What is the concordance rate for schizophrenia in monozygotic and dizygotic twins? What is general level of concordance for twins and is it higher for monozygotic twins?
What research is available on this?

The Wikipedia article seems to provide a summary of this information with links to the primary literature

http://en.wikipedia.org/wiki/Causes_of_schizophrenia#Genetics

  Concordance rates between monozygotic twins vary in different studies,
  approximately 50%; whereas dizygotic twins was 17%. Some twin
  studies (Koskenvuo et al; Hoeffer et al) have found rates as low as 11.0%–13.8% among
  monozygotic twins, and 1.8%–4.1% among dizygotic twins, however.

References

Koskenvuo M, Langinvainio H, Kaprio J, Lönnqvist J, Tienari P; Langinvainio; Kaprio; Lönnqvist; Tienari (1984). "Psychiatric hospitalization in twins". Acta Genet Med Gemellol (Roma) 33 (2): 321–32. PMID 6540965.
Hoeffer A, Pollin W; Pollin (November 1970). "Schizophrenia in the NAS-NRC panel of 15,909 veteran twin pairs". Arch Gen Psychiatry 23 (5): 469–77. doi:10.1001/archpsyc.1970.01750050085012. PMID 5478575.


Can a person be brilliant even though slow at resolving problems? Can a person be very intelligent, able to solve difficult problems if given enough time, yet really a slow thinker? Especially if nervous. Could such a slow thinking brilliant person get all the questions on an IQ test correct even though they were 20 minutes beyond the required end of the test?

Another way of putting this question is regarding the validity of time limits on IQ tests.  How have these been arrived at?  Have other (extended) time limits been tested?  Have such time limits yielded different (higher) scores?

There are many definitions of intelligence. I find the one given by David Wechsler (1944) useful in the context of this question:

  The ... capacity of the individual ... to deal effectively with his environment

Finding a solution quickly is sometimes necessary if you want to deal with your environment effectively. Not all problems will wait for you to solve them slowly. Which is why the concept of intelligence usually includes a time component and a person solving the same problem slower is considered less intelligent.

"Brilliance" is not a psychological concept.

Source:

Wechsler, D (1944). The measurement of adult intelligence. Baltimore: Williams & Wilkins.


What self-image do most people have? There seem to be a lot of studies about the influence of self-image on our psychology, but I've been wondering: Is there research on what type of self-image (positive, negative) most people have? Do people in Western countries tend to have a positive or a negative self-image?

Short answer:

  ... on the balance, most people tend to view themselves positively.

Longer answer:

Not much is clear about self-image.  One thing that is clear is that self-image is not one thing.  In the research literature, it can refer to a conglomerate of fairly independent / mildly correlated constructs, such as body image, self-schema, self-valuation, self-esteem, self-perceived physical attractiveness, self-worth, etc...  That is to say, one can score positively on some of these measures and negatively on others, with little relationship between the scores.

Culture may indeed play a role as well:

  More recent research investigating self-esteem in other countries
  suggests that illusory superiority depends on culture. Some studies
  indicate that East Asians tend to underestimate their own abilities in
  order to improve themselves and get along with others.

The uncertainty between positive and negative self-image is underscored by the existence of both an above-average-effect, and a worse-than-average effect.  Each may refer to different aspects of self-image, but may even refer to the same aspects!

  For example, while college students rate themselves as more likely
  than average to live to 70, they believe they are less likely than
  average to live to 100. People regard themselves as above average on
  easy tasks such as riding a bicycle but below average on difficult
  tasks like riding a unicycle.


Is it possible to be completely impartial when considering yourself? Consider the following quotation by Poulain de la Barre:

  Everything that has been written by men about women should be viewed with suspicion, because they are both judge and party.

Is it possible to be completely impartial when considering yourself, or matters in which you have a significant vested interest, or will one always be biased?

For most people, I would say no, they lack the self-awareness and self-control to be able to make such a judgement. Those who have practiced a good amount of meditation would, on average, be better candidates. Moreover, nearly anyone experiencing strong emotions would have extra trouble thinking objectively and detached from personal interest. Those who can turn their emotions off would be better candidates.

Another method to consider is creating an objective measuring system that does not rely on subjective information. Technology or strict definitions may be needed for the method to be reliably applicable. If the person making the measurement system created it with the intent to use on others, it could be good to use back on the creator. Some simple examples here are those measurement systems intended to assess physical abilities and strength. Granted one had reasonable self-control and integrity, it would be pretty easy to accurately measure one's own physical strength using a weight set, for example. A fair person could also measure his or her own maximum running speed with pretty good accuracy.

As for matters of "significant vested interest", I would need some specific examples to really be able to say whether it would be reasonable to expect a person to be able to self-assess. The only example that comes to mind right now is that of whether the world would be a better place without oneself. That would be difficult for many people to answer accurately since, at least it seems to me, many people do not consider their own value to society when considering their career or other choices that affect others. Some people have a net positive effect on society while others have a net negative.


What is an interstitial personality trait? The HEXACO and some other measures of personality describe certain traits as "interstitial". What does it mean for a personality trait to be "interstitial"?

Many personality measures are organised hierarchically where broad traits are defined as the combination of multiple narrow traits. Broad traits are often called domains and narrow traits are often called facets.

Two influential examples are the NEO-PI and the HEXACO models of personality. For example, the NEO-PI has five broad traits and each broad trait is composed of 6 narrow traits. The HEXACO model includes six broad traits and each broad trait is composed of four narrow traits.

However, some measures include narrow traits that do not fit so neatly within a particular hierarchical framework. For example, factor analytic research may indicate that the trait loads substantially on more than one broad trait.

Interstitial traits are narrow traits that are meaningfully correlated with two or more broad traits.

The terminology comes from the word "interstices" meaning "a small space that lies between things". Thus, such traits occupy a narrow unique space that overlaps with more than one broad trait.

I'm not sure whether the term "interstitial" could be used to describe traits that are relatively unrelated to any broad trait.


Is good short term memory correlated with good long term memory? Is there any link between one's ability to store information in their short term memory, with their ability to store information in their long term memory?

There is a functional dissociation between short and long-term memory.

It was observed by Milner (1966) that a patient (case H.M) can have a normally working short-term memory with an impaired long term one; and by Shallice & Warrington (1970) that a patient (K.F.) can have correct long-term memory performance while a severe impairment in short-term memory.

So there is no simple relationship between the two, if at all. Nevertheless, it could be a correlation but probably mediated by other factors such as attentional processes, explicit learning strategy etc.


Psychological explanation for perceptions of the Loch Ness monster I previously asked about whether physics could explain the occurrences of the rogue waves which could psychology explain the eyewitnesses' perceptions of the Loch Ness monster? (The Physics.SE question has been put on hold because not all of it is about physics.)

So the question:

What is the psychological explanation for reports of Loch Ness monster?
Could it be related to the dark, undulating pattern under the crests of the white-caps?

Edit You are walking along a country lane, when a sudden motion on the water catches your eye. Followed by the sound of a crashing wave. Within seconds, only ripples remain on the surface. You remember the image as shown above. It could be a white-cap on a wave, but everyone who has been to the beach knows that waves come in one-after-another, and there are no other waves, so it can't be a wave. You notice the darker area under the white-cap and realize the only possible explanation is: you have just seen a large animal dive under the surface. Like a sounding whale. (Or monster?).
Loch Ness is located near a major fault line that has seismic activity. Physicists can explain that a wave created by seismic activity is a rogue wave or tsunami. They can also explain why the wave does not reach shore and, why the area under the white-cap is always darker.
So, could a collaboration between physics and psychology show this illusion is a possible explanation for Nessi?

Herd mentality and hallucinations can explain many things like the Loch Ness monster, ware wolves, vampires and ghosts.

  Hallucinations involve sensing things while awake that appear to be real, but instead have been created by the mind.

Extreme emotional states can cause psychosis which leads to hallucinations and delusions and other thoughts which are removed from reality. Many things can stir an otherwise normal person into a frenzy which then provides the vulnerability for psychosis. Then at the sight of wave their imagination is more real than what their eyes see and the image of a monster is imprinted in their memory. If the monster is attacking them or something else it might be an intrusive thought as well.

After the initial hallucination the story is repeated and herd mentality will cause others to experience something similar at the sight of the wave. As more people experience the sighting it becomes more popular continuing and expanding the myth.


Why do people hide wealth? I was reading about Panama leaks and I was wondering why do people keep their wealth secret? What's the psychology behind it?

