What makes something relevant to an argument and how can people improve in determining relevance? Are there any books that examine questions about relevance in general like the following?
Relevance Theory seems something else and inapplicable.

What makes something (ir)relevant to an argument or discourse?
How can humans improve on deciding whether something is (ir)relevant?

The Wikipedia article on relevance references a couple of books and a few journal articles.

The Wikipedia article says

  Cognitive science and pragmatics

  Further information: Relevance theory

  In 1986, Dan Sperber and Deirdre Wilson drew attention to the central importance of relevance decisions in reasoning and communication. They proposed an account of the process of inferring relevant information from any given utterance. To do this work, they used what they called the "Principle of Relevance": namely, the position that any utterance addressed to someone automatically conveys the presumption of its own optimal relevance. The central idea of Sperber and Wilson's theory is that all utterances are encountered in some context, and the correct interpretation of a particular utterance is the one that allows most new implications to be made in that context on the basis of the least amount of information necessary to convey it. For Sperber and Wilson, relevance is conceived as relative or subjective, as it depends upon the state of knowledge of a hearer when they encounter an utterance.

The books referenced are:

Sperber, D. & D. Wilson (1986/1995). Relevance: Communication and Cognition 2nd edition. Oxford: Blackwell. ISBN-13: 978-0631198789Available from:
Amazon UK
Amazon US
Amazon Canada

and

Sperber, D. & D. Wilson (2004). Relevance Theory, In: Horn, L.R. & Ward, G. (eds.) 2004 The Handbook of Pragmatics Oxford: Blackwell: pp 607-632. ISBN-13: 978-0631225485Available from:
Amazon UK
Amazon US
Amazon Canada

There is free access to this part of the book on Dan Sperber's website

When going to the amazon pages for the relevant books, it also suggests other books other people have bought with these books along with other possible related books.


What are the key predictive traits of therapeutic success? In my answer here, to this question : Does hypnotherapy/hypnosis, in any form, for any type of disorder, work?

It brought up the valid question of why people quit therapy. Obviously, if the therapy is not helpful, it is could be construed as a straightforward cause and effect.

People stop therapy or positive coping techniques for a vast number of reasons.

What are the the key predictive factors that cause people to succeed or fail a longer term therapy which has been giving shorter term successes for that individual?

There is a substantial body of literature addressing each of these questions (why do people quit therapy and what predicts positive outcomes); unfortunately there are no easy answers. In part, this is because the literature has looked at these questions from a range of angles, including client characteristics (age, race, gender, motivation, education level, diagnosis), therapist characteristics (demographics, years of experience, therapeutic orientation [cognitive vs psychodynamic]), therapeutic dynamic characteristics (client-therapist demographic match, therapeutic alliance),  and treatment characteristics (whether treatment is manualized, group vs individual therapy, type of therapy). I’ve provided brief answers to both below, but you’ll likely need to do additional literature searches if you have a question about a specific group of patients or therapy.

Why do people quit therapy?

Swift & Greenberg (2012), conducted a meta-analysis of 699 studies and found a nearly 20% dropout rate for therapy. They found that younger clients, clients who were attending university clinics, those with personality or eating disorders, and those seen by providers-in-training had higher dropout rates. Some of these factors may be correlated; younger clients may be more likely to attend university clinics, and those clinics often use graduate student therapists-in-training to provide services. The study also found dropout rates were higher in studies where the therapist rated/decided if a client had dropped out, which may reflect the therapists’ perspective. Additionally, therapy that was not time-limited and not manualized had higher dropout rates. Whether it was group vs individual therapy, the orientation of therapy, provider race or gender, and client race or employment status had no effect. Results were mixed for other client demographic variables such as gender, education and marital status.

Another meta-analysis of 11 studies found that dropout was higher when therapeutic alliance, the relationship between the client and therapist, was weaker (Sharf, Primavera, & Diener, 2010). However, the authors noted that this was moderated by the client’s level of education and the length of treatment. Clients with more education were less likely to dropout. The longer the treatment the higher the dropout rate, though, as in the Swift & Greenberg (2012), it may also reflect the perception of the person reporting dropout. Clients may have felt the therapy was completed, while therapists may have felt the client “dropped out.”

Finally, a recent meta-analyses examined the impact of accommodating client preferences on treatment outcomes and dropout rates (Swift, Callahan, Ivanovic, & Kominiak, 2013). There is extensive literature exploring the importance of client preferences related to type of therapist (sex, race), type of treatment (therapy and meds, therapeutic orientation), or style (collaborative, prescriptive) on therapeutic outcomes. Swift and colleagues (2013) found that accommodating client preferences resulted in better outcomes and decreased dropout; these effects did not vary based on client demographic characteristics (age, sex, marital status, etc.). They also noted that clients who were not accommodated were especially likely to dropout of short term therapy.

What predicts therapeutic outcome?

Several recent studies examined the role that therapeutic alliance had on outcomes. A Swedish study of 646 patients found that alliance impacted symptom level in the next therapy session in a feedback loop, such that stronger alliance predicted stronger change in symptoms, which in turn strengthened alliance (Falkenstrom, Granstrom, & Holmqvist, 2013). However, the authors noted that the effect was stronger for some clients (personality disorder patients), than others, indicating that client factors also impact outcomes. Therapy type (supportive, CBT, psychodynamic) did not impact symptom reduction.
Another study found only a weak indication that therapeutic relationship impacts outcomes in complex treatment for psychosis (Priebe, Richardson, Cooney, Adedeji, & McCabe, 2011); these results may reflect a similar finding to Falkenstrom and colleagues (2013), in that diagnosis impacts the role of alliance in outcomes. McEvoy, Burgess, & Nathan (2014) found that another client factor, level of interpersonal problems, predicted dropout and poorer outcomes, regardless of alliance. They also found that type of treatment impacted this relationship, as those patients in CBT who had better alliance were more likely to stay in treatment, but that neither alliance nor personal problems predicted outcomes in those clients.  A 2012 meta analysis questioned previous findings that found alliance predicted outcomes (Fluckiger, Del Re, Wampold, Symonds, & Horvath); they found small effects of alliance and outcomes early in therapy, but not for longer-term therapy and did not find sustained relationships with any other commonly noted predictors, such as type of therapy. In contrast, a recent study (Gullo, Lo Coco, & Gelso, 2012) found that a genuine and real (i.e. accurate and not distorted by past conflict or bias) therapeutic relationship predicted successful outcomes for those clients who stayed with treatment, but not those clients who terminated early.

In terms of other client characteristics that can impact outcomes, one study of 60 Caucasian and Asian American clients found that those with more somatic symptoms and who used avoidant coping had poorer psychosocial functioning and psychological discomfort at end of treatment (Kim, Zane, & Blozis, 2012). They also found that those who preferred Non-English language therapy had worse outcomes and that this was mediated by avoidant coping. The authors proposed that Asian American patients who preferred non-English language therapy may have used coping styles that were culturally relevant to them, but which fit poorly with the style of therapy they received. The expression of psychological symptoms and illness is culturally defined, and should be kept in mind when reading meta-analyses that may reflect the dominant culture.

Another meta-analysis of 23 studies found a small to medium effect of homework compliance (completing therapeutic assignments given by the therapist) on client outcomes, which was present regardless of the client’s primary symptom presentation (Mausbach, Moore, Roesch, Cardenas, & Patterson, 2010). This may reflect the importance of client buy-in and effort in therapy, though it should be noted the effect size varied according to certain methodological factors.

Other analyses have examined the importance of therapist characteristics or client-therapist match on outcomes. A meta-analysis of 64 studies found therapist sex did not impact client outcomes or dropout (Bowman, Scogin, Floyd, & Mckendree-Smith, 2001). As noted in my answer to the dropout question above, Swift and colleagues (2013) noted a range of domains in which clients can prefer to be matched in regards to therapy. A 2011 (Cabral & Smith) meta-analyses of 52 studies found almost no effect for race-ethnicity matching and outcomes when looking across all studies. However, the authors did note that African Americans had mildly better outcomes when matched with African American therapists, a trend which did not hold for the other racial and ethnic groups in the study (Caucasians, Hispanics, and Asian Americans). A second meta-analyses of 7 studies found similar results, with a negligible effect size for ethnic match across all samples, though matching had a greater effect for ethnic minority samples than Caucasians in terms of preventing dropout and increasing the number of sessions attended (Maramba & Hall, 2002). Again, these findings call attention to the importance of multicultural conceptualization when identifying treatments and approaches for clients; this diversity is also an excellent example as to why your questions have no simple answers.

Note: None of the studies I found, focusing on recent, meta-analytic literature, addressed whether the clients found the therapy “helpful” (as indicated in your question) as a primary research question.

Bowman, D., Scogin, F., Floyd, M., & Mckendree-Smith, N. (2001). Psychotherapy length of stay and outcome: A meta-analysis of the effect of therapist sex. Psychotherapy, 38(2), 142-148

Cabral, R. R., & Smith, T. B. (2011). Racial/Ethnic matching of clients and therapists in mental health services: A meta-analytic review of preferences, perceptions, and outcomes. Journal of Counseling Psychology, 58(4), 537-554. DOI: 10.1037/a0025266

Falkenstrom, F., Granstorm, F., & Holmqvist, R. (2013). Therapeutic alliance predicts symptomatic improvement session by session. Journal of Counseling Psychology, 60(3), 317-328. DOI: 10.1037/a0032258

Fluckiger, C., Del Re, A. C., Wampold, B. E., Symonds, D., Horvath, A. O. (2012). How central is the alliance in psychotherapy? A multilevel longitudinal meta-analysis. Journal of Counseling Psychology, 59(1), 10-17. DOI: 10.1037/a0025749

Gullo, S., Lo Coco, G., & Gelso, C. (2012). Early and later predictors of outcome in brief therapy: The role of real relationship. Journal of Clinical Psychology, 68, 614-619. DOI: 10.1002/jclp.21860

Kim, J. E., Zane, N W., & Blozis, S. A. (2012). Client predictors of short-term psychotherapy outcomes among Asian and White American outpatients. Journal of Clinical Psychology, 68, 1287-1302. DOI: 10.1002/jclp.21905

Maramba, G. G., & Hall, G. C. N. (2002). Meta-analyses of ethnic match as a predictor of dropout, utilization, and level of functioning. Cultural Diversity and Ethnic Minority Psychology, 8(3), 290-297. DOI: 10.1037//1099-9809.8.3.290.

