# Question
Title: Link between visual-spatial + verbal working memory and intelligence/academic achievement?
What is the link between someone's visual and spatial working memory, their verbal working memory, and different types of cognitive abilities or tasks? More specifically, intelligence tests (WAIS, Stanford Binet, etc.) and would this relate to educational outcomes in different fields (maybe SAT scores, graduation rates in different fields, and GPA, etc.)? Is there a relationship between these variables? Some cite working memory as the most important predictor of early academic success.

Somebody who has a strong verbal working memory may generally perform well on other types of verbal tasks included on intelligence tests: vocabulary, verbal reasoning, analogies, antynoms, etc. And be better suited to learn about fields such as literature, biology, foreign languages, etc. because there is a lot of linguistic mastery required in these disciplines.

Or on the other hand, if somebody has a strong visual-spatial working memory they may generally perform well on intelligence tests on other types of visual-spatial tasks that also recruit reasoning ability and long-term memory. And would be better suited to learning about fields such as physics, mathematics, art, architecture, etc. because there is more of a visual-spatial component in these disciplines.

Of course, there are many other factors that affect ability and learning. Working memory would be a small determinant but a determinant nonetheless. Furthermore, there is research which shows a link between spatial ability and achievement in STEM subjects up to graduate level studies for example.

Cognitive abilities from both of these broad areas (overall visual-spatial and verbal ability) certainly overlap highly — same with other types of reasoning abilities such as numerical and logical. However, I assume each area has a bias as to what types of cognitive abilities are used more.

There seems to be a very strong correlation between the two types of working memory or short-term memory. That's what I wanted to find out mainly: **What is the relationship between the different types of working memory or short-term memory and other types of reasoning abilities (non-working memory reasoning tasks including verbal ability, numerical, spatial, etc.)? Are the different measures of short-term and working memory measuring approximately the same thing?**

How common is the occurance of individuals that have poor verbal working memory and high verbal reasoning scores on intelligence tests for example? How about for visual-spatial working memory and non-working memory visual-spatial scores on intelligence tests?

I've read a few papers on this subject but am unsure of the answer.

Hopefully, someone can point me in the right direction. Thanks.

**References:**

Timothy F. Brady, Talia Konkle, George A. Alvarez; A review of visual memory capacity: Beyond individual items and toward structured representations. Journal of Vision 2011;11(5):4. doi: 10.1167/11.5.4.

Teixeira, Rosani Aparecida Antunes, Zachi, Elaine Cristina, Roque, Daniela Tsubota, Taub, Anita, & Ventura, Dora Fix. (2011). Memory span measured by the spatial span tests of the Cambridge Neuropsychological Test Automated Battery in a group of Brazilian children and adolescents. Dementia & Neuropsychologia, 5(2), 129-134. https://dx.doi.org/10.1590/S1980-57642011DN05020012

Spatial Ability: A Neglected Talent in Educational and Occupational Settings Harrison J. Kell & David Lubinski Roeper Review Vol. 35 , Iss. 4,2013

# Answer
Work in progress -

> What is the relationship between the different types of working memory or short-term memory and other types of reasoning abilities (non-working memory reasoning tasks including verbal ability, numerical, spatial, etc.)? Are the different measures of short-term and working memory measuring approximately the same thing?

This is a good question, but you are a funny person: say hello to *positive manifold*.

The concept of the general factor of intelligence emerges from the observation that all cognitive tasks are positive correlated with one another, or display positive manifold. It's as though they're all *tapping into* this invisible phlogiston, the general factor of intelligence/psychometric g. Perhaps the following puts it more succinctly:

From: Sternberg, R. J., & Kaufman, S. B. (Eds.). (2011). The Cambridge handbook of intelligence. Cambridge University Press.

> Is there a relationship between these variables?

As above. The reason why WM is most predictive of academic achievement is essentially because it's thought that it's tapping into the general factor most.

> Somebody who has a strong verbal working memory may generally… Or on the other hand, if somebody has a strong visual-spatial working memory they may generally perform well on intelligence tests on other types of visual-spatial tasks

What you are saying *sounds* perfectly cogent, but you are making one important assumption here that I don't necessarily agree with: that visuo-spatial WM and verbal WM are so thoroughly dissociable that one can have one that is stronger than the other in the way that I kick a ball real good with my right foot, but am a total ponce with my left foot. Although they are considered separate cognitive structures, I would anticipate that they're still very highly correlated in most people, individual differences notwithstanding.

Here is a snippet I have found:

However, later in the same reference, there is an interesting chapter on individual differences in visuo-spatial WM ability. In it, the authors describe a sample comprising children with learning disabilities where the deficit could be characterised as High Verbal/Low Visuo-Spatial intelligence, and vice-versa. Under some circumstances, the abilities can be dissociated:

From: Cornoldi, C., & Vecchi, T. (2004). Visuo-spatial working memory and individual differences. Psychology Press.

> Of course, there are many other factors that affect ability and learning. Working memory would be a small determinant but a determinant nonetheless.

Here, I disagree. Have you ever attempted to entertain a complicated concept comprising multiple components, only to have it "fall out of your mind" for lack of a better word? In order to process complicated concepts, you need to have some. Working memory is king, and all other abilities are subservient to it.

> How common is the occurance of individuals that have poor verbal working memory and high verbal reasoning scores on intelligence tests for example?

I am going to make a bold a priori claim: it is simply not possible for this to occur.

To argue my point, consider what you are implying: suppose someone was reading a passage of text with a long sentence. If they had very low verbal WMC, what would happen is that the beginning of the sentence would decay before they got to the end; they could never hold the information in the fore of the mind sufficiently long enough to process it, prod it, and synthesise an idea. Likewise for a sophisticated verbal reasoning task; a complex reasoning item has multiple components that must be considered simultaneously.

This reference describes it perfectly:

From: Cowan, N. (2012). Working memory capacity. Psychology press.

Effectively, what I am saying is that robust WMC is a necessary but insufficient component of verbal reasoning ability.

> How about for visual-spatial working memory and non-working memory visual-spatial scores on intelligence tests?

I'm a little confused by this, but I think you're making the same analogy as above. Same deal. However, I will make the point that WMC would represent the bottleneck in cognitive resources that would predict performance.

Having made this claim simply from first principles, let me dig up some evidence for my claims.
> 3 votes

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Tags: intelligence, working-memory, short-term-memory, spatial-cognition
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# Question
Title: How exactly does transcranial direct current stimulation (tDCS) work?
The method of **transcranial direct current stimulation (tDCS)** involves the flow of electric charge from a positive electrode to a negative one.

This method is not exactly a stimulation method because the current applied do not provoke neurons firing such as TMS (transcranial magnetic stimulation), it just **modulate** the level of excitability of neurons. **How happens this modulation of excitability?**

Precisely, my question is:

**How that positive or negative current interferes with electric fields generated by neurons?**

*references:*

# Answer
> 4 votes
I'm not sure at what level of sophistication you expect this answer, but the basic theory of how tDCS works at a cellular level is that neurons oriented roughly parallel to the electric field lines suffer a (partial) depolarization of the axon hillock cell membrane when the dendrites of the neuron are oriented toward the anode of a constant electric field, and the a reverse effect (hillock membrane hyperpolarization) occurs when the dendrites are oriented toward the cathode. (*Niedermeyer's Electroencephalography*, 6th ed., p. 1136) And on this basic theory, not much happens if the neuron is perpendicular to the electric field. Another way of saying the same thing (but more concisely) from Lefaucheur et al.:

> The primary effect of tDCS on neurons is a subthreshold shift of resting membrane potentials towards depolarization or hyperpolarization, depending on current flow direction relative to axonal orientation.

The simple theory above applies to a cell in isolation. I'm even less sure I understand your detail question "How that positive or negative current interferes with electric fields generated by neurons?" In more sophisticated approaches, the cell shapes also affect the electric field influencing nearby cells; see for instance Ye & Steiger. Ultimately, in a nonhomogenous medium like the brain, it's quite nontrivial to determine the local electric field orientation induced by some distant electrodes. To get a solution one needs to simulate the entire brain as done by Wagner et al. for instance.

To verify that tDCS basically works like this (i.e. as a modulation, as you correctly observed) one can experimentally add another stimulus that can trigger neuronal activation, for instance TMS, and measure how much of this extra stimulus is required to obtain the same effect with and without tDCS. This was done for instance in the highly-cited study of Nitsche and Paulus. They observed excitability changes of up to 40% using this method.

The basic theory doesn't quite explain everything relating to tDCS, in particular it doesn't explain why some effects persists for a time after the DC current is turned off; the extent of these effects is dependent on the current intensity and the duration of the stimulation. Nitsche and Paulus discuss some theories relating to this, mentioning that perhaps tDCS induces changes in the spontaneous discharge rate as well.

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Tags: neuroscience, cognitive-neuroscience, methodology, tdcs
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# Question
Title: Precise term for a sort of social pressure
**Context**: It is known that some pubs and the like usually offer free drinks for females. The owner of the place expects then that more males will come and pay for a drink for themselves because a considerable amount of females are already there, so that the payout for the owner is positive. To put another example, in some casinos, people get paid to play slots machine so that the sound of it and seen people getting money from it encourages other people to play slots machine as well.

> Is there a precise term for that effect/social behavior?

I apologize if the question is not too narrow and I will happily make it more precise if it is required. Thank you (and happy new year!).

# Answer
> 2 votes
The first practice (sometimes called ladies' nights or similar) is a form of sex-based pricing and is seen by some as a form of commoditization (aka commodification) of women. It's illegal in the UK and parts of US.

The casino design part of your question is mostly unrelated, although some casinos surely use even more blatant commodification of women as part of their strategy \[for attracting men\], such as skimpy outfits for their female employees. The things you ask about such having slots right in your face at the entrance has been (traditionally) considered to be superior to empty entrance lobbies at attracting more bets, but it's not totally clear if that works by peer pressure, exposure or a combination. This type of (heavy) gaming casino design with machines everywhere starting from the entrance is also called Friedman-type after Bill Friedman who wrote a book-size document promoting it.

