# Question
Title: How can I run a placebo medication pills study? Practical advice needed
I am a lab manager looking to design a placebo experiment in a behavioral lab with a medical doctor. I believe our study needs to be credible and professional. I'd appreciate any recommendations on details of placebo manufacturer or retailer, type of pill bottle to use, how to create brochures of information about the purported effect of the placebo pill. Info on points of methodology is also appreciated.

# Answer
> 3 votes
Ethical procedures are specific to your country and even differ between universities and sometimes even per department. Of course you know everything about the Declaration of Helsinki, being immersed in the city of its origins (you seem to (have) be(en) affiliated to the University of Helsinki). You seem to be located in NY now, but I'm unsure to your affiliation. So I started wandering on the sites of the uni of Helsinki and the New York University for some information. But note you should look into the local requirements yourself (although your study has likely long since started :-)

First, you need to find out the **IRB** (or here for NY) you will be dealing with, often operating under a university, or affiliated hospital. These folks can tell you anything you need to know. Here is a site of the IRB with all the specifics you need to submit an IRB proposal to NY Uni. Note that the best thing is for specifics such as pill bottles and placebos is to talk to the IRB, or try to find investigators that have done such a thing recently in your neighborhood. For example, there's a study from Segal *et al* (2017):

**Randomised, double-blind, *placebo-controlled trial* with azithromycin selects for anti-inflammatory microbial metabolites in the emphysematous lung**,

that was conducted by the New York University School of Medicine and by the looks of it it is exactly the thing you are planning to do. These guys can likely help you out, and reading the papers and related ones may help you as well. For example the linked paper says in the Methods:

> Both placebo and AZM were prepared in an opaque capsule by the NYU pharmacy...

Hence, the NYU pharmacy, apparently, assists in these kinds of matters - the place to go!

<sub>**Reference**
**-** Segal *et al*., *Thorax* (2017); **72** :13-22</sub>

# Answer
> -1 votes
This might seem a bit random at the moment, but if you run a 15 minutes personality test on a placebo group you'll be to have a better understanding how it works, so it might help with the methodology and overall conclusion.It might also help the process: a person is likely to cooperate if they believe that you genuinely care. Doing and analyzing test for each subject might come handy for gaining that trust.

I strongly believe that people who have trust in authority are likely to be treated successfully with the placebo. Just like faith healing, but 'modern' one. (No data to back it up, unfortunately.)

---
Tags: reference-request, experiment-design, behavioral-economics, placebo
---


# Question
Title: I want to find event1 in my EEG data, followed by event2 and then extract reaction time between them
```
for i=1:length(subjects)
    EEG = pop_loadset([sub_name{i},'.set'],folder);
    for k = 1:length(EEG.event)-1
        disp(k);
        if strcmp(EEG.event(k).type,con1)
            k = k+1;
            if strcmp(EEG.event(k+1).type,con2)
                rt = EEG.event(k+1).latency-EEG.event(k).latency;
            end
        end
    end
end

```

# Answer
> 1 votes
I'm guessing you are using Matlab. Your code is mainly sound, but a few comments:

* don't use "i" or "j" as they are function names in Matlab.
* don't change the value of a for loop variable inside the loop.

Here is you code, corrected:

```
for sub=1:length(subjects)
    EEG = pop_loadset([sub_name{sub},'.set'],folder);
    trial = 0;
    for eve = 1:length(EEG.event)
        if strcmp(EEG.event(trial).type,con1)
            trial = trial+1;
            trialonset(trial) = EEG.event(trial).latency;
        elseif strcmp(EEG.event(trial).type,con2)
            trialoffset(trial) = EEG.event(trial).latency;
        end
    end
    rtlist{sub} = trialoffset-trialonset;
end

```

---
Tags: eeg, reaction-time
---


# Question
Title: How do we imagine? How do images have qualia?
After reading a bit about qualia and hard problem of consiousness, I came up to theoretical solution. The reason why we have this problem is because we can imagine. We can imagine an object visible to us as red being green, for example. Green fire. Even if we never saw it in the reality.

But how do we imagine? How do those images have properties named by people as qualia? I can imagine a blue cube or a red cube, or a red sphere, and visual periphery is not involved here, I can do it with closed eyes.

What parts of our brain are responsible for imagination? How does the brain "give" qualia (form, color, smell, etc.) to images? What differs in my brain when I imagine a red cube from when I imagine a blue cube? And are qualia stored in our memory?

# Answer
This is hardly settled science, but one hypothesis with some empirical support is that

> Visual mental imagery and perception share similar cortical representations (Cichy et al., 2012; Kosslyn, 2005; Pylyshyn, 2003). It has been proposed that, **while brain forward connections convey information from the outside world, backward connections might have a dominant role during the forming of mental images in the absence of external bottom-up inputs** (Ganis and Schendan, 2008; Ishai et al., 2000; Kalkstein et al., 2011; Kosslyn, 2005).

For more theoretical speculation on the neural basis of qualia you could read Orpwood (2017), although by his own admittance, his ideas (at least in the past) were not terribly clearly presented. He does discuss a theoretical example of olfactory qualia. (I'm mentioning this because you said in the comments that you want to go beyond visual ones.)

Also note that some neuroscientists think the problem of qualia is ill-posed, in that it is intrinsically dualist:

> Typically, qualia are defined by four characteristics. Qualia are private, meaning they cannot be known unless they are experienced through the first-person perspective. Qualia are intrinsic, which indicates that they are self-sufficient and independent of other items in experience. Qualia are also ineffable, signifying that the experience of qualia cannot be sufficiently conveyed through words alone. Finally, qualia are immediately accessible through consciousness, which means that knowledge of qualia is direct and certain, as opposed to knowledge of the physical world, which is indirect and logically deduced. \[...\]
>
> This definition, unfortunately, leads us down a murky path towards dualism, a philosophical position which asserts that there are two kinds of real substances: the physical substance out of which the universe is composed, and the non-physical substance out of which the mind is composed.

Since you asked in the past about the private conceptions of word meanings (as a barrier to common sense), that kinda has the same problem.

If we just stick to qualia as brain processes/representation, regarding pain-related words, for example

> Language is more than a mere medium when it comes to share our pain experiences. In fact, it has been shown that processing pain-related words is associated with enhanced activation of part of the neural circuitry underlying physical pain experiences. \[citing four references in support\]
>
> * Richter M, Eck J, Straube T, Miltner WH, Weiss T. Do words hurt? Brain activation during the processing of pain-related words. Pain. 2010 Feb;148(2):198–205. pmid:19846255
> * Richter M, Schroeter C, Puensch T, Straube T, Hecht H, Ritter A, et al. Pain-related and negative semantic priming enhances perceived pain intensity. Pain Res Manag. 2014 Mar-Apr;19(2):69–74. pmid:24716197
> * Gu X, Han S. Neural substrates underlying evaluation of pain in actions depicted in words. Behav Brain Res. 2007 Aug 6;181:218–23. pmid:17512615
> * Osaka N, Osaka M, Morishita M, Kondo H, Fukuyama H. A word expressing affective pain activates the anterior cingulate cortex in the human brain: an fMRI study. Behav Brain Res. 2004 Aug 12;153:123–127. pmid:15219713

I think this is somewhat analogous to the issue of V1 involvement in visual imagery.
> 3 votes

---
Tags: neuroscience, memory, philosophy-of-mind, qualia
---


# Question
Title: Body temperature increasing when trying to solve difficult problems
\[ *I am unsure if this is the correct site to ask this question* \]
I am a HS student, currently studying IT and personally I focus on the field of software (programming) and of course where there is programming there are problems which require you to have the skills to solve problems that occur. So I wanted to improve my skills by trying to solve problems and I've been doing some on hackerrank.

However, whenever i try to solve a problem which is difficult to me and that I'm not capable of understanding it, I begin "*overheating*", literally. This keeps me from taking further steps to learn about the problems and different ways to approach to the solution. Basically, I feel like a moron and stop working on the problem.

**my question to you is, why do I "overheat" (body temp. increases) when i try to solve problems that are difficult to me?**

is it because I don't have a goal which motivates me hard enough or am I just... a moron ?
Is there are way to "turn off" this overwhelming feeling?

EDIT :

After some more research i've come across this article which I believe could be the answer to my question (not sure).

# Answer
The "overheat" (flushing of the skin) you experience is a common-enough reaction to stress, part of the fight-or-flight response. It's not uncommon for people to experince it during exams; generally exam/test axniety is related to both internal and external factors (or perception thereof)

> Self-esteem was a significant and strong predictor of test anxiety. Perceived difficulty of the test and the high-stakes nature or consequences of the test was also related to higher test anxiety.

It's beyond the scope of this site to suggest individualized treatments, but generally you may want to read about anxiety disorders and panic attacks, more specifically.

Although there are vast amounts of academic publications about the measurement and the effects of test anxiety, the amount of publications trying to assess coping strategies appears a lot more limited. E.g. I found a small study about relaxation techniques, Larson and Rose (2011), which found them effective on reducing the anxiety, but ultimately having no impact on test resuts.

Although I usually recommend Wikipedia as a good first read on many topics, their article on test anxiety is pretty bad, especially in the treatment section, with a heavy emphasis on medication... almost entirely sourced from a poor-quality site. That's in sharp contrast for instance with NHS' take on the matter, which makes virtually no mention of medication. Even the (US) Mayo clinic for instance doesn't place much emphasis on medication for test anxiety.