Mausbach, B. T., Moore, R., Roesch, S., Cardenas, V., & Patterson, T. L. (2010). The relationship between homework compliance and therapy outcomes: An updated meta-analysis. Cognitive Therapy Research, 34, 429-438. DOI: 10.1007/s10608-010-9297-z

McEvoy, P. M., Burgess, M. M., & Nathan, P. (2014). The relationship between interpersonal problems, therapeutic alliance, and outcomes following group and individual cognitive behavior therapy. Journal of Affective Disorders, 157(20), 25-32. DOI: 10.1016/j.jad.2013.12.038.

Priebe, S., Richardson, M., Cooney, M., Adedeji, O., & McCabe, R. (2011). Does the therapeutic relationship predict outcomes of psychiatric treatment in patients with psychosis? A systematic review. Psychosomatics, 80(2), 70-77. DOI: 10.1159/000320976

Sharf, J., Primavera, L. H., & Diener, M. J. (2010). Dropout and therapeutic alliance: A meta-analysis of adult individual psychotherapy. Psychotherapy Theory, Research, Practice, Training, 47(4), 637-645. Doi: 10.1037/a0021175

Swift, J. K., Callahan, J. L., Ivanovic, M., Kominiak, N. (2013). Further examination of the psychotherapy preference effect: A meta-regression analysis. Journal of Psychotherapy Integration, 23(2), 134-145. DOI: 10.1037/a0031423

Swift, J. K., & Greenberg, R. P. (2012). Premature discontinuation in adult psychotherapy: A meta-analysis. Journal of Consulting and Clinical Psychology, 80(4), 547-559. doi: 10.1037/a0028226


Why is MATLAB so common in Neuroscience? It is common knowledge that neuroscience -- particularly experimental neuroscience -- uses MATLAB more than any other programming language. I have always just taken this as a given, and pointed to existing toolboxes, legacy lab codebases, and social pressure as the reasons why this continues to be the case, even though concrete reasons to switch are widely known.

I want to go past these general reasons and pin down the exact causes of MATLAB's stronghold in Neuroscience. Things like

file formats that can only be read in MATLAB
acquisition systems that are highly coupled to MATLAB
toolboxes that are widely regarded as the "gold standard" for something
labs or companies that train many researchers on MATLAB and advocate for it
introductory neuroscience programs / textbooks that teach concepts through MATLAB examples

or any other tangible things to point to would be excellent.

I think the major reason is inertia, in the sense that many labs use Matlab, so many Matlab toolboxes are available, so many labs train people in the use of Matlab...

However, as a trained software engineer turned Neuroscientist who has been programming in various languages for close to 30 years, there are several reasons why I actually enjoy using Matlab. One can also make arguments for why it's a good fit for labs filled with people who aren't programmers.

(As an aside, the .mat file format is actually a standard file format called "HDF". So I don't think that file format lock-in is a real reason.)

Things Matlab does well

Very good cross-platform support. Matlab runs out of the box on every major platform. In research, when you want something to just work, spending days getting a python distribution configured with a mutually-compatible set of package versions is just ridiculous. Caveat: I haven't tried anaconda, which hopefully has solved this problem.
Very low housekeeping overhead. No other serious language (is BASIC a serious language?) lets you start writing code without having to include headers, define namespaces, allocate memory... For biologists without programming experience, this is a godsend.
Integrated debugging environment. Non-programmers will not easily be able to learn a language that does not come with an IDE. R, I'm looking at you. Python has very nice options now.
Intrinsic vectorisation of operations. for loops are kind of ugly and error-prone, when what you really want to do is perform an operation on every element of a matrix or perform matrix operations. I know that Python has some add-ins to accomplish matrix operations, but Python itself is not vectorised.
Support for object-oriented software design. As a legacy language, Matlab has a whole bunch of baggage. Mathworks is slowly improving the design of the language and adding other niceties (the parallel computing toolbox is pretty great): the class system; tables with named columns; the ability to ignore return and input arguments in function calls; function handles; namespaces...
Ability to work across machine abstraction levels. Matlab used to be slow, but the JIT compilation works wonders and keeps improving. You can operate at a very high level of abstraction with classes and objects; if you need something fast and low-level, you can write a small amount of C code and call it natively from Matlab.

Things Matlab does badly

Graphics and GUIDE. Oh my god. Handle graphics is pretty horrible. I know they are working on version 2, and it can't come soon enough. matplotlib in Python looks much better, and R makes amazing graphs out of the box. GUIs are pretty ugly to design in any language, but GUIDE makes it very easy to write some really horrible code.
Global namespace. This is sort-of true, and sort-of makes sense for convenience's sake. It's an inherent tradeoff between ease of use and nice encapsulation. Matlab does provide namespace support now, but I think it's still true that the vast majority of toolboxes don't use it.
First-class functions. If the anonymous function system could be upgraded slightly to handle multiple return arguments and to handle currying... Also, intrinsic support for named arguments and parameters would be greatly helpful, especially considering that many Matlab functions accept named parameters as part of their calling syntax.


Are there any models of human cognition that do not depend on physicalism or materialism? Are there any models of Human Cognition that do not depend on Physicalism or materialism? Could Cognition models that say 'mind' states are actually 'brain states' and that we are therefore neuro-chemical mechanisms ; could these models miss important factors like how 'behavioral algorithms' of the 'mind-brain' are organised and how they interact and how the mind-brain 'makes new 'behavioral algorithms'. What I call Behavioral Algorithms could be called 'mental programs' or 'mental software'. So are there models of Cognition that do not focus on Physicalism ( the philosophy that everything that exist has a physical basis and nothing else like  emergent qualities or something 'intangible')?

Algorithms can be seen as rules defined on various states of the system. Thus, there must be a mapping of the physical states to the abstract states, as well as a mapping of the physical rules/transitions to the abstract rules. David Chalmers is one of the most popular philosophers who discusses the notion of when a physical system implements an abstract computational system. [1] It seems like you are asking for theories of cognition that are truly emergent, however. These do exist - for an overview, see [2]. "Models governed by simple laws, especially models that learn, can give rise to emergent patterns that were not predicted in advance and that, even after they have been observed, may not be fully comprehended by the modeler. To what extent such patterns can or ever will be fully understood remains an open question." This vision of the cognitive sciences falls under the epistemological framework of explanatory pluralism - the view that properties exist on many levels, but their physical basis is the same. However, this is still physicalism - everything supervenes on the physical. [3] Furthermore, we are often required to simulate the basic rules in order to even see the emergent properties in the first place. [4] I think the take home message of this situation is that we can't have science without physicalism.

[1] Chalmers, David J. "A computational foundation for the study of cognition." (1993).

[2] McClelland, James L. "Emergence in cognitive science." Topics in cognitive science 2.4 (2010): 751-770.

[3] http://plato.stanford.edu/archives/fall2009/entries/physicalism/

[4] Baker, Alan. "Simulation-based definitions of emergence." Journal of Artificial Societies and Social Simulation 13.1 (2010): 9.


If the color black reflects no light, how are we able to see it? If color as we perceive it is dependent on the wave lengths that are reflected by an object, with white reflecting all hues and black absorbing all, how do we detect a black object?

I do understand there is no such thing as a perfect black. Is it this physical imperfection of black surfaces that provides the visual system with a cue about its shading?

Objects are visually perceived when they reflect light. A black object does not reflect any light. In other words, no photons are reflected to be detected by the photoreceptors in the retina. A black shape on a colored background appears black because its brightness approaches zero relative to its surroundings.

Black, as any other perceived hue, is a relative perception. The visual system, as any other sensory system, detects physical stimuli in a relative way. For example, under bright daylight (photopic conditions) a camera flash might appear as a weak source of light. That same flash viewed under dark (scoptopic) conditions may appear as a blinding flash. When the visual system is light-adapted, it needs a lot of photons to be able to respond to a visual stimulus. Under this condition, dark colored objects may appear black, simply because the photoreceptor's thresholds are too high. Conversely, that same dark object may appear as gray under scotopic conditions when the retina is dark-adapted (colors are not perceived under scotopic conditions - note here that black and white are not colors, but the two extremes on the perceived gray-scale).

An important thing to realize is that colors are perceptions and subject to neurophysiological processing imperfections. For example, blind people rarely perceive the world as black, despite the fact that their visual system cannot detect photons. Instead, they may perceive the world as a grayish hue, they often experience illusionary spontaneous flashes of light (phosphenes), or even entire visual scenes (Charles Bonnet syndrome). Hence, while a black object is physically defined as an object that emits/reflects no photons, it does not mean that the corresponding area in the neural representation of the visual field is silent. Perhaps on the contrary.


Is it possible that people perceive time differently than others do? All of my life I have been told to be more patient, to stop "racing through life", etc.  Happily, I am finally mature enough to accept that as solid advice, but I am curious as to whether it is possible that I perceive time differently than others do.

Today, for example, I was stuck at a red light in traffic on a road that was three lanes wide.  I was in the second row of cars that were stopped at the intersection.  When the light turned green, it seemed to me like 10-20 seconds elapsed before any of the three cars in the first row began to move forward.  Obviously, it is unlikely that all three cars in the front row reacted this slowly--hence my question.

Short Answer

Yes. People estimate time differently, by focusing their attention on time in more or lesser degree. Also within a person, time estimation may vary due to stochastic variations.

Long answer

This is a really nice paper that tries to explain time-perception in a cognitive architecture called ACT-R. It is a model of human cognition that tries to explain human behavior with only basic functions (declarative and procedural memory, vision, working memory a.o.).