More recent studies such as Finlay et al. (2009) found however that creating a playground atmosphere is what encourages most bets from most people, simply because they spend more time in the casino. This type of casino design was promoted by Roger Thomas although the playground name for it apparently came from an academic, David Kranes. Interestingly the crowding (of people) in this type of playground casino design is reduced compared to the traditional "gaming" one. Apparently this gets women to bet more than they had planned, but has little effect on men; quoting from the Finlay (2009) study:

> Relative to a densely crowded casino (high information load), a sparsely crowded casino (low information load) was more harmful for females who reported higher levels of intention to gamble beyond planned levels in the less crowded condition. For males, at-risk intention was not affected by crowding. For both genders, crowding had no significant impact on restoration and pleasure. Tuan (1977) characterized crowding as “an awareness that one is observed” (p. 60). A sparsely crowded gambling venue may increase gambling intentions among females because they feel unobserved. This release from inhibition is not characteristic of males. Loo (1978) indicated that female adults tend to react more positively to a dense crowd than do males. Females are more inclined to be cooperative which is conducive to a dense crowd. In contrast, males are more inclined to be competitive which will be enhanced with a dense crowd. These results suggest that females should be counseled to avoid gambling in relative isolation. Note that in the case of crowding, a high information load is protective for females.

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Tags: social-psychology, terminology
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# Question
Title: Give me 5 simple reasons why Applied Kinesiology is bogus
I'm a Ph.D. candidate in molecular biology, I can handle science. But my mom and grandma are armchair experts in neuro-psycho-biology. What are 5 ways I can convince them holding vitamin cans and assessing their grasping arm strength will not tell them what ones to take or not to take? I'm concerned about them overdosing on the vitamins that come in the heaviest bottles.

If you're wondering exactly what I'm talking about, please see the second paragraph on "claims": https://en.wikipedia.org/wiki/Applied\_kinesiology#Claims

Thanks!

# Answer
Here is more than 5 reasons:

Applied Kinesilogy a Fraud

Here are some findings that point to Applied Kinesiology being fraudulent:

> 1. Three practitioners testing eleven subjects made significantly different assessments; their diagnoses of nutritional deficiencies did not correspond to the nutrient levels obtain by blood serum analysis; and that the responses to nutrient substances did not significantly differ from responses to placebos \[10\].
> 2. Another study found no effect from administering the nutrients "expected" to strengthen a muscle diagnosed as "weak" by AK practitioners \[11\]."
> 3. Researchers who conducted an elaborate double-blind trial concluded that "muscle response appeared to be a random phenomenon \[12\]."
> 4. Another study showed that suggestion can influence the outcome of muscle-testing. During part of this experiment, college students were told that chewing M&M candies would give them instant energy that would probably make them test stronger. Five out of nine did so \[13\].
> 5. Four AK practitioners tested seven patients were extremely sensitive to wasp venom. Altogether, 140 muscle tests were done to see how the patients responded to preparations of venom or salt water in a bottle. If the test were valid, the venom bottles should result in "strong" reactions and the salt-water bottles should produce "weak" test reactions. However, the practitioners were unable to identify which bottles contained which \[14\].
> 6. Several chiropractors were tested at a medical office while under unblinded and blinded conditions. During the volunteers could resist downward pressure when a drop of glucose was placed on their tongue but could resist when fructose was administered. The the arm tests were repeated using substances in coded test tubes so that the volunteer, the chiropractors, and the onlookers could not tell which solution being applied to the volunteer's tongue. When the code was revealed, There was no connection between ability to resist and whether the volunteer was given the "good" or the "bad" sugar \[15\].

\[10\] Kenny JJ, Clemens R, Forsythe KD. Applied kinesiology unreliable for assessing nutrient status. Journal of the American Dietetic Association 88:698-704, 1988.

\[11\] Triano JJ. Muscle strength testing as a diagnostic screen for supplemental nutrition therapy: a blind study. Journal of Manipulative and Physiological Therapeutics 5:179-182, 1982

\[12\] Haas M and others. Muscle testing response to provocative vertebral challenge and spinal manipulation: a randomized controlled trial of construct validity. Journal of Manipulative and Physiological Therapeutics 17:141-148, 1994.

\[13\] Applied kinesiology - Double-blind pilot study. Journal of Prosthetic Dentistry 45:321-323, 1981.

\[14\] Ludtke R and others. Test-retest-reliability and validity of the kinesiology muscle test. Complementary Therapy in Medicine 9:141-145, 2001.

\[15\] Hyman R. The mischief-making of ideomotor action. by ideomotor action. The Scientific Review of Alternative Medicine, Fall-Winter issue, 1999. Republished on Quackwatch, Aug 26, 2003.
> 1 votes

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Tags: psychology, placebo
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# Question
Title: Can a person do things against their own will and be conscious of it at the same time?
I am a firm believer of the principle of free-will, but wanted to see if there was any examples(or case examples) of people knowingly doing things against their own will.

I know that we can be pressured to do things and make hard choices, but the choice is still that of the individual.

Can a person do things they know they are not willing to do?

# Answer
> Can a person do things against their own will and be conscious of it at the same time?
>
> Can a person do things they know they are not willing to do?

This is a little tricky to answer without parsing it as follows: *can someone's earnestly stated desires be different to the desires implied by their actions?*

Phrasing your question this way is important because what someone wants is unknowable: people could be lying to themselves, or lying to us, or simply lacking the insight to fully understand the motivations underpinning their behaviour. The intent behind a behaviour is even more unknowable: it can only be inferred from observation. Thus, although we presume that a dog eats because its hungry, and drinks water because it's thirsty, we need to be careful in recognising that while this is certainly a reasonable inference, nonetheless it is still only an inference.

I am sure you will also find some very rare syndrome that is sexier e.g. alien claw hand or similar, but conceptually I would suggest drug addiction is the best example of this.

Although not immediately apparent, the phenomenology of the drug-taking behaviour is very reminiscent of what you're describing. The two core features of addiction are craving and compulsion -- the latter is of relevance to your question. At its core, compulsive drug-taking behaviour is a decoupling of an earnestly stated (or believed) desire and action that suggests something entirely to the contrary.

> I am a firm believer of the principle of free-will, but wanted to see if there was any examples(or case examples) of people knowingly doing things against their own will.

Typically, drug addicts will consciously state that they do not want to consume drugs, but that they are lead to do so by some uncontrollable compulsion. That is, they continue to consume drugs despite the clear acknowledgement that it is no longer in their interests to do so and conveying an earnest desire to not consume drugs.

> I know that we can be pressured to do things and make hard choices, but the choice is still that of the individual.

The concept of drug addiction creates problems for proponents of free will: if addiction is a choice, then so are the harms. The moral culpability of the addict came be framed in either two ways:

*Deviancy.* The drug addict values the wrong things. They belong in prison.

*Weakness.* The drug addict has the same values as us, but is too weak-willed to pursue/obtain/keep them. In recognising their weakness, they deserve help.

Generally, to reconcile the concept of addiction as choice (free will) versus addiction as disease (addiction) those in the literature will attempt to describe the initial use of drugs as a volitional act, but one which becomes less and less *freely chosen* over time. The adaptive changes that are observed in the brain with repetitive drug administration i.e. addiction support are generally used to argue this point.
> 0 votes

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Tags: consciousness, brain, free-will
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# Question
Title: Study on likability, weakness, and competence?
I heard a podcast about a study (I think it was Radiolab or similar) that found that people are viewed as more likable after they reveal a weakness or a shortcoming, but the effect only occurs if they have established that they are competent.

What is that study? The podcast said it is influential and well known.

In the podcast, a professor told a story about how when he was a graduate student made a fool of himself in front of his PhD advisor and he joked that he did it on purpose to improve his likebility and she retorted that he hadn't yet established himself as competent. I remember hearing it in late 2014. Any help enormously appreciated!

# Answer
> 3 votes
Thank you all for your responses. I found the answer independently - I was looking for the *Pratfall Effect* described in Elliot Aronson's 1966 paper "The effect of a pratfall on increasing interpersonal attractiveness" in Psychonomic Science.

The paper's abstract reads:

> An experiment was performed which demonstrated that the attractiveness of a superior person is enhanced if he commits a clumsy blunder; the same blunder tends to decrease the the attractiveness of a mediocre person. We predicted these results by conjecturing that a superior person may be viewed as superhuman and, therefore, distant; a blunder tends to humanize him and, consequently, increases his attractiveness.

More information on the Pratfall Effect can be found here: Wikipedia, Psychology Archive

<sub> Aronson, E., Willerman, B., & Floyd, J. (1966). The effect of a pratfall on increasing interpersonal attractiveness. Psychonomic Science, 4(6), 227-228. </sub>

# Answer
> 2 votes
I'm not convinced the effect is even true in general, and appears to be false in job/task-related contexts particularly when the boss does the disclosure; according to a recent paper:

> It is generally believed that self-disclosure has positive effects, particularly for relationships; however, we predict and find negative effects in the context of task-oriented relationships. Across three laboratory experiments, we find that both task-relevant (Study 1) and task-irrelevant (Studies 2 and 3) weakness disclosures, made by a higher (versus peer) status coworker during an interdependent task, negatively affected the receiver’s perception of the discloser’s status and consequently undermined the discloser’s influence, encouraged task conflict, and led to lower relationship quality with the discloser. Peer status disclosers did not trigger these negative responses. We find support for perceived vulnerability as the proposed psychological process (Study 3). Specifically, higher (but not peer) status disclosers experience a status penalty after weakness disclosures because these disclosures signal vulnerability, which violates the expectations people have for higher (but not peer) status coworkers. These findings provide insight into the effects of self-disclosing weakness at work and the ways in which high status employees may inadvertently trigger their own status loss.