And what I discovered in the last two paragraphs turns out is also reflect in others' conclusions e.g. UCLA's Center for Mental Health in Schools:

> In a 2013 review, von der Embse, Barterian, and Segool (2013) concluded that “there are few studies that have examined test-anxiety interventions with elementary and secondary school students. However, techniques including biofeedback, behavior therapy, cognitive behavioral therapy, priming competency, and mixed approaches have demonstrated promising results.” While medication also is discussed, it is not the preferred treatment and, if prescribed, is to be used in conjunction with psychological interventions (Tracy, 2012).

Alas this UCLA source/quote is focused on pre-university education and tests. However the paper of von der Embse pointed to an older meta-analysis that didn't have this narrower focus, Eregne (2003), which concluded that

> The treatment of test anxiety has been quite successful in reducing the test anxiety level of clients. The most effective treatments appear to be those that combine skill-focussed approaches with behaviour or cognitive approaches. Individually conducted programs, along with programs that combined individual and group counselling formats, produced the greatest changes.

And this older paper (whose primary studies were almost exclusively aimed at university students) has a fairly detailed assessment of the effectiveness of various types of interventions (although I personally wonder if there was enough statistical power for each kind to draw such definitive conclusions):

> Test anxiety reduction groups was categorized into 21 different interventions. The observed differences among these interventions were significant. Type of the intervention was related to the effectiveness of the intervention. Behavioural treatments included systematic desensitization, relaxation training, anxiety management training, hypnosis and other behavioural treatments such as modelling and extinction. Systematic desensitization and other behavioural techniques were found to be effective, E+ = 0.90 and E+ = 1.01 respectively. Relaxation training alone and hypnotherapy were moderately effective, E+ = 0.50 and E+ = 0.52 respectively. Although Hembree’s (1988) meta-analytic study supported the effectiveness of relaxation training, this finding has been contradicted in the literature. Among cognitive therapies, cognitive restructuring produced the largest effect size (E+ = 1.11). However, rational-emotive therapy and other cognitive techniques produced moderate effect sizes, E+ = 0.54 and E+ = 0.48 respectively. These findings are also consistent with previous studies (DiTomasso, 1980; O’Bryan, 1986; Thompson, 1987). These interventions may be effective on the emotionality and ‘worry’ components of the test anxiety construct as proposed by Spielberger and Vagg (1995). The result of this meta-analysis indicate that effectiveness of cognitive therapies increased when they were combined with skill-focussed techniques. This finding is consistent with O’Bryan’s (1986) metaanalytic study. Clients may increase their sense of readiness and their confidence level by learning different study and test taking skills. Cognitive behavioural interventions were found to be small to moderately effective in reducing test anxiety. This contradicts the findings of the studies conducted by DiTomasso (1980) and Gambles (1994). Study skills training alone had a small effect size (E+ = 0.28). This indicates that test anxiety cannot be explained by a learning deficit model which indicates the lack of effective study skills and test taking skills. While cognitive and behavioural treatment techniques focus on relieving symptoms of test anxiety that interfere with an individual’s ability to perform well or be comfortable in testing situations, other researchers have conceptualized test anxiety as a result of a deficit of knowledge, training, ability to study, or test-taking skills. These theorists suggest that improving an individual’s skills in these areas will result in improved performance and comfort. Results of this meta-analysis indicate that this may not necessarily be the case. Study skills training when measured by test anxiety show only small and moderate effect sizes (E+ = 0.28, E+ = 0.43, E+ = 0.45). These results indicate that subjects treated with study skills training have only moderate improvement when compared with individuals who receive no treatment. However, a trend is indicated for significant improvement when study skills training is combined with cognitive or behavioural interventions. One of the significant findings of this study is that effectiveness of behavioural or cognitive interventions is increased whenever they are combined with study skills training. Although a number of interventions have been suggested and tested in test anxiety reduction, an integrated approach, utilizing various strategies in combination, is likely have special value. Such a combined program might include such components as: (1) applicable information about studying and test taking skills; (2) opportunity to observe someone take tests, or test-like problems; (3) increasing self-monitoring and practice self-control especially of behaviour and thought in test-taking situations; (4) practice in attending to the task in hand, attentional training and (5) learning how to relax under test specific conditions. Modality. The test anxiety reduction programs which were done with groups and individuals together produced larger effect sizes (E+ = 0.84); second, the group format had an effect size of (E+ = 0.67). The individual format had the smallest effect size (E+ = 0.34). Most of the intervention programs (83 percent) were conducted in the group format. It is highly likely that clients in groups can get other students’ perceptions and get alternative solutions to their problems. They may see that they are not the only person who has problems related to test anxiety; they may gain therapeutic benefit in group formats and easily transfer it into their daily lives.

Also his ("E+") measure of effect size is based on Hunter and Schmidt (1990) methodology, which itself has been criticized by some for allegedly inflating effect sizes.
> 3 votes

---
Tags: neuroscience, brain-training, problem-solving, brain-development
---


# Question
Title: How does caffeine work as an analgesic adjuvant?
Caffeine is used an adjuvant in over-the-couner pain medication, e.g. added to paracetamol and/or aspirin.

A brief look at the Wikipedia page on caffeine doesn't indicate any analgesic effect of caffeine itself. So, what mechanism/pathway allows it to attain this adjuvant effect for pain relief?

# Answer
Zhang (2001) reports that the analgesic activity of caffeine is due to

* a blockade of peripheral pro-nociceptive actions of adenosine;
* the activation of the central noradenosine, pain-suppressing pathways;
* stimulation of the central nervous system with subsequent actions on pain perception;
* inhibition of PG (prostaglandine) E2 synthesis, just like the primary mechanism of paracetamol and caffeine by blocking the COX enzyme;
* disinhibition of inhibitory adenosine actions on central cholinergic nerve terminals, leading to increased acetylcholine release and activation of cholinergic mechanisms involved in analgesia;
* lastly, caffeine-induced changes in mood may help in in pain relief.

Concerning the direct COX inhibitory action (which highly surprised me, personally) - Aspirin-like drugs act on the catalytic site of the COX enzyme. Paracetamol is believed to act at a different site, such as the peroxidation site of COX, while caffeine may block synthesis of the COX-2 protein, probably at the transcriptional level,thereby leading to enhanced COX-2 inhibition. Caffeine is a nonselective antagonist of adenosine A1 and A2 receptors. Adenosine A2a receptors induce intracellular signalling events that cause an upregulation of the COX-2 gene and the release of PGE2 in rat microglia, which is antagonized by caffeine.

Tavares & Sakata (2012) also provide an interesting review on the analgesic effects of caffeine, without it being used in conjunction with other medications.

**References**
**-** Tavares & Sakata, *Rev Bras Anestesiol* (2012); **62**(3): 387-401
**-** Zhang, *Drug Safety* (2001); **24**(15): 1127–42
> 3 votes

---
Tags: neurophysiology, psychopharmacology, pain
---


# Question
Title: What is an empirical proof that two concepts are not independent/orthogonal?
Given there are two psychological concepts A and B that are considered to be independent/orthogonal.

Would the following empirical results proof the opposite? If not why?

In the first experiment A is the independent variable with two conditions: high and low A. B is identically induced in both conditions and measured as the dependent variable. In the high A condition high B is measured. In the low A condition low B is measured. The second experiment is analog to the first one, except with A and B reversed: in the high B condition high A is measured, and in the low B condition low A is measured.

References to papers that use similiar arguments would be very helpful.

# Answer
> 2 votes
Since the data show a two-way dependence (low A -\> low B, hi A -\> hi B and the reverse) this would prove the variables are not independent, as

> Linearly independent, orthogonal, and uncorrelated are three terms used to indicate lack of relationship between variables.

<sub>**Reference**
**-** Rodgers *et al.*, The American Statistician (1984); **38**(2): 133-4</sub>

---
Tags: terminology, experimental-psychology, experiment-design
---


# Question
Title: Are people who believe they are of average intelligence mentally ill?
A psychology professor of mine said that anyone who believes themselves to be of only average intelligence is likely suffering from depression or another mental illness that impacts their self-esteem. Is there any source that would corroborate this claim?

# Answer
Studies show that the overestimation of one's intelligence is both gender and culture/country dependent.

I don't know of any studies which tried to relate the over/under-estimation of one's intelligence (in measurable terms, rather than generic statements like "I'm stupid") to depression.

There is one recent (2017) study in older adults that found a self-reported measure of cognitive abilities to be a stronger predictor of (Big Five) personality than of actual cognitive abilities. Fairly predictably, the correlations were with Extraversion (positively), Openness to Experience (positively) and Neuroticism (negatively). Although not reporting it in its abstract, a slightly older (2012) study, Jacobs et al. also found a (negative) correlation between neuroticism and self-reported fluid IQ (but not for two other kinds: visual and comprehension-knowledge).

As it's fairly well known, neuroticism predicts depression (and anxiety).

Personality traits also correlate with each other though, and the estimate of one's IQ also correlates with the measured IQ. So, Jacobs et al. also regressed the relationship between self-estimated and measured IQ on the personality traits that looked promising. And alas in this model, Neuroticism failed to predict anything in addition what extraversion and agreeableness did (that probably explains why Neuroticism is not mentioned in their abstract.)

In their discussion section, Jacobs et al. chalk this off to their sample having a fairly restricted range of IQ.
> 4 votes

---
Tags: reference-request, confidence
---


# Question
Title: How can two-way dependencies in factorial designs be interpreted?
**Scenario:** Given there are results from two factorial experiments that show a two-way dependency between two variables A and B.

**Details:** In the first experiment A is the independent variable with two conditions: high and low A. B is identically induced in both conditions and measured as the dependent variable. In the high A condition, high B is measured. In the low A condition, low B is measured. The second experiment is analog to the first one, except with A and B reversed: in the high B condition high A is measured, and in the low B condition low A is measured.

**Question:** What can be reasoned or assumed about the relationship between the two variables A and B, and why?

References to example papers would be excellent.