Quiet simply: loss aversion

People are adverse to loss, the majority of people who are wealthy pay into a system they get little direct benefit from, in comparison to poorer people who tend to get back what they put in or more depending on circumstance. However the rich, and everyone else, benefit from being in wealthy westernised societies with higher levels of tax, because people have more money in these countries. It is the tax system which allows these countries to develop their citizens, poor countries have lower levels of education and poor infrastructure as a result of low taxation and poor distribution of expenditure. However people do not calculate costs and indirect benefits together..."individuals bracket indirect benefits and costs separately. This is the case when the primitive utility function"..."satisfies the decomposability property (Tversky and Kahnemann, 1991)" Alesinay and Passarelliz (2015). Basically as indirect benefits are not calculated directly from costs individuals will look to avoid loss, its quiet natural to avoid loss. If you think about inheritance tax, money and property that have already been taxed are taxed again, surely an individual should be able to decide what to do with their property? Of course the state would agree for redistributing wealth for the benefit of society. Although this would seem unfair to the individual who saved in comparison to those that spent all they had. The point is that its just as easy to justify tax avoidance as it is to promote taxation, we could easily get into the principles of collectivism and individualism here but that is for the politics and philosophy areas of stackexchange.


How long can a person stay happy, excited and motivated about something new? I'm interested in learning more about studies or experiments that determine how long a typical person can stay excited about something new:

New job
new project
new relationship
new idea
new purchase/toy

Is there any evidence to support the hypothesis that humans are excited by new things/prospects, but only for a short time? If so, how short? Is it days, weeks or a "honey moon"?

A while ago I've heard a talk on TED.com that happy people are up to 30% more productive (Does happiness affect productivity?), and I'm wondering if this is applicable to "being excited about something new" - i.e: are people more effective/smart when they are taking on new project, new job or a new relationship? Are people more excited, energized and engaged when they conceive new ideas?

It would also help if I get to learn what the search term for "being excited about something new" is.

Update:
Looking into happiness and productivity produced two terms: "Happiness economics" and Hedonic Adaptation. The article on hedonic adaptation says that happiness is homeostatic in nature

  a system that regulates its internal environment and tends to maintain
  a stable, relatively constant condition of [its] properties

Reading that happiness regulates itself (as in negative feedback) sounds very reasonable to me, and I recall reading about antidepressants and Serotonin, which also mentioned that Serotonin production uses negative feedback, where more Serotonin released now inhibits release of more Serotonin, thus antidepressants dont work immediately and require a couple weeks to take effect[looking for a link].

I'm wondering if the process of being excited about something new is also homeostatic in nature?

Probably the most striking evidence of "happiness homeostasis" is a now classic study by Brickman, Coates and Bulman (1978) which compared the self-reported happiness of lottery winners and accident victims with a control group. The following quote describes the part of the outcome you'd be interested in succinctly:

  Lottery winners and controls were not significantly different in their ratings of how happy they were now, how happy they were before winning (or, for controls, how happy they were 6 months ago), and how happy they expected to be in a couple of years.

Except for one, the lottery winners were between one and 18 months removed from their winnings, while the group of accident victims were one to 12 months removed from their accident. This seems to indicate that yes, happiness is broadly speaking a homeostatic process (but as with most homeostatic processes, it's likely complex).

That's probably not the precision level you were looking for, but there's quite a literature--almost 1600 citations on Scholar for this paper alone. One other limitation of it is that it uses interviews instead of ecological momentary assessment, which a more modern paper would likely want to employ. That might be another term to keep in mind.

References

  Brickman, P., Coates, D., Janoff-Bulman, R. (1978). Lottery winners and accident victims: Is happiness relative?. Journal of personality and social psychology, 36(8), 917-927.


Does hypnotherapy/hypnosis, in any form, for any type of disorder, work? Does Hypnosis Work for Treating, or Curing, any Form of any Mental Disorder?

Let's say my definition of hypnosis is related mostly to the classical way people think about it.  This is subjective of course, but I've purposefully made it that way. I do realize at times it may overlap into other types of therapy as well.

If there are other forms of hypnosis I'd like to hear about those too though!

Citation/Research Wise:

I'd like to know if its backed by literature.  I want the specific citation's abstract   quoted.
I'd like to know their findings, conclusions, and methodologies and your analysis of that.
I'd like to know how long the treatments lasted after they stopped being hypnotized.
I'd like to know how effective it was for whatever specific goals that it was used to treat.  How long did the affects last if there were any?
I'd like to know if you found any potential errors or flaws in the study - and you're overall analysis of that.

Citing Wikipedia is not an acceptable answer or comment as it is not a reputable source, it's citations are.  If you are going to do that, pick the most compelling and valid studies (no matter the disorder), or something like a meta analysis that Wikipedia cites and then post that along with the answer to the above questions.  Thanks.

Anecdotally:

I'd like to know what it feels like to be hypnotized if you've had the experience of it.
I'd like to know why if it worked really well for you then why did you stop doing it or have you actually continued?

It can be any disorder of any kind, just as long as someone could classify it as a psychological "problem" in some context.  The more angles you come at it with the better though.

Hypnosis "works" only insofar as it induces1 a trance. Hypnosis is not a type of therapy. Hypnosis does not cure any disorders or do anything at all, except induce a trance.

Hypnotherapy, from the perspective of psychodynamic theory, utilizes this trance to directly access the subconscious. In traditional hypnotherapy (of the Victorian era), direct suggestions were "planted" in the "unprotected" subconscious; in modern Ericksonian hypnotherapy, the unconscious is stimulated to participate in the healing process.

So the question we are dealing with asks:

Does hypnotherapy work for any type of disorder?

Yes, it does. Standard works (Burrows & Dennerstein, 1980; Brown & Fromm, 1986; Cheek & LeCron, 1968; Crasilneck & Hall, 1985; Hammond, 1990; Kossak, 1989; Kroger & Fezler, 1976; Peter et al., 1991; Revenstorff, 1993; Lynn et al., 1996; Wester & Smith, 1984; Erickson, 2007-2010; O'Hanlon & Hexum, 1990) show that hypnosis has been successfully applied to a multitude of psychosomatic, psychiatric and somatic cases including:

behavioral problems

nail biting
enuresis (bedwetting)
smoking
overweight
academic and athletic increase in performance

psychoneurotic disorders

phobias, obsessive-compulsive disorders
depressive reactions
post-traumatic stress disorder
dissociative disorders
sleep disorders

psychosomatic disorders

chronic pain
migraine, tension headache
morbus crohn, ulcers
asthma, hay fever
hypertonia (high blood pressure)

somatic disorders

immunology: warts, dermatosis, ichtyosis, tumors
vasomotoric: bleeding control, morbus raynaud, wound healing
acute pain: obstetrics, dentistry, postoperative pain
neurology: amnesia, rehabilitation after brain lesions

In addition to case studies, there is a growing number of controlled group studies on the effectiveness of hypnotherapy which show empirically confirmed indications for this method. Meta-analyses have become the accepted method of judging the effectiveness of a therapeutic procedure, so I will confine myself to these in the following overview.

In a meta-analysis (Rominger, 1995) of 36 control group studies with more than 1200 patients  the effect sizes ranged from g = .54 to g = .952. This corresponds (converted after Rosenthal, 1984) to a correlation between treatment and effect ranging from r = .26 to r = .44. From this a success rate (in %) can be estimated for treated and untreated patients (table 1).

                 Number of Studies    Success Rate    Success Rate
                                      untreated (%)   treated (%)
all studies      36                   31              69
smoking           4                   30              70
anxiety           6                   29              71
pain             14                   37              63

Table 1. Results of a meta-analysis of hypnotherapy (after Rominger, 1995).

In a more recent meta-analysis, Bongartz et al. (1999) found comparable results in 112 studies with 5600 patients (table 2).

                       Number of Studies    Success Rate    Success Rate
                                            untreated (%)   treated (%)
psychotherapy (all)    85                   32              68
addiction               6                   37              63
somatoform disorders   11                   35              65
anxiety                11                   26              74
behavioral problems     4                   33              67
pain (all)             27                   35              65
pain (cancer)           6                   36              64
pain (surgery)          8                   38              62
pain (birth)            5                   36              64

Table 2. Results of a meta-analysis of hypnotherapy (after Bongartz et al., 1999).

In a new meta-analysis (2002), Bongartz et al. again confirmed the effectiveness of hypnotherapy. The abstract recapitulates:

  From 193 studies published until 1998 that investigated the efficacy
  of hypnosis 43 randomized clinical studies were selected that compared
  a patient group treated exclusively by hypnosis with an untreated
  control group (or with a group of patients treated by conventional
  medical procedures).The 43 studies were integrated into a
  meta-analysis that yielded a weighted average post-treatment effect
  size of d=.60 (medium effect size) for hypnotic treatment of ICD-10
  coded disorders (24 studies; average treatment period: 5.1 weeks)
  and d=.38 (small effect) for hypnosis as an adjunct for supporting
  medical procedures (19 studies).These estimates are conservative
  since all variables of a given study were used. Most of the studies
  employed methods of the classical approach to hypnosis. In order to
  obtain an estimate to which extent non-clinical factors
  (design-quality, way of comparison of dependent variables) have an
  influence on the effect sizes, effect sizes were computed for all
  studies of the original 193 studies that reported the necessary
  statistical information (N=89). For those studies with an average
  effect size of d=.80 a mas- sive influence of non-clinical factors was
  demonstrated with a range from d=.51 for randomized studies with group
  comparisons to d=2.0 for non-randomized studies using
  pre-post-comparisons.