Very shortly, the model is as follows: There is a pacemaker. This pacemaker creates pulses that are counted and saved in memory, and this memory is coupled to a particular time-frame. Each time you start counting, you reset the pacemaker to zero. So, for instance, after some practice, you learn that five seconds consists of 23 pulses, and eight seconds is equivalent to 30 pulses.

The pacemaker has two properties however. First, the pacemaker is not perfect. There are minor variations in the duration of each interval between the pulses. Five seconds may thus sometimes be perceived as 22 pulses and sometimes as 24 pulses. This is the reason variability exists in time estimations.

Secondly, the duration of intervals between pulses increases over time. Where the time between a pulse may be 200 ms (+- random value) when you start to count, it may be 400 ms (+- random value) after ten seconds. On top of that, the effects of random noise also becomes larger. If you count the pulses, the precision of the counting will thus decrease. Therefore it is increasingly difficult to estimate longer periods of time as compared to shorter periods of time. In figure 2 in the paper, this is depicted with the increasing width of the normal distributions.

Attention
So far I have only explained how one person may perceive time differently due to stochastic differences in pulse productions. What I left out so far is the attentional component of the model. When you focus your attention on the pulses your estimates will be rather good, because you perceive these pulses more consciously. However, as anyone may know, "time may fly" (when you're having fun). This is believed to be caused by the lack of attention to the pulses, therefore being unaware of how time passes. It is however not entirely clear how this attentional component works, and the debate is still ongoing.

Neuro-biology:

The model was based on a paper written by Mattel and Meck (2004), which provide a neuro-biological explanation for the pacemaker. The model they propose is the "striatal beat frequency model", which states that there is neuronal activity oscillating at different rates in different networks of neurons. The oscillations are then detected by Striatal Spiny Neurons, which result in a sort of "barcode"(i.e. an array neurons being active and inactive; see Figure 1A). It is these barcodes that are memorized and associated with a particular duration (See Figure 1B).

Figure 1: Striatal beat frequency model. Picture taken from Researchgate

As mentioned earlier, the pacemaker needs to be reset when you start counting from zero. It is theorized that this is done by a burst of dopamine.

Here is a review about the neural pathways for time-estimation by Buhusi and Meck (2005). My neuro-biology is a little rusty though, so if there is anyone that could comment/elaborate on this, that would be highly appreciated.

References

Buhusi, C. V., & Meck, W. H. (2005). What makes us tick? Functional and neural mechanisms of interval timing. Nature reviews. Neuroscience, 6(10), 755.

Matell, M. S., & Meck, W. H. (2004). Cortico-striatal circuits and interval timing: coincidence detection of oscillatory processes. Cognitive brain research, 21(2), 139-170.

Taatgen, N. A., Van Rijn, H., & Anderson, J. (2007). An integrated theory of prospective time interval estimation: The role of cognition, attention, and learning. Psychological Review, 114(3), 577.


Why did humans develop the "sense of humour"? Speaking from the point of view of evolutionary psychology, is there any research that demonstrates why a 'sense of humor' may be a part of our mental mechanisms?

Does research show that it is a way to quickly decrease stress levels?

Interestingly, the same question you asked has been asked since quite some time:

The Act of Creation, 1964 - Arthur Koestler

  What is the survival value of the involuntary, simultaneous contraction of fifteen facial muscles associated with certain noises
  which are often irrepressible? Laughter is a reflex, but unique in
  that it serves no apparent biological purpose; one might call it a
  luxury reflex. Its only utilitarian function, as far as one can see,
  is to provide temporary relief from utilitarian pressures. On the
  evolutionary level where laughter arises, an element of frivolity
  seems to creep into a humorless universe governed by the laws of
  thermodynamics and the survival of the fittest.

Firstly, like all other narratives built by evolutionary psychologists, it is difficult to back up speculations with empirical evidence. Since we are going back far back into the evolutionary history of homo sapiens, we will be dealing with what I would call "well-informed speculation".

Quoted from The Mating Mind (2001) by Geoffrey Miller.

  To traditional evolutionary psychologists, human abilities like music,
  humor, and creativity do not look like adaptations because they look
  too variable, too heritable, too wasteful, and not very modular. But
  these are precisely the features we should expect of fitness
  indicators. If a human mental trait shows large individual
  differences, high heritability, high condition-dependence, high costs,
  and high correlations with other mental and physical abilities, then
  it may have evolved through sexual selection as a fitness indicator.
  (pg. 132-133)

Sexual Selection

Notice that he also mentioned your speculation about decreased stress levels:

  Some theories of humor have proposed that laughter evolved to promote
  group bonding, discharge nervous tension, or keep us healthy. The
  more laughter the better. Such theories predict that we should laugh
  at any joke, however stupid, however many times we have heard it
  before, yet we do not. A good sense of humor means a discriminating
  sense of humor, not a hyena-like shriek at every repetitive pratfall.
  Such discrimination is easy to understand if our sense of humor
  evolved in the service of sexual choice, to assess the joke-telling
  ability of others.

Furthermore, I recommend that you read this review of Robert Mankoff of “Inside Jokes”: The Hidden Side of Humor. (2011) and of course the book itself. It sheds a strong light onto your question.

Sources:

Matthew M. Hurley, Daniel C. Dennett, and Reginald B. Adams Jr., Inside Jokes: Using Humor to Reverse-Engineer the Mind. MIT Press, 2011, 376 pp., ISBN-13: 978-0262015820

Koestler, Arthur. 1964. The Act of Creation, Penguin Books, New York

Miller, G. (2000), The Mating Mind: How Sexual Choice Shaped the Evolution of Human Nature, London: Heineman, ISBN 0-434-00741-2 (also Doubleday; ISBN 0-385-49516-1)


When counting a given letter in sentences, why do people tend to omit occurrences in certain common words? I have noticed that when I, and presumably others, count the number of times the letter F appears in the following passage:

FINISHED FILES ARE THE RESULT
OF YEARS OF SCIENTIFIC
STUDY COMBINED WITH THE
EXPERIENCE OF YEARS

They typically get a count of three, yet the real answer is six. The letter F in the the word "OF" tends to be omitted from the count.

I imagine that this effect has something to do with top-down processing.

Questions

Have there been any scientific studies of this or a similar task?
What proportion of people complete the task successfully?
What explains the tendency of people to not count the letter F's in the word "OF"?

What explains the tendency of people to not count the letter F's in the word "OF"?

One possibility to explain this effect is related to the phenomenon of word skipping. When we read, we do not fixate every word, but skip a certain proportion of words while making educated guesses instead. Whether or not a certain word is skipped seems to depend on its length and its predictability, that is, how likely a word is given its predecessor (e.g, Rayner et al., 2011). For your example, the preposition "of" might be very likely to be skipped because it is very short and some grammatical clauses always ask for this preposition.

Please see PubMed for a more comprehensive literature search on word skipping: http://www.ncbi.nlm.nih.gov/pubmed?term=%22word%20skipping%22

References
Rayner K, Slattery TJ, Drieghe D, Liversedge SP. (2011). Eye movements and word skipping during reading: effects of word length and predictability. J Exp Psychol Hum Percept Perform. 37(2):514-28


Relationship between social psychology and educational psychology For some time I have been trying to figure out what the connection between social psychology and educational psychology is. By their definition, it seems that there at least one (major) point of connection. Both disciplines have the term "psychology" in their title.

However, if you go further to investigate the connection, you might find that Wikipedia entry on educational psychology seems a bit confusing:

"Educational psychology is the study of how humans learn in educational settings, the effectiveness of educational interventions, the psychology of teaching, and the **social psychology of schools as organizations."

Does it mean that social psychology should be considered as a part/subdiscipline of educational psychology?

No, social psychology is not a subfield of educational psychology. Social psychology is one of the basic disciplines of psychology (like e.g. personality psychology or developmental psychology), whereas educational psychology is an applied discipline (like e.g. clinical psychology or industrial/organizational psychology). A sort of standard definition of social psychology is, that it is the

  the study of the manner in which the personality, attitudes, motivations, and behavior of the individual influence and are influenced by social groups. (Merriam-Webster, 2013)

This means that as soon as there is some sort of social interaction involved in an educational setting, both disciplines are concerned.

References:

Merriam-Webster. (August 2013). Social Psychology. Retrieved from http://www.merriam-webster.com/dictionary/social%20psychology


What correlation research has been done on MBTI vs Big5? Big5 is probably the most used personality model in research, while MBTI has not gained status of being scientifically supported.

What exact research has been done on correlating the two models?
Could someone give me links to full research reports with correlations between the two models?
Correlations between subfacets would be especially useful (i.e MBTI extroversion vs Big5 extroversion).

The MBTI can be considered to be subsumed by the Big5/Five-Factor Model. McCrae and Costa examined this back in the late 1980’s. First of all, they showed that the types do not interact in a statistically meaningful way indicating that there isn’t a reason to interpret four type categories (e.g., ESTJ vs INFP). The categories (e.g., extraversion vs introversion) describe some meaningful amount of variance themselves but combining them into the types and interpreting the whole is not statistically warranted (McCrae & Costa Jr., 1989). Statistically, false dichotomization/median splits (here called types) reduces the predictive power of a measure in general.

To further examine the universality of the Five-Factor Model, they examined how the MBTI dimensional raw scores related to the FFM/Big5 scores. They showed that FFM-Extroversion was highly correlated to MBTI-Introversion (r = -.74), FFM-Neuroticism was weakly correlated to MBTI-Introversion (r = .16), FFM-Openness was correlated to MBTI-Intuition (r = .72), and to MBTI-Perception (r = .30), FFM-Agreeableness was correlated to MBTI-Feeling (r = .44), FFM-Contentiousness correlated to MBTI-Perception (r = .49). These correlations were for men only, but are reported to give as an example of how the FFM can account for MBTI measures. The MBTI does not capture trait Neuroticism which could be considered a fault because Neuroticism is strongly predictive of many negative outcomes (Barlow, Sauer-Zavala, Carl, Bullis, & Ellard, 2014). The other factors of the MBTI are accounted for in the FFM, but captures additional variance above and beyond the MBTI. Validity and universality of the Five-factor model is another question but, briefly, it is empirically derived from factor analysis of the entire English dictionary (lexical approach) a factor structure which has been replicated in over 40 languages (McCrae & Costa, 2008).