# Answer
> 1 votes
In the full-generality land of arbitrary A and B, the 'details' section of the question gives the grand total of all the conclusions that can be drawn here. What you have is that when A was fixed to be high, B was observed to be high, when B was fixed to be high, A was observed to be high etc etc, and this is the complete total of things you know about A and B. Full-generality land is super harsh. You can observe an arbitrarily large number of points falling on an exact line and full-generality land will insist that the true function might bounce around like a roller-coaster that just happens to pass through the points you've observed. Full generality-land doesn't have to make sense. In full-generality land, fixing A at 0.1 units higher than you did in this experiment might cause the value of B to plummet, or turn into a turkey dinner.

Reality tends to make a lot more sense than full-generality land, except when brains or quantum particles are involved. Some things you might know in reality:

The units A and B are measured in.

Whether A and B are smoothly-varying or can contain discontinuities.

Whether A or B have ceiling/floor caps, and maybe where they are.

Whether the 'fixing' intervention is likely to be monotonic in its effects on A, B, or both (this is a big one, and it's quite likely that you do know this).

The 'causal depth' you plausibly care about (A and B are both caused by X might be interesting, that A and B are both products of the big bang probably not, how far you want to ride that train is domain specific)

That some particular theory of A and B is incompatible with A and B being high simultaneously.

All these things would give you some traction to move beyond the bare-bones statement of the exact results you observed, which is all full-generality land will let you do. Full generality land won't even let you claim that you'd get the same results from the exact same experiment performed tomorrow. Full-generality land has the attitude normally associated with honey badgers.

There's definitely a version of your argument that makes sense. If you have five blind people arguing over whether an elephant is a snake or a wall or a bit of rope, firing a starter's pistol so the elephant runs away is an excellent experiment. Under the theory that an elephant is five different things it is vanishingly unlikely that they will all run in exactly the same direction. Observing that they do all go in the same direction at the same speed should cause the blind scientists to propose a bunch of strongly-connected elephant theories. Only this argument is inductive not deductive, so it requires you to supply a hypothesis space. It's always possible that there were five animals who all ran in the same direction, to make the inductive argument it's critical to guess how likely that scenario is. If you do the experiment in a narrow valley there might acutally only be one direction it's possible to run in. If you do the experiment out in the open plain there's 360 degrees of freedom and coincidences are much more inductively compelling. In the real world, you almost always have some information about the landscape, making results of the kind decribed here strong ones. But you stripped all of that information out to ask the question! Reducing the variables to A and B brings you into full-generality land, where nothing is certain. Maybe you are standing in a narrow valley. Maybe you're underwater. Who knows?

It is possible to operate in full-generality land despite its Dadist tendencies, sometimes you can get away with some impressively weak assumptions. Try these:

Dunn, J. C., & James, R. N. (2003). Signed difference analysis: Theory and application. Journal of Mathematical Psychology, 47(4), 389-416.

Pearl, J (2014). Probabilistic reasoning in intelligent systems: networks of plausible inference.

---
Tags: experimental-psychology, experiment-design
---


# Question
Title: Which personality test has a name that sounds like "Max C?"
I was listening to a podcast about personality tests and I heard someone mention a test that phonetically sounded like it was called "Max C." Looking this up yields no answers. I've also tried a few similar-sounding words, but no dice. Does anyone know of which test this is and what its *actual* name is?

# Answer
> 1 votes
Could be "\[maximum\] Conscientiousness," one of the core traits in the Big Five \[personality index\]. The Big Five traits are the best-known personality models in modern academic psychology, and frequently referred to by their initials (O C E A N).

> https://en.wikipedia.org/wiki/Conscientiousness

---
Tags: personality, test
---


# Question
Title: Does the subconscious mind communicate its analysis through emotions?
I'm reading this article by Marianne Cantwell, in the middle of the article, she quotes Jonah Lehrer's book *How We Decide*:

> “When a person is drawn to a specific item on the menu or a particular romantic prospect, the mind is trying to tell him that he should choose that option.
>
> It has already assessed the alternatives – this analysis takes place outside of conscious awareness – and converted that assessment into positive emotion.
>
> The world is full of things and it is our feelings that help us choose among them.”

How correct is this statement from the perspective of psychology and neuroscience?

# Answer
First, there's not complete agreement in psychology nor neuroscience: you can find support for most any imaginable position. But in terms of the consensus of recent peer-reviewed work, here are some thoughts.

> “When a person is drawn to a specific item on the menu or a particular romantic prospect, the mind is trying to tell him that he should choose that option."

There's a false dichotomy here between a person's motivation and some external (?) agent called "the mind". Thoughts, feelings, and behaviors emerge from biological and cognitive processes, and if you dig into those operations there is no level that reveals a separate agent. See this link for a related theory called the Homunculus https://en.wikipedia.org/wiki/Homunculus#Terminological\_use\_in\_modern\_science , or chapter 2 of the book, *Waking Up* by Sam Harris, for a deeper dive into agentic selves in the brain.

> "It has already assessed the alternatives – this analysis takes place outside of conscious awareness – and converted that assessment into positive emotion."

There were early reports of complex weighing of alternatives by unconscious minds by Dijksterhuis and others, but the higher-quality recent replication attempts suggest these claims were overblown. The unconscious mind may or may not be able to do basic arithmetic. That's the current level: nothing so fancy as suggested here. Recent coverage of this replication: https://retractionwatch.com/2017/05/08/can-math-unconsciously-replicators-prominent-2012-study-doubts/

> "The world is full of things and it is our feelings that help us choose among them.”

This is true, but is already well known. Feelings, thoughts, and motivations operate together to urge our organisms towards desired outcomes and away from unwanted outcomes. Here's an article that goes into more depth on how the body (including our mind) pursues desired states: https://www.tandfonline.com/doi/pdf/10.1080/00332747.1955.11022996
> 5 votes

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Tags: emotion, decision-making
---


# Question
Title: What does "they tend within and between classes" mean in 'The Irreducible Mind'?
I am a philosophy student but I'm also interested in philosophy of mind, a field that overlaps issues in psychology and neuroscience these days. This passage is taken from a similar multidisciplinary book but this particular passage is mentioning various neuroimaging techniques. I have difficulty understanding what is meant by the embolden phrase. I am not sure whether "within and between" has a technical or simply a semantic/grammatical significance. In either case I remain confused. And hence I was not sure which site if at all is appropriate for asking clarification.

Within page 17 of the book *Irreducible Mind: Toward a Psychology for the 21st Century* by Kelly, et al. (2007), it says...

> The third development was the advent and maturation of the functional neuroimaging technologies mentioned in the Introduction, which enable us to observe directly, without opening up the skull , the activity of the working human brain. Two principal classes of such methods are currently available, although others are under development.12 The first provides measures of the electric and magnetic fields directly generated by neuroelectric activity in populations of suitably located and oriented cortical neurons (electroencephalography \[EEG\]; magnetoencephalography \[MEG\]). The second provides measures of hemodynamic or metabolic consequences of neural activity such as local changes of blood flow, glucose consumption, or blood oxygenation (especially positron emission tomography \[PET\]; and functional magnetic resonance imaging \[fMRI\]). All these technologies are complex and expensive, and **they tend within and between classes to have complementary strengths and weaknesses** (see, e.g., Nunez & Silberstein, 2000; Toga & Mazziotta, 1996; Wikswo, Gevins, & Williamson, 1993). Together, they undoubtedly constitute a major methodological advance for cognitive neuroscience. Indeed, scarcely an issue now goes by of any cognitive neuroscience journal that does not contain one or more papers featuring images outfitted with colored spots identifying regions of "significant" brain "activation" produced by some stimulus or task.13

I first posted the passage to esl and english.se but the answers I got were not definitive.

An answerer on esl.se told me it may have to do with within-subject and between-subject experiment methods or convey a similar meaning.

On english.se I was told it could simply be the common phrasal verb "tend to" with "within and between" breaking it up as a parenthetical clause with commas missed. That is it can be rewritten as "they tend, within and between classes, to have..."

In either case I don't know what "classes" the author is talking about. Are these classes of the imaging devices he enumerates? This latter question could be quite technical. Still excuse me if this was not the right question for this site.

## References

Kelly, E. F., Kelly, E. W., Crabtree, A., Gauld, A., & Grosso, M. (2007). *Irreducible mind: Toward a psychology for the 21st century*. Plymouth, UK: Rowman & Littlefield.

# Answer
This is kinda unclear so I'm not sure my reading is the correct one. But for me the two classes are the electric/magnetic class of imaging techniques and the hemodynamic/metabolic class of imaging techniques, and each class has multiple methods within it. It's a world that looks like this: {\[EEG,MEG\],\[PET,fMRI\]}. Within a single class, the multiple methods have complementary strengths and weaknesses, at the same time, the two classes have complementary strengths and weaknesses relative to each other. Within a class, you can be looking at the same type of information but have different trade-offs in terms of temporal and spatial resolution, or image quality and expense, depending on the method. Between classes, you're looking at fundamentally different types of information, so you get a different (complementary) picture of the brain's activity.
Squashing both of those contrasts down into one sentence, you have "they tend within and between classes to have complementary strengths and weaknesses"

Probably.
> 2 votes

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Tags: neuroscience, neuroimaging
---


title: Nature vs. Nurture

text:
# Question
Title: Nature vs. Nurture
In the following I have 4 questions which I think are too interleaved to separate into 4 different posts. I hope it's not a duplicate, but I didn't find here similar posts.