(Doi link; free full-text from one of the authrors.)

What this study (alas) didn't address is whether a low-status peer would be seen in a more positive light by a higher-status one after a disclosure, like in your last paragraph. So we don't seem to have experimental evidence on whether "sucking up" by (more or less machiavellian) disclosures or even faking less competence (as to diminish perceived threat) works as intended. I suppose the latter is quite contextual. In a hierarchy where the lower status individual could conceivably take the place of the higher status individual (say in a military junta or an apparatchik system) feigning a less threatening attitude (via some but not complete incompetence) perhaps does work. I'm having doubts that feigning partial incompetence does much good to a subordinate in a context where the high-status individual does not see any direct threat to his position (like when hiring a contractor for a non-core task). But this is just me theorizing. More empirical research is needed, as the saying goes. In general, other forms of "sucking up" do seem to work through, with the caveat that while "sucking up" may have a positive effect on the relationship with the boss, it's also likely to have a negative effect on the relationship(s) with same-status peers/colleagures.

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Tags: cognitive-psychology, social-psychology, emotion, reference-request, personality
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# Question
Title: Why do scientists say brains are faster than computers?
Supposing that neurons function similarly to transistors: A neuron able to fire $200$ times per second and transistors can be switched on and off more than $100,000,000,000$ ($10^{11}$) times per second. Let's say it fires 1 out of 2 times in average. We have $86,000,000,000$ ($8.6 \cdot 10^{10}$) neurons in a brain, and $4,000,000,000$ ($4 \cdot 10^9$) transistors in medium CPU.

$\text{Units count} \cdot \text{firing probability} \cdot \text{firing rate} = \text{total fires per second}$

A brain's total fires per second: $(8.6 \cdot 10^{10}) \cdot 1 \cdot 200 = 1.72 \cdot 10^{13}$.

A CPU's total fires per second: $(4 \cdot 10^9) \cdot \frac{1}{2} \cdot 10^{11} = 2 \cdot 10^{20}$.

A CPU is faster than a brain by $\frac{2 \cdot 10^{20}}{1.72 \cdot 10^{13}} = 1.16 \cdot 10^7$, or about 12 million times faster. I gave the brain an advantage that every neuron is firing non-stop instead of just 1%, and that they fire at the rate of the fastest neurons.

Why isn't this argument valid?

# Answer
There is a basic epistemological problem here that was only touched upon by Chuck Sherrington - everyone is making the assumption that the brain processes the same kind of information as a digital computer. There is no real evidence to suggest that it does, in fact. A digital computer is an instantiation of a Turing machine, which is equivalent to certain kinds of automata. **In order for the "processing power" of the brain to be compared to that of a digital computer in the first place, one needs to show that the brain employs representations (discrete entitites/states like bits) and rules (well-defined transitions between states/bits).** Nobody has even come close to doing this, *even for a subsection of the brain*. This would be done by showing that the brain implements some digital computation - David Chalmers' famously \[1\] explains how this needs to be done. **According to current the state of research, the brain seems to be a complex biological system, operating at multiple levels of measurement, and does not process information in discrete terms!** And yes, Chuck Sherrington says it, neurons are not simply on/off!

\[1\] Chalmers, David J. "A computational foundation for the study of cognition." (1993).
> 7 votes

# Answer
Have you ever seen IBM's Watson? Watson is composed of a cluster of *ninety* IBM Power 750 servers, each of which uses a 3.5 GHz POWER7 eight core processor, with four threads per core. In total, the system has 2,880 POWER7 processor cores and has 16 terabytes of RAM. It must be kept in a (very) large refrigerated room.

> Watson is a question answering (QA) computing system that IBM built to apply advanced natural language processing, information retrieval, knowledge representation, automated reasoning, and machine learning technologies to the field of open domain question answering. According to John Rennie, Watson can process 500 gigabytes, the equivalent of a million books, per second.

Watson's official debut was on the game show *Jeopardy*, where it was pitted against two of *Jeopardy's* best players. It won, but the humans gave it a run for its money. Most believe the win was more due to Watson's faster response time (it was electronically keyed into the buzzer; Watson could activate the buzzer within about eight milliseconds, whereas the human response time to the *go ahead* light signal is several tenths of a second. In addition, to access memory more quickly, content was stored in Watson's RAM for the game because data stored on hard drives are too slow to access.

Watson was devised as a medical diagnostician (as well as other applications). With many years, scores of technicians, who knows how many billions of dollars, and access to medical encyclopedias, books, medical journals and the internet, it can outperform *third year medical students* in only one area: oncology (and even then, only lung, prostate and breast CA).

So, one average medical resident (4 years of medical school, and, say, second year of residency) can outperform a very, very fast medical supercomputer 99% of the time. I specialize in Primary Care medicine: Family and Emergency Medicine. With a few exceptions per year, within minutes of initiating a conversation with a patient, by watching the patient, reading his vital signs, and hearing answers to perhaps a dozen questions, I already have narrowed down my diagnoses to 2 or 3 top candidates and several other lesser considerations. I am one individual with one brain which accesses only to the information to which I've been exposed, yet I will outperform a medical supercomputer \>99% of the time. In under 10 minutes. (This does not mean that I only spend 10 minutes with a patient. Medicine is about more than the correct diagnosis.)

This is Watson:

My brain is about the size of the "W" etched on the room's window.

You tell me: Which is "faster", a supercomputer or a human brain? It really does depend on your definition of "faster", doesn't it?

References:
Wikipedia
Putting Watson to Work: Watson in Healthcare. IBM.
IBM's Watson is better at diagnosing cancer than human doctors
IBM Watson's impressive healthcare analytics capabilities continue to evolve
> 9 votes

# Answer
I'm not sure the math checks out in the question (the CPU cycles per second seems awfully high), but I think there are some useful principles to keep in mind regardless of the details of the math.

So let's assume that we do have a computer that can perform more operations per second than the combined sum of all action potentials in the brain per second. Is the computer faster than the brain?

The answer is it depends on what the question is. There are certainly types of information processing that computers are much faster at than human brains. A cheap calculator can solve the problem 2854 x 239 much faster than the average human brain. But brains tend to be much faster than computers at pattern recognition type problems.

The main point is that looking at the speed of transistors and neurons is the wrong level -- or at least it provides an incomplete picture -- to be thinking about the speed of information processing. Not that the 'hardware' doesn't matter, but other factors matter too. For a computer, the software matters. For a brain, the network of connections between neurons matters.
> 5 votes

# Answer
**Anology** Taking the analogy and calculations directly, you are assuming that the fundamental computing unit of the brain is the neuron; we do not know if this is true. It could be a cortical column, a group of several neurons, the neuron, a dendritic branch (a fascinating review paper!), a synapse, receptors or neurotransmitter vesicles (how about glial cells?). This paper describes the somewhat accidental fascination with the historical view of a neuron being 'the unit'.

So, to the numbers. If one treats a singular neuron's action potential as a 1/0 like a transistor, sure you're numbers kind of make sense. (Not sure where you got the 1% figure from?) However this is making the assumption I eluded to above. If you were to run the numbers with synapses, the brain might win.

You are further assuming that a 1/0, spike or no spike, representation of a neuron is all that the brain does. We do not know how the brain encodes information -- as others have said, it might not work in the same serial 1/0 fashion that we have engineered computers to operate. Information/processing in the brain could be via individual neurons firing rates, population firing rates, spike timing, etc. (sections 1.5, 1.6 and 1.7 review some). Imagine that the timing of when a transistor flipped compared to another was important! Moreover, this only considers action potentials (or EPSPs if one redoes the numbers with synapses). Neurons (and synapses) are extremely non-linear and a lot of information/processing might be undertaken before or after an action potential (EPSP). This is the age old question of analogue (brains) vs. digital (modern computers).

**Serial vs. parallel** I think an important point missing from previous answers is the fact that the brain is massively parallel. That is, there is not one processor serially undertaking instructions.

A typical CPU (core to be specific) in a computer may be very fast in terms of calculations per second -- arguably a great deal faster than a single neuron -- however, there are very few of these individual units when compared to the brain. This is why supercomputers take advantage of hundreds of CPUs (and cores). However, the numbers of these cores is extremely low when compared to the brain (if we are assuming that a neuron is the fundamental unit, see above), where an analogy might be that each core/neuron is a lot slower, there are however millions (trillions if 'the unit' is a synapse) of cores.

Yes, you have considered that a CPU has many many transitors on it, however the CPU itself it still only processing information in a serial fashion. It does this operation, then this operation, then this etc. As I said above, this is why supercomputers use many CPUs as this allows them to do a somewhat parallel process. However this is more complicated as in reality, a computer's parallel programme is typically just a serial one split a few times. For example, you want to calculate what A+b is where A is a huge matrix and b is a constant. One can do this in serial by iterating through all the elements in A and adding b; or, one can 'parallelise' this by using 10 CPUs and splitting the matrix in to 10 subsets and having each CPU do a serial operation on their own subset and finally concatenate the resulting subsets back in to A again. This isn't really parallel computing but rather smaller serial operations (parallel programming is hard). The brain is truly parallel. (The quote in the answer to this previous question has a great analogy in it.)

To compare the two is fundamentally flawed as the way we quantify the performance of a CPU does not apply to the brain. It might be possible to compare them if a common metric could be devised, but this would mean we would need to understand how the brain processes information in the first place, which is a long long way off.

As a final note, have a look at this article.