                                **References**

Barlow, D. H., Sauer-Zavala, S., Carl, J. R., Bullis, J. R., & Ellard, K. K. (2014). The Nature, Diagnosis, and Treatment of Neuroticism: Back to the Future . Clinical Psychological Science , 2 (3 ), 344–365.

McCrae, R. R., & Costa Jr., P. T. (1989). Reinterpreting the Myers-Briggs Type Indicator From the Perspective of the Five-Factor Model of Personality. Journal of Personality, 57(1), 17–40.(https://www.researchgate.net/profile/Paul_Costa3/publication/20447534_Reinterpreting_the_Myers-Briggs_Type_Indicator_From_the_Perspective_of_the_Five-Factor_Model_of_Personality/links/00b49515b9ad847e86000000.pdf)

McCrae, R. R., & Costa, P. T. (2008). Empirical and Theoretical Status of the Five-Factor Model of Personality Traits. The SAGE Handbook of Personality Theory and Assessment: Volume 1 — Personality Theories and Models. SAGE Publications Ltd (pp. 273–295).


What is the evidence for the efficacy of Internal Family Systems (IFS) therapy? I've been reading about Internal Family Systems therapy recently. It's claims seem quite appealing, since it suggests it can do the work of other therapies like psychoanalysis only faster and more directly.
Has it been studied to determine how effective it is? Whether in comparison to to other therapies or not.

Internal Family Systems therapy have not been subjected to large rigorous clinical trials. Most of the studies were pilots with no confirmatory studies as yet. I am just repeating the IFS website which best summarises the three existing studies in rheumatoid arthritis, PTSD and depression. I could not find any decent trials in my preliminary search.
A pilot study of 13 patients with PTSD and comorbidities found a 92% improvement after completing 16 sessions.
A randomised trial of 79 patients with rheumatoid arthritis, the 39 patients receiving IFS had reduced pain and depressive symptoms, while improving physical function and self-compassion.
A study of female college students did not find any difference in the 17 students treated with IFS compared with the 15 students treated with usual care of IPT or CBT, which supports IFS's efficacy, but the therapists in the IFS arm mainly only had 1 year of IFS training and experience.
https://ifs-institute.com/resources/research


Is meaning-seeking behavior a biological optimization problem? In short, I'm interested in cognitive, neuroscientific, biological and/or computational perspectives on what we vaguely refer to as meaning seeking. Of course, this is a large topic, but any information would be highly appreciated.

Background

Humans tend to desire meaning in their lives. While it would be hard to agree on a precise definition of meaning, it often refers to positioning oneself in a way that is compatible with one's beliefs, ambitions and values, allowing the individual to make sense of the world and of himself, and to pursue whatever (often transcendental) goals he considers worthy (i.e. meaningful). In simpler words, meaning could refer to making peace with the perceived reality of the world and with oneself. At first glance, it seems to me that a meaningful existence requires the absence of cognitive dissonances, but I wonder what science would have to say about this, and if there is any empirical basis for claiming this. Or perhaps the questions is misformulated and such behavior should not be put into the domain of meaning?

Possible explanations

A simple evolutionary argument could be that meaning-seeking behavior originates from our impulse to belong (isolation means death), but how do we then explain hermits or dissidents or all other individuals who have effectively made themselves suffer/die in order to uphold meaning in their lives (i.e. dying for one's beliefs)? So the argument that meaning-seeking behavior is a purely evolutionary phenomenon that serves only to maximize one's potential for reproduction doesn't appear sufficient.

Questions

Can meaning seeking be thought of as an optimization problem of some
biological parameters on an individual level, e.g. in terms of
energy required for various cellular processes, homeostatic gene
expression dynamics etc.? For example, depression (which can have an
existential origin) is damaging to health and has been linked to
epigenetic modifications (Sun et al. 2012), so having a mechanism that would seek
to minimize such damage would seem to be beneficial for an organism.
Can we construct a more formal definition of meaning that would be
less anthropocentric? In other words, how far would we need to curb
the definition so that humans would no longer qualify as the only
meaning-seeking organisms? Or are we indeed the only species with the required neural capacity to express such behavior?
Could modern experimental methods such as EEG, fMRI, gene
expression profiling and epigenome sequencing be used to answer some of these questions at
least to a degree? E.g. would a comparison of individuals who claim
to live a meaningful life vs those who don't make any sense? Of
course, even if a some significant differences were observed, an
obvious next question would be what caused them, i.e. a mind-body-environment
problem ...

I'd be happy to know at least if there are some research groups or labs that try to tackle such questions.

it seems to me that a meaningful existence requires
  the absence of cognitive dissonances, but I wonder what science would
  have to say about this, and if there is any empirical basis for
  claiming this.

The difficulty, as you've pointed out, is that there isn't agreement on the definition of "meaning" in this context.  Meaning can be interpreted by different people (and cultures) variously as: "accomplishment", "social good", "altruism", "realizing potential", "inner peace", "knowledge", and on and on.

  the argument that meaning-seeking behavior is a purely evolutionary
  phenomenon that serves only to maximize one's potential for
  reproduction doesn't appear sufficient.

Read about evolutionary explanations for altruistic behaviour for example to see how this can be addressed: "Every single instance of altruistic behavior need not always increase inclusive fitness; ... it would be beneficial to err on the side of caution and usually be altruistic even if in most cases there were no benefits."

  how far would we need to curb the definition so that humans would no
  longer qualify as the only meaning-seeking organisms?

"Social good" and "altruism" are examples of meaning-seeking behaviours commonly found in many animal species.

  Could modern experimental methods such as EEG, fMRI, gene expression
  profiling and epigenome sequencing be used to answer some of these
  questions at least to a degree?

Sure, why not.  For example: "Altruism, the experiment suggested, was not a superior moral faculty that suppresses basic selfish urges but rather was basic to the brain, hard-wired and pleasurable."

  I'd be happy to know at least if there are some research groups or
  labs that try to tackle such questions.

The area of psychology most likely to address such an abstract concept as meaning-seeking is probably Humanistic Psychology: "Human beings are intentional, aim at goals, are aware that they cause future events, and seek meaning, value, and creativity."

You can read about research done in this field - there isn't very much of it though - and also about self-actualization (another common interpretation of meaning-seeking in psychology).


Is a network of neurons the only factor in memory? Background

I'm actually writing a science fiction novel set a couple decades in the future. Brains are not my field. I've done as much research as I could.

In the story, the protagonist finds out he has died, but to have his deceased brain scanned, mapping out all the nuerons and synapse connections. Perhaps with an advanced MRI.

Then a "system" essentially iterates over many various stimuli. Simulating to the brain the visual sensation of seeing a bird, for example. The machine looks for the corresponding neurons to fire when seeing a bird. The machine iterates over many birds to understand how this brain stores "birds", and repeats this process for basically anything that could be detected from the senses.

Then this brain could be stored in a computer and bioprinted.

I've seen videos of researchers today simulating a primitive network of neurons, so this seems vaguely possible. I know we are also currently capable of bioprinting blood vessels and skin today.

Question

If a brain was bioprinted with the exact neuron network and synapse connections as a host brain, would this brain theoretically hold the previous memories from the host it's made from?

Answer
Yes, theoretically.

Now
According to my ongoing informal research, there are two sides of brain preservation innovation: 1) the preservation and mapping (building) the connectome; and 2) the reinstantiation of memories and/or creating consciousness from a connectome.
From http://www.brainpreservation.org/overview/:

[N]euroscience is now identifying the synaptic and nuclear structures
that contain our unique memories and identity, and new electron
microscopy (EM) imaging techniques are allowing us to verify when
these structures have been successfully preserved, from gross
connectivity in the connectome, all the way to particular synaptic
features, receptor distributions, and even the signal states
(phosphorylation, methylation, acetylation, etc.) of individual brain
proteins and epigenomic DNA.
[…]
Recently, MRI machines have been built that can image individual cell
proteins, improbable as this sounds. Such technology may one day give
us the ability to inexpensively and nondestructively scan preserved
brains to upload the molecular features of memory and identity.

From http://www.brainpreservation.org/content-2/connectome/:

What is a Connectome?
A connectome* is the complete map of the neural connections in a
brain. It is sometimes referred to as a “wiring diagram” of the
molecular connections between neurons, trading on the analogy of a
brain to an electronic device, where axons and dendrites are wires and
neuron bodies are components. Depending on the scientist, the term
connectome may or may not also include learning-relevant molecular
states at each synaptic connection (the “synaptome”) and any
learning-relevant changes in the nucleus of each neuron (the
“epigenome”).

Progress
Recently, "The Small Mammal BPF Prize" was won. It's one in a series of competitions for brain preservation (BP) achievements. This competition is doing for BP what XPRIZE is doing for space innovation with competitions like the Ansari X Prize.
The winning team used a combination of plastination (chemopreservation) and cryonics (cryopreservation) to preserve a rabbit brain. From the press release http://www.brainpreservation.org/small-mammal-announcement/:

The Small Mammal Brain Preservation Prize has officially been won by
researchers at 21st Century Medicine. Using a combination of ultrafast
chemical fixation and cryogenic storage, it is the first demonstration
that near perfect, long-term structural preservation of an intact
mammalian brain is achievable.

Future
In regard to reinstantiation of memories and/or creating consciousness: when progressive innovations in technology enable mapping of the entire connectome, the next step is applying a "runtime" to the structure. This runtime is described as "cycles" by György Buzsáki in his book Rhythms of the Brain.

In a sequence of "cycles," György Buzsáki guides the reader from the
physics of oscillations through neuronal assembly organization to
complex cognitive processing and memory storage.

