the second hypothesis, but not for the first. Observations regarding these findings and suggestions for future explorations are given.

The article expands upon this, but I can't access the paper, because it's pay-walled.

Reference:

Hannah M. T., Domino G., Hanson R. Hannah R. (September 1994) Acting and Personality Change: The Measurement of Change in Self-Perceived Personality Characteristics during the Actors Character Development Process, Journal of Research in Personality, 28(3):277-286


Whats the difference between BDD and hypochondriasis? I'm a new psychiatry trainee. I've run through the literature available to me (plus google), and the descriptions of body dysmorphic disorder (BDD) and hypochondriasis seem too similar. Here's what I've understood so far:

Hypochondriasis represents a general anxiety of disease/symptoms whereas BDD happens to revolve around a single issue. The former is more about somatic symptoms whereas the latter is about physical appearances. But I wonder if this understanding is correct and whether there is a clearer differentiation.

DSM-5 is the go to book for psychiatric dignoses and I would strongly recommend you pick up a copy if you are studying Psychiatry.

I am going to split my answer in 3 as you are talking about two different disgnoses and the 3rd part will be making a comparison between the two.

Hypochondriasis

The more recently approved Diagnostic and Statistical Manual of Mental Disorders (DSM-5) contains many revisions, but few are as sweeping as those involving somatoform disorders. In the updated edition, hypochondriasis and several related conditions have been replaced by two new, empirically derived concepts: Somatic Symptom Disorder and Illness Anxiety Disorder. They differ markedly from the somatoform disorders in DSM-IV.

To meet the diagnostic criteria for Somatic Symptom Disorder under DSM-5 (Page 311), patients must have:

The Somatic Symptom Disorder is considered persistant if it is characterised by severe symptoms, marked impairment, and long duration (more than 6 months).

The DSM also goes on to say that there are 3 levels of severity, which are:

Mild if only one of the symptoms specified in Criterion B is fulfilled.
Moderate If two or more of the symptoms specified in Criterion B are fulfilled.
Severe If two or more of the symptoms specified in Criterion B are fulfilled, plus there are multiple somatic complaints (or one very severe somatic symptom).

Patients with illness anxiety disorder may or may not have a medical condition but have heightened bodily sensations, are intensely anxious about the possibility of an undiagnosed illness, or devote excessive time and energy to health concerns, often obsessively researching them. Like people with somatic symptom disorder, they are not easily reassured. Illness anxiety disorder can cause considerable distress and life disruption, even at moderate levels.

In DSM-5 Page 315 it states that the diagnostic critera for Illness Anxiety Disorder is

  Preoccupation with having or acquiring a serious illness.
  Somatic symptoms are not present or, if present, are only mild in intensity. If another medical condition is present or there is a high
  risk for developing a medical condition (e.g., strong family history
  is present), the preoccupation is clearly excessive or
  disproportionate.
  There is a high level of anxiety about health, and the individual is easily alarmed about personal health status.
  The individual performs excessive health-related behaviours (e.g., repeatedly checks his or her body for signs of illness) or exhibits
  maladaptive avoidance (e.g., avoids doctor appointments and
  hospitals).
  Illness preoccupation has been present for at least 6 months, but the specific illness that is feared may change over that period of
  time.
  The illness-related preoccupation is not better explained by another mental disorder, such as somatic symptom disorder, panic
  disorder, generalised anxiety disorder, body dysmorphic disorder,
  obsessive-compulsive disorder, or delusional disorder, somatic type.

The DSM goes on to say that there are two types of Illness Anxiety Disorder

  Care-seeking type: Medical care, including physician visits or undergoing tests and procedures, is frequently used.
  Care-avoidant type: Medical care is rarely used.

  Diagnostic Features

  Most individuals with hypochondriasis are now classified as having
  somatic symptom disorder; however, in a minority of cases, the
  diagnosis of illness anxiety disorder applies instead...

Body Dysmorphic Disorder (BDD)

In DSM-5, BDD is described under Obsessive Compulsive Disorders.

BDD as described in DSM-5

  Preoccupation with one or more perceived defects or flaws in physical appearance that are not observable or appear slight to others.
  At some point during the course of the disorder, the individual has performed repetitive behaviors (e.g., mirror checking, excessive
  grooming, skin picking, reassurance seeking) or mental acts (e.g.,
  comparing his or her appearance with that of others) in response to
  the appearance concerns.
  The preoccupation causes clinically significant distress or impairment in social, occupational, or other important areas of
  functioning.
  The appearance preoccupation is not better explained by concerns with body fat or weight in an individual whose symptoms meet
  diagnostic criteria for an eating disorder.