A table listing all 43 analyzed studies and their area of application ("Störungsbild/Anwendungsbereich"), number of patients ("Patientenzahl"), type of hypnosis ("Hypnoseart"), treatment period in weeks ("Behandlungszeitraum") and effect sizes ("Effektstärke") is included in the publication which is available online at http://bscw.rediris.es/pub/bscw.cgi/d4416025/Bongartz-Effektivitat_hypnose.pdf (in German). It gives a more discriminating view and shows the large variance in effect sizes among the studies, but does not add anything new to this overview.

All the studies included in the meta-analysis used a control group, randomized assignment of patients to the groups, and used hypnotherapy as the only psychotherapeutic treatment (and not in conjunction with other forms of psychotherapy), but sometimes in conjunction with the medical standard therapy. As such, from my point of view, the meta-analysis is quite flawless. Some of the studies included measurements taken some time after the end of the treatment, but these were not considered in this meta analysis, because the 193 studies from which the ones included in the meta-analysis were selected are all the studies that the authors could find in relevant databases and literature ("footnote chasing") between 1974 and 1998, and the number of studies including "longer-term" effects were apparently not enough for a separate analysis. Thus, the authors of the meta-analysis considered only the immediate post-treatment measures of all studies.

In summary, it seems to me that the effectiveness of hypnotherapy has been shown especially for behavioral, anxiety and (psycho)somatic disorders and symptoms, while it seems not to have been applied, or not successfully, to psychotic, affective, dissociative, sexual, eating, sleep, impulse control, adjustment and personality disorders.

Footnotes:

1 Sometimes. An attempt by a clinical psychologist and trained hypnotist to hypnotize me did not lead to any trance.

2 In an analysis of 302 meta-analyses of psychologica, pedagogical and behavioral therapies, Lipsey and Wilson (1993) found 90% of effect sizes to be above 0.10, and 85% above 0.20. A more methodically severe selection of 156 meta-analyses returned a mean effect size of 0.47.

Sources:

Bongartz, W., Flammer, E., & Schonke, R. (1999). Die Effektivität der Hypnotherapie: Eine meta-analytische Studie. Vortrag auf der Jahrestagung der M.E.G., Bad Orb.
Bongartz, W., Flammer, E., & Schonke, R. (2002). Die Effektivität der Hypnose: Eine meta-analytische Studie. Psychotherapeut, 47, 67-76.
Brown, D. P., & Fromm, E. (1986). Hypnotherapy and Hypnoanalysis. Hillsdale, NY: Lawrence Erlbaum.
Burrows, G. D., & Dennerstein, L. (Eds.) (1980). *Handbook of hypnosis and psychosomatic medicine. Amsterdam: Elsevier.
Cheek, D. B., & LeCron, L. M. (1968). Clinical hypnotherapy. New York: Grune & Stratton.
Crasilneck, H. B., & Hall, J. A. (1985). Clinical Hypnosis: Principles and Applications* (2nd ed.). New York: Grune & Stratton.
Erickson, M. H. (2007-2010). Collected Works (10 vols.). Milton H. Erickson Foundation Press.
Hammond, D. C. (ed.) (1990). Handbook of Hypnotic Suggestions and Metaphors. New York: Norton.
Kossak, H. C. (1989). Hypnose: Ein Lehrbuch. Weinheim: PVU.
Kroger, W. S., & Fezler, W. D. (1976). Hypnosis and Behavior Modification: Imagery Conditioning. Philadelphia: Lippincott.
Lynn, S. J., Kirsch, I., & Rhue, J. W. (eds.) (1996) *Casebook of Clinical Hypnosis. Washington, DC: APA.
Lipsey, M, L., & Wilson, D. B. (1993). The efficacy of psychological, educational, and behavioral treatment: Confirmation from meta-analysis. American Psychologist, 48, 1181-1209.
O'Hanlon, W. H., & Hexum, A. L. (1990). An Uncommon Casebook: The Complete Clinical Works of Milton H. Erickson. New York: Norton.
Peter, B., Kraiker, C., & Revenstorf, D. (eds.) (1991). Hypnose und Verhaltenstherapie. Bern: Huber.
Revenstorff, D. (1993). Klinische Hypnose (2nd ed.). Heidelberg: Springer.
Rominger, M. (1995). Metaanalyse der Hypnotherapie (Diploma thesis). University of Tübingen.
Rosenthal, R. (1984). Meta-Analytic Procedures for Social Research*. London: Sage.
Wester, W. C., & Smith, A. H. (1984). Clinical Hypnosis: A Multidisciplinary Approach. Philadelphia: Lippincott.


Can people improve their memory by training themselves to recall previously forgotten memories? Apparently, somebody has recalled previously forgotton memories and become able to speak fluent french after a coma. I'm wondering if people can also train themselves to be good at recalling previously forgotten memories by training themselves to recall information they've forgotten that there's a record of.

For example, if a cell phone gets invented where you can type in somebody's name and then type what their phone number was and when you want to phone them, you have to go to their name and then start typing digits from beginning to end from memory and as soon as you type a digit incorrectly, you get notified and then you have to type that digit followed by the next digit and will be notified when you do so correctly, I wonder if the people using it would train themselves to recall memories of what phone numbers were.

I wonder if people would become even smarter if some of the memories they trained themselves to recall were memories from before they started the training because that way, their brain has to form complex connections in order to recall memories that were lost in the brain than to just not forget stuff they learn from then on. That's probably because lost memories get scattered to unrecognizability in the brain but that doesn't mean there isn't a complex method of extracting the memory from the disorder. Maybe unlike the man in the previously linked video who thought he was somebody else, with sufficient training, they'll learn how to properly extract their past experience correctly from the disorder and have undistorted memories. Maybe getting an actual defect in the connection suppressing ability making you do something like only have suppress unimportant connections from an accident like in that video could make it so easy to recall previously forgotten memories cause of not suppressing the connections for extracting them that much and be superior to any possible training to recall previously forgotten memories because you'll be hyper-aware thinking about a large amount of your past all at once because it's just as easy as thinking about a single past experience because the memories of the individual experiences were already lost in the brain, and the you can recall memories that were even more badly lost with the defect in the connection suppressing ability than you would with training alone.

I wonder if in general, it's easier for autistic people to train themselves to recall previously forgotten memories.

Memory is not fixed - it is very plastic.  If you look at Amnesia, there are many different causes and many different ways it can manifest itself. It can also be anywhere between mild and severe.  There are methods which can be used to try and prevent further memory loss - by abstaining from alcohol when it is caused by alcohol abuse such as with Korsakoff's syndrome, by using diaries, calendars, wall planners etc. But just like with Alzheimer's Disease there is no effective (and ethical treatment) for memory loss.

Which brings me onto the ethics of memory recall therapy or training.  If you look at studies into memory and PTSD (Post Traumatic Stress Disorder) - also found in category F43.1 in ICD-10 - methods used to try and help sufferers to remember the traumatic events for this example, have been found through research to cause False Memory Syndrome.  Although as with many pieces of research, there are opponents to the idea.

From what I know, and believe from looking at research, once memory is lost, it is lost for good.  You may recall parts of the memory through various ways but to try and recall the whole memory can lead to a change in what actually happened as @Arnon pointed out in his comment.


Is there any strong empirical support that "casual" (10-20 minutes per day) mindfulness meditation leads to lasting cognitive improvements? I want to emphasize that I'm not referring to the intense mindfulness-based cognitive therapy (MBCT), but instead just 10-20 minutes of daily mindfulness meditation (MM), perhaps guided by a smartphone app.

It's usually claimed that MM leads to improvements in the prefrontal cortex (enhanced focus, working memory etc.) and the amygdala (reduced depression, anxiety, stress etc.).

I have read recent studies claiming that mindfulness meditation is no more effective than watching a documentary, is counterproductive at work etc. (Some of these studies may have been context-specific.) Anecdotally, I've done MM myself on-and-off for several years and didn't notice any significant improvements in the areas listed above.

Due to publication bias, p-hacking, the reproducibility crisis etc. and my own personal experience, I'm skeptical that MM does anything significant (noticeable changes) and/or lasting (after the meditation, during the day).

Is there a large-scale, pre-registered replication effort to support the benefits of 'casual' MM (i.e., not the more intense MBCT)?