Book resources:

Amazon: https://www.amazon.com/Rhythms-Brain-Gyorgy-Buzsaki/dp/0199828237
EDU (PDF): http://www.caam.rice.edu/~yad1/miscellaneous/References/Neuroscience/Papers/Hippocampus/RythmsOfTheBrainBuszaki.pdf

Example 1
The OpenWorm project is an example of contemporary connectome innovation, which is a necessary step for the memory/consciousness side of BP. From http://www.openworm.org:

OpenWorm is an open source project dedicated to creating the world’s
first virtual organism in a computer, a C.elegans nematode. Throughout
the years we have built a network of relationships with with many
biologists and neuroscientists interested in C. elegant.

From http://www.scientificamerican.com/article/c-elegans-connectome/:

Because a lone connectome is a snapshot of pathways through which
information might flow in an incredibly dynamic organ, it cannot
reveal how neurons behave in real time, nor does it account for the
many mysterious ways that neurons regulate one another's behavior.
Without such maps, however, scientists cannot thoroughly understand
how the brain processes information at the level of the circuit. In
combination with other tools, the C. elegans connectome has in fact
taught scientists a lot about the worm's behavior; partial connectomes
that researchers have established in the crustacean nervous system
have been similarly helpful. Scientists are also learning how to make
connectomes faster than before and to enhance the information they
provide. Many researchers in the field summarize their philosophy like
this: "A connectome is necessary, but not sufficient."

Example 2
I believe Stanford's computer model of an organism is in the scope of BP and could be the foundation of what eventually becomes entire brain/connectome virtualization. This breakthrough is an example of the technological capabilities in 2012. Now, in 2016 with AI tech on the rise, exponential progress in this field may become a reality in our lifetime.
From http://news.stanford.edu/news/2012/july/computer-model-organism-071812.html:

[In 2012] Stanford researchers produce first complete computer model
of an organism. A mammoth effort has produced a complete computational
model of the bacterium Mycoplasma genitalium, opening the door for
biological computer-aided design.

From http://www.cell.com/cell/abstract/S0092-8674(12)00776-3:

Understanding how complex phenotypes arise from individual molecules
and their interactions is a primary challenge in biology that
computational approaches are poised to tackle. We report a whole-cell
computational model of the life cycle of the human pathogen Mycoplasma
genitalium that includes all of its molecular components and their
interactions. An integrative approach to modeling that combines
diverse mathematics enabled the simultaneous inclusion of
fundamentally different cellular processes and experimental
measurements. Our whole-cell model accounts for all annotated gene
functions and was validated against a broad range of data. The model
provides insights into many previously unobserved cellular behaviors,
including in vivo rates of protein-DNA association and an inverse
relationship between the durations of DNA replication initiation and
replication. In addition, experimental analysis directed by model
predictions identified previously undetected kinetic parameters and
biological functions. We conclude that comprehensive whole-cell models
can be used to facilitate biological discovery.


What personality traits does sexy and revealing clothing correlate with? Is there some unifying characteristic that distinguishes women who wear form-fitting, lowcut, see-through and other kinds of revealing outfits?

Are they more extroverted, do they rate higher in (sexual) sensation seeking, do they have high or low confidence etc.?

Is there any research on this?

This question is primarily about Feminine psychology. Men identify less with their clothing than women and are stereotyped as promoting self-objectification many times.

In American society clothing norms are for women are very complex and are difficult to navigate. Because sexuality is indeed related to which parts of your body you do or do not reveal there is direct clinical quality relationships between certain clothes and states of mind. However generalizations made about a persons state of mind based on their clothing can often be faulty. People experience stimuli in their lives which prompt individual responses that do not match their overall personality.

Active research along these lines has been published. In Enclothed cognition it is reported that a lab coat is able to change the perception and increase attention when associated with a doctor. Likewise in More Than a Body: Mind Perception and the Nature of Objectification studies were done comparing the agency viewed by people on clothed, naked and sexualized pictures. In conclusion they said:

  Whatever the positive or negative effects of focusing on someone’s body, its effect on mind perception seems clear. Those perceived in terms of their physical characteristics are not completely stripped of mind but are, instead, seen to possess a different kind of mind, one lacking in self-control and moral responsibility but relatively more capable of pain, pleasure, and emotion.

In "You Are What You Wear: What Your Clothes Reveal About You" shopping for clothes is treated as a therapy to correct negative schemas. Though its validity has not been proven it seems rational.

To directly answer your questions about "Are they more extroverted, do they rate higher in (sexual) sensation seeking, do they have high or low confidence etc.?" according to You Are What You Wear it largely depends on age and the norms for that age. A college age girl in a revealing dress would have a different state of mind than an older woman in a similarly revealing dress.


What is the evidence to suggest that the introvert/extrovert distinction is a shallow distinction? The author here claims:

  A great leader knows that making room for both extroverts and introverts to share their thoughts could be the key to whether or not their next project succeeds or fails.

This document purports:

  Carl Jung and the authors of the Myers–Briggs provide a different perspective and suggest that everyone has both an extraverted side and an introverted side, with one being more dominant than the other. Rather than focusing on interpersonal behavior, however, Jung defined introversion as an "attitude-type characterised by orientation in life through subjective psychic contents" (focus on one's inner psychic activity); and extraversion as "an attitude type characterised by concentration of interest on the external object" (the outside world)

The commentator writes:

  The distinction between introvert and extrovert is shallow psychology. They are sometimes used condescendingly by angsty individuals at either side of the imaginary spectrum. The truth isn't even that most people fall somewhere in between. There is no gray area, because these matters are not black and white. Their use leads to generalization and over-simplification of delicate subject matter. Introvert vs. extrovert is always a sledgehammer where a scalpel is required.

My question is: What is the evidence to suggest that the introvert/extrovert distinction is a shallow distinction?

I think it is safe to say that in psychological research on personality differences, extraversion (vs. introversion) is one of the most important personality dimensions. In fact, extraversion (along with neuroticism) has been included in "virtually all major dispositional models" (see Watson,
Clark, & Harkness, 1994; Zuckerman, Kuhlman, Joireman, & Teta, 1993; as cited in Watson et al. 1999). Extraversion can be reliably measured with personality questionnaires (e.g. Costa & MaCrae, 1992), it is a heritable trait (e.g., Jang et al. 1996) and it meaningfully predicts other important variables such as trait positive affectivity (Watson et al. 2009) or job satisfaction (Judge et al., 2002) to pick two arbitrary examples.

Of course, neither does this mean that it is useful to categorize people into introverts and extraverts (personality research has long moved away from "type" approaches to investigate gradual differences) nor does this mean that extraversion is the only personality difference that matters (it is an important one, but there are others).

In conclusion, extraversion-introversion is a robust and widely replicated personality dimension that features in almost all models of personality.

References

Costa, P.T.,Jr. & McCrae, R.R. (1992). Revised NEO Personality Inventory (NEO-PI-R) and NEO Five-Factor Inventory (NEO-FFI) manual. Odessa, FL: Psychological Assessment Resources.

Jang, K.; Livesley, W. J.; Vemon, P. A. (1996). Heritability of the Big Five Personality Dimensions and Their Facets: A Twin Study. Journal of Personality 64 (3): 577–591.

Judge, T. A., Heller, D., & Mount, M. K. (2002). Five-factor model of personality and job satisfaction: A meta-analysis. Journal of Applied Psychology, 87, 530–541. doi:10.1037/0021-9010.87.3.530

Watson, D., Wiese, D., Vaidya, J., & Tellegen, A. (1999). The two general
activation systems of affect: Structural findings, evolutionary consider-
ations, and psychobiological evidence. Journal of Personality and Social
Psychology, 76, 820–838.


Do humans only dream of things they have actually witnessed/seen? Is it necessary for humans to have dreams that only contain things they have witnessed/seen in their consciousness?

People often report dreaming about  things that they have not experienced in the real world (e.g., monsters, flying, falling off a building).

With our own imagination while awake most people can visualise many things that they have never actually seen. It seems likely that dreams would be at least as flexible as our own imagination.

Videos, stories, images, and other media might inform this imagination. Likewise, in general, daily thoughts, emotions, and experiences are often weaved into dreams.

This is just a basic common sense answer. It takes for granted an information processing model of cognition that denies the existence of true psychic power in dreams. That said, a weak form of what might be labelled "psychic" or "premonitions" in dreams is still possible in the form of insight that was only first achieved in a dream. More deeply, it would be interesting to see another answer that compared the kinds of creative imagination exhibited in dreams relative to creative imagination while awake.


Is there a scientific definition of "fairness"? The concept of fairness, in my opinion, is somehow defined by the concept of empathy through some searches by Daniel Goleman in his book Social Intelligence.

The book deals with scientific measurement through MRI.

Ethic and Moral are also trying to define what is fair.

Can you give me some hint achieving a definition of what is fair?

i.e. why killing people, slavery, exploiting are not fair stuff?

I would also urge you to think about equality vs. equity as two important facets to understanding fairness, especially in the context of heterogeneous societies.

Simply put, Equality is the idea that all individuals are exactly equal. If X people work on a project, all of them would get remunerated exactly the same amount.

On the other hand, Equity is the idea that there exists a quid pro quo i.e. if X people work on a project individuals would get paid proportional to the amount of work they put in.

Both could be considered "fair" depending on your perspective. In fact, it has been shown that individuals tend to switch between equity and equality when self-presentational concerns are made salient.
(Ref: http://www.sciencedirect.com/science/article/pii/0022103176900792)

Needless to say, this "fairness" debate guides discussion on Affirmative Action in the West and social reservation policies in countries like India.  I like the following piece which sums up this discussion nicely:

http://www.ala.org/offices/oif/iftoolkits/toolkitrelatedlinks/equalityequity


What is the definition of sanity? How can I prove someone either sane or insane? In my experience the definition of insanity is thus:

  Insanity: The state of being seriously mentally ill, mad, and/or irrational.

Is there a proper scientific definition of this term? While mentally ill is relatively easily to pin down, the others criteria seem subjective.

Is there any test or method that can be used to prove a subject to be either sane or insane? How can any such test give objectively accurate results for this or another similar definition of insanity?