(Edited to include more detail as there was interest/comments.)
> 3 votes

# Answer
The computer analogy fails on several counts. Most notably, the status of a "bit" in a computer system is completely determined at any one time by the running program. Neurons and synapses are quantum entities, whose state at any one time is a superposition. Both neurons and synapses are living things, to some extent acting independently. Each ***synapse*** is a quantum nanocomputer, vastly more powerful than any existing computer and performing a "calculation" that cannot, even in principle, be carried out by a computer.

https://diaryofachristianskeptic.blogspot.ca/2018/01/the-synapse-as-quantum-nano-computer.html
> 0 votes

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Tags: neuroscience, theoretical-neuroscience
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# Question
Title: Is this brain map scientifically correct?
I'm not an expert in neuroscience but always read about information that seems conflicting to me. On one side I hear that the idea of single brain functions localized in specific brain areas is incorrect since everything is processed globally and on the other side I come up permanently with such kind of depictions of the brain

Can someone tell me how far this is correct or incorrect?

# Answer
The diagram is a somewhat simplistic representation of brain functions, but it is accurate. The diagram given shows the primary areas that complete the actions listed. However, the entire brain is connected and communicates with itself extensively, so it isn't like the occipital lobe is the only brain region active when you see something.

For example, when you see an object, it is first processed in the occipital lobe as this is where the primary visual cortex is located. However, after the actual image itself has been processed, signals are sent to other brain regions for further interpretation. So if you see an angry dog running at you, the signal will begin in your occiptal lobe to process the visual image itself, but signals will then be sent to the temporal lobe to create an emotional response and to the frontal lobe to begin defensive motor activity.

> On one side I hear that the idea of single brain functions localized in specific brain areas is incorrect since everything is processed globally and on the other side I come up permanently with such kind of depictions of the brain

While these two explanations may seem conflicting, they are both somewhat correct. The diagram shows where primary processing of each task takes place, but it takes global communication to accomplish many of the complex tasks carried out by the brain. If there is a disconnect between the occipital lobe and parts of the temporal lobe, you will still be able to see just fine but may not have an emotional reaction to what you see. Vision is technically intact, but the full visual experience is damaged.

Just remember that diagrams like the one shown show you primary processing locations, but signals are sent between many brain regions to accomplish the full range of tasks carried out by the brain.

For further reading on the topic, this website offers a longer but still easy to understand explanation of current findings in brain connectivity: https://www.livescience.com/40855-brain-connections-no-neuron-is-an-island.html

Reference: Kolb, B. & Whishaw, I. Q. (2009). *Fundamentals of Human Neuropsychology: Sixth Edition*. New York: Worth Publishers
> 6 votes

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Tags: neuroscience, brain, neuropsychology
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# Question
Title: Does the taste of sugar replenish willpower?
In a post titled Willpower Depletion vs Willpower Distraction the claim is made that:

> Basically, for a while some researchers believed that willpower depletion "is" glucose depletion in the prefrontal cortex, but some more recent experiments have failed to replicate this, e.g. by finding that the mere taste of sugar is enough to "replenish" willpower faster than the time it takes blood to move from the mouth to the brain:

Is that claim representative of the knowledge we have from studies?

# Answer
> 4 votes
I'm not sure what you mean to ask here, but there is a recent (2016) meta-analysis by Vadillio, Gold and Osman just on the topic of glucose and willpower. Abstract:

> The idea behind ego depletion is that willpower draws on a limited mental resource, so that engaging in an act of self-control impairs self-control in subsequent tasks. To present ego depletion as more than a convenient metaphor, some researchers have proposed that glucose is the limited resource that becomes depleted with self-control. However, there have been theoretical challenges to the proposed glucose mechanism, and the experiments that have tested it have found mixed results. We used a new meta-analytic tool, p-curve analysis, to examine the reliability of the evidence from these experiments. We found that the effect sizes reported in this literature are possibly influenced by publication or reporting bias and that, even within studies yielding significant results, the evidential value of this research is weak. In light of these results, and pending further evidence, researchers and policymakers should refrain from drawing any conclusions about the role of glucose in self-control.

It's not too far in its conclusions from a 2014 meta-analysis on the mere existence of ego/willpower depletion.

As Vadillo et al. use p-curves, the interpretation of their result is somewhat subjective.

Here is their interpretation:

> The results of our analyses suggest that the relationship between glucose levels and self-control behaviors might be unreliable. Figure 1 shows that the key p values of the 19 studies included in the present analyses follow a surprisingly flat distribution. This is exactly the pattern of results that one would expect to find if those results were false positives. These results remain unchanged regardless of whether glucose-rinsing studies are included or excluded from the sample. These results may not come as a complete surprise given the empirical challenges to the glucose hypothesis suggested by failed replications (Job et al., 2013; Kelly et al., 2015; Lange & Eggert, 2014; Lange et al., 2014) and theoretical critiques regarding its biological plausibility (Kurzban, 2010; Osman, 2014). Furthermore, a detailed analysis of the seminal article suggesting the glucose hypothesis showed that the number of significant findings reported in that article was too large, given the low power of each study (Schimmack, 2012). In other words, the results were too good to be true (Francis, 2012). Nevertheless, the findings from the present study are a surprise in the context of the wide acceptance of the glucose hypothesis in general scientific research and its popularity, as evidenced by the number of citations of Gailliot et al. (2007) in the literature and the continued influence of this hypothesis in recent reviews on ego depletion (e.g., Baumeister, 2014; Baumeister & Alghamdi, 2015).
>
> \[...\]
>
> It is worth noting that, as with any other statistical test, p-curve analysis is not a flawless indicator of bias (Bishop & Thompson, 2016; Bruns & Ioannidis, 2016; Lakens, 2015). Our results suggest that, on average, these studies have little or no evidential value, but they do not allow us to determine whether the significant results are due to publication bias, selective reporting of outcomes or analyses, p-hacking, or all of these. It is not impossible that some of these studies are exploring small but true effects and that their evidential value may be diluted by the biases that pervade the rest of the studies. Perhaps future research will show that glucose does play a role in egodepletion effects, but our conclusions are based on the analysis of the extant literature in this area. Thus, our contribution must be seen as an additional piece of information in the wider context of attempts to verify the reliability of the glucose model of ego depletion. Note that the kind of biases explored in the present study are prevalent in other (but not all) areas of psychological research (e.g., Bakker, van Dijk, & Wicherts, 2012) and that low reproducibility is not exclusively a problem of psychological research (Camerer et al., 2016; Errington et al., 2014).

---

The meta-analysis had a special category for glucose-rinsing studies:

> Glucose-rinsing studies examine the impact of simply rinsing one’s mouth with a glucose solution before exerting self-control (Hagger & Chatzisarantis, 2013; Lange & Eggert, 2014; Molden et al., 2012; Sanders, Shirk, Burgin, & Martin, 2012). Results from these studies suggest that the signal of glucose from the mouth to the brain is sufficient to neutralize the ego-depletion effect. This mechanism is consistent with the results of the ingestion manipulations but suggests that the effect does not depend on a metabolic explanation.

Here's the full table of studies included, which included an indicator column for whether the study was rinsing-only:

But there's no separate p-curve just for the rinsing studies. You can probably make one yourself though...

Actually I just did that with the 8 studies in the "yes" column:

Note that they've changed the test somewhat since that meta-analysis was published.

The meta-analysis did note that whether the rinsing studies were added or removed made no difference on the p-curve testing of the rest. And from my graph you can kinda see why: ignoring the 0% bins, the rinse group has roughly the same shape as the whole group.

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Tags: willpower
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# Question
Title: Name of the psychological condition for someone who creates dramas because they need it in their lives
I know someone who is very dramatic, sometimes I think they create dramas because they need it in their life, I’ve heard of other people describe the same thing, is there a name for this type of behaviour

# Answer
According to a recent (2016) paper that proposed seemingly the first specialized scale for measuring this trait (which they call NFD = need for drama):

> Clinicians have studied individuals who engage in clinically relevant dramatic behaviors and labeled them with borderline or histrionic personality disorders (BPD and HPD, respectively). Borderline personality disorder is defined by impulsivity, self-harming behaviors, chaos and instability in interpersonal relationships, and feelings of victimization; and HPD is defined by extreme sensitivity to criticism, excessive attention seeking, and need for approval from others.
>
> Whereas BPD and HPD offer a framework for understanding dramatic personalities, they may not be the most effective for examining dramatic personalities in samples that are not clinically relevant; and may not be suitable as predictors of work-related performance and counterproductive work behaviors (Guenole, 2014). A compound personality trait, such as NFD, is more suitable to assess individuals within work environments. Furthermore, whereas BPD and HPD have a troubled history as sex-biased diagnoses that may be unsuitably applied to organizational and social research questions, we hypothesize that NFD is prevalent equally in men and women in the population and that our measure of NFD is suitable for non-clinical research

Note that both HPD and BPD belong to the so-called "dramatic" cluster (B) of persnoality disorders. Also, there has been criticism of the HPD construct, particularly in that it overlaps BPD too much, but HPD was nonetheless kept in DSM-5... and this basically a decision of the board of trustees, which overruled their own working group that had agreed to the deletion of HPD. Also interesting is that an independent survey of personality disorder experts had found HPD the lowest validity (if we go by the "very valid" ranking) of all DSM-IV personality diagnoses, but nonetheless they saw it as valid enough to be kept.

Moving on to the new kid, NFD, its compound aspect refers to three subscales:

* Interpersonal manipulation (IPM)
* Impulsive outspokenness (IO)
* Persistent perceived victimhood (PPV)

And they correlated their NFD measure with the big 5 personality factors

and with a host of other scales, in particular a measure of the dark triad

The also found that there was no bias for either sex in the samples they used to validate their NFD scale. But they did not correlate with clinical scales for either BPD or HPD, leaving that for future research.

Time will tell if this NFD scale will see adoption by other researchers. If you want to use their terminology "high NFD individual" would be the scientifically sounding term, or maybe just 'high drama' individuals. Given their finding that men and women are equally prone to this... the received term "drama queen" seems somewhat inappropriate (sexist).
> 2 votes

# Answer
Generally this would be a histrionic personality type. More information can be found here.
> 0 votes

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Tags: behavior
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# Question
Title: How to detect which memory is being used when answering a yes or no question?
I am asking participants some questions on a form. I have to know which kind of memory they are using when answering these questions. I am having difficulty deciding this. Is there any special technique to determine this?