The following is the empirical support I can find

Beauchemin, J., Hutchins, T. L., & Patterson, F. (2008). Mindfulness meditation may lessen anxiety, promote social skills, and improve academic performance among adolescents with learning disabilities. Complementary Health Practice Review, 13(1), 34-45. DOI: 10.1177/1533210107311624
Free PDF
All outcome measures showed significant improvement, with participants who completed the program demonstrating decreased state and trait anxiety, enhanced social skills, and improved academic performance. Although not directly assessed, the outcomes are consistent with a cognitive-interference model of learning disability and suggest that mindfulness meditation decreases anxiety and detrimental self-focus of attention, which, in turn, promotes social skills and academic outcomes.

Moore, A., & Malinowski, P. (2009). Meditation, mindfulness and cognitive flexibility. Consciousness and cognition, 18(1), 176-186. DOI: 10.1016/j.concog.2008.12.008
Free PDF
Overall the results suggest that attentional performance and cognitive flexibility are positively related to meditation practice and levels of mindfulness. Meditators performed significantly better than non-meditators on all measures of attention. Furthermore, self-reported mindfulness was higher in meditators than non-meditators and correlations with all attention measures were of moderate to high strength. This pattern of results suggests that mindfulness is intimately linked to improvements of attentional functions and cognitive flexibility. The relevance of these findings for mental balance and well-being are discussed.

Zeidan, F., Johnson, S. K., Diamond, B. J., David, Z., & Goolkasian, P. (2010). Mindfulness meditation improves cognition: Evidence of brief mental training. Consciousness and cognition, 19(2), 597-605. DOI: 10.1016/j.concog.2010.03.014
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Our findings, with naïve participants learning mindfulness techniques by means of a brief training format, are consistent with those that have been reported for adept meditators. Four days (20 min/day) of MM training was effective in signifi- cantly increasing mindfulness scores in comparison to an active control group. Our brief MM training protocol promoted sig- nificant effects on several cognitive tasks that require sustained attention and executive processing efficiency (Symbol Digit Modalities Test, verbal fluency, and the hit runs on n-back task). However, no specific benefits from MM training were found with many of the mood scales, the forward and backward digit span or speed on the n-back task. It is important to note that the groups did not differ at baseline on any of the measures and had no prior meditative experience.

Chiesa, A., Calati, R., & Serretti, A. (2011). Does mindfulness training improve cognitive abilities? A systematic review of neuropsychological findings. Clinical psychology review, 31(3), 449-464. DOI: 10.1016/j.cpr.2010.11.003
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[T]he results of the present review provide preliminary support for the notion that MMPs could provide significant benefits on several measures of cognition which seem specific for the phase of meditation training under investigation. However, further higher quality studies focusing on more standardized MMPs are needed to replicate available findings, to more deeply explore the effects of mindfulness training on further domains of cognition and to reduce discrepancies of findings deriving from systematic differences in mindfulness protocols.


How long does it take for electrical impulses from neurons to travel in the human brain? Consider the maximal distance between two separated areas in the human brain. How fast can information via neuronal excitement travel between these two locations?

This is hard to say because not as many studies measuring this in humans have been done as have been done in other primates, like macaque monkeys, and when it is done, it is usually done in patients who have some brain issue like epilepsy and have recording electrodes implanted for preparation for a procedure, and so may not have a typical response. Also it is hard to know how best to satisfy your requirement "the maximal distance between two separated areas in the human brain".

That said, here's my attempt: about 25 to 30 ms. I get this from two sources:

1) a 1983 paper using epileptic patients with microwire electrodes in their brain at various regions. I pick the data of measurements of the visual response arriving in the occipital lobe because--thinking simply--it is at the back of the head on the other side of the head from the eyes, and so the "maximal distance" is the entire front-to-back length of the brain (the pathway being retina -> thalamus -> V1 of visual cortex). From the paper (page 490, bottom):

  Occipital Lobe Units: Using diffuse flash stimuli...the shortest
  latency of the 11 responsive occipital cortex cells was 31 ms; the
  mean latency was 63.6 ms (range, 31 to 110 ms, SD, 25.1).

2) A 2009 paper, also using epileptic patients which found, among other things:

  the evoked potential started ~20 ms earlier in V1 (25
  ms after stimulus onset;


Is the effect related to shutting your eyes when a car is turning well known? Since I was little I realized that when you close your eyes when being in a car and the car turns in a street to the side, you perceive the car turning more in one direction than it actually does.

Does this effect have a name? Is it an example of some well known effect? If so, what is it and where can I learn more about it?

Short answer
In general, sensory systems are not well equipped to perform absolute estimations of a stimulus level, especially since they adapt to the ambient level of stimulation, i.e., their baseline is re-set continuously. Nonetheless, the vestibular system is quite well capable of estimating the degrees of rotation, as shown in blindfolded subjects that were rotated along the vertical axis.

Background
Rotation initiated by an object you are sitting or standing on is sensed by the visual system and the vestibular system. The visual system is the most accurate, as it immediately senses a change in the visual scene. When the eyes are closed, only the vestibular organ is functional.

Movement in the horizontal plane is sensed by the semicircular canals in the inner ear (Fig. 1). One fundamental principle in sensory organs in general is that they operate on a relative scale. In other words, sensory systems excel in comparing two stimulus intensities. They are, however, poorly equipped to provide an absolute measure of stimulus intensity. How bright is bright? Only through experience does one know the absolute value of a stimulus. I'm in the hearing sciences, and I can pretty well tell what the absolute stimulus level is of a stimulus between 20 and 70 dB. But that's only because I spent hours and hours providing well-defined stimuli to study subjects. If you ask me how bright a certain flash of light is, I surely can't tell you.

What's more - sensory systems adapt quickly (Webster, 2012). For example, if you keep on moving in circles then the sensory end organs in the semicircular organs (hair cells and associated vestibular nerve) adapt and become less responsive to the ongoing stimulus (St. george et al., 2011). However, short circular movements in a car are typically short accelerations and decelerations, which are pretty well encoded by the vestibular system. Indeed, blindfolded subjects do pretty well in regaining their original position when rotated about a head-centered vertical axis. It is not until adaptation comes into play that things start to deteriorate. (St. george et al., 2011).

Reference
- St. george et al., J Physiol (2011); 589(4): 843–53
- Webster, F1000 Biol Rep (2012); 4: 21

Fig. 1. Inner ear. source: MedScape


Need to define observation/phenomenon in order to study it, same replies to same political topics, different individuals I was wondering if anyone could help me define my observation, in order to read some literature on the subject. I have some Cog. Psych. background but have never encountered this during my studies. It is a social, behavioral and a cognitive phenomenon, that I have observed reading the news and political forums. Every time N Korea is mentioned, people start talking about how hungry their nation is, and make jokes about Kim's weight. Almost every time a popular topic appears on the news regarding the subject, these kinds of posts can be seen. I can provide many examples, if necessary. It is always different individuals with the same kinds of replies/responses.

Is there anything I can read to inform myself about this phenomenon ?

EDIT: as pointed out, not all observations/phenomena need a term.  However, I do need some references to read more about it, so I am not completely lost.

I doubt there's anything deeper than a meme or stereotyping at play here. See https://knowyourmeme.com/memes/hungry-kim-jong-un

  On December 23rd, the "Kim Jong-Un is Hungry"[4] single topic blog launched on the microblogging site Tumblr with the tagline "He's always thinking about food. For himself… not for his people."


Why can't we do the things we know instantaneously? In the following video eventhough people know that when handlebar of the bicycle is turned left the wheel of that bicycle is turned towards right and vice versa, they can't ride that new bicycle instantaneously without any practice. Why is that so? Why can't we do something even though we know how it works? what is the scientific explanation behind it?

Detailed video link

Short video

One more hypothetical question relating to this. Let us consider a boy who never swam in his life, if theoretically came to know each and every aspect of swimming ,learning for several years. If one day after these years he fell into a large swimming pool, can he decently swim by applying his theoretical knowledge.

This is not a thought experiment as in philosophy.I want to know scientifically how his knowledge and doing of swimming correlate?

Motor learning is a complex process (Wolpert & Flanagan, 2010). Oftentimes the process is broken up in elements (Weaver, 2015):

a cognitive phase;
an associative phase;
an autonomous phase.

The process you describe as having the 'knowledge' is part of phase 1, namely cognitively analyzing what is needed to do the job. However, the associative phase is necessary, where one actively practices and obtains feedback through observation and instructions by a teacher of what is correct, and what still needs work. Lastly, the motor behavior needs to be automated, such that it can happen without conscious control (Weaver, 2015).

This process needs a lot of time and hence the scene in the Matrix where Neo learns Kung Fu in a split second is obviously not possible. In fact, mastering martial arts, and in fact any skill, leads to profound changes in the brain, including gross structural changes that can only happen over the course of days, weeks, or even months. For instance, jugglers have been shown to increase gray matter over time in specific areas of the brain (Fig. 1).