My understanding (as a layman, based on few non-professional books and some googling) is that the current "state of the art" regrading the age-old question in the title, is essentially as following:

For pretty much any reliable measurement researchers could come up with (in relation to cognitive capabilities, personality traits, interests, confidence, success, etc), 100% of the variance could be attributed to heredity and nonshared-environment (typically in approximately 50-50 split between the two), and effectively 0% of the variance is attributed to shared-environment.

My impression is that the research is vast, the data is ample, and the conclusions are overwhelmingly consistent and accepted.

My first intermediate question: is the above description correct?

Now, that trichotomy, as I understand it, goes like this: by "heredity" people refer to anything identical twins that grow separately share (so mainly genetic and epigenetic factors), by "nonshared-environment" people refer to anything identical twins that grow together do not share (specific social interactions, different life experience, etc), and by "shared environment" people refer to the things non-sibling that grow together share (same parents and family, same home, same neighborhood, same school, same lifestyle etc).

My second intermediate question: is this description correct?

If so, it basically means that a pair of identical twins that grew up together, is indistinguishable from a pair of identical twins that grew up separately, and that a pair of any two random people is indistinguishable from any two non-sibling that grew up in the same home with the same parents.

In shorts, sharing home does not make people more similar, with respect to most reliably measurable properties.

My third intermediate question: are there any notable exceptions? Known traits whose variance is meaningfully explained by the shared-environment?

My forth and last question: Is the socioeconomic status of the family is part of the shared-environment? It seems as it should be (if my description above is not too-wrong), but then it implies that it has no effect on anything other than the future socioeconomic status of the children. Is this really case?

Do things like the neighborhood and schools quality have no intrinsic effect (e.g. on intelligence, inclination to violence, occupational aptitude, religiousness, etc)?

# Answer
> 3 votes
Actually, you are misunderstanding twin studies when it comes to shared vs. non-shared environments. These are defined only in terms of outcomes:

> The environmental influences on personality are divided into two main types in the behavior genetic literature: “shared” versus “nonshared” environment. In typical behavior genetic studies, actual measures of environmental factors are not obtained, but influences are inferred from the outcome pattern of observed similarities between subjects. Plomin, DeFries, et al. (2001; pp. 378–379; p. 300) define shared environment as “environmental factors responsible for resemblance between family members” or “family resemblance not explained by genetics”, and nonshared environment as “environmental influences that contribute to differences between family members” or “variance not explained by genetics or by shared family environment”. \[...\]
>
> It is important to note that the distinction between shared and nonshared environment is made solely in terms of outcome, i.e., if an environment has the effect of making siblings more similar, it is defined as a shared environment, and if an environment has the effect of making siblings more different, it is defined as a nonshared environment.

But your confusion is common enough

> Not only textbook authors, but even reports from behavior genetic studies oscillate between the outcome-based shared/nonshared distinction, and the causal-event-based variety. A recent description of the nature of “shared environment” is given by Reiss et al. (2000) in their book from the well known NEAD (Nonshared Environment and Adolescent Development) twin and sibling study, in explaining the results of minimal influence of “shared environment” (p. 68): “This analysis tells us that the major environmental influences on adolescents’ proneness to anxiety must be different for sibs in the same family. This rules out a number of influences, such as the family social class or the level of parents’ anxiety, all of which are *shared* by siblings in the same family.” According to the definition of “shared environment” this interpretation is incorrect when it comes to siblings living in their original family, since two siblings perfectly well can have different responses to a parent’s anxiety. Such gene-environment interaction would be accounted as a nonshared environmental effect in many commonly used behavior genetic models, in which nonshared environment incorporates interaction effects.

With this in mind however

> The results of many heritability studies of the Big Five personality dimensions show that most of the environmental influence is attributable to nonshared environment. \[As defined in the first quote\].

Also note that since (according to the review of Turkheimer and Waldron) Plomin's group work was seminal, it makes sense to refer to defer to their definitions.

> In what may have been the most influential article ever written in the field of developmental behavior genetics, Plomin and Daniels (1987) reviewed evidence that a substantial portion of the variability in behavioral outcomes could not be explained by the additive effects of genotype or the environmental influences of families. They suggested that this residual term, which they called the nonshared environment, had been neglected by environmentally oriented researchers who assumed that the most important mechanisms of environmental action involved familial variables, like socioeconomic status and parenting styles, that are shared by siblings raised in the same home and serve to make siblings more similar to each other. Indeed, Plomin and Daniels argued, once genetic relatedness has been taken into account, siblings seem to be hardly more similar than children chosen at random from the population. An important indicator of the influence of Plomin and Daniels' (1987) article is that an entire field of empirical research was generated in an attempt to answer the question posed in its title: Why are children in the same family so different? The content of this research was strongly influenced by Plomin and Daniels, building on earlier theoretical work by Rowe and Plomin (1981), who suggested that the causes of outcome differences among siblings were to be found in differences in the environments they experienced.

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Tags: developmental-psychology, nature-nurture
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# Question
Title: Is Paul's Churchland claim about qualia supported by science?
Knowledge argument:

> Mary is a brilliant scientist who is, for whatever reason, forced to investigate the world from a black and white room via a black and white television monitor. She specializes in the neurophysiology of vision and acquires, let us suppose, all the physical information there is to obtain about what goes on when we see ripe tomatoes, or the sky, and use terms like "red", "blue", and so on. She discovers, for example, just which wavelength combinations from the sky stimulate the retina, and exactly how this produces via the central nervous system the contraction of the vocal cords and expulsion of air from the lungs that results in the uttering of the sentence "The sky is blue". \[...\] What will happen when Mary is released from her black and white room or is given a color television monitor? Will she learn anything or not?

Paul's Chuchland answer is:

> According to Paul Churchland, Mary might be considered to be like a feral child. Feral children have suffered extreme isolation during childhood. Technically when Mary leaves the room, she would not have the ability to see or know what the color red is. A brain has to learn and develop how to see colors. Patterns need to form in the V4 section of the visual cortex. These patterns are formed from exposure to wavelengths of light. This exposure is needed during the early stages of brain development. In Mary's case, the identifications and categorizations of color will only be in respect to representations of black and white.

But can't I really see new color if I never experienced some mixture of wavelengths prior? I thought that the person who saw only 90% of spectrum for the whole life still would gain new experience when seeing something from remaining 10%.

I know cone cells are responsible for color perception. They are located on retina of eyes. Most people have three of them, but there can be more or less. Signals from them travel to parvocellular cells and to koniocellular cells. It's not clear how color is processed there, as far as I am aware. Then signals travel to visual cortex from there. And V1 is said to be the most influential part of visual cortex. But I am not sure how V4 is responsible for color perception.

Is there scientific support for his claim? Or instead, is there scientific support for the opposite?

# Answer
> 3 votes
Read further down to

> The neural basis of qualia
>
> V.S. Ramachandran and Edward Hubbard of the Center for Brain and Cognition at UCSD argue that Mary might do one of three things upon seeing a red apple for the first time:
>
> 1. Mary says she sees nothing but gray.
> 2. She has the "Wow!" response from subjectively experiencing the color for the first time.
> 3. She experiences a form of blindsight for color, in which she reports seeing no difference between a red apple and an apple painted gray, but when asked to point to the red apple, she correctly does.
>
> They explain further: "Which of these three possible outcomes will actually occur? We believe we've learned the answer from a colorblind synesthete subject. Much like the theoretical Mary, our colorblind synesthete volunteer cannot see certain hues, because of deficient color receptors. However, when he looks at numbers, his synesthesia enables him to experience colors in his mind that he has never seen in the real world. He calls these "Martian colors." The fact that color cells (and corresponding colors) can activate in his brain helps us answer the philosophical question: we suggest that the same thing will happen to Mary."\[21\]

So it is possible to see in your mind colors you've never seen in reality, due to defective receptors. But it's possible that synesthesia in this subject caused some pathways to form that do not exist in someone who never experienced any color even even due to "fake" inputs like synesthesia.

One fairly recent (2012) fMRI study on a late-blind synaesthete found that

> The colour area hOC4v was engaged when the synaesthetic experience included colour. These results confirm the continued recruitment of visual colour cortex in this late-blind synaesthetes.

So it's technologically possible to determine/confirm when color "perception" in the brain is occurring in the blind. All it would take now is a subject for whom the order of events is reversed (born blind, but acquired/induced synesthesia.) The last paper notes however that.

> It is known that differences in the functional neuroanatomy of sighted and early-blind subjects reflect predominantly early recruitment of visual cortical areas for tactile \[...\] and auditory stimulation \[...\], and during verbal \[...\], and memory processing \[...\]. However, in late-blind individuals, visual cortical areas seem to retain some aspects of their original specificity. For instance, tactile perception of motion and faces activates visual cortical areas previously involved in analysis of equivalent visual stimuli \[...\]. And in a late blind synaesthete (the subject of the present report), both striate and extrastriate visual areas appeared to be engaged in the synaesthetic perception of coloured and spatially located concurrents \[...\].

So it's not a foregone conclusion that the early- or congenitally-blind could still/even experience synaesthetic color.

One 2018 study (Dell'Erba et al.) on the subjective experiences of a congenitally-blind man on psychedelic drugs reported that these include "synesthetic hallucinations", but of the tactile kind, and the complete absence of visual hallucinations, in line with their (previously reported) absence from the congenitally blind in general.

A Harlow-type experiment in monkeys (for the development of color vision in a black-and-white environment) might barely clear ethics boards nowadays. However, monkeys with natural \[partial\] color blindness can get the "full version" though gene therapy, suggesting that at least the color machinery in the brain, if developed for two colors/sensors, can quickly accommodate three thereafter. This result however (besides the coolness of gene therapy) isn't terribly surprising on a phenomenological level, given the reports of synesthesic "martian colors" in the color blind humans. (More interestingly, giving mice three-colored vision doesn't work as well.)