  Diagnostic Features

  Individuals with body dysmorphic disorder (formerly known as
  dysmorphophobia) are preoccupied with one or more perceived defects or
  flaws in their physical appearance, which they believe look ugly,
  unattractive, abnormal, or deformed...

Comparison between Hypochondriasis and BDD

When you compare the two within the DSM they do differ as you suggest where Hypochondriasis is more about somatic symptoms as it is about perception of illness whereas BDD is about physical appearances.  However when you look at the International Statistical Classification of Diseases (ICD) produced by the World Health Organisation, which is linked to in the DSM with the ICD codes at the top of each Diagnostic Criteria (for example 300.82 (F45.1) for Somatic Symptom Disorder - see image above), the 10th revision ICD code - ICD-10 - which is in brackets, refers to Section F45 of the ICD and this adds to the definitions.

  F45 - Somatoform disorders

  The main feature is repeated presentation of physical symptoms
  together with persistent requests for medical investigations, in spite
  of repeated negative findings and reassurances by doctors that the
  symptoms have no physical basis. If any physical disorders are
  present, they do not explain the nature and extent of the symptoms or
  the distress and preoccupation of the patient.

...

  F45.2 - Hypochondriacal disorder

  The essential feature is a persistent preoccupation with the possibility of having one or more serious and progressive physical
  disorders. Patients manifest persistent somatic complaints or a
  persistent preoccupation with their physical appearance. Normal or
  commonplace sensations and appearances are often interpreted by
  patients as abnormal and distressing, and attention is usually focused
  upon only one or two organs or systems of the body. Marked depression
  and anxiety are often present, and may justify additional diagnoses.

  Body dysmorphic disorder
  Dysmorphophobia (nondelusional)
  Hypochondriacal neurosis
  Hypochondriasis
  Nosophobia

  Excl.:
  delusional dysmorphophobia (F22.8)
  fixed delusions about bodily functions or shape (F22.-)

When reading this it confuses things as F45.2 considers BDD to be a somatic disorder as it is about perception rather than fact, however in my view, as psychiatry uses the DSM to distinguish between the two, in a psychiatric sense you get a definitive answer which you already have.

With psychosomatic disorders your mind can make your body act like it actually has the medical problem or make an actual problem like pain worse, where as in BDD your mind cannot alter the physical shape of the body.


Can habits be implemented by playing mental scenarios or playing things in your head? A significant amount of people say that you need to do things over and over again to implement a habit into your subconscious mind where you no longer have to think to do it. If, let's say, I want to implement a habit of drinking water when I walk in my bathroom in the morning but fail to do it due to the fact that this is attempted in the morning 2 minutes after waking where I'm still tired and less awake, would it be possible for me to implement this habit or at least become much more conscious of it by playing the scenario in my head, maybe even acting it out mid-day, or just thinking about why I should do it, etc. ?

The answer is yes and can be supported by a theory called implementation intention.

  An implementation intention is a self-regulatory strategy in the
  form of an "if-then plan" that can lead to better goal attainment, as
  well as help in habit and behavior modification. It is subordinate to
  goal intentions as it specifies the when, where and how portions of
  goal-directed behavior. The concept of implementation intentions was
  introduced in 1999 by psychologist Peter Gollwitzer. Studies
  conducted in 1997 and earlier showed that the use of implementation
  intentions can result in a higher probability of successful goal
  attainment, by predetermining a specific and desired goal-directed
  behavior in response to a particular future event or cue.


What are the effects of negative self image on cognition and brain function? All other things considered equal, what are the effects of a negative self image, on cognition and brain function?

Are there any studies that would have specific data supporting cognitive outcomes (concentration times, memory, mind body awareness) rather than just pointing to self-esteem?

In addition, what cognitive effect does positive self image have on cognition and brain function? Are there qualities in either of them that are not inverses of the other?

Some information that partly answers your questions.

There have been some studies based on these questions, a significant article related to this type of study is Self-esteem, locus of control, hippocampal volume, and cortisol
regulation in young and old adulthood (Pruessner et al. 2005).

This article makes the link between self image and the individual's 'locus of control', they found that:

  our results clearly demonstrate that self-esteem and
  locus of control are significantly linked to the volume of the
  hippocampus in healthy young and elderly subjects. Further, we
  found evidence that these two factors are also related to the acute
  and chronic regulation of the major stress hormone in humans,
  cortisol.