For example, consider these questions :

1. *Is your name Majid?* Is the memory used semantic or episodic? I know that most probably everyone would say semantic because there is no event being recalled, but I am not sure if remembering own's name is possible without recalling an event.
2. *Is your hair black?* This one is only available while thinking of a memory, but like the last one it could be semantic too.
3. *Do you know how to ride a bike?* This one could be semantic or episodic because I might recall an event of riding a bike and then answer. Or it could even be procedural memory as I might simulate riding a bike and then say, "Yes".

I am trying to figure out how do I assign each question one or more of the memory types?

I am using the memory types introduced by Squire in 2004. The picture is from *Fundamentals of Cognitive Neuroscience* by Bernard Baars.

# Answer
> 2 votes
**It depends** whether the answers are well known facts. If I know well my name, the color of my hair and whether I can ride a bike then semantic memory is used to answer these questions. If I have a doubt whether I can ride a bike, then I may use other types of memory like episodic or even procedural to come up with an answer.

Also, I may use episodic memory to answer a specific question today, but if I have to answer the same question tomorrow I will probably use semantic memory because it has become a general fact that is stored in semantic memory.

> Semantic memory reflects our knowledge of the world around us, hence the term 'general knowledge' is often used. It holds generic information that is more than likely acquired across various contexts and is used across different situations.

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Tags: memory, long-term-memory, semantic-memory, procedural-memory, episodic-memory
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# Question
Title: What was creativity called before the 1950s, i.e. before Guilford coined the term?
It is known that Guilford coined the term, but the concept is much older. What did people in Freud's time call it? Genius? innovation? Something else?

# Answer
> 2 votes
Let me open this by saying that it's not clear to me that Guilford coined the term, as the Google n-gram viewer shows use well before 1950:

Freud wrote an essay on creative writers (and day-dreaming) in 1908 but he does not talk of creativity as a noun/concept in itself at least in the English translation. Likewise Jung wrote a fair bit about the "creative impulse", but like in the case of Freud he doesn't seem much concerned how comes people are creative but just why they start to manifest it outwards as art. Another similar term Jung used was the "creative fire". At my level of understanding, the reason for this lack of concern in the psychoanalytic tradition is that they explained (away) the source of the creative process as the unconscious. And once they get to the unconscious as the ultimate explanation, all effort for further understanding what goes under that seems to stop, and the their efforts are directed at understanding the manifestations of the unconscious. It's a bit like saying that you can't understand God, but you can study his works. I'm probably exaggerating that, but part of the issue surely is methodological; Jung and Freud did not apply (or even outright rejected) a systematic scientific method.

The stated motivation of Guilford's work on creativity was that he thought the IQ tests were only good at discriminating elementary school performance, but not good for discriminating what he called "creative potential". In "Creativity: Yesterday, today, and tomorrow" Guilford credits Catharine Patrick with the first experimental studies of creativity; she wrote several papers from 1935 to 1941 with "Creative thought" in their title. Guilford says Patrick attempted to systematically test the anecdotal evidence of Graham Wallas (1926) related in his book titled "The art of thought". There doesn't seem to be an on-line record of Patrick's earliest (1935) paper on the topic. Her 1937 "Creative thought in Artists" and 1941 paper "Whole and Part Relationship in Creative Thought" are available on-line. Neither paper uses "creativity" as a term in their text, so in this narrow sense Guilford was the first to use the term in the nascent field.

# Answer
> 1 votes
The premise of this question is mistaken. As early as 1875, A W Ward referred to Shakespeare's "poetic creativity". (Source: Oxford English Dictionary, under "creativity"). That was eight decades before the 1950s and two decades before J P Guilford was born.

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Tags: terminology, creativity, history-of-psychology
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# Question
Title: 'Always Give a Reason Why' - How to describe this subject area?
I summarise http://rayedwards.com/always-give-a-reason-why/:

> In Dr. Robert Cialdini’s book, *Influence*, he cites a research study showing that simply adding the word “because” to a request multiplies the likelihood of compliance.
>
> Interestingly, the study seems to indicate that the legitimacy of the reasons supplied did not seem as important to the outcome as you might suppose. In fact, it seems hardly necessary to have a real reason at all.
>
> For example, you might ask to cut line at the post office, and be more likely to get a “yes” response from the person in front of you if you simply frame your question by saying something like, “Would it be possible for me to please cut a front of you in line, **because I’m really in a hurry**.”

I recognise the lack of substantiated evidence in the above quote, but I'm interested in learning about such empirically, scientifically proven behaviour and human psychology (eg through reputable peer-reviewed articles). To clarify, I seek not the hard data itself, but only conclusions and tips supported by credible evidence. I only chanced upon that above link, so to discover more in this area methodically and productively, what are some key words terming this subject? Where should I start?

I've no training in sciences, so I'd cherish answers and advice written in lay, simple, readable language.

# Answer
This particular study, sometimes called the "Xerox Experiment", was done by Ellen Langer, who studies "mindfullness", but that may not be what you are looking for. It is also cited on Wikipedia under Attitude Change - Heuristic Processing:

> For example, people are more likely to grant favors if reasons are provided. A study shows that when people said, "Excuse me, I have five pages to xerox. May I use the copier?” they received a positive response of 60%. The statement, “Excuse me, I have five pages to xerox. I am in a rush. May I use the copier?” produced a 95% success rate.

It is worth noting however, that a study published in the same year by Stanley Milgram (famous for his obedience experiments in the 60's), cited on Wikipedia under "Breaching Experiments", about people giving up their seats in the subway found a similar success rate when no reason was given, but a significantly lower compliance rate if a trivial reason was provided:

> the second condition, the trivial justification ... a much lower number gave up their seats.

A related field that a layman might find more accessible, is called "behavioural economics", and there is also a lot of overlap with "cognitive bias". Search YouTube for Dan Ariely, you'll learn lots of neat tips and tricks just like this one, backed by peer-reviewed studies, about how easily people can be manipulated.
> 6 votes

# Answer
Cialdini's book *Influence* is great, I wish I hadn't lost my copy of it...I always considered that to be a social psych book, so perhaps you should study social psychology if you have an interest in this sort of thing. You could also consider glancing at his Wikipedia page for more information about where his journal articles were published...this could provide some clues as to which journals/textbooks to look into.

Also note, the idea of adding the word "because" to a request is related to the idea of **pretexting,** which is studied by social engineers. While (I think) this isn't technically considered part of psychology, I would imagine that social engineering is considered relevant to cognitive science.

Disclaimer: I am not a professional psychologist, just an enthusiast.
> 3 votes

# Answer
Summary:

* Don't just give *any* reason. a certain type of "grating" reason (as explained in 2nd half of my post) has been shown to backfire and be worse than none.
* A syntactically correct but semantically (fairly) meaningless reason could be classified as a *peripheral route to persuasion*. In low stakes situations, a vacuous (but not grating) reason may work better than none, but as the stakes increase so does the scrutiny applied to the reason.

---

Let me start by elaborating on experiments mentioned by Arnon Weinberg (because I think some of the details are necessary before trying to conclude from the perspective of later works):

Actually Wikipedia doesn't detail the Xerox experiment well enough. The actual result was a bit more complicated: for small favors (in which the requester had fewer \[actually 5\] pages to copy than the recipient of the request \[who had 20\]) it made no difference whether the reason given was non-informative ("placebic") or real/plausible. But when the favor was "big" (the requester had more copies \[20\] to make than the recipient \[who had 5\]), the reason given did make a difference... and in fact giving a "placebic" reason was no better than no reason at all for big favors.

Also (contra to what Ana said) in the xerox experiment the reasons were terse, either bare request "Excuse me, I have 5 (20) pages. May I use the xerox machine?" or +"because I have to make copies" ("placebic") or +"because I'm in a rush" ("real"). I think that Cialdini’s logic for always giving a reason is that in this experiment giving a reason was not worse than giving none (in any scenario), but also keep in mind that "not worse" does not equal "always better"; giving a "placebic" reason for a big favor didn't work (but also didn't hurt).

I think that in the Milligram subway experiment the reason given was worse than "placebic" though. In the xerox experiment you cannot really refute the "placebic" reason "because I have to make copies" with respect to the use of the xerox (you can't \[easily\] make copies otherwise). So while it may sound weird it's not that grating (to me). On the other hand in the Milligram subway experiment, the reason was "I can't read my book standing up" which is something that most people can mentally refute as probably fake right away... But this is just me theorizing. It would be nice if someone redid one of the experiments with 4 arms for the argument given: none, implausible, neutral/repetition, and plausible.

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In the (very highly cited ~8K cites in GS, ~10x the Xerox experiment) "Elaboration Likelihood Model of Persuasion" of Petty and Cacioppo (1986), giving a "placebic" argument would probably be classified as a **peripheral route to persuasion**. They note (actually it's one of their "postulates") that

> As motivation and/or ability to process arguments is decreased, peripheral cues become relatively more important determinants of persuasion.

By peripheral cues they mean among other things repetition (Trump being a good recent example, heh), distraction etc. I guess a "placebic" reason counts as a form of distraction. But also note that in the Xerox experiment the placebic reason is also a form repetition "I need X because I need X", alhouth with a slightly different formulation for the 2nd X.

Petty and Cacioppo actually discuss the Xerox experiment of Langer on p. 159, remarking after summarizing it that

> Folkes (1985) provided a partial replication of this effect. In two field studies using the inconsequential request (making five copies), respondents were equally willing to comply whether the request containing the valid or the placebic reason. In a thind study, however, the subjects were asked to guess how they would respond to the requests and to "think carefully before answering". When instructed to think before responding, the valid reason produced significantly more anticipation of compliance than the placebic reason.