Fig. 1. Expert jugglers show increased gray matter volume in several brain areas, including the secondary visual cortex and the hMT +/V5 (Gerber et al. , 2014)

References
- Gerber et al., NeuroImage (2015); 95: 320-5
- Weaver, PLoS Biol (2015); 13(12): e1002313
- Wolpert & Flanagan, Curr Biol (2010); 20(11): R467-72


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

What bias am I guilty of?

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

Fallacy of the single cause:

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

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

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


Is autism caused by genetics? Is autism and Asperger's syndrome caused by genetics or some other factor such as the environment?

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

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

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

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

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

The NHS webpage on Autism states (Emphasis mine)

  Most researchers believe that certain genes a child inherits from their parents could make them more vulnerable to developing ASD.

  Cases of ASD have been known to run in families. For example, younger siblings of children with ASD can also develop the condition, and it's common for identical twins to both develop ASD.

  No specific genes linked to ASD have been identified, but it may be a presenting feature of some rare genetic syndromes, including Fragile X syndrome, Williams syndrome and Angelman syndrome.

On environmental causes the NHS say that

  Some researchers believe that a person born with a genetic vulnerability to ASD only develops the condition if they're exposed to a specific environmental trigger.

  Possible triggers include being born prematurely (before 35 weeks of pregnancy), or being exposed in the womb to alcohol or to certain medication, such as sodium valproate (sometimes used to treat epilepsy during pregnancy).

  No conclusive evidence has been found linking pollution or maternal infections in pregnancy with an increased risk of ASD.

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

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

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

There has been research into autoimmune disorders causing ASD.

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

  there are likely multiple, biologically defined subgroups within the ASD spectrum(3–7). Specifically, there is growing evidence that supports maternal immune dysfunction may underlie the behavioral abnormalities observed in a subset of children affected with the disorder(8). Several immunologic risk factors have been described including: genetic associations with immune-related genes(9–16), family history of autoimmune disease(15, 17–21), maternal inflammation and infection during pregnancy(22–27), and altered immune responses in the children, and are associated with increased impairments in core and associated features of ASD(28). More specific to this review, maternal anti-brain autoantibodies, which are thought to access the fetal compartment during gestation, have been identified as one risk factor for developing ASD and are proposed to contribute to early neurodevelopmental perturbations in the developing fetus(29–31).

  References

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

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

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

References

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


What are ERP components such as N400? A lot of research uses ERP, which is time-locked EEG. I am reading about semantic and syntactic anomalies. So when a semantic anomaly occurs there is supposed to be a negative peak in ERP at 400ms. I have some questions how this this component was established and how the data is collected?
Is there an assumption that these peaks happen in all individuals always at the same time? Is it only an assumption or is there evidence of invariability? Let's say the peak happens at 420 ms would you than use the amplitude from 400 ms or from 420?
Is the data collected from the whole brain and averaged out?

The semantic N400 and syntactic P600 are some of the most well established ERP components in the literature. They were discovered decades ago and the results have been replicated hundreds of times in other papers. There is just no question that they are present and very robust. That's not saying they are there 100% of the time in 100% of people. All we know is that it's a very easy response to get out and by now it would be surprising / worthy of investigation if people didn't show them in the standard paradigm.
There is a paper from a few years ago that looks at the 30 years of N400 research and all the papers that found the effects. It's probably a bit out of date now but it does a great summary of the research up until that point.
I think Hillyard & Kutas (1983) is the original paper.
ERP components are not always so tightly linked in time. You can module them based on task context and shift them by all sorts of ways so it's never that the peak is exactly at 400 ms post-stimulus. It can start WAY before then and end WAY after then. Broadly, we use N400 to talk about a large response that peaks "in that time window" (so, from 300-500ms). I wouldn't get too fixated on the specific milliseconds. Therefore you don't "use" the amplitude for anything (not sure I understood that part of your question).
Typically you see N400 over central-parietal electrodes. There is a bit of confusion over exactly what the cortical sources are but MEG and fMRI do support the idea it's a strong dipole with the positive component slightly in the LH and therefore EEG electrodes over central and parietal sites pick up the strongest signal. This also gets at what you use as your reference electrode because EEG potentials are differential and the patterns you see on the head are very dependent on reference / ground settings.
Typically you would group electrodes over general position and look at central-parietal ones or you could plot individual responses (both ways would still show the N400). As with anything in science, it's up to you what you show.


What happens with stress, if there's distraction before a story reaches it's end? I remember reading of a study where children were told stories. During the telling of the story tension rose and the heart rate increased. After the story was over the heart rate went back to normal.

There was another experiment where the story wasn't told to the end. During the telling of the story, attention shifted elsewhere while the tension was still up and the story never reached its end. In that condition, the heart rate stayed elevated.

Unfortunately, I don't remember the exact source. Can you tell me whether the described effect exists and if so, point me to the studies about it?

When stress is chronic it could provoke bad effects:

High blood pressure
Impaired cognition (maybe it explains the distraction)
Lowered immune system

In my opinion, the distraction could be the effect of the increased level of cortisol... I wish my intervention will be useful.

REFERENCES
Michael S. Gazzaniga, Richard B. Ivry, George R. Mangun (2013),  "Cognitive Neuroscience: The Biology of the Mind: 4th Edition"


How does personality moderate or mediate the relationship between stress and burnout? My research is on work related stress and burnout amongst healthcare professionals and the role that personality play in either reducing or increasing levels of stress and burnout. I'm using the big five personality factors to research how each of these factors affect the relationship between stress and burnout.

How does personality affect levels of stress in individuals?
Can a person's personality be a mediating or moderating factor?

Personality is generally theorised to be a stable individual difference variable. Research has shown it to be highly stable over time. Thus, from a theoretical perspective it typically has a primacy in causal models.

Stress can be an ambiguous construct. It can refer to the objective existence of stressful stimuli or the way that individuals perceive those stresses.

From a theoretical perspective, personality is related to both the objective experience of stressors and the subjective perception of stressors. In particular, neuroticism refers to dispositions to experience negative emotions. Personality influences the world. For example, people put themselves into situations that may elicit more stressful experiences. Likewise, personality can influence the experience of stress through various mental models, interpretive schemas, rumination tendencies, and so on.

While one can imagine in the extreme that stress can alter personality (e.g., PTSD), in general personality makes more sense as a factor that has a causal influence on both the objective experience and perception of stressful experiences. In this sense, it personality does not mediate the effect of stress on burnout. This theoretically based conclusion is important. Statistical tests of mediation will provide rubbish information if you just plug in three intercorrelated variables like stress, personality, and burnout.

From a theoretical perspective personality should causally influence the objective presence of stress, the subjective perception of stress, and whether someone experiences burnout. It also makes sense that certain personality traits such as neuroticism would causally increase the relationship between objective stressors and subjective stress and ultimately more extreme forms of subjective stress such as burnout. However, in order to really test this idea, you need to get very good measures of objective stressors. Subjective measures of stress are likely to be influenced directly by personality which is likely to reduce the potential moderator relationship. Alternatively, you might just find that main effects are enough; i.e., that personality and objective stressors mutually contribute to burnout, but that there is no interaction effect (as would be implied by the moderator hypothesis).

There are thousands of empirical articles looking at correlates of personality, stress, strain, burnout and so on. I have read a lot of them many years ago. This answer focuses more on the theoretical underpinnings of any relationship.


Face-Blindness: Have I seen you before? Sometimes when I meet new people, I feel like I have seen them before. Their faces might look similar to people's faces, I have really have met before.

The wiki article on Difficulties with Facial Recognition states that:

  Prosopagnosia is an inability to identify faces and face-like objects. This represents a failure to encode incoming visual information. Neurological studies indicate that prosopagnosia is associated with bilateral lesions of the central visual system, primarily located in the mesial occipitotemporal region.

I don't have problems with identifying faces, I just group them too often.

Questions

Why do novel faces sometimes look familiar?
Is this related to a kind of face-blindness?
What is the neural basis for this phenomena?

Related questions

Does the fusiform face area in patients with Prosopagnosia (face blindness) show lower activity under an fMRI?

Feeling as though you have seen a face before is perfectly normal. It may reflect actual similarities between the new face and the face you have seen before. There are people who genuinely look like each other, an example being celebrity look-a-likes. It may also reflect a commonly observed cultural/ethnic effect where people of a different ethnicity look more similar (Meissner & Bringham, 2001).

In terms of what happens in the brain, besides processing by the basic visual system (LGN, V1), the ventral visual pathway and areas associated with object and face recognition are involved with identifying the face. Particularly, these three core regions show space-specific responses: fusiform gyrus, lateral inferior occipital gyri , and posterior superior temporal sulcus (Haxby et al., 2000; 2001).

  A model of the distributed human neural system for face perception (Image from Haxby et al., 2000.)