(Note: the authors of the article acknowledge that their data does not allow them to make firm conclusions).

Cortisol affects, amongst other things, memory, learning and concentration.  A specific study about this is in the article "Cortisol differentially affects memory in young and elderly men." (Wolf et al. 2001) and "Impaired memory retrieval correlates with individual differences in cortisol response but not autonomic response" (Buchanan et al. 2006).  From the second article/study:

  [This study] suggest that individual differences in cortisol reactivity affect memory retrieval performance, and help to explain the differential effects of stress on memory.

I will say that this is not the complete picture, but the link between self image and cortisol levels seem to be a major factor about how self image affects cognitive abilities such as learning, memory etc.


What is the test-retest improvement in Block Design test? Background:

My lab is conducting a research on perceptual training. We train participants on different tasks, and assess them pre- and post- training on a large battery of tests. Obviously, people improve in tasks that are very similar to what they trained on, but we are interested in the generalization of training. One of the tests in the pre/post battery is Block Design. We currently do not have a control group that did not train at all. We noticed that all groups improved significantly in Block Design, and we are now wondering if that's only test-retest improvement, but were not able to find data on expected improvement in the literature.

Question:

When testing subjects in the Block Design test twice, with the 2 sessions separated by roughly 4 months, what is the expected improvement?

Ronnlund and Nilsson (2006) studied performance on the WAIS block design test in a large sample of adults both longitudinally and cross-sectionally. The time difference was about 5 years. They wanted to tease out age related changes from practice effects. I believe they estimated the 5-year practice related improvement to be about 0.6 of a T score (i.e., about .06 of a standard deviation).

Benefits of practice presumably decay as a monotonically decreasing function of time between practice and retest. Thus, presumably, any practice effects would be a fair bit greater at two months than they would be at five years.

Dikmen et al (1999) performed a study involving 384 adult participants who completed several test including the WAIS Block Design on two occasions separated by between two and twelve months.
Specifically see Table 2 that reports time 1 and time 2 results:

Time 1 M (SD): 11.3 (3.0)
Time 2 M (SD): 12.0 (3.2)

Thus, the standardised increase was $d = 0.7 / 3.0 = 0.23$.

The study also reports in Table 5 practice effects for various test-retest intervals (less than 3 months, 4 to 9 months, and > 10 months). See Table 5 for more information, but in general greater practice effects were observed for WAIS performance IQ for shorter time periods. Thus, you might expect, given your two month period a slightly larger effect than the overall effect (perhaps $d=.30$ or some such).

References

Dikmen, S.S., Heaton, R.K., Grant, I., Temkin, N.R. & others (1999). Test--retest reliability and practice effects of expanded Halstead--Reitan Neuropsychological Test Battery. Journal of the International Neuropsychological Society, 5, 346-356.
Ronnlund, M. & Nilsson, L.G. (2006). Adult life-span patterns in WAIS-R Block Design performance: Cross-sectional versus longitudinal age gradients and relations to demographic factors. Intelligence, 34, 63-78.


Quit smoking supported by mental training Given that mental training/workout releases acetylcholine (something I read in a popular-scientific book and on Wiki, see also below) , and that acetylcholine and nicotine bind to the same receptors. Is it possible to reduce the craving for nicotine by doing a brain-training task such as mathematics or memorising poetry?

There is many methods to change craving for nicotine. You can train your brain by the suggesting to yourself (or by hipnotherapeutists) something as: I don't need nicothine. When you are in the trance state for exemple or when you have highly good responses for hipnosis suggestions it will be usefull. In trance people have diffrent reality and their body tell them that i can do that and people can change even chemical responses of their bodies. https://en.wikipedia.org/wiki/Hypnotherapy

Another thing is that you can focus on mathematic or poetry so much that you forget about your bad habit and when you do it again and again its Pavlov's Dog effect that it will be automatic response for your psyche. For example - your mathematics will be the cure for the craving for nicotine. However if you stop doing your mathematic, you probably will be smoking again (old habits activate again without mathematics or poetry cure).


Does the brain's reward system also work when the reward comes before the experience? Here's how I understand how the brain rewarding system works, as described by behaviorism:

When I eat a chocolate after learning, there's a chance that I'll connect the learning with the pleasurable experience of eating chocolate, which can eventually make me love learning.

Does this mechanism work even when I eat the chocolate before the learning? Is the brain connecting of cause and effect time-dependent?