Sanity is an explicit legal definition. It is generally not a psychological term. This is Wikipedia's definition of Sanity which aligns perfectly to my understanding of abnormal psychology. (emphasis mine):

  In criminal and mental health law, sanity is a legal term denoting that an individual is of sound mind and therefore can bear legal responsibility for his or her actions. The official legal term is compos mentis. It is generally defined in terms of the absence of insanity (non compos mentis). It is not a medical term, although the opinions of medical experts are often important in making a legal decision as to whether someone is sane or insane.

Psychologists are often called in to determine "sanity" but they deduce whether one fits the legal definition based on any psychological disorders the individual might have. "Insanity" in this sense could be considered to be one of many psychological disorders that would cause one to be unable to function in a court room and understand their rights.

"Temporary Insanity" was a previously common but largely ill regarded legal excuse in the earlier days of psychology. It is not a psychological term nor does it have a psychological definition.

You'll note the DSM does not include diagnostic criteria for sanity. It is not a term commonly used in research or psychiatry because as you suggest it is much too broad of a concept.

Research on "insane" people is as uselessly broad as it would be on "silly" or "dumb" people. Instead research is conducted on specific conditions or measures.

Wikipedia has some information on Sanity in Psychiatry and Psychology but note these are very outdated ideas and I'm not aware of any current researchers who respect these theories as valid.


Does smoking counterbalance the effect of Belladonna? Atropine, the main ingredient of Belladona, is the stuff that makes you dump, by blocking the action of acetylcholine at muscarinic receptors.

Would smoking or applying a nicotine patch, by introducing additional nicotine, which also binds to the acetylcholine receptors to some extend counterbalance the effect of atropine?

Disclaimer: I do not work with receptor bindings very often.

First point binding sites...
Both Atropine and Nicotine bind to Cholinergic receptors. However receptor binding is not competitive as the rector sites for each neurotransmitter is different (NT): Atropine is a direct-antagonist of Muscarine binding with AChRm (muscarinic receptors) while nicotine is a direct agonist of AchRn (nicotinic receptors).

Atropine however does inhibit the action of nicotine in mediating ion currents on cholinergic receptors in the Central Nervous System (CNS). However this depends on the concentration of each NT in the neural system, low does of Atropine are enough to block high concentrations nicotine. So while a high concentration nicotine, say from an e-lite might be enough to save your life from Belladonna poisoning, I wouldn't personally go out of my way to test the theory! However the Nicotine from a cigarette probably wouldn't be a high enough dose to counter 1um of atropine. However say you did drink some belladonna because you have evil 'friends', but then you smoked a cigarette with enough nicotine to save your life. You then encounter another problem...half-life. The half-life of atropine is 2 hours, the half-life of nicotine is 1-2 hours! Do you want to risk that last hour if it takes two hours to see a medic or if you are transported back in time to medieval england!? Incidentally if you were poisoned with belladonna being transported back to medieval England would make sense. Your only option at this point, after the first hour, is to keep smoking (nicotine metabolites have 20 hour half-life, but there action is reduced), this is one of only a few situations that smoking may prolong your life! Although you will need some pretty potent tobacco to achieve this, better make sure you land in Tudor England instead.

Moral of the story...don't time travel! I'm looking at you 'doctor' with the blue box.

If you do believe you are in medieval England or the Roman empire please ask someone to call a Neurologist or a psychiatrist! If they say "what's a neurologist/psychiatrist?" you are completely sane, congratulations you have achieved time-travel.

Specifically information about competition between atropine and nicotine concentrations...

"At the holding potential of 80 mV, 1 mM atropine inhibits 1 mM acetylcholine- induced inward currents mediated by rat a2b2, a2b4, a3b2, a3b4, a4b2, a4b4, and a7 nicotinic receptors by 12–56%. Inward currents induced with a low agonist concentration are equally inhibited (a3b2, a3b4), less inhibited (a2b4, a7), or potentiated (a4b2, a4b4) by 1 mM atropine. Effects on the more sensitive 44 nicotinic receptors were investigated in detail by systematic variation of acetylcholine and atropine concentra- tions and of membrane potential. At high agonist concentration, atropine inhibits 44 nicotinic receptor-mediated ion current in a noncompetitive, voltage-dependent way with IC50 values of 655nM at80mVandof4.5M at 40mV. At low agonist concentration, 1 M atropine potentiates 44 nicotinic recep- tor-mediated ion current. This potentiating effect is surmounted by high concentrations of acetylcholine, indicating a competitive interaction of atropine with the nicotinic receptor, and potentiation is also reversed at high atropine concentrations...The apparent affinity of atropine for the agonist recognition sites of the a4b4 nicotinic acetylcholine receptor is estimated to be 29.9 mM." Zwart and Vijverberg (1997)


Anorexia nervosa as an anxiety management tool Talking to people with anorexia nervosa, I noticed that some of them have actually much bigger problems than their aforementioned condition.

In some cases it looked as if the person was spending daily an insane amount of time on food, having no time left to deal with other more serious issues in his life. Removing his anorexia, would leave him "helpless" against his real fear, so why would he want that? He would rather keep postponing facing his fear... indefinitely.

Question:

Are there any studies related to the above conditions being used by a person, as a way to divert his attention away from other events that are actually even more stressful?

Note:
I'm not implying that distraction is always the only (or even the main) reason these conditions appear; I'm simply wondering if they are sometimes used subconsciously as another anxiety management tool.

If I'm understanding your question, you're wondering if anorexia nervosa is a symptom of other underlying problems in a person's life.

This is a current theory being supported by "Mental disorders as complex networks: An introduction and overview of a network approach to psychopathology" written by Nuijten et. al. The paper describes how instead of seeing a disorder as a single "latent variable" connecting all the symptoms, all the symptoms should just be considered as a network reinforcing themselves. This is demonstrated in the figure below taken from the paper:

For a discussion of the paper, see "Mental Disorders As Networks" by SlateStarCodex.


What is the definition of affective cueing? In contrast to affective priming, what is affective cueing? I'm not sure how to differentiate between the two.

I found a good review on affective priming in Karl Christoph Klauer (1997) in the European Review of Social Psychology, and from this I gather that affective priming simply is a priming which is targeted at emotions instead of at reactions. I did not find any definition of affective cueing so far. The best I could manage was from this question, however it does not help me at all, nor do the reference in there.

There is no agreed-upon definition of affective cueing because it's not a proper name. If you google for "affective cueing" you only find a handful of hits and in them the term is used differently, mostly to indicate that some cue (a stimulus that carries information) is of positive versus negative valence.

In contrast, affective priming refers to a specific, experimental research paradigm:

  Affective priming investigates whether the evaluation of a first stimulus, the prime, that is to be ignored, affects the processing of subsequent stimuli.

(as described in the article you found)


Does thinking or focusing on something alter a neuron's speed? I Googled about this but couldn't find any thing precise to be that does thinking about something hard alters the speed of neurons impulses? I have heard of neurons velocity being variable but want to understand the exact circumstances in which the velocity varies.

There are, as far as I know, 2 main factors that determine the speed of action potential propagation:

Diameter: Axons with a large diameter have lower resistances, and hence higher conduction velocities;
Myelination: Myelin prevents passive diffusion of ions through the cell's membrane and increases charge separation across the cell membrane, speeding up conduction. Additionally, the spaces between the myelin sheaths, known as the nodes of Ranvier, facilitate saltatory conduction, which is akin to the action potential 'jumping' from node to node with a net increase in propagation as a consequence.

These factors are physical properties of a neuron and hence are pretty much constant under physiological conditions, and are not influenced by thinking or focus.


Is it good to take playful breaks at work? I read this Washingon Post article about groups that are trying to encourage play in "workaholic" adults. I'm curious if anything is known on the psychological effects of taking playful breaks at work.

From personal experience, taking playful breaks seems to improve my productivity and resistance to distractions. On the other hand, maybe taking playful breaks makes work seem even more drab by comparison, lessening motivation?

Building on @caseyr547's answer, and especially the second link in the first reply to your comment, yes!

From Cook's (2009) abstract (emphasis added):

  Over the past decade, there have been numerous claims in the popular media relating to having fun at work, touting a plethora of benefits for both individuals and organisations that have to date not been empirically investigated. Thus far, any research related to fun in the workplace has often been indiscriminate with its use of terms, interspersing fun with humour and play, thus adding confusion to an already inadequately defined construct. The aim of this research is two fold: to develop a more comprehensive understanding of the construct to differentiate and define fun in a work context, and to measure the perceived impact of having fun in the workplace. In order to locate fun as a unique construct, literature related to fun, humour and play/playfulness was reviewed and positioned in a nomological net utilising a three phase framework consisting of presage, process and product (3P). Four studies in this research program investigated the domain of fun activities in the workplace, the underlying structure of the construct, the process of having fun and the perceived impact of fun specifically in relation to job satisfaction, stress reduction, effectiveness and workplace relationships. Results identified a domain of 15 distinct fun activities. Using multidimensional scaling, an underlying structure of four neighbourhood clusters (humour and play, informal socialising, formal socialising and organisational activities) and two dimensions (contextual connections with others and activity structure and intensity) were identified. The investigation of the process of fun was conducted by examining case vignettes using the 3P framework. Results suggest the experience of fun at work is activity based, with an emotionally qualitative dimension that is highly socially interactive and engaging. The organisational context for fun appears to be embodied in supportive management and colleagues, positive team dynamics and a non stressed environment. The participant experiencing the fun is usually in the role of contributor rather than observer, is highly engaged, experiencing amusement, laughter, flow, social connection and as an outcome, an increase in positive mood. While humour and play contribute to the process of fun, fun appears to be a uniquely distinct construct. Finally, the present results suggest the perceived impact of having fun at work, while positive, was not reported globally to the extent suggested in the popular press. The most significant outcome of having fun was the reporting of improved positive mood after the fun event, with the related cascading organisational effects discussed. Complimentary to this, having fun at work was perceived to positively influence workplace relationships to a moderate-high degree, contribute to managing stress to a moderate degree, improved job satisfaction to moderate degree and was reported to have a little more than neutral, direct impact on workplace effectiveness. These outcomes must however be examined in the context of results, suggesting not only are different types of fun activities enjoyed more, but different types of activities are highly salient in relation to the particular organisational variable measured. Results of this series of studies have provided a revised nomological net that can be used in further research to define the construct of fun in a workplace context. Supplementary to this, outcomes suggest having fun at work has positive impacts for both individuals and workplaces and therefore further
  investigation, at multiple organisational levels is required, ranging from individual
  disposition in relation to fun, to the effects of fun on workplace culture.