There is ongoing debate that the fusiform area plays a broader role in that of visual expertise, rather than just face perception (Gaulthier et al., 2000; Xu, 2005). Although less is known about temporal aspects of face processing, this is starting to be the focus of newer studies such as Zheng et al., 2012.

I haven't found any known explanation but if you feel that the way you perceive similarity in faces is not normal, then you may be interested in reading about false facial recognition problems following brain damage (*Rapcsak et al., 1996) or (slightly different) misidentification syndromes (Hudson & Grace, 1999; Breen et al., 2000).

*Unfortunately I could not access this article to summarize it.

References

Breen, N., Caine, D., Coltheart, M. (2000). Models of face recognition and delusional misidentification: A critical review. Cognitive Neuropsychology. 17(1/2/3):55-71.
Gauthier, I., Skudlarski, P.,  Gore, J. C.,  Anderson, A. W. (2000). Expertise for cars and birds recruits brain areas involved in face recognition. Nature Neuroscience 3:191-197.
Haxby, J. V., Hoffman, E. A., Gobinni M. I. (2000). The distributed neural system for face perception. Trends in Cognitive Science, 4(6):223-233.
Haxby, J. V., Hoffman, E. A., Gobinni M. I. (2001). Human neural systems for face recognition and social communication. Biological Psychology, 51(1):59-67.
Hudson, A. J., Grace, G. M. (1999). Misidentification syndromes related to face specific area in the fusiform gyrus. J Neurol Neurosurg Psychiatry, 69(5):645-648.
Meissner, C. A.; Brigham, J. C. (2001). Thirty years of investigating the own-race bias in memory for faces: A meta-analytic review. Psychology, Public Policy, and Law, 7(1):3-35.
Rapcsak S. Z., Polster M. R., Glisky M. L., Comer J. F. False recognition of unfamiliar faces following right hemisphere damage: neuropsychological and anatomical observations. Cortex; a Journal Devoted to the Study of the Nervous System and Behavior. 32(4):593-611.
Xu, Yaoda. (2005). Revisiting the role of the fusiform face area in visual expertise. Cereb Cortex. 15(8):1234-1242.
Zheng, X., . Mondloch, C. J.,  Segalowitz, S. J. (2012). The timing of individual face recognition in the brain. Neuropsychologia, 50(7):1451-1461.


Could neuroscientific knowledge and techiques be used to optimise peoples' education and learning? Expanding upon this, I have two ideas behind this question - 1) that current knowledge of the brain and its workings (biochemically, biomechanically, physiologically etc) is in its infancy and that we are a long way from fully understanding the mechanisms of cognition and brain function......

and 2) There are people in this world that have amazing cognitive and mental capabilities and I believe they show off what the brain can achieve in terms of singular focussed abilities such as autistic savants.

These people are amazing at one or two abilities such as mental calculations, eidetic memory, polylingualism, prodigious musical ability etc and I realise these people have some sort of deficit or disability but I think it simply displays the potential that everyone could have if they had the right stuff (whatever this may be!).

Thinking of this potential when the time comes when we understand a whole lot more about the brain:

Will it be possible to use neuroscientific  knowledge to personalise each child's cognitive learning at each stage in their lives from say age one onwards through to school level to allow them to develop savant like capabilities, even if it isn't as impressive as actual savants?

Thank you, sorry for the long winded question but my thinking is that the brain is capable of lots more and if we are today basing some of our education curriculum and structure on current scientific knowledge then surely in the future this could snowball for such sciences to fulfil our cognitive potential.

There is an emerging trend in cognitive science called neuroeducation - the wikipedia page is of interest, especially the section "Neuroscience and education: A bridge too far" (I removed the question mark).
https://en.wikipedia.org/wiki/Educational_neuroscience

Another thought that came while reading your interesting question. It is about the desire to enhance the human mind, a desire that we find for example in the "transhumanism" movement (http://en.wikipedia.org/wiki/Transhumanism). If I understand the role of cognitive science as a science to describe how the mind works, I have a hard time thinking about it as a science that aim at modifying how the brain works. Cognitive science would not be a science anymore, but a technology.


Can addiction develop to the absence of a normally present negative stimulus? I am wondering, can someone become addicted to the absence or the removal of a negative stimulus? Normally, addiction is associated with pleasure-inducing drugs, like opiates and amphetamines as notorious examples. These compounds induce massive release of dopamine in the limbic system, ultimately leading to addiction. Addiction is a collection of behaviors:

  Addiction is characterized by inability to consistently abstain,
  impairment in behavioral control, craving, diminished recognition of
  significant problems with one’s behaviors and interpersonal
  relationships, and a dysfunctional emotional response. Like other
  chronic diseases, addiction often involves cycles of relapse and
  remission.

It is known that training can be assisted by positive reinforcement (well done! here's a candy), or by negative reinforcement (wrong! here's an electroshock). Can addiction be caused by either? In other words, suppose someone is constantly aware of something unpleasant (pain, itching, unwanted perceptions such as tinnitus (ringing in the ears), negative emotions or thoughts) can the removal/lessening of such a stimulus lead to an addiction of the means to remove it?

For the sake of the question I think it is sufficient to focus the question on one (e.g., craving), or several of the symptoms, as existing studies, if any, may have focused on only one or few of the symptoms of addiction.

In short: are there studies on the addiction to the absence / removal of a negative stimulus?

This question was fueled by the comments to an earlier question

In short, the answer to your question

  can someone become addicted to the absence or the removal of a negative stimulus?

is most definitely yes.

Whilst not intended to be used as “diagnostic criteria” for determining if addiction is present or not, the characteristics of addiction provided through the American Society of Addiction Medicine (ASAM) are widely present in most cases of addiction, and gives an outline of the mechanism required for what you could be talking about, and therefore your hypothesis definitely has legs.  You only have to look at alcoholism as an example.

The mechanism works through positive reinforcement, which as you put it, "Well done! here's a candy" in which the "candy", as you will see below, can be pain relief.

The same ASAM link you gave also points out that

  Addiction is a primary, chronic disease of brain reward, motivation, memory and related circuitry.

Although experimental studies have produced mixed results, there has been a long-standing belief in the analgesic properties of alcohol and a meta-analysis of controlled experimental studies conducted by Thompson et al. (2016) found that alcohol has the ability to provide a sense of relief from pain.

  Alcohol resulted in a small increase in pain threshold.
  A moderate-large decrease in pain ratings was also observed.
  Higher blood alcohol content is associated with greater analgesia.
  Analgesic effects may contribute to alcohol dependence in those with persistent pain.

Alcohol is also a big problem amongst many seeking help from severe stress, depression and/or anxiety through negative urgency which is correlated with greater caudate nucleus activity to alcohol cues (Chester, et al. 2016).

This is because, as pointed out by Sharot (2012)

  The caudate nucleus is one of the major targets for the brain’s dopaminergic system (Wise & Rompre, 1989). Dopamine is a principal neuromodulator for reward learning and reward-seeking behaviour (Bayer & Glimcher, 2005; Belin & Everitt, 2008; Schultz, 2001). In particular, dopamine is suggested to signal predictions of rewards, and errors in such prediction–providing a learning signal when predictions do not align with outcomes (Montague, Hymann & Cohen, 2004; Schultz, 2001, 2007).

Through the dependency on the false friend called Alcohol, there is the inability to consistently abstain from seeking relief from pain (emotional or physical) which is part of the impairment in behavioural control.  The feelings of escape from physical pain or the emotional attachment to life's hardships, after a while, can lead to craving for the same feeling, either to remove the returning pain, or to prevent its return.

Diminished recognition of significant problems with their behaviours and interpersonal relationships forms another part of the impairment in behavioural control and can arise from this constant "need" for an alcoholic drink, and dysfunctional emotional responses develop.

References

Chester, D. S., Lynam, D. R., Milich, R., & DeWall, C. N. (2016). Craving versus control: Negative urgency and neural correlates of alcohol cue reactivity. Drug and alcohol dependence, 163, S25-S28. doi: 10.1016/j.drugalcdep.2015.10.036

Sharot, T. (2012). Chapter 3 - Predicting Emotional Reactions: Mechanisms, Bias and Choice. In R. Dolan & T. Sharot (Ed.), Neuroscience of Preference and Choice (pp. 53-72). Academic Press doi: 10.1016/B978-0-12-381431-9.00003-6

Thompson, T., Oram, C., Correll, C. U., Tsermentseli, S., & Stubbs, B. (2017). Analgesic effects of alcohol: a systematic review and meta-analysis of controlled experimental studies in healthy participants. The Journal of Pain, 18(5), 499-510. doi: 10.1016/j.jpain.2016.11.009


Can anyone provide a modern source for the average college student IQ of 115? I've read in various places that the average college student IQ is about 115, and the various estimations of IQ by college major reached by converting SAT to IQ all use 115 as the starting point for college students. However, the most recent source for this number is The Bell Curve, which was in the early 1990s. It is also just about the only source of the last 40+ years. Can anyone provide a more recent documentation of the average IQ of college students? (that isn't just a reference to an older study)

Ok I finally found the official demographic norming data from the WAIS-IV on page 104 of this book:

"WAIS-IV Clinical Use and Interpretation: Scientist-Practitioner Perspectives"

You can see a preview of this book at http://tinyurl.com/z3vr44e.