Much more interesting for our discussion is achromatopsia and its (genetic) treatments:

> Achromatopsia is a rare (1 in 30,000 to 80,000) congenital visual condition characterized by diminished or absent cone photoreceptor function. Patients have severely reduced visual acuity (~20/200), nystagmus and photophobia. Causative autosomal recessive mutations affect genes of the cone phototransduction cascade, CNGA3, CNGB3, GNAT2, PDE6H, PDE6C, \[...\] or the transcription factor ATF6. A subset of patients have unidentified causative mutations. Patients typically show complete cone function loss, as shown by absent cone-isolating electroretinogram (ERG) recordings. An incomplete phenotype occurs more rarely, but is not clearly correlated to the underlying mutation. Achromatopsia affects all three classes of photoreceptor and hence, by definition, relates to genes that are expressed in all cone subtypes, as listed above. Conversely, blue monochromatism, tritanopia, and red-green color blindness (deuteranopia and protanopia) are caused by mutations in genes specific to certain subtypes of cone photoreceptors; an important difference to achromatopsia. \[...\]
>
> A well reported achromatopsia population lived on the South Pacific island of Pingelap. A genetic bottleneck following Typhoon Lengkeki in 1775 created a founder effect and over 10 percent of the island population had complete achromatopsia. The story is notably recorded in The Island of the Colorblind by the neurologist and author, Oliver Sacks. \[...\]
>
> phase I clinical trials to treat achromatopsia using an AAV vector to deliver CNGA3 have already started in Germany (NCT02610582), CNGA3 in the USA and Israel (NCT02935517), CNGB3 in the USA (NCT02599922), and CNGB3 in the UK (NCT03001310) \[...\]

These are in the wake of partially successful animal knockout models & treatments thereof.

> Carvalho et al. (2011) explored the therapeutic age window for gene therapy in achromatopsia. A mouse model caused by a premature stop codon was rescued with human CNGB3 transgene packaged in an AAV8 capsid. The use of a cone arrestin promoter fragment resulted in universal expression in all cone subpopulations, an alternative solution to the use of the ubiquitous CBA promoter. The subretinal vector rescued retinal function, as tested by ERG, at a range of ages, but again there were poor visual responses in mice treated at later ages. This confirmed that there is an optimal therapeutic window at a younger age. The limited benefit at later ages may be a result of slow retinal degeneration in this model or amblyopia. Cone outer segment abnormalities have also been noted in achromatopsia animal models and it has been shown that regenerating the outer segments with intravitreal ciliary neurotrophic factor just before achromatopsia gene therapy may improve the responses significantly in older Cngb3 deficient mice.

The treatments were also successful for serendipitous "models" found in some sheep (age of the animals is not discussed in this latter context, alas):

> Two serendipitous discoveries of day blindness in unrelated Awassi sheep flocks in Israel yielded two new large-animal models of Cnga3 achromatopsia. Both models—a premature stop codon and a missense mutation—were rescued using the same human PR2.1-CNGA3 vector described by Komaromy et al. (2010). As expected, photopic ERG was restored. Treated animals were also able to use the restored cone function to navigate a maze in photopic conditions. A mouse Cnga3 transgene also provided a similar rescue effect.

The authors of this review generally conclude/speculate that

> The implications for human achromatopsia gene therapy are that the treatment will most likely need to be applied in early childhood to be maximally effective. \[...\]
>
> The \[four human\] trials are designed to initially test the safety profile in adult patients, but three of the trials plan to include patients as young as 6 years in later groups. By comparing older and younger patients, the trials will examine differences in integrated functional cone rescue between age groups. If the pattern observed in the animal trials holds true, there may be a difference in benefit due to patient age at time of treatment. Such a difference may arise from reorganization of cortical pathways or foveal hypoplasia.
>
> In the one other therapeutic trial registered for achromatopsia (ClinicalTrials.gov number, NCT01648452), six CNGB3 achromatopsia patients received intraocular implants that released Ciliary Neurotrophic Factor (CNTF). CNTF provides neuroprotection to rod and cone photoreceptors in degenerative retinal disease. Concurrent treatment with intravitreal CNTF in a canine model of CNGB3 achromatopsia potentiated gene therapy rescue. CNTF improved ERG rescue in older animals, overcoming a notable inability of gene therapy alone to benefit most dogs over 1 year of age. Limited evidence suggested that CNTF pre-treatment de-differentiated the cone photoreceptors by elongating the outer segments to facilitate CNGA3/B3 tetrameric protein assembly. As mentioned above, in the CNTF only trial, no functional improvement in cone function occurred. There are no current plans to include CNTF pre-treatment in any of the registered human gene therapy trials. This discussion may be reignited if the early trials show difficulty in rescuing cone function in older patients.

So the aforementioned (ongoing as of mid-2017) human trials should have interesting things to say about human color vision development in the absence of all three color "sensors"...

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Tags: neuroscience, perception, developmental-psychology, sensation, color
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title: Nature vs. nurture in irritability?

text:
# Question
Title: Nature vs. nurture in irritability?
For example, personally I'm quite irritable. It's not hard to irritate me and I swear either through an inner voice or whisper very often, but not out-loud. That does not happen very often. This is hardly likely due to some temporal cause.

But at the same time it seems there are people who are less irritable. How much of this is due to nature and how much is due to nurture? Are there any studies?

# Answer
Irritability is a pretty broad concept. Various aspects/measures of it have shown various degrees of heritability. For example, just in one twin study (Coccaro, 1997):

> To determine the degree of genetic and environmental influences on assessments of aggression and irritability in male subjects, the "Motor Aggression" subscales of the Buss-Durkee Hostility Inventory (BDHI) were mailed to 1208 male twins in the Vietnam Era Twin Registry. Data from monozygotic 182 and 118 dizygotic twin pairs were available and were analyzed using model-fitting procedures. Three of the four BDHI subscales demonstrated significant heritability of a nonadditive nature: 40% for Indirect Assault, 37% for Irritability, and 28% for Verbal Assault. Additive genetic variance accounted for 47% of the individual differences for Direct Assault. Nonshared, but not shared, environmental influences contributed to explaining the variance in the model, with estimates ranging from 53% (Direct Assault) to 72% (Verbal Assault). Because some of these BDHI scales have been shown to correlate with indices of central serotonin function, it is possible that impulsive aggression, as reflected by these scales, is heritable in men.

And a study from the genomic era (Riglin, 2017), alas only on irritability in children:

> Severe irritability is one of the commonest reasons prompting referral to mental health services. It is frequently seen in neurodevelopmental disorders that manifest early in development, especially attention-deficit/hyperactivity disorder (ADHD). However, irritability can also be conceptualized as a mood problem because of its links with anxiety/depressive disorders; notably DSM-5 currently classifies severe, childhood-onset irritability as a mood disorder. Investigations into the genetic nature of irritability are lacking although twin studies suggest it shares genetic risks with both ADHD and depression. We investigated the genetic underpinnings of irritability using a molecular genetic approach, testing the hypothesis that early irritability (in childhood/adolescence) is associated with genetic risk for ADHD, as indexed by polygenic risk scores (PRS). As a secondary aim we investigated associations between irritability and PRS for major depressive disorder (MDD). Three UK samples were utilized: two longitudinal population-based cohorts with irritability data from childhood (7 years) to adolescence (15–16 years), and one ADHD patient sample (6–18 years). Irritability was defined using parent reports. PRS were derived from large genome-wide association meta-analyses. We observed associations between ADHD PRS and early irritability in our clinical ADHD sample and one of the population samples. This suggests that early irritability traits share genetic risk with ADHD in the general population and are a marker of higher genetic loading in individuals with an ADHD diagnosis. Associations with MDD PRS were not observed. This suggests that early-onset irritability could be conceptualized as a neurodevelopmental difficulty, behaving more like disorders such as ADHD than mood disorders.

Note that since polygenic risk scores currently only cover a small fraction of the heritability found in twin studies (for almost any psychiatric/psychological issue/construct), genomic results are rather tentative. Usually the presence of a gene overlap means something, but the absence of a genetic overlap can simply mean there hasn't been enough data.

And Riglin point out to a recent review Vidal-Ribas (2016) of which they are aware they cannot explain genomically. The latter found/concluded that

> irritability forms a distinct dimension with substantial stability across time, and that it is specifically associated with depression and anxiety in longitudinal studies. Evidence from genetic studies reveals that irritability is moderately heritable, and its overlap with depression is explained mainly by genetic factors. \[...\]
>
> The genetic contribution to the variation of irritability is approximately 30% to 40% in both adults and adolescents. This is close to the heritability estimates for depression and anxiety. Genetic influences on irritability increase slightly over time in males and decrease in females, and unique (as opposed to shared) environmental factors explain most of the remaining (non-genetic) variance in both.

I highly suggest reading this review if you're unfamiliar with the psychiatric approach to irritability because it has a good, detailed background on that (including the substantial changes in DSM-5, which were applied only to children though.) And since the focus on irritability as separate entity is pretty new in psychiatry, the authors of this review note for instance that

> Probably the main limitation in the study and treatment of irritability so far is the lack of high-quality measures. Most of the measurement of irritability has been done with instruments created ad hoc, that is, through extracting items from existing scales or interviews that were not intended primarily to measure irritability.

For instance, the heritability data on adults they cited from Coccaro (1997) with which I started this answer, whereas for adolescents (as you probably guessed by now), there are newer studies available; the data cited on the latter in the review is from Stringaris (2012) and there's more specific longitudinal data in Savage (2015).
> 2 votes

# Answer
You will have to investigate quite a few factors:

1. There must be a genetic/epigenetic factors to this because we know that personality trait neuroticism has genetic and environmental factors.
2. You should also investigate into stress - biological and psychological stress.
3. Investigating theories of psychological development can also come in handy, especially, Freudian theories.