Short answer
Operant conditioning through positive reinforcement is always established by applying a stimulus after the behavior. Negative reinforcers can, however, be deployed before the wanted behavior is initiated.

Background
The reward system can be seen as positive reinforcement.

In experimental paradigms (and everyday life in general), reinforcement is established by a certain stimulus presented after a certain behavior, termed operant conditioning. There are various forms of operant conditioning (Fig. 1). Without exception, the stimulus always follows the behavior.

Your example of the chocolate is an example of positive reinforcement: If you want your dog to sit on command, you may give him a treat every time he sits for you. The dog will eventually come to understand that sitting when told to will result in a treat. This treat is reinforcing because he likes it and will result in him sitting when instructed to do so.

Now, if we reverse the traditional operant conditioning process from behavior-reward to reward-behavior, then any behavior would lead to a reward because the reward has already been given. So also no behavior at all or, even worse, adverse behavior (the dog starts ripping apart the trainer) would be reinforced in this way. By definition, reinforcement is always given after the behavior, otherwise there can be no link established between stimulus and associated behavior.

Note, however, that negative reinforcement can be established with the stimulus starting before the wanted behavior has been shown. The familiar example here is the nagging parent that the kid should finally clean up its room. When done, the nagging finally stops. So a negative reinforcer can be started before the behavior. But also here, the change in the stimulus switches only after the intended behavior has been evoked.

Fig. 1. Operant conditioning. source: wikipedia

Further reading
1. Learning Theories: An Educational Perspective, Sixth Edition, Dale H. Schunk:
Page 81 (Section: Informational Variables: Pavlov believed that stimuli non-pairing would extinguish the conditioning. Giving the reward before the conditioned behavior in the question seems a lot like unpairing stimulus and behavior)


Are hallucinations mostly 'real' fantasies or are they 'real' memories? When someone has a hallucination of a person or odor does is that a fantasy which one have never seen before (so a kind of construction) or can it be a remembering but then more real as seen in the mind?

Are they considered to be the same or is there made a distinction in therapy (if necassary)?

Hallucinations involving a person or odour can be either from memory or completely made up (constructed) within the mind.  Where they are from memory they generally, but not always, take the form of flashbacks which are very intrusive in the sense that they are unwanted, and can be triggered by something the person sees or hears, but again, not always.

Neuroses and psychoses which involve flashbacks can take on any form in any combination of any 1 or more of the senses of the body:

Sight (Visual flashbacks)
Sound (Auditory flashbacks)
Smell (Olfactory flashbacks)
Touch (Kineasthetic flashbacks - sometimes referred to as tactile flashbacks)
Taste (Gustatory flashacks)

Psychoses such as Schizophrenia can involve the same hallucinations but they are different to flashbacks as they are not necessarily recalling an event from the past.  They can be completely constructed.

When a psychiatrist is making a diagnosis, using their knowledge of ,or through reference to, the DSM, they will need to be aware of the form and source of the hallucinations which will play a part in how they will form the diagnosis and treatment plan through medication and/or therapy.  The latest edition of the DSM is the Fifth Edition (DSM-5)

Therapists will need to be aware of how the hallucinations form with their client in order for the therapist to effectively help their clients to deal with them.


If a specific neuron is present in my brain, will it be present in another person's brain? For example if I have a neuron cell that fires when I say the letter 'A' and is located at a specific place in my brain, will another person have that cell at the exact same place and will it fire when he/she says 'A'?

No, unless you are a C. elegans (or have a similarly simple nervous system), and even then maybe not quite.

Wild-type C. elegans has exactly 302 neurons and they are the same neurons in different members of the species. However, even then, learning can change their nervous system so that it isn't exactly identical in two individuals.

Mammals including humans, however, have brains that are much more shaped by experience and learning. Only the general structure is the same, and even that differs somewhat. It has even been shown that different parts of the brain can be different sizes in individuals with different occupations (see Maguire et al., 2000, for example).

Maguire, E. A., Gadian, D. G., Johnsrude, I. S., Good, C. D., Ashburner, J., Frackowiak, R. S., & Frith, C. D. (2000). Navigation-related structural change in the hippocampi of taxi drivers. Proceedings of the National Academy of Sciences, 97(8), 4398-4403.

White, J. G., Southgate, E., Thomson, J. N., & Brenner, S. (1986). The structure of the nervous system of the nematode Caenorhabditis elegans. Philos Trans R Soc Lond B Biol Sci, 314(1165), 1-340.