The answer to my question is: Some college:      102.28
                                College graduates: 110.77


Are there ways to accelerate the recovery from depression via novel pharmacological antidepressants? Are there any scientists making substantial progress in the development of far more effective antidepressants? Are there any groups of people interested in developing antidepressants based on genetic tests?

Depression: How effective are antidepressants?

"It can take a long time for a medication to start helping some people. Other people still have symptoms even after trying several different medications. They can then discuss the alternative treatment options with their doctor."
https://www.ncbi.nlm.nih.gov/books/NBK361016/

Wikipedia maintains a list of potential antidepressants currently under investigation.

Of some note, the US FDA recently approved esketamine for clinical use.  After being banned in the 1970s, psychedelics have become available for research purposes again in the past 20 years or so.  Esketamine, a derivative of the psychedelic drug ketamine, which was already approved as an anesthetic, is an early result of this resurgence.  Other psychedelics (eg, psylocibin, LSD, mescaline, DMT, MDMA) are being investigated as potential treatment for a variety of mental disorders, including depression.

Also of note, transcranial magnetic stimulation (rTMS) is a relatively new treatment for some types of depression.  The notion that depression comes in several forms or sub-types, responsive to different treatment options, has lead to the investigation of a variety of genetic tests that may help personalize treatment in the future.  Additionally, several labs (example) are investigating the possibility of using fMRI to distinguish such sub-types using brain scans.


What transient factors affect performance on IQ tests? While performance on intelligence tests aim to measure an underlying relatively stable trait, there are presumably a range of transient factors that could temporarily lower or possibly even raise scores on such tests.

Possible factors might be: alcohol, sleep deprivation, mood, test taking anxiety, etc.

Are there any studies so far that have assessed the degree to which such transient factors can influence performance on intelligence tests?
Do such studies suggest such affects depend on other factors such as gender, personality, and presence/absence of ADD/Asperger's?

I had a course which was about IQ; I never read an article about it, so I can't quote studies (I can look up the references if you like).

There are indeed a lot of factors that can influence ones score on an IQ test. These are some transient factors that came to my mind:

The setting: was the test taken at home, at school, at a totally unfamiliar place? Test scores tend to be higher when a child can take it at home.
The part of the day: was the test taken in the morning, in the afternoon, or in the evening? I think (I should look this up) that scores tend to be lower if IQ tests are taken in the evening. Perhaps if you're a morning type, you're better in the morning than 'evening people', who are better in the afternoon than in the morning. But this is speculation (I know I've read something about it, but I can't seem to find it now).
Motivation/Attention: this really can play a big role in the results. That's why good tests (e.g. the WISC) have a zone for remarks. Children with ADHD score better when they are given more pauses during the examination.
Hormones: there is some evidence that there's a hormonal influence (testosteron, estrogen, congenital adrenal hyperplasia).
Test taking anxiety: this can indeed influence the score negatively. It's important that the test leader says 'good job' or something like that. Normally, this isn't according to the guidelines of the test, but it's acceptable here, since you would underestimate the ability.


Do researchers and laypeople understand statistics differently? I'm looking for references related to how researchers and laypeople understand concepts of statistical inference. In particular, I'm looking for articles in which subjects could demonstrate statistical competence by evaluating statistical claims. Does anyone have a relevant reference?

Even among researchers there is widespread misunderstanding of core statistics ideas. Look at the work by Geoff Cumming. Example paper title: 'Researchers misunderstand confidence intervals and standard error bars.'


Theories of Emotion: Schachter's Two Factor Theory Example I'm currently in AP Psychology and studying for the exam using the College Board's course description, which contains sample psychology multiple choice questions. Here is one question, taken from the document:

Lee is about to skydive for the first time. He interprets his racing heart to be the result of his eager anticipation and excitement. This best represents which theory of emotion?
(a) Cannon-Bard
(b) James-Lange
(c) Drive reduction
(d) Schachter’s two factor
(e) Arousal

Immediately, I ruled out A, B, C, and E, leaving "D" as the choice. But per the definition of the Schachter two factor theory of emotion (alternatively known as the Schachter-Singer model), an emotion is felt only after there has been a physiological response and a cognitive appraisal of the situation. Here is one source that explains this, but our AP Psychology textbook also explains it in that way. I don't see how that matches the given scenario. Why is this correct?

I think it's because he interprets his emotion as anticipation and excitement because of the context - because he's about to go skydiving which is fun and exciting.  If he was at home watching a boring TV show and had the same physiological experience, he might think he was having a symptom of some kind of heart disease.  If he'd just tried a new drug and had the experience, he'd think it a side effect of the drug.  If he'd just met a new person and had the racing heart, he might think he was in love.  The physiological response (racing heart) is necessary, but it needs to be defined cognitively according to the context (skydiving), that's the two-factor theory.


What is the role of Chloride (Cl- ions) in membrane potential? This Membrane Potential article mentions only that Cl- ion is used to model inhibitory GABA synapses. Does it have another role besides hyper-polarizing the cell due to inhibitory neurotransmitter binding?

For example, Cl- ions are not taken into consideration in the Pinsky & Rinzel 1994 Model or in Pospischil et. al. 2008 Models.

In normal neurons, Chloride's reversal potential is near the resting potential for the neuron and also happens to be near the leak conductance reversal potential for the neuron. While not exactly the same these three are sometimes confused.

The difference between these three reversal potentials is subtle.

Chloride Reversal Potential: is the potential carried only by the chloride ion. Therefore it given by the Nernst Equilibrium Potential.
Leak Reversal Potential: The conductance that remains (relatively) constant. As useful metaphor the leak conductance is the passive conductance of ions through the membrane. This current can be carried by any Ion.
Resting Potential: The voltage where the neuron is at rest, usually when it is at a steady state. It is defined by all ion's that permeate the membrane at rest. (see GHK)

Because these three reversal potentials are approximately the same that means many computational neuroscience papers will consider only consider the leak current like the two paper's you linked. However, if there is reason to consider Chloride conducting channels specifically (like GABA receptors) then there will be a specific term for the Chloride Ion's Reversal potential.

From a computational perspective, the fact that the Chloride reversal potential is close to the rest potential is actually important. It is capable of shunting inhibition. In short this means that the neurons membrane potential is moved closer to rest, rather than more negative as is the case with regular hyperpolarizing current carried by Potassium Ions. Thus if the membrane potential is below the driving potential for chlorine the shunting inhibition will actually slightly depolarize the cell. Note that this small depolarization  will not pass the chlorine reversal potential, thus keeping the cell at rest and preventing firing, despite "depolarizing the cell"

While it is generally true that hyperpolarizing current suppresses firing, there are exceptions to this rule. For example, if a neuron is a resonator (fires in response to certain frequency of input) then hyperpolarizing inputs at the right frequency will cause the neuron to fire. Note, However this is only true for the current carried by Potassium Ions, and shunting inhibition will prevent this type of hyperpolarize-induced firing. The reasoning for this is quite complex, but a good (albeit math-heavy) explanation see Dr. Izhikevich's book Chp 7.


What can clinical psychologists do that psychiatrists can't do? From Yahoo Answers:

  For example, I know that psychiatrists can prescribe medicine and
  psychologists CAN'T, but are there any things that clinical
  psychologists are specialised in that psychiatrists aren't? If not,
  then why do we have psychologists and not just psychiatrists? Sorry if
  it sounds like a stupid question, I'm just a little confused lol.

Is it correct to say that people who don't or might not need drugs for their problems would go to psychologists instead psychiatrists because it is significantly cheaper?

There's an answer:

  they are also able to provide meditation and breathing techniques for
  things such as panic attacks.

So psychiatrists can't do that? The only thing I can see psychologists doing outside the academia is being a cheaper alternative to a psychiatrist. If clinical psychologists (is that the same as non-academic psychologists?) charged the same as psychiatrists, why doesn't everyone go to psychiatrists?

Short answer is that psychiatrists are medical doctors and (more often than not) medical researchers, and thus psychiatrists themselves often do not practice psychotherapy.

Psychiatrists

Psychiatrists are physicians, which means they have received a medical degree (M.D.) and have completed medical training, along with an additional four-year residency in psychiatry. Some psychiatrists pursue additional fellowship training after their residency. Thus, it takes at least twelve years of practice to become a psychiatrist.