In my personal view, I think a combination of genetic and environmental factors should play role in shaping irritability tolerance, however, additionally environment plays a role of stressor.

In other words, you should have genetics, epigenetics and upbringing as a predictors of general irritability. Immediate state of being can also have influence, but stressor is like a trigger.
> 4 votes

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Tags: emotion, personality, behavior
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# Question
Title: Confidence rating in cognitive experiments
Does a confidence rating included in a post task measure the likelihood of correctness to the answer or likelihood of occurrence of an event.

To give an example: participants are given a picture of clouds and they are provided with the binary question if they think it might start raining; the answer is thus either a '*yes*' or a '*no*'. Then they have to give an estimate of how confident they are of their decisions on a rating scale that indicates how confident they were; for example they might say '*70%*'.

**Does the confidence rating reflect their estimate of likelihood of rain, or rather the likelihood that the choice is correct?**

# Answer
If the question is *'Will it start to rain based on this cloud cover?*' and the answer is a binary *'yes'* or *'no'* and the subsequent question is *'How sure are you about that?'*, then the answer to your question

> Does the confidence rating reflect their estimate of likelihood of rain, or rather the likelihood that the choice is correct?

is the latter: it reflects t**he likelihood that the choice is correct**, because when they say *'no it will not rain'*, with a confidence of 60%, then the chance it will rain is 40% and not 60%. Hence, it reflects the confidence they have in their answer.
> 1 votes

# Answer
The question you ask is at the heart of confidence judgments, i.e. whether they reflect objective truth or an observer belief of the truth. There is currently no answer to your question. All you can do is read the literature and please do experiments to give us an answer to this question. Start with: Fleming & Frith (2014) The Cognitive Neuroscience of Metacognition

Another paper very relevant to your question is: Pouget, A., Drugowitsch, J., & Kepecs, A. (2016). Confidence and certainty: distinct probabilistic quantities for different goals. Nature neuroscience, 19(3), 366.
> 0 votes

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Tags: methodology, task-analysis, confidence
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# Question
Title: What is the basis of the belief that modern psychology demonstrates that words themselves can be hurtful and verbal aggression should be wed out?
I'm sorry for the length of this question, but to ask it I'll need to refer to two concepts.

Firstly, we see the escalating trend to weed out any and all examples of even very minor negativity or aggression in words. Those are deemed unacceptable, addressees of such messages may be called 'victims', and telling people to 'grow a thicker skin' is explicitly declared a non-solution to the problem. Examples of this are many: StackExchange's new Code of Conduct, strict rules of communication Riot Games is trying to enforce in League of Legends, punishing people for jokes, firing employees for not being nice enough to their colleagues, etc etc.

It is claimed that such policies are backed up by modern psychology:

> One major mistake in this reasoning is "unlike with sticks and stones, with words the addressees have the choice: to accept the message or to drop it". They do not, the message will be received and the emotional reaction will happen, emotions are not subject to conscious control. One can choose to "get over it", but the same can be said of sticks and stones, so the real issue is the damage assessment. One reason for the new consensus is the undermining of folk misconceptions that heavily weigh physical damage over emotional one (as in the saying) by modern psychology.

-- @Conifold

> Humans are social creatures. If a grief stricken person can be consoled by words and interactions. Why would you not expect the opposite to be equally effective that is turning a happy person depressed and mentelly unwell? To say that people should just "ignore it" is to assign all blame to the victim but that's not fair and ignores everything we know about human behaviour.

-- @Cell

Here I have to jump for a short while to the second concept... Monika and Marcin Gajda, in their book "Rozwój. Jak współpracować z łaską" (which is a Polish book on self-development that claims to be based on psychology and is written from an extensive Christian angle) introduces the concept of "emotional sovereignty". It distinguishes five levels of this sovereignty:

1. **Submission.** For example, if a bum insults me, I'll have the rest of my day screwed because I'll think how useless I must be that even a bum holds me in contempt.
2. **Entering a symmetrical conflict.** Here I'll insult back the bum or even start physically fighting him to defend my good name.
3. **Ignoring aggressively.** Here, feeling superior to the bum, I'll walk away, maybe mumbling something silently to myself.
4. **Assertiveness.** As described by modern psychology.
5. **Merciful love.** Told you the book is written with an extensive Christian angle. Here, with no contempt, feelings of superiority, aggression, urges of vengeance, or anything of this sort on my side, I'll look at the bum with compassion, seeing how miserable he must be to behave that way.

The book claims that people can - and should - work themselves from the lower levels to the higher levels, for their own good. Staying on the lower levels is harmful, also from the psychological point of view, for the people who stay there. Also the book claims that a person may be on different levels in relation to different people: for example, a person may be on the 5th level with regard to this exemplary 'bum', but on the lowest level with regard to one's own mother. (Important: This self-development is not supposed to include trying to control one's own emotions).

And here is where the two concepts meet, at least in my mind. If such 'abusive' words and messages are treated as 'big deal', if growing a thicker skin is not to be advised, if, having received such messages, the correct action to take is deemed to be to report the offender to whoever is in charge of the community, if, as psychologists want, not attempting to stop receiving these messages is not respecting oneself enough… Then such beliefs and policies seem to me to hurt, rather than protecting, 'victims' of verbal abuse, because effectively they teach them to stay at the lower levels of emotional sovereignty. If, instead of attempting to cleanse the word of all verbal 'negativity', the emphasis was on empowering the addressees of such messages to be 'sovereign' over them, then the old adage that '*sticks and stones can break my bones, but words can never hurt me*' would become true. On the other hand, the current emphasis of fighting the 'abusive' messages themselves seems to me to give the abusers the power to actually hurt the receivers of the verbal abuse: and that's a lot of power to place in improper hands.

I understand that my reasoning may be very well wrong, as the general consensus seems to be in the opposite. Then do both models not contradict themselves, regardless of whatever would seem to me to be the case? Or is Gajdowie's model of emotional sovereignty wrong?

EDIT: Just to clarify: The precise point that is hard to reconcile for me is this one: It is impossible for the receiver of the 'abusive' messages to avoid being damaged by such messages (the quoted comments) vs it is possible (Gajdowie)

# Answer
> 2 votes
Most of your post is hard to follow and mixes a lot of topics. On the issue whether pain and social rejection have something in common, a highly-cited (2003) fMRI study found that

> In summary, a pattern of activations very similar to those found in studies of physical pain emerged during social exclusion, providing evidence that the experience and regulation of social and physical pain share a common neuroanatomical basis.

Likewise a newer (2011) study concludes that:

> rejection and physical pain are similar not only in that they are both distressing—they share a common somatosensory representation as well.

An even more recent study (Woo, 2014) has challenged these though:

> Pain- and rejection-related representations are uncorrelated within regions thought to encode pain affect (for example, dorsal anterior cingulate) and show distinct functional connectivity with other regions in a separate resting-state data set (N=91). These findings demonstrate that separate representations underlie pain and rejection despite common fMRI activity at the gross anatomical level. Rather than co-opting pain circuitry, rejection involves distinct affective representations in humans.

Since most of the "hurtful" words on SE are of the kind that lead the receiver to experience some level of exclusion (not being "good enough" to be part of the site\[s\] etc.)... it seemed appropriate to mention this. Of course you can make someone feel excluded while being perfectly polite.

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I'm less familiar with research on the effects of verbal abuse, but at least one study found it has long-term negative consequences for some children. In fact there's more than one study with the same conclusions.

I don't know if there are studies on the extent to which adults are just able to shrug off verbal abuse. But there certainly are books arguing for not tolerating it in the workplace, e.g. Bob Sutton's "No asshole" series.

And despite what your Polish Zen psychologists would like the reality to be, it just doesn't work like that in practice. Verbal abuse does have some effect, even on people (e.g. nurses) who encounter it often. Granted the effect is not huge. On a scale of 0 (no reaction) to 6 (extreme feeling), the average effects of verbal abuse (on nurses) are reported below:

There are a lot more studies on the effects bullying, which combines verbal abuse with other behaviors. Actually a problem with work-related constructs including verbal abuse is that there's perhaps a bit too many of them. But there's a slightly narrower one that was studied namely incivility; from Hershcovis (2011):

> Incivility has recently emerged as one of the most studied variables in the workplace mistreatment \[long list of citations\]. It was defined by Andersson and Pearson (1999) as low intensity deviant acts such as rude and discourteous verbal and non-verbal behaviors enacted toward another organizational member with ambiguous intent to harm. This construct differentiates itself from other constructs on several dimensions. First, it is defined as a low intensity behavior. Andersson and Pearson explicitly argue that minor forms of mistreatment can have a significant impact on employee attitudes toward the organization. In contrast, most other mistreatment constructs are not defined in terms of their intensity, though intensity may be inferred by their definition or measurement. For example, bullying can be assumed to be of higher intensity than incivility because of its persistence and frequency. A second differentiating feature of incivility is the explicit statement that intent is ambiguous. Researchers in the workplace mistreatment literature have frequently debated the notion of intent. For instance, Neuman and Baron (2005) argued that when defining mistreatment from the perspective of the actor, intent is crucial. Otherwise, accidentally harmful behaviors such as being hurt by a dentist during a dental procedure may be considered aggressive. On the other hand, from a target’s perspective, perceived intent may be all that matters because victims will react based on their perception, whether or not their perception is accurate.