Furthermore!! Folkes pretty much did what I hoped someone would do, and also tested with an obnoxious reason:

> Although providing a partial replication of Langer et al.(1978), Folkes takes issue with Langer's assertion that the placebic information is processed "mindlessly". Folkes argues that if the reasons are processed automatically under low consequences conditions, then a poor reason should as effective as a valid one. However she found a that a poor reason (e.g. "because I don't want to wait") was significantly less effective than a valid or placebic one under low consequence conditions.

So the conclusion is: **don't just give *any* reason**!

I'm not sure from which book of Cialdini the give-any-reason advice came. If it's from his 1984 *Influence*, then that could not have covered research that was published (a year) later. Cialdini has a 2001 book with the same title but a different subtitle though; hopefully that's more up-to-date, but I haven't checked.

Here's the actual data from Folke:

All requests were small in the Falke experiments (4 or 5 pages to copy) and also took place at two different locations; her experiment 2 was in the UK, the rest in the US. In Falke's experiments 1-3, she attempted to directly replicate (the small favor) experiment of Lange but with varying questions. Only in experiment 4 were the subjects instructed to think carefully before deciding.

The reason why Falke calls the grating reasons "controllable" is based on the level of volitional control (of the requester) implied in the reason:

> Attribution research suggests that one distinction between good and bad excuses is in perceived controllability. An excuse can suggest one is compelled to perform an action or imply volitional control (Weiner, 1980). Lack of control mitigates responsibility for a transgression more than volitional control. Thus, when people ask favors for reasons they cannot control, their requests are more frequently complied with than when reasons for the requested favor are controllable (Barnes, Ickes, & Kidd, 1979; Weiner, 1980). In the copying machine paradigm, requests to go first because of controllable reasons (e.g., "because I don't want to wait") should be complied with less—they do not mitigate responsibility for needing the favor. When a person lacks control over the reason for wanting to go first (e.g., "because I feel really sick"), compliance should be greater.

Finally, Petty and Cacioppo also distinguish some personality factors affecting the result, in particular what they call "need for cognition". Individuals that rated higher on a self-reported measure for this factor had (objectively) more polarized attitudes on an argument than individuals who scored low on this measure.
> 2 votes

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Tags: cognitive-psychology, social-cognition, persuasion
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# Question
Title: Can the effectiveness of antidepressants be explained by a placebo effect?
A friend of mine showed me a paper (Kirsch, 2014) where the author claims that antidepressants work mostly through a placebo effect (backed up with relevant citations). Antidepressants are generally serotonin enhancers and their mechanism of action hinges on the premise that there is a chemical imbalance of serotonin in the brain. But not only do they not work significantly better than placebos, but also there are antidepressants that do not enhance serotonin but suppress it. There are some that do nothing to serotonin at all, but their therapeutic effects are all the same, according to Hirsch. So the effect is independent of the chemical composition. That means the chemical imbalance theory is wrong. Is my understanding, as a layperson, correct?

If all of this is legitimate, does that makes any sense to take medicines for an ADHD patient as well? I mean, does the placebo effect, if true, affect ADHD patients, too?

I fear that if people get to see this paper, they may misinterpret the results and may refuse to go to a psychiatrist and get treated even if they have legitimate issues. This is alarming, IMO.

**Reference**
**-** Kirsch, Antidepressants and the Placebo Effect, *Zeitschrift für Psychologie* (2014); 222(3): 128–134

# Answer
**Short answer**
Don't believe everything you read.

**Background**

* The article cited (Kirsch, 2014) appears in a German journal with a mediocre impact factor. Not the most convincing platform.
* I'll cite parts of the abstract, starting with

> But analyses of the published data and the unpublished data that were hidden by drug companies reveals that most (if not all) of the benefits are due to the placebo effect.

His reference list includes some 40+ references; if I type in "antidepressant AND serotonin" in Scopus (an established academic search engine I often use) I get 23k+ hits. With a bold statement like Hirsch makes, he might be skipping the literature proving him wrong.

> Some antidepressants increase serotonin levels, some decrease it, and some have no effect at all on serotonin. Nevertheless, they all show the same therapeutic benefit.

The new generation of antidepressants, the SNRIs, also have action on nor-epinephrine and may be more effective than the regular SSRIs. Serotonin may and likely is not the whole story. Depression is a complex disease with variable etiologies. Thinking it's all about serotonin is a bit short-sighted.

> Even the small statistical difference between antidepressants and placebos may be an enhanced placebo effect, due to the fact that most patients and doctors in clinical trials successfully break blind.

Oh come on - when you put forth such a line in the abstract that other researchers can't successfully perform a proper masked clinical trial, only testifies of a lack of proper data to back his \[flawed\] claims up.

> The serotonin theory is as close as any theory in the history of science to having been proved wrong.

This is a totally subjective thing to say. I don't care where it ranks in a ladder. Especially not in an abstract. Saying stuff like this only testifies he has nothing better to say in the abstract.

> Instead of curing depression, popular antidepressants may induce a biological vulnerability making people more likely to become depressed in the future.

This would need carefully planned prospective clinical studies to prove. Until this is addressed, he shouldn't be going down this path.

Lastly - Hirsch has been **criticized** proclaiming the same stuff since the 1990's, without changing the contents of his message. Perhaps he should stop theorizing and start experimenting to put his conspiracy theories to the test.

According to Klein (1998), Kirsch bases his claims on a flawed study (Kirsch & Sapirstein, 1998), where Kirsch claims that the substantial majority of drug effect is due to placebo effect and the rest is either measurement error or active placebo effect. Klein criticizes the article, because it was derived from a relative small group of unrepresentative, inconsistently and erroneously selected articles arbitrarily analyzed by an obscure, misleading effect size. Further, he identifies problems with the meta-analytic approach in general, such as the lack of attempts to further segment the placebo response. Lastly, he points to the lack of peer review and the opportunity provided by an electronic journal for rapid publication.

**References**
**-** Kirsch, *Zeitschrift für Psychologie* (2014); **222**(3): 128–34
**-** Kirsch & Sapirstein, *Prevention & Treatment* (1998); **1**: 0002a
**-** Klein, *Prevention & Treatment* (1998); **1**: 0006c
> 10 votes

# Answer
Let me supplement Alice's nice answer with a few more points. Regarding

> there are antidepressants that do not enhance serotonin but suppress it.

That seems to be tianeptine; it is often brought up such discussions as *the* counterexample to SSRIs being "real" anti-depressants. More recent research on tianeptine suggests it acts on the opioid receptors... and that's not a new line of antidepressant treatment, but rather an old one, potentially sharing the same addiction risks as other opioid-acting medications (e.g. painkillers).

Which brings us to the next point

> There are some that do nothing to serotonin at all, but their therapeutic effects are all the same, according to Hirsch.

Surely there are; bupropion is a more widely used (at the least in the US) anti-depressant that is not an obvious SSRI.

> So the effect is independent of the chemical composition. That means the chemical imbalance theory is wrong.

That's basically jumping to conclusions (and more than once). The effect is not *totally* independent of the chemical composition of the medication. An alternative conclusion is that depression, which is diagnosed based on a checklist of symptoms, is a heterogeneous disease with multiple causes producing somewhat similar symptoms (which, by the way, don't all have to be present to get a diagnostic).

Actually almost every individual neurotransmitter that is suspect to be involved in depression, including serotonin, but also catecholamines (norepinephrine and dopamine) have been subjected to experimental manipulation typically via dietary changes (in live humans). You can read more details in my answer on skeptics, but the main pattern seems to be that while we can't cause healthy individuals to get (majorly) depressed by lowering the aforementioned neurotransmitters, in previously depressed individuals (and to a lesser extent in their relatives) such interventions that lower these neurotransmitters do produce more significant mood changes; the most significant changes are seen in patients who are taking exactly the medication that the diet intervention counteracts. (see e.g. Kumar et al.).

Also current anti-depressants are only 30% to 60% effective (depending who reviews the evidence and more importantly whether substituting medications \[several times\] counts etc.)

So what to conclude from this? The most sensible conclusion to me is that not everything is understood about the neurochemistry of depression, but surely concluding that neurotransmitters are not involved is rubbish.

Almost every researcher who works in this field has some favorite hypothesis that explains better the current non-quite-satisfactory simple explanations based on one neutrotrasmitter or antoher, e.g. a 2008 review in *Nature* by Krishnan and Nestler said:

> It is now thought that acute increases in the amount of synaptic monoamines induced by antidepressants produce secondary neuroplastic changes that are on a longer timescale and involve transcriptional and translational changes that mediate molecular and cellular plasticity.

I doubt that's the ultimate word on the topic (all such narrative reviews have their biases when it comes to the less investigated aspects, no matter how prestigious the venue or the author), but it's clear that the "brighter bulbs" keep looking for more satisfying answers than the monoamine hypothesis (this what's called in the mass media "chemical imbalance"). I think any ultimately useful answer has to account for how the current antidepressants work... which is by acting on neurotransmitters, which in turn does alleviate depression (better than placebo) in some people but alas does not in quite a few others.