Psychiatrists are legally allowed to prescribe psychotropic medications to patients. This is because they are medically trained to do so, having completed a medical degree and medical training. A large portion of this medical training is dedicated to learning how psychotropic medications work in the brain and in the body, particularly in those of patients with mental illnesses. For this reason, psychiatrists are generally more aware of the physical symptoms of illness (much like a doctor would be) as well as the mental symptoms, and thus must make an informed evaluation to determine whether the patients' symptoms are due to physical or mental factors (or both).

Though psychiatrists can perform psychotherapy, the vast majority are purely medical researchers. A psychiatrist may thus refer a patient to a clinical psychologist or a specifically-trained therapist for their individual psychotherapy needs. A physician or psychiatrist (both trained in psychopharmacology by definition) who both practices psychotherapy and prescribes psychoactive medication may refer to themselves as a "psychopharmacologist", though this is more of a distinction than a formal occupation.

Clinical psychologists

Clinical psychologists are PhDs who have received several years of graduate training in the science and theory of psychology-based dysfunction and mental illness. They do not receive medical training, but they do undergo 2-4 years of supervised clinical practice before they are licensed as clinical psychologists.

A clinical psychologist's job description is a bit more broad than that of a psychiatrist. While many provide psychotherapy to patients suffering from mental illness, other clinical psychologists may opt to teach, administer psychological testing, conduct research, work with administrators, develop treatment and prevention programs, or work as psychological consultants.

Though there is very little that a clinical psychologist can do that a psychiatrist simply can't do, a clinical psychologist is trained in mental health and well-being first and foremost, and thus is typically called on to perform tasks related to mental health (such as psychotherapy or psychometric testing). The difference may be comparable to that of a professor versus a teacher. Though the professor typically undergoes more training, they split their focus between their research and their students (and may prioritize research first), whereas high school teachers are often teachers through-and-through, and thus their primary focus is on the students. Thus the teacher role is a bit more interpersonal.


With the brain's propensity for homeostasis, how can some drugs be labelled addictive and others not? The human body is always striving for homeostasis. One of the purposes of the brain is to maintain homeostasis, but also the brain needs to maintain homeostasis within itself.

Ergo:
Given the use of any drug, that acts of the brain, will cause a change in brain chemistry.

Why are some drugs are regarded as addictive and others are not?

Here is a part answer to your question.

According to the article Drug Facts: Understanding Drug Abuse and Addiction and Drugs, Brains, and Behavior: The Science of Addiction, addiction is a disease caused by some types of drugs.  Specifically, they rewire the brain to cause an overstimulus of the 'reward' centres and by imitating some of the pre-existing neurochemical messengers in the brain - essentially, 'tricking' the brain that homeostasis is maintained.

Related, the article "Why does the rapid delivery of drugs to
the brain promote addiction?" (Samaha and Robinson, 2005) concluded that the rate of delivery is an important factor:

  that rapidly
  delivered drugs might promote addiction by promoting
  forms of neurobehavioural plasticity that contribute to
  the compulsive pursuit of drugs.


What is runaway excitation? Can someone give me a brief explanation of this term? Found it in a paper but there doesn't seem to be an explanation that is consistent out there to my knowledge.

When I have used (or seen) this term, it usually means that recurrent excitatory connections in a network have become stronger than the inhibitory feedback. This means that excitatory activity will grow stronger and stronger, without inhibitory influences to keep it in check. Eventually, the activity within the network will be limited only by spike-rate saturation. This type of network configuration is sometimes used as a model for an epileptic seizure.


Categorisation of attributes according to OCEAN I've read about OCEAN (or The big five or FFM) on Wikipedia and I'm intrigued. I would like to have a categorisation of attributes describing a personality according to the model. Since we have a lot of attributes and this is a potentially subjective for each attribute if you were to add any measure of intensity, I wanted to ask if you know any source, preferably a scientific one, where this has been done already. (A non-scientific source could be a categorisation done in a blog about character design in novels, for example.)

It's unclear what is your definition of attributes.
But the Big Five emerged from the lexical hypothesis whereby adjectives in the dictionary that describe people were systematically examined and categorised using approaches such as factor analysis. Some of the papers in this area would contain lists of terms.

Equally, for briefer lists, you could look at the domain-facet frameworks of various Big 5 personality models, such as the NEO. In this context, the facets help to define the Big 5 Domains.

Here are a few such domain-facet/aspect frameworks, summarised in Anglim & O'Connor (2018, PDF). That article also provides a brief review of the lexical approach with some further references.

Anglim, J., & O'Connor, P. (2019). Measurement and Research Using the Big Five, HEXACO, and Narrow Traits: A Primer for Researchers and Practitioners. Australian Journal of Psychology, 71, 16-25. https://psyarxiv.com/a78g2/download


Punishment v.s Negative Reinforcement Consider the following scenario:

  Every time I do the groceries with my son he constantly asks for a packet of lollies. I find this constant asking for lollies very annoying, so I always end up buying him the lollies.

For the parent, the textbook states that this an example of negative reinforcement. Now this seems very intuitive, but I am wondering why this could not be an example of a punishment?  The definition of punishment that I have been given is:

  "If the behaviour brings about a negative outcome, it's less likely to occur in the future".

I would've thought that the if the son's behaviour changed from misbehaving, this is an example of a punishment (albeit a tasty punishment). If the son continued to misbehave after receiving the lollies, then this would be typical of a reinforcer.

Am I on the right track?

Operant Conditioning

The general topic you are referring to is called operant conditioning.

Positive/negative refers to whether you are adding something or taking it away.

Reinforcement/punishment refers to whether you are causing a behavior to increase or decrease.

Positive punishment is adding (positive) a bad thing (punishment) like yelling at or slapping the kid.

Negative reinforcement is taking away (negative) a bad thing (reinforcing).

Negative punishment is taking away (negative) a good thing (punishing), like limiting access to a certain toy or the television.

Both positive punishment and negative punishment tend to reduce a behavior, though often positive punishment is less effective and more likely to produce off-effects.

Importantly, in operant conditioning everything is relative to the consequences of a behavior by the one behaving ("operating"). If someone is not "operating" you cannot describe it in operant conditioning terms.

Your example scenario

Your first example is positive reinforcement from the perspective of the child: their behavior (begging) leads to getting rewarded with lollies. One would expect that this would increase future begging for candy rather than reduce it.

The only way to think of this as negative reinforcement is from the perspective of the parent, for whom giving the child lollies (the parent's behavior) has removed a noxious stimulus (the begging by the child), which might lead the parent to again purchase lollies to reduce complaining.

However, in parenting or training a dog or most any other context where there is a power relationship, you are usually more concerned with thinking about how behaviors affect the child/dog/whomever. In this situation, if a parent wants to stop the begging long term, likely the best approach is to target extinction of the behavior, which occurs when a behavior (e.g., begging) does not achieve a positive outcome (e.g., no lollies are obtained).

When you write:

  I would've thought that the if the son's behaviour changed from misbehaving, this is an example of a punishment (albeit a tasty punishment)

From the perspective of the son, this is not an example of operant conditioning, because the behaviour change (stopping begging) is not causing the 'stimulus' (getting candy), but rather the other way around. You could only consider this operant conditioning from the perspective of the parent, who is being trained to do an action ("give candy") to remove an aversive stimulus (child begging).


Possibility of increasing brain speed In science fiction stories, we often see the use of virtual reality, a 3d world that allows you to actually 'be' there. The writers often use a pod or helmet to signify the use of some sort of computer that reads and sends information to the brain. What many, if not all, of them have in common is that time is sped up. If it isn't double then it's triple or much more. Now, while this is science fiction and far removed from any real basis, I'm curious. Is it possible to speed up brain in such cases? I.e. Would we be able to make time move faster in a virtual space?

My gut, deduction, and the meagre amount of information I found online, says it's impossible. I know very little about the brain, but processing information at a much faster speed would force a much bigger strain on the organ, thus overtaxing it. Not to mention, if the brain could actually run faster, wouldn't it have it's own mechanisms for running faster, considering it would be quite the advantage when you want to survive as a cavemen against a lion that's in need of some breakfast.

There are just too many ways to answer this question. But I suspect all of them will be proxies to the ultimate answer - the goldilocks principle.

To give an example, for the human brain to be faster, it would either have to be smaller, or would consume more energy. There is an optimal balance between the size of the brain and its energy ratio (to the rest of the body). Like many factors, these were heavily shaped by evolution (which in turn is heavily affected by our environment).

You can also argue that a faster brain will accumulate processing residues faster, thus we'll have to sleep more frequently, which may have adverse effect on survival chances. I know it sounds far-fetched, but you can actually argue that the size of the brain is correlated to the distance of earth from the sun. That's the goldilocks principle for you.

Would strongly recommend:

What is so special about the human brain? (TED Talk)

And the first chapter in:

Gibb, B., 2012. The Rough Guide to the Brain, 2 edition. ed. Rough Guides, London.