Nonetheless, the effects of incivility were comparable with that of bullying in a work environment:

Infante (2009) points out that the negative effects of verbal aggresion have been seen in multiple contexts:

> Verbal aggression is message behavior which attacks a person's self-concept in order to deliver psychological pain (Infante & Wigley, 1986). Researchers in recent years have given considerable attention to verbal aggression in numerous contexts such as interpersonal, family, organizational, political, and intercultural. This research has been unequivocal in suggesting that verbal aggression is a highly destructive form of communication. For instance, it can result in violent crimes (Toch, 1969; Zillmann, 1979), it is a catalyst to interspousal violence (Infante, Chandler, & Rudd, 1989), it is associated with adolescents having problems when they are the victims of their parents' verbal aggression (Straus, Sweet, & Vissing, 1989), and it is a very negative factor in superior-subordinate communication (Infante & Gorden, 1991). \[...\]
>
> The types of verbally aggressive messages, derived deductively from theory and research, are: character attacks, competence attacks, background attacks, physical appearance attacks, maledictions, teasing, swearing, ridicule, threats, nonverbal emblems (Infante, 1987). However, other types also can be specified: blame, personality attacks, commands, global rejection, discontinuation, negative comparison, sexual harassment, and attacking the target's significant others.
>
> Continuation of verbal aggression after it is initiated, largely is due to reciprocity. People often feel compelled to return acts of aggression to save face and to discourage future attacks (Felson, 1978, 1982). Reciprocating verbal aggression can escalate tensions to the point of physical aggression (Berkowitz, 1962, 1973). Even if reciprocity does not result in violence the destructiveness nevertheless is more than what would have occurred had one party not reciprocated.

I.e. a tit-for-tat exchange or verbal aggression can result is what is nowadays more colloquially called a "toxic environment".

> The research has focused on effects of verbal aggression in different communication contexts. Two basic effects are self-concept damage and aggression escalation. These can lead to reduced trust, relationship deterioration, and relationship termination in interpersonal communication. Organizational communication research has found that the verbally aggressive behavior of supervisors has negative effects (Infante & Gorden, 1985, 1987, 1991). Verbally aggressive subordinates are evaluated unfavorably by their supervisors (Gorden, Infante, & Izzo, 1988; Infante & Gorden, 1989). Family communication research has suggested that children may be harmed by their parents' verbal aggression (Straus et al., 1989). Other research suggests husbands of verbally aggressive wives are more depressed (Segrin & Fitzpatrick, 1992). Verbal aggression in a marriage is negatively related to marital satisfaction (Payne & Sabourin, 1990; Rancer, Baukus, & Amato, 1986). Several studies indicate verbal aggression sometimes leads to interspousal violence (Gelles, 1974; Infante et al., 1989; Straus, 1974). The use of verbal aggression in political communication has negative effects on source credibility (Downs, Kaid, & Ragan, 1990). A study which manipulated verbal aggression in an experiment suggests that the relationship with lowered source credibility is causal (Infante, Hartley, Martin, Higgins, Bruning, & Hur, 1992). It should be emphasized that the results of research have been remarkably consistent in suggesting that the effects of verbal aggression are negative, supporting the ethical stance that verbal aggression is a destructive form of communication that should be discouraged.

Infante also discusses mitigation strategies, although the existence of these doesn't justify your point that verbal aggression is harmless:

> Once verbal aggression does occur in a situation, basic concerns are how the effects can be neutralized and how escalation of aggression can be prevented. \[...\]
>
> \[An\] approach is based on symbolic interactionism and involves the strategies that victims may use to "dismiss" verbal attacks or render them ineffective (Wagner, 1980). Protecting self from abuse by manipulating symbols, according to this view, is one of the most highly developed functions of our symbol system. Wagner (1980) conceives of these as "strategies of dismissal." He presents numerous strategies that the victim of an attack can use while interacting with the attacker or while interacting with self in order to restore the attacked self to a state of equilibrium. Some of these strategies are reviewed below (see Wagner, 1980, for a more complete discussion).
>
> Many dismissals of an attack rely upon finding an exception to the locus of attack. These can pertain to the situation of the attack, the victim, or the attacker. Dismissal strategies for the situation invoke misinformation (claim that the attack was based on incorrect information) or coercion (contend that the data which attacks self s judgment was obtained by coercion). Dismissals based on the victim involve one's conception of self and utilize the idea that the object of attack was not the "true" self. Some of these strategies are personal growth (maintain that the self characterized in the attack no longer exists because of change), the unconscious (agreeing with the unfavorable characterization by the attacker but claiming the matter is beyond personal control because the unconscious mind is responsible), and excuse (claim the behavior which suggests an undesirable self "was not my fault"). Strategies that focus on the attacker seek to derogate the source. These are based on ignorance (the attacker does not know what he/she is talking about), the dark side (the attack was motivated by lesser human tendencies to be jealous, envious, resentful, vicious, sadistic), and unacknowledged motives (the attacker has a hidden agenda). These strategies of "dismissal" seem aimed mainly at neutralizing the effect of verbally aggressive remarks so that the victim does not experience a sense of dissonance with self. This can be done to a considerable extent at the intrapersonal level.

Unlike your Christian-motivated book, Infante doesn't try to order these strategies. And these are just the purely self-oriented strategies. He spends even more space discussing (non-aggressive) communicative response strategies.

I'd also note that the paper Infante cites for dismissal strategies, Wagner (1980), doesn't have much in the way of citations (in Google Scholar).

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Tags: emotion, aggression
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# Question
Title: Is mapping sound frequencies to the vertical axis universal?
Shrill notes are said to be "high", and rumbles are said to be "low". Humans seem to metaphorically map frequency to the vertical axis, and in the cultures that I know of, high frequency is considered "up".

* Is this a universal phenomenon? Are there any cultures that map it upside-down, or in a completely different way? (For example, smaller objects tend to produce higher pitches. Are there any cultures that say that a pitch is "small" instead of "high"?)
* Does this convention pre-date the scientific understanding of sound waves?
* If it is universal (or nearly so), is there any neurological hard-wiring that would cause that mapping?

# Answer
Humans technically don't perceive frequencies, they perceive pitch. According to Wikipedia:

> the idiom relating vertical height to sound pitch is shared by most languages.

citing a 1930 article by Pratt, which in turn says that:

> Stumpf has found that adjectives meaning high and low (or words closely related in meaning) have been applied to tones in almost every known language.\[2\] But why should tones be characterized as high or low? Do these characteristics refer to differences in spatial height and depth? The answer to this second question has been almost without exception in the negative. A high tone does not mean a tone which is high in space. The phrase is merely figurative, and must be accounted for in terms of secondary criteria such as, e.g., the apparent localization of high vocal tones in the head and low ones in the chest. The composer Berlioz makes sport of such explanations and reminds his readers that high and low tones for the pianist lie in the horizontal directions of right and left and that the violoncellist must reach downward to produce high tones, and suggests that those composers of opera who use descending passages for a person falling downstairs have stupidly transferred to the tones the arbitrary downward character of the printed notes on the staff. And yet Stumpf, convinced that there can be no intrinsic height and depth in tones, has felt obliged to argue that here again some associative mechanism, strangely obscure and elusive, has been at work. Even Wundt was forced to agree with Stumpf in calling these terms metaphorical when applied to tones \[3\], and most psychologists who have given the matter any thought have expressed similar views \[4\].
>
> \[2\]: C. Stumpf, Tonpsychologie, 1883, I, 192 ff.
>
> \[3\]: W. Wundt, Grundzüge der physiologischen Psychologie, 1910, 11, 78.
>
> \[4\]: J. Redfield, Music: a Science and an Art, 1928, 42 ff.

All these sources are pretty dated alas.

There are however some newer papers on this; e.g. Fernandez-Prieto et al. (2017) which do qualify such statements, e.g.:

> Higher frequency and louder sounds are associated with higher positions whereas lower frequency and quieter sounds are associated with lower locations. In English, ‘‘high’’ and ‘‘low’’ are used to label pitch, loudness, and spatial verticality. By contrast, different words are preferentially used, in Catalan and Spanish, for pitch (high: ‘‘agut/agudo’’; low: ‘‘greu/grave’’) and for loudness/verticality (high: ‘‘alt/alto’’; low: ‘‘baix/bajo’’). Thus, English and Catalan/Spanish differ in the spatial connotations for pitch. To analyze the influence of language on these crossmodal associations, a task was conducted in which English and Spanish/Catalan speakers had to judge whether a tone was higher or lower (in pitch or loudness) than a reference tone. The response buttons were located at crossmodally congruent or incongruent positions with respect to the probe tone. Crossmodal correspondences were evidenced in both language groups. However, English speakers showed greater effects for pitch, suggesting an influence of linguistic background.

They also cite an older review paper (Cassanto, 2013) which highlights a similar studies (co-authored by Cassanto) on Dutch vs Farsi:

> Like English, Dutch describes pitches as ‘high’ (hoog) or ‘low’ (laag), but this is not the only possible spatial metaphor for pitch. In Farsi, high pitches are ‘thin’ (nāzok) and low pitches are ‘thick’ (koloft). Dutch and Farsi speakers’ performance on non-linguistic pitch reproduction tasks reflects these linguistic differences (Dolscheid, Shayan, Majid, and Casasanto 2013). Participants were asked to reproduce the pitch of tones that they heard in the presence of irrelevant spatial information: lines that varied in their height (height interference task) or their thickness (thickness interference task). Dutch speakers’ pitch estimates showed stronger crossdimensional interference from spatial height, and Farsi speakers’ from the thickness of visually presented stimuli. This effect was not explained by differences in accuracy, or in musical training. When trained to talk about pitches using Farsi-like metaphors (e.g. a tuba sounds thicker than a flute) for 20-30 minutes, Dutch speakers’ performance on the non-linguistic thickness interference task became indistinguishable from native Farsi speakers’. Experience using one kind of spatial metaphor or another in language can have a causal influence on non-linguistic pitch representations. \[...\]
>
> infants as young as four months old are sensitive to the height-pitch mapping found in Dutch-speaking adults (but not in Farsi-speaking adults), and also to the thickness-pitch mapping found in Farsi-speaking adults (but not in Dutch-speaking adults; Dolscheid, Hunnius, Casasanto, and Majid 2012). There is no need, therefore, to posit that using linguistic metaphors causes people to construct these mappings de novo.