What Krishnan and Nestler favor is another fairly circulated notion (but not so much in the mass media!) that a final common pathway for depression exists. But alas, the case is far from being closed on that. Here are a few textbook paragraphs that contrast diabetes (another heterogeneous disease) with depression, which also gets to this final-common-pathway issue, as well as the difficulty in distinguishing cause from effect with individual neurotransmitter systems:

> Researchers have compared MDD \[major depressive disorder\] to other chronic, heterogeneous diseases such as diabetes mellitus (Krishnan & Nestler, 2008), which, like MDD, is projected to increase in prevalence in the coming decades. \[...\] Like depression, diabetes can present with a variety of symptoms, such as polyuria, polydipsia, polyphagia, as well as with cardiovascular, digestive, and nervous system dysfunction. Unlike MDD, however, these symptoms are a product of a known molecular basis of the disease: a deficit in the production or utilization of insulin. The involvement of insulin—due to the lack of the hormone or to failure of its intended signaling—represents a final common molecular pathway (FCMP) in diabetes that unites the involvement of disparate physiological systems. This FCMP has allowed researchers to begin to use powerful animal models to understand the symptoms, risk factors, and complications of this disorder. In addition, the identification of insulin and the pancreatic ß-cells involved in insulin production have led to dramatic improvements in the prevention and treatment of diabetes. At this point, however, an FCMP is absent in the study of MDD; presently, there is no neurobiological equivalent in depression of insulin from ß-cells.
>
> Over the past few decades, many molecular systems have been implicated in depression. \[...\] Because of the wide array of molecular systems that are disrupted in MDD, or in which disruption leads to depression, it has been difficult for researchers and clinicians to cleanly link molecular and behavioral systems. Investigators have noted limitations with all these single-system theories of MDD; indeed, to date, there is no known single molecule that is both necessary and sufficient to explain all the varied combinations of symptoms that can be present in individuals diagnosed with MDD. Genetic studies of MDD, too, have not been definitive in determining consistent risk loci, due to heterogeneity, environmental factors, and nosological limitations (Shyn & Hamilton, 2010). Even evidence of successful antidepressant action is not sufficient to demonstrate the primacy of the targetted molecular system in the pathophysiology of MDD. In fact, some researchers have argued that anomalies in traditional molecules implicated in the pathophysiology of MDD, like monoamines or glutamate, are unlikely to be at the etiological core of depression (Krishnan & Nestler, 2010). This difficulty disentangling the causal links between symptoms profiles and molecular systems has historically led to simplifications and misconceptions of the neurobiology of depression (Lacasse & Leo, 2005).
>
> A primary challenge for investigators is differentiating between molecules that are disrupted as a consequence of depression and molecules that, when disrupted, are involved in the etiology of MDD. Demonstrating that a particular molecule—for example, a metabolite of a neurotransmitter— is up- or down-regulated in MDD is not sufficient to claim that disruption in this molecule causes MDD. Even when molecules can be causally linked to depression, the heterogeneity of this disorder prevents researchers from linking that molecule to all forms of MDD. For example, showing that interferon alpha (IFN-) can cause MDD is not equivalent to proving that IFN- underlies all cases of the disorder. Indeed, whereas some molecular systems may be strongly associated with one particular domain of impairment (e.g., dopamine and deficits in motivation and behavior), the effects of other molecular systems, like norepinephrine, may be less specific. Adding to this complexity is the fact that MDD is a moderately heritable disorder (Levinson, 2009) in which preexisting vulnerabilities interact with stressful life events to increase risk for initial and recurrent depressive episodes in a manner similar to the kindling model of epileptogenesis (Kendler, Thornton, & Gardner, 2000). Moreover, different symptoms and symptom clusters in MDD are inherited at different rates. For example, sleep and appetite disruption have higher heritability estimates than does psychomotor retardation (Jang, Livesley, Taylor, Stein, & Moon, 2004).

Reproduced from Chen and Gotlib "Molecular Foundations of the Symptoms of Major Depressive Disorder" in *The Oxford Handbook of Molecular Psychology*, OUP 2015
> 2 votes

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Tags: depression, psychopharmacology, adhd, serotonin, placebo
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# Question
Title: Do "overview" sections increase learning outcome?
Suppose a math textbook contains an overview chapter for each part of the textbook. The intent of those overview chapters is to motivate and introduce the new mathematical concepts which will be discussed in the respective part of the textbook. For example, why do we need the mathematical concept? How did the concept evolve in history? What will be the content of the next chapters?

In this context, will the overview sections facilitate learning? How important are overview chapters in textbooks for the success of learning?

*Note:* I reasked this question on matheducators.stackexchange.com.

# Answer
> 2 votes
There is something called "advance organizer", that traces back to Ausubel (1960). It is some kind of overview, in which a short summary is given and (more important), in which the following topic is connected to prior knowledge (= Associations are being activated). In that sense it activates schemes, in order to assimiliate the new knoweldge to the old one or to accomodate/correct the prior knowledge. So, to be useful, advance organizers should have certain features:

* Connections between the following topic and prior knowlege
* Catch the attention of the student
* Be concret, insted of abstract

F.e. Before teaching equations the teacher could give the analogy of a scale.

From a scientific perspective it is known, that advance organizers can have supportive effects on learning and retention (see f.e. Luiten, Ames & Ackerson, 1980)

Luiten, J., Ames, W., & Ackerson, G. (1980). A meta-analysis of the effects of advance organizers on learning and retention. American Educational Research Journal, 17(2), 211-218.

# Answer
> 2 votes
Yes, an overview chapter helps for most people.

An overview chapters allows the reader to develop a stronger associative network, for instance this read:

> Sowa, J. F. (2006). Semantic networks. Encyclopedia of Cognitive Science.

Considering the importance that one is able to *connect the dots* while learning math, facilitating the development of the associative network is beneficial for learning. This effect is further elevated by visual learners.

I can suggest you these:

> Presmeg, N. C. (2006). Research on visualization in learning and teaching mathematics. Handbook of research on the psychology of mathematics education, 205-235.
>
> Gilbert, J. (2005). Visualization: A metacognitive skill in science and science education. Visualization in science education, 9-27.

For less visual learners, or those too lazy to appreciate the overview pages, I personally believe it will not reduce learning or provide any other harm for that matter.

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Tags: cognitive-psychology, learning, motivation, educational-psychology
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# Question
Title: Is there a case of multiple personalities that is not a disorder?
Is there a case of multiple personalities that is not a disorder? For some reason everything I found about "multiple personality" comes in a "disorder" form. Or is it a given that one mind can only have one personality?

Is there any information on cases where multiple personalities coexist in the mind of a single individual, without the adverse effects such as disassociation, memory loss or self harm, that is **not** the product of a trauma?

Note that I do not ask in the context of "social context" personality, but two distinct personalities that persist throughout different social settings. Also it might be worthy to note that even though they are vastly different in the way they perceive and react, there is no pronounced conflict or any adverse side effects as far as I can tell, if anything it appears to have a wide array of benefits.

# Answer
> 3 votes
Well, this is mostly a technicality (but then so is the DSM definition of any mental disorder). The DSM allows for a DDNOS; actually in DSM-5 that would be OSDD "Other Specified Dissociative Disorder" diagnosis:

> This category applies to presentations in which symptoms characteristic of a dissociative disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the full criteria for any of the disorders in the dissociative disorders diagnostic class. The other specified dissociative disorder category is used in situations in which the clinician chooses to communicate the specific reason that the presentation does not meet the criteria for any specific dissociative disorder. This is done by recording “other specified dissociative disorder” followed by the specific reason (e.g., “dissociative trance”). Examples of presentations that can be specified using the “other specified” designation include the following:
>
> 1. Chronic and recurrent syndromes of mixed dissociative symptoms: This category includes identity disturbance associated with less-than-marked discontinuities in sense of self and agency, or alterations of identity or episodes of possession in an individual who reports no dissociative amnesia.
>
> \[more types follow but are not relevant here\]

So OSDD type 1 would include any cases of multiple personalities/identities without dissociative amnesia, so in this (DSM) sense you can't have your cake and eat it, i.e. multiple personalities/identities would always be a disorder, albeit with not-so-obvious name, assuming the extent of these personalities/identities is sufficient to be deemed clinically relevant (by the diagnostician). For reference, the brief DID definition (without all the usual caveats of the full def such as not being caused by drugs or other medical conditions, but being clinically relevant in terms of distress/impairment etc.) is

> Dissociative identity disorder is characterized by a) the presence of two or more distinct personality states or an experience of possession and b) recurrent episodes of amnesia.

So clearly if (b) is dropped from DID resulting in OSDD type 1, we're left with what you're asking for (again as long as it's clinically relevant distress/impairment, not caused by drugs or other medical issues etc. These are common verbiage caveats added to most definitions of disordes in the DSM.) So then this is pretty much an issue what is clinically relevant distress/impairment so that a cluster of symptoims is a disorder. There is only one additional, unusual caveat added to DID in DSM-5 (and this would apply to OSDD as well):

> Note: In children, the symptoms are not better explained by imaginary playmates or other fantasy play.

On the topic of prevalence and presentation, a 2014 review notes

> Chronic complex DD \[dissociative disorders\] include dissociative identity disorder (DID) and the most common form of dissociative disorder not otherwise specified (DDNOS, type 1), now known as Other Specified Dissociative Disorders (OSDD, type 1).
>
> \[...\]
>
> The most common type of DDNOS, which has been replaced in the Diagnostic and Statistical Manual of Mental Disorders-5, called other specified dissociative disorder (OSDD), is typically found to be the most prevalent DD in general population and clinical studies with a prevalence rates up to 8.3% in the community reviewed in \[...\]. Across general population studies, the most severe DD, dissociative identity disorder (DID) has a prevalence of approximately 1% and has been found in .4 – 14% of psychiatric inpatients and outpatients, depending on the sample \[...\]. Most DDNOS/OSDD patients are similar in presenting symptoms, history, clinical course, and treatment response to DID patients, so DDNOS/OSDD is combined with DID here \[...\].
>
> Many clinicians and lay people believe that DID presents with dramatic, florid personality states with obvious state transitions (switching). These florid presentations are likely based on media stereotypes, but actually occur in only about 5% of DID patients \[...\]. The vast majority of DID patients have subtle presentations characterized by a mixture of dissociative and PTSD symptoms embedded with other symptoms such as posttraumatic depression, substance abuse, somatoform symptoms, eating disorders, personality disorders, and self-destructive and impulsive behaviors \[...\]. A classic presentation includes a history of multiple treatment providers, numerous serious suicide attempts resulting in repeated hospitalizations, and good medication trials typically with limited or no benefit \[...\].
>
> Although the media and public are often overly fascinated with DID dissociated self-states, the complex symptomatic presentation of DID receives more clinical attention from trained clinicians \[...\]. Under-recognition of DID is common because the most obvious and pressing aspect of a patient’s clinical presentation may be one of the many comorbid disorders (e.g., severe mood disorders, posttraumatic stress disorder \[PTSD\], eating disorder, substance abuse, BPD), or the pseudopsychotic symptoms related to the overlap and intrusions of self-states into consciousness. This overlapping influence of self-states causes “passive influence” phenomena or Schneiderian first rank symptoms, which are more common in DID than overt, obvious “switching” of states. DID patients experience more first rank symptoms than do individuals with schizophrenia, with the exception of thought broadcasting or audible thoughts \[...\]. Intrusions into consciousness may be partially excluded from consciousness (e.g., hearing voices of states, thought insertion/withdrawal, “made” actions/impulses) or fully excluded from consciousness (e.g., time loss, fugues, disremembered behaviors; \[...\].