In summary, @what is right to be concerned about the definition of "playful break". The particular kind of fun activity in question seems to moderate the effects quite a bit. Popular media seems to have over-hyped the effects somewhat. Still, overall, fun is indeed fun – i.e., the behavior affects affect and cognition. It may also improve coworker relations, reduce stress, and make people happier with and better at their jobs...but these results may be too subjective to trust on their own, and deserve replication and reexamination.

Reference

Cook, K. (2009). Fun at Work: Construct Definition and Perceived Impact in the Workplace. (Doctoral dissertation.) Griffith University. Retrieved from https://www120.secure.griffith.edu.au/rch/file/16034620-6834-02f5-2d07-79df62b21e6c/1/02Whole.pdf.


Does physical aerobic exercise ameliorate depression? Studies seem to find correlation, but has the causal link been established?

There are different theories about the causes of depression. Three of them assume a cause that could be affected by aerobic exercise.

Neurochemical theory of depression:

It seems that depression might be caused by low serotonin and/or noradrenalin levels. Physical activity releases both neurotransmitters, thus alleviating depressive symptoms.

Cognitive theory of depression:

It seems that negative cognitive schemata cause depression. Sports improves self-efficacy and other schemata.

Diathesis–stress model of depression:

Depression is the result of a predispositional vulnerability combined with stress from adverse life experiences. Aerobic exercise relaxes the sympathetic nervous system thus alleviating stress and, as a consequence, depression.

Maybe someone else will come up with studies showing a causal connection. These (and other) theories might explain the connection.


Do people who lose their faith tend to replace it with other non-evidence-based reasoning? I was watching this talk by Phil Plait given at TAM(The Amazing Meeting) 8. You can find a partial transcript here. It will help provide some context.

In the talk he makes the following claim:

  Studies have shown that people who lose their faith tend to replace it with something else, with a different type of belief. If you start out religious and lose your faith in God, you’ll replace that with something else, some other non-evidence-based reasoning.

My questions:

Q1: Which studies is he referring to?

Q2: How much evidence is there to support the claim ?

This is an interesting question, so I'll take a stab at it.  Direct evidence for the claim is hard to come by.  Generally, religious affiliations, conversions, and loss of faith are self-identified in surveys.  The reliance on self-identification makes it difficult to test the claim that people move to some other non-evidence-based reasoning, as they may not be aware of it.  Indirect evidence is easier to find.

The extensive Religious Landscape Survey (2009) by the Pew Forum on Religion & Public Life for example, asks the self-identified "unaffiliated" who grew up religious to explain their reasons for leaving their faith.  Only about 40% leaving Christianity cite not believing in God as their reason, and less than 30% leaving Catholicism cite no longer being religious in some way.  Looking at specific survey responses, most converts leave their religion for reasons other than relying on science and logic, and remain "spiritual" in some way.

Another way to test the claim is to ask people about their beliefs, as is nicely summarized here, from the same survey.  A large proportion of non-religiously affiliated participants - even some self-identified atheists - believe in God, the afterlife, or some other type of spirituality.


Is StackExchange.com Addiction Dangerous? I recently looked at the meta.math.stackexchange.com and found the second anniversary was celebrated. As in the last year's Happy-Birthday post (linked therein) , some people declared the addiction to the site.

My question is: What kind of addiction is this?

Certainly some kind of internet addiction, combined with a good portion of gamification, represented by reputation, badges, ...
But in this case, I think there is also some kind of altruistic helper-syndrome.

Does this make math addiction a good one? Are there examples of helpful, let's say in a social sense, addictions?

For something to be considered a mental disorder worthy of it's own definition,  it needs to have some really strong effects that are consistently different from others definitions and are not explained by co-morbidity of others.

ADHD, OCD, and Tourettes all exhibit co-morbidity and common brain regions, but since the symptoms and treatment differ so radically, we treat them as distinct from each other.

In short, you are asking the wrong question : )  I'm sure there is plenty of good lit out there on helping people to the point of harming oneself.  Usually, however, this type of "addiction" is a better understood as a generalized form of something else and you would be hard pressed to come up with symptoms and treatments that would generalize only to help addicts of sites like stack exchange.

It's like talking about "breast cancer" instead of categorizing it according to cell types, treatment, etc.  Sure, you will get more money for breast cancer than a-morphic-sciency-sounding cancer, but that doesn't help one predict what could kill it.


Basic definition of incongruence Question:

Regarding Carl Rogers' Person Centered Therapy, which of the following is the correct definition of incongruence:

Inconsistency between ideal self and real self.
Inconsistency between ideal self and self-image.

My Understanding:

Self-Worth: How we value ourselves.

Self-Image: How we see ourselves.

Ideal Self: Who we'd like to be.

Real Self: Who we actually are.

Problem:

The explanations I'm finding online interchangebly use real-self and self-image as part of the definition of incongruence however it is my understanding that these are these two terms mean different things.

The terms congruence and incongruence are used in the 2nd and 3rd core conditions in Person-Centred Therapy.

Carl Rogers developed PCT, and outlined in a Journal of Consulting Psychology (1957) that 6 core therapeutic conditions are needed for constructive personality change and that all 6 must be present in therapy. Rogers considered that no other conditions are necessary.  The 6 core conditions are:

2 people are to be in psychological contact
The client is to be incongruent
The therapist is to be congruent or integrated in the relationship
The therapist experiences Unconditional Positive Regard (UPR) for the client
The therapist has empathetic understanding of the client’s internal frame of reference and endeavours to communicate the empathy to the client
The communication to the client of the therapist’s empathy and UPR is to a minimum degree achieved.

Incongruence
This term used in the 2nd core condition refers to a discrepancy between the client’s perception and the reality of the situation.  The client will be aware of the reality but perceives it differently.

It refers to a discrepancy between the actual experience of the organism and the self picture of the individual insofar as it represents that experience… [An] instance would be the mother who develops vague illnesses whenever her only son makes plans to leave home. The actual desire is to hold on to her only source of satisfaction. To perceive this in awareness would be inconsistent with the picture she holds of herself as a good mother.  (Rogers, 1957, p. 2)

Congruence
This term used in the 3rd core condition refers to the exhibition of genuineness, transparency and wholeness.  The therapist will not give perceptions of professionalism which disguises the humanity of the therapist.  However, the therapist will convey any feelings of confusion, dislike or any other feelings arising within themselves through advanced empathy, in order to be transparent and genuine.

  Can I be real in the relationship?  This has come to have an increasing amount of importance to me over the years.  I feel that genuineness is another way of describing the quality I would like to have.  I like the term congruence by which I mean that what I am experiencing inside is present in my awareness and comes out through my communication.  In a sense, when I have this quality, I am all in one piece in the relationship. (Rogers, et al., 1965)

 -- Edit to clarify more as requested in comments --

The situation with the mother in Rogers' example shows that the mother sees her ideal self to be a good mother but her perception of her self image is that she is not a good mother as she develops vague illnesses whenever her son plans to leave home.

References

Rogers, C., 1957. The Necessary and Sufficient Conditions of Therapeutic Personality Change. [Online]
Available at: http://www.shoreline.edu/dchris/psych236/Documents/Rogers.pdf
[Accessed 15 March 2016]

Rogers, C., Perls, F. & Ellis, A., 1965. Video: Three approaches to psychotherapy. [Online]
Available at: https://www.youtube.com/watch?v=SgiX0QLnpBM
[Accessed 15 March 2016].


How to measure emotional intensity? This is a follow-up question to: Do people feel emotions less strongly as they grow older?

Basically - I'm wondering - has anyone ever made an empirical measurement of how strongly someone felt happiness, sadness, anger or grief? Is it also possible to compare intensities of emotion between different people? And if so, how?

Since things like happiness, sadness, and grief are highly subjective, so I don't think there's any way you could measure those variables directly.

You could operationally define those emotions, such as measuring happiness by the number of hours someone spends doing something they enjoy, but you can imagine all of the confounds involved with that.

Or, you could define a general scale (see here for a list of those having to do with pain) and rank how people score on it.  Then, you could use principles of non-parametric statistics to compare your rankings.

You could also measure known anatomical correlates (e.g., activity in the amygdala as a basis of fear via fMRI), but so many emotions/feelings/other background processing overlap in certain brain regions that the validity would have to be shown through good controls.


Do lucid dream eyemasks work? There seems to be a few eyemasks available that claim to help the wearer achieve lucid dreaming.  For example:

  The NovaDreamer lucid dream mask works by detecting Rapid Eye Movement
  (REM) while you are asleep and dreaming. The mask then flashes a
  series of lights through your closed eyelids; a stimulus which becomes
  incorporated into your dream. [...] This is your cue to recognize that
  you are dreaming and become lucid.  -- NovaDreamer

Another examples is Remee.

Is there peer-reviewed evidence (or even preliminary data) that lucid dream eyemasks can promote lucid dreaming in a laboratory?

There doesn't seem to be much material about these outside of sales material and news items (which makes me suspicious).

I will take a stab at this question, because lucid dreaming is somewhat of an area of expertise of mine.

The first thing that you will notice as you explore the lucid dreaming is that the phenomenon is poorly recognized by modern sleep science. There are hundreds of articles that use scientific methods to study sleep disorders, like sleep apneas, restless leg, delayed sleep phase, etc. But I've yet to find a scientific, peer reviewed article that has touched upon lucid dream induction with external devices.