So yeah, weirdly, the otherwise specified DDs are much more common than the "flagship" DID... and (thus) the transitions between personalities/identities are mostly non-abrupt.

And finally whether DDs can occur without trauma, the DSM-5 says yes, but also acknowledges that DDs commonly occur after trauma:

> The dissociative disorders are frequently found in the aftermath of trauma, and many of the symptoms, including embarrassment and confusion about the symptoms or a desire to hide them, are influenced by the proximity to trauma. In DSM-5, the dissociative disorders are placed next to, but are not part of, the trauma- and stressor-related disorders, reflecting the close relationship between these diagnostic classes.

And going back to the review for some empirical quantification:

> Epidemiological studies have found that mood, somatoform, anxiety disorders, and substance abuse are commonly associated with antecedent trauma, as well as PTSD \[...\]. These disorders are also common co-morbidities of patients with chronic complex DD \[...\]. For example, in a prospective treatment study of DID and dissociative disorder not otherwise specified (DDNOS) patients, 89% also had PTSD (n = 242), 83% had a mood disorder (n = 226), 50% had an anxiety disorder other than PTSD (n = 136), 30% had an eating disorder (n = 81), 22% had a substance abuse/dependence disorder (n = 61), and 22% had a somatoform disorder (n = 59).

But you have to keep in mind that a study like the last one is restricted to subjects who are seeking treatment, so they experience one or more distressing symptoms.

On the other hand, I'm guessing your question might have been motivated by a Vice article that has a similar title to your question, but which is mainly talking about the "multiplicity community" whose members are appanretly not distessed by their experiences. Likewise there's a "Plural Activism" movement, the mission statement of which is apparently

> Plural Activism will bring public awareness to the fact that multiples, no matter their origin, are able to live healthy, successful lives without integration.

So that goes back to what I was saying about psychiatrists (and their studies) mostly seeing people who are distressed. Quoting from Vice:

> The multiplicity community insists on being seen as healthy—even normal. This is our reality, they argue. Why are you imposing your reality onto us? Dissociative Identity Disorder (DID)—and its controversial precursor, Multiple Personality Disorder—are terms roundly rejected by the community, and most of them don't feel that they belong in the Diagnostic and Statistical Manual (DSM) at all. It's not that they don't believe people can suffer from DID (or, more broadly, Dissociative Disorder Not Otherwise Specified \[DDNOS\]). They just don't accept that they suffer from it. To them, all those with DID/DDNOS are multiple, but not all multiples are DID/DDNOS. Contrary to what a DID/DDNOS diagnosis implies, multiples want everyone in their system to be seen as people. Not fragments, alters, or personalities, but distinct individuals who happen to be inhabiting the same physical body.
>
> \[...\]
>
> "The multiplicity community's history with the MPD/DID/DDNOS labels is complicated, and full of contention," says Falah Liang \[an exponent of this community\]. "There's a lot of resentment towards psychiatry for pathologizing what is seen as simply a neurological difference like being left-handed, for painting multiplicity as freaks and invalids, and for pushing integration as a necessary 'cure' that all multiplicity must undergo." On the flip side, the anonymous psychologist I spoke to expressed mild resentment at the idea of healthy/empowered multiplicity distracting from people who actually need a DID diagnosis. "People with DID need to be recognized, as it's a genuine disorder," she said.
>
> \[...\]
>
> Dr. Max Krucoff, a neurosurgery resident at Duke University Medical Center, would be the first to acknowledge the potential slipperiness of DSM diagnoses. "Most medical diagnoses are defined by a pathophysiology—something identifiable, anatomic," he says. "Psychiatric diagnoses have no known underlying cause. I can't take a biopsy of somebody's brain and look at it under a microscope and say, 'You have Multiple Personality Disorder.'"
>
> Still, the controversial term "disorder," he says, is a means to an end: effective treatment for those who want and/or need it. "If people aren't hurting anybody or dangerous to anybody or asking for help, there's no reason to go looking for them and treating them," he says. "Everybody's on a spectrum, and what's considered a psychiatric illness is often evolving. If you feel like you're sick, if you feel like you need help, then doctors may be able to label you with a disorder only so they can figure out a good way to treat and help you."

And I was going to say that no academic publications have looked at this multiplicity community, but I'm glad to be proven wrong, there's a 2017 paper: "Multiplicity: An Explorative Interview Study on Personal Experiences of People with Multiple Selves" mostly exploring the on-line communities:

> Results: Multiplicity is discussed on Twitter, Tumblr, Google+ and several other personal websites, blogs, and forums maintained by multiples. According to the study's estimates, there are 200–300 individuals who participate in these forums and believe they are multiple. Based on the six interviews, it appears that multiples have several selves who are relatively independent of each other and constitute the personality's system. Each “resident person” or self, has their own unique behavioral pattern, which is triggered by different situations. However, multiples are a heterogeneous group in terms of their system organization, memory functions, and control over switching between selves.
>
> Conclusions: Multiplicity can be placed along a continuum between identity disturbance and dissociative identity disorder (DID), although most systems function relatively well in everyday life. Further research is needed to explore this phenomenon, especially in terms of the extent to which multiplicity can be regarded as a healthy way of coping.

And a few more details relating to antecedent trauma (or lack thereof),

> Typically, multiples use their unique terminology to refer to common experiences, for example, “system” (which is the term used to refer to themselves, i.e., a system of persons), “resident persons” (or “alters,” who are alternative personalities sharing the body), “fronting” (when one resident person takes control over the behavior in a particular moment or period of time) and “host” (the original personality, often the one who has been present from birth). \[...\]
>
> Most systems do not report amnesic barriers or recall traumatic events, and they insist that their multiplicity is something they were born with. Many of them call this healthy or a natural state of identity.
>
> Multiples are a heterogeneous group. According to their posts, their triggers, how they switch between resident persons and the way they organize real-life behaviors differ greatly from one system to another.
>
> A recurring topic on forums is the gender identity of multiples. Many multiples experience transgender issues and gender dysphoria because their residents have different genders and sexual preferences. There are many similarities between multiplicity and lesbian, gay, bisexual, transgender, and queer (LGBTQ) rights activism. Multiplicity uses many of the terms that the LGBTQ community uses, such as “coming out,” which means “revealing themselves” to the outside world as a multiple.

The first 3 vignettes (interviews) in the paper do involve antecedent trauma (two of them quite clearly) or report switching being somewhat stress-related. The 4th vignette is perhaps an example where trauma is not involved, but it does involve autism. The 5th vignette is perhaps the one with the least co-morbidity:

> “I'm the host. I'm agender, because I don't like to be identified by gender. We've decided, it's better that I talk because I've been here the whole time,” a 22-year-old female voice introduced herself. She lives in a small town with family and currently studies psychology in college. \[...\]
>
> The system started about seven years ago, when the body was 15 years old. “We are not traumagenic; it just happened,” she stated. “In the very beginning, there were only two people who argued. One day I woke up and felt as if someone was possessing me. First I thought that I was losing my mind. It was crazy.” Then, a couple of months later, another person switched in, but it did not communicate with her. A little later, someone else came in and established order. Then, more switched in. There are fairly original members, and there are other ones who gradually showed up.
>
> Her parents know about the system, but they have never met other members. “My mum asked me if I wanted to kill her,” she stated. Her teachers do not know about her system because she would never allow switching in the classroom. She talked to professionals, and they do not think it is a problem; they see it as a sort of help. Given that she has not had trauma or amnesia, they do not believe it is DID. She added, “It isn't interfering with my life now. On the contrary, it is helpful.”

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Tags: abnormal-psychology, personality
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# Question
Title: What is the best unobtrusive and objective method to measure mental workload?
What is the current research/industry standard on measuring mental workload using objective measurements (e.g. EEG, eye-tracking)?

Do you have any suggestions for specific tools and techniques? Are there combinations of physiological measurements one should consider?

# Answer
> 4 votes
There are different parameters you can use, but as the question is not clear what exactly you want to do , I think with EEG and Task Load Index (TLI) you are good to go.

> The Task load index (TLI) is the so called engagement-index and is defined by two formulas, TLI1 and TLI2. However, these indices were calculated as follows:
>
> where Pθ and Pα denote the theta- and alpha-band power, respectively. Pθ,Fz and Pθ,AFz are the theta activities of Fz and AFz electrodes respectively. The θ (theta) activity was calculated by averaging the power spectrum of the θ frequency range (4-7.5 Hz). Similarly, Pα,Pz and Pα,CPzPOz are the α (alpha) activities of Pz and the pool of CPz and POz electrodes, respectively. The α activity was calculated by averaging the power spectrum of the α frequency range (8- 12.5)

This section is exactly quoted from this paper.

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Tags: measurement, methodology, workload
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