Outside Dr. LaBerge and another scientist whose name escapes me at the moment, the majority of lucid dream induction research is done by independent agents, like myself. Such people have very little formal scientific education, poor access to tools, and are unlikely to publish papers to scientific, peer reviewed journals. Did I mention that a night of laboratory sleep study with Polysomnography costs somewhere around 3000$ ?

There's a lot of anectodatal evidence and other first hand accounts of what works and what does not, but if science is a subject to publication bias, then such self reported experiences are extremely affected by the desire to find an approach that works.

This is why you hear a lot about methods that worked once or twice, but cannot be demonstrated to work reliably over extended periods of time, and for different people.

Lucid Dreaming Masks are a good example of technology that was developed outside the mainstream science. It uses primitive methods of detecting rapid eye movement sleep, which are still effective, but are disconnected from the data analysis tools. I'm not aware of any sleeping masks that log data, so the user cannot even look at when the signaling took place to adjust the signaling. It is like stabbing blindly with random patterns and hoping that something will happen.

But detecting REM sleep is only the first part of the equation, the good thing is that REM detection is getting to be practically free with iPhone and inexpensive lucid dreaming masks.  The second part is that a stimulus must be found that is effective at "inducing a lucid dream".

My own experiments can hardly be called laboratory, and most of them use iPhone actigraphy. I can tell you that I tried various types of audio, light and vibration cues, which were delivered as close to REM as I could manage.  As much as I wanted to say that they work, they don't. My lucid dreaming smartphone apps have been published to the app store and have tens of thousands of users.

For all the customization options that I included in the apps, I've yet to hear a single "Yes, I'm absolutely certain that an external cue has triggered a lucid dream for me" from the users.

Occasionally there may be some connection noticed or something that happens in a dream may be linked to the external cue playing in the real world. But the majority of lucid dreams that are experienced by the device users can just as well be linked to the fact that a user is more interested and aware of the phenomenon of lucid dreaming.

If you read about first hand experiences with lucid dream inducing masks, then you will find out that the statements above are echoed many times - once in a while there's something that flashes in a dream, but it is very difficult to recognize. This is what people who spent 500$ on a mask say over and over again.

To conclude, I'd say that regardless of what you look at - Remee, NovaDreamer, REM Dreamer or various iPhone/Android apps for lucid dream induction, there's nothing currently at the market that can put a novice into a state of lucid dreaming on the first night, without training.

I would love to test them in a real lab though.


Where could I collect UK participants for my survey? I am looking for survey participants from the UK. Is there a place I can publish my survey in order to get UK participants?

You could obtain paid participants from https://www.prolific.ac/

That site allows you filter by country.

The prices are reasonable, especially if your survey is short and you don't need too many participants.


"Dependence" in DSM-5 I've read with some interest and amusement the following first-hand account (2006) on the confusion surrounding the DSM-IV meaning of "dependence" :

One of us (C.O.) was a member of the committee who attended every one of the [DSM] committee meetings throughout the 1980s. There was good agreement among committee members as to the definition of addiction, but there was disagreement as to the label that should be used. The proponents of the term “addiction” believed that this word would convey the appropriate meaning of the compulsive drug-taking condition and would distinguish it from “physical” dependence, which is normal and can occur in anyone who takes medications that affect the CNS. Those who favored the term “dependence” felt that this was a more neutral term that could easily apply to all drugs, including alcohol and nicotine. The committee members argued that the word “addiction” was a pejorative term that would add to the stigmatization of people with substance use disorders. A vote was taken at one of the last meetings of the committee, and the word “dependence” won over “addiction” by a single vote.
Experience over the past two decades has demonstrated that this decision was a serious mistake. The term “dependence” has traditionally been used to describe “physical dependence,” which refers to the adaptations that result in withdrawal symptoms when drugs, such as alcohol and heroin, are discontinued. Physical dependence is also observed with certain psychoactive medications, such as antidepressants and beta-blockers. However, the adaptations associated with drug withdrawal are distinct from the adaptations that result in addiction, which refers to the loss of control over the intense urges to take the drug even at the expense of adverse consequences. For example, research has shown that when opiates are administered to a naive animal, adaptation begins to occur after the first dose so that the second dose has a discernibly decreased effect from the first. After several days of taking the medication, abrupt cessation produces a withdrawal syndrome varying with the duration of treatment and the dose level. This is an expected pharmacological response, and although it may occur among addicts, it is quite distinct from compulsive drug-seeking behavior. This has resulted in confusion among clinicians regarding the difference between “dependence” in a DSM sense, which is really “addiction,” and “dependence” as a normal physiological adaptation to repeated dosing of a medication. The result is that clinicians who see evidence of tolerance and withdrawal symptoms assume that this means addiction, and patients requiring additional pain medication are made to suffer. Similarly, pain patients in need of opiate medications may forgo proper treatment because of the fear of dependence, which is self-limiting by equating it with addiction.
The authors are now in the planning stages for DSM-V. There will be careful reviews of the criteria, but in the case of substance use disorders, the medical world drastically needs a change in labeling. Addiction is a perfectly acceptable word. It is used by the American Society of Addiction Medicine, the American Association of Addiction Psychiatrists, the American Journal on Addictions, and the oldest journal in the field, simply known as Addiction. It is clear that any harm that might occur because of the pejorative connotation of the word “addiction” would be completely outweighed by the tremendous harm that is now being done to the patients who have had needed medication withheld because their doctors believe that they are addicted simply because they are dependent.

So what (if anything) has DMS-5 done with respect to the dependence/addiction terminology?

To me, the copy of DSM-5 follows the idea put forward by proponents of the term “addiction” in the meetings mentioned in your quote whereby

proponents of the term “addiction” believed that this word would convey the appropriate meaning of the compulsive drug-taking condition and would distinguish it from “physical” dependence, which is normal and can occur in anyone who takes medications that affect the CNS.

In the second page of the preface to DSM-5 (page xlii), the following is stated.

Restructuring of substance use disorders for consistency and clarity. The categories of substance abuse and substance dependence have been eliminated and replaced with an overarching new category of substance use disorders—with the specific substance used defining the specific disorders. "Dependence" has been easily confused with the term "addiction" when, in fact, the tolerance and withdrawal that previously defined dependence are actually very normal responses to prescribed medications that affect the central nervous system and do not necessarily indicate the presence of an addiction. By revising and clarifying these criteria in DSM-5, we hope to alleviate some of the widespread misunderstanding about these issues.

The section on Substance Use Disorders is within the section titled Substance-Related and Addictive Disorders which starts on page 481.

The substance-related disorders encompass 10 separate classes of drugs: alcohol; caffeine; cannabis; hallucinogens (with separate categories for phencyclidine [or similarly acting arylcyclohexylamines] and other hallucinogens); inhalants; opioids; sedatives, hypnotics, and anxiolytics; stimulants (amphetamine-type substances, cocaine, and other stimulants); tobacco; and other (or unknown) substances. These 10 classes are not fully distinct. All drugs that are taken in excess have in common direct activation of the brain reward system, which is involved in the reinforcement of behaviors and the production of memories. They produce such an intense activation of the reward system that normal activities may be neglected. Instead of achieving reward system activation through adaptive behaviors, drugs of abuse directly activate the reward pathways. The pharmacological mechanisms by which each class of drugs produces reward are different, but the drugs typically activate the system and produce feelings of pleasure, often referred to as a "high." Furthermore, individuals with lower levels of self-control, which may reflect impairments of brain inhibitory mechanisms, may be particularly predisposed to develop substance use disorders, suggesting that the roots of substance use disorders for some persons can be seen in behaviors long before the onset of actual substance use itself.
[...]
The substance-related disorders are divided into two groups: substance use disorders and substance-induced disorders. The following conditions may be classified as substance-induced: intoxication, withdrawal, and other substance/medication-induced mental disorders (psychotic disorders, bipolar and related disorders, depressive disorders, anxiety disorders, obsessive-compulsive and related disorders, sleep disorders, sexual dysfunctions, delirium, and neurocognitive disorders).


How can different ion channels of the same type have different cell responses? The NMDA receptor is an ion channel and contributes to synaptic plasticity and memory. It is said that calcium ion flux through the receptor is critical for this mechanism. However, there are other ion channels that let calcium ions into the cell, how come they don't contribute to synaptic plasticity (to my knowledge)?

Quibbling about other types of LTP (not mediated by NDMA receptors) aside, this is a good question, with a rather intricate answer.
Basically (NDMAR mediated) LTP is not merely activated by calcium, but rather by CaMKII, which essentially acts a sort longer-term chemical memory for calcium that was once "detected" in a spine. A couple of points quoted from a fairly recent review paper:

[a] bulk calcium signal, when produced by depolarization of voltage-dependent calcium channels, is not sufficient to activate CaMKII.

a calcium signal will stay largely within the activated spine. The next step in the long-term potentiation cascade is the binding of calcium to the four binding sites on calmodulin. Calcium-saturated calmodulin keeps calcium bound for ~1 ms, a long enough time for calmodulin to diffuse within the spine and to bind CaMKII, but too short a period of time to diffuse out of the spine. [...] CaMKII diffuses at a very slow rate (for CaMKII to exit spines may take many minutes), activated CaMKII is mostly localized to the activated spine.

So basically a fast signal (calcium) gets converted into a (spatially) slow but locally persistent CaMKII signal (via calmodulin). As I understand it, anyway.


Need a perspective on science, philosophy, religion, etc Consider the following five "things":

science | philosophy | religion | spirituality | politics

I have no training in psychology beyond high school Psych 101 long ago. I would like to know how a cognitive scientist or psychologist would likely define or categorize these things.

For example, would a psychologist call them "disciplines" or something else?

My grouping may not be the most logical. For example, some people may treat religion and spirituality as the same thing, while others might exclude either or both from the group. Politics is another strange one, as it draws from all the other groups.

In summary I'm jut trying to get a social scientist's perspective on this so I can better analyze, research and write about them.

I see where you're coming from, I would argue that they are all based around ideologies or philosophies and to disband the "philosophy" heading in favour of another title.