A somewhat similar paper on infants, perhaps with stronger claims is from Walker et al., 2010:

> Stimulation of one sensory modality can induce perceptual experiences in another modality that reflect synaesthetic correspondences among different dimensions of sensory experience. In visual-hearing synaesthesia, for example, higher pitched sounds induce visual images that are brighter, smaller, higher in space, and sharper than those induced by lower pitched sounds. Claims that neonatal perception is synaesthetic imply that such correspondences are an unlearned aspect of perception. To date, the youngest children in whom such correspondences have been confirmed with any certainty were 2- to 3-year-olds. We examined preferential looking to assess 3- to 4-month-old preverbal infants’ sensitivity to the correspondences linking auditory pitch to visuospatial height and visual sharpness. The infants looked longer at a changing visual display when this was accompanied by a sound whose changing pitch was congruent, rather than incongruent, with these correspondences. This is the strongest indication to date that synaesthetic cross-modality correspondences are an unlearned aspect of perception.

Cassanto and colleagues also develop a Hierarchical Mental Metaphors Theory (HMMT) according to which

> correlational mental metaphors develop in two stages, the second of which may extend throughout the lifetime. The mental metaphors that adults typically use are specific instances of more general families of mappings. These families may be evident in behavior from infancy, and reflect regularities in humans’ experiences of the physical and social world, many of which may be universal. As children are exposed to peculiar aspects of their languages, cultures, or even their own bodies, certain mappings from a given source-target family become strengthened through repeated use, which weakens ‘sibling’ mappings as a consequence. The result is that people tend to think in language-specific, culture-specific, or body-specific mental metaphors: Relativity emerges from universals. \[...\]
>
> One prediction of HMMT is that specific source-target mappings should be easy to activate via linguistic training so long as they are members of one of the families of source-target mappings encoded in our minds (over phylogenetic or ontogenetic time) on the basis of observable sourcetarget correspondences in the world. Mappings that are not members of a pre-linguistically established family (and that do not reflect correlations in our experience) should be relatively hard to activate via training, because these mappings would need to be created, not just strengthened.
>
> In a test of this prediction, Dutch speakers were trained to used a thickness- pitch mapping that is the reverse of the mapping found in Farsi, and in the natural world: thin=low and thick=high. These ‘reverse-Farsi’ trained participants received the same amount of training as the participants trained to use the Farsi-like mapping. Whereas Farsi-like training had a significant effect on participants’ nonlinguistic pitch representations, reverse-Farsi training had no effect (Dolscheid et al. 2013). Thus, brief linguistic experience caused participants to use the thickness-pitch mapping that reflects correlations between thickness and pitch in the world (and is evident in prelinguistic infants). Yet, the same amount of linguistic experience was not effective at instilling the opposite thickness-pitch mapping, which has no obvious experiential correlates, and is therefore not predicted to be among the pre-linguistically established space-pitch mappings.

That's referring to the same paper as the first citation in the previous quote. Oddly this experiment isn't summarized in the paper's abstract, but does appear in the paper (as Experiment 4). Cassanto has a free pdf of that paper as well.

A 2014 PNAS paper by Parise et al. proposes that the low-high pitch metaphor has a natural basis in the elevation of the sources of such sounds in nature.
> 5 votes

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Tags: language, music, hearing
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# Question
Title: Help to find the International Trauma Questionnaire (ITQ)
I'm looking for the *International Trauma Questionnaire (ITQ)* as per ICD-11 proposals, but I can not find it. It was previously called *the ICD-11 Trauma Questionnaire (ICD-TQ)*. Can someone help me?

# Answer
You can find the ITQ at the following site that we've made for the scale:

https://www.traumameasuresglobal.com/
> 0 votes

# Answer
I would suggest going to the source which is Cloitre, et al. (2018)

> The ITQ is a brief, simply worded measure of the core features of PTSD and CPTSD. It is consistent with the organizing principles of the ICD‐11 to maximize clinical utility and international applicability through a focus on a limited but central set of symptoms. The measure is freely available and can be found in the body of this paper.

## References

Cloitre, M., Shevlin, M., Brewin, C. R., Bisson, J. I., Roberts, N. P., Maercker, A., ... & Hyland, P. (2018). The International Trauma Questionnaire: development of a self‐report measure of ICD‐11 PTSD and complex PTSD. *Acta Psychiatrica Scandinavica.* (In Press: September 2018) doi: 10.1111/acps.12956
> 3 votes

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Tags: measurement, personality
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# Question
Title: How can be explained from an evolutionary perspective the fact that some successful people do not want to have children?
According to David Funder, Douglas Kenrick proposed a revised version of Maslow's hierarchy from an evolutionary perspective (1). He said that human beings will strive to move from 1 to 7 in a pyramid.

1. Immediate physiological needs.
2. Self-protection.
3. Affiliation.
4. Status-esteem.
5. Mate acquisition.
6. Mate retention.
7. Parenting.

But my questions are:

How can we explain from an evolutionary perspective that some "successful" species, choose consciously to avoid parenthood at all? Does it conflict with the evolutionary perspective that every human would try to parenting? If not, how is it supposed to be interpreted?

(1) The personality puzzle by David Funder (2013), Chapter 13, page 452.

# Answer
> 4 votes
Before addressing your true question, I just want to say that you can find individuals with almost any characteristic, even non-adaptive ones. Variation can exist for many reasons including genetic (e.g. mutations), or non-genetic reasons such as developmental problems or other environmental causes.

But back the true question:

> How can it be explained from an evolutionary perspective that some people have no desire to want children?

Evolutionary psychologists do not perceive the brain to be a conscious fitness calculating machine. To address such a question, it is fundamental to understand the difference between proximate and ultimate causation.

It is true that humans who didn't have any children would, by definition, be less reproductively successful in the past. Therefore, you would expect traits that lead to not having children be slowly selected out.

But you have to analyze this at the *proximate* level: What caused people in the past to have children? It was not mainly people thinking "I really want a child," rather it was people thinking "I desire sex with that person." What I am getting at here is that it was *sex drive*, rather than explicitly wanting children per se, that has been selected for.

It can often be helpful to compare us to other animals, especially animals who don't have as powerful cognitive faculties as us. Do you think that all other animals really think that "they want a child," or do you think that by some strange mechanism two individuals are attracted to each other to copulate (It might be scent, visuals, strength, or anything really)?

Of course, I have simplified things substantially. Probably there have been many psychological traits that have been helpful for reproduction other than simply sex drive. Probably also social bonding, and perhaps even the "desire for having children." However, my point here is that the desire to have children is not required, if another mechanism leads to people having children. However, it gets even more complex, because an infinitely strong sexual drive is not necessarily good, either. Being selective in who you mate with can be important as well for ultimate reproductive success.

Next question:

> How can we explain from an evolutionary perspective that some "successful" species, choose consciously to avoid parenthood at all?

There is a fundamental trade-off between how much effort and energy you invest in each offspring, and the number of offspring you have. If you have 10 children, you simply do not have as much time or resources to spend on each of them compared to if you had 2 children. This can lead to differences in how many of your offspring survive and eventually have their own offspring (Especially in conditions where resources are scarce). These differences in reproductive patterns were originally explored in r/K selection theory and now in Life history theory. Ignoring parenthood has its benefits in that it allows for more offspring and investing less energy into each.

Now you may ask the following:

> But what about after the child comes? For humans, if there is no one there to take care of the child, then it's guaranteed that the child will not survive.

It is clear that humans are a species where parenthood is important, because human infants are so helpless when born and for a long duration. Therefore, you would also expect it to have been selected for that people would invest time and resources in (i.e. to parent) the child when it shows up. You would probably expect this especially for women, because the child can survive without the father, but it is very difficult for it to survive without the mother (in the first few years, especially in ancient environments).

But, in fact, it is very rare that mothers have no desire to protect or care for their offspring after having it. So rare that it does not conflict with the evolutionary perspective. We also know that certain hormones are important for developing social bonds between the parent and offspring such as oxytocin.

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Tags: evolutionary-psychology, parenting
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title: System 1 and 2 thinking and unconcious

text:
# Question
Title: System 1 and 2 thinking and unconcious
Research says there is system 1 and 2 thinking.

My question is how is system and and 2 thinking related to unconcious mind? Can we say for example system 1 thinking is unconcious mind?

# Answer
> 2 votes
Peter Carruthers argues (2014) that system 1 doesn't quite overlap with unconscious thinking:

> I shall argue that there is, indeed, a real, scientifically valid, distinction between a set of intuitive, unconsciously operating reasoning systems, on the one hand, and a reflective system whose operations are partly conscious, on the other. But I shall argue that this division fails to line up with many of the other properties generally associated with Systems 1 and 2. In particular, some intuitive systems can be slow, some can be controlled, and some can approach the highest normative standards; so the moniker «quick and dirty» is certainly inappropriate when applied to intuitive reasoning as such.

And Jonathan Evans (2014), a dual-process theorist but also strong critic of UTT, writes:

> It is true that the distinction between conscious and nonconscious processing has been emphasised by some social psychologists (e.g., Wilson 2002), but it is emphatically not the foundation for contemporary dual-process theories of reasoning and decision making. As a dual-process theorist, I have argued, in common with others, that the conscious/unconscious decision cannot be the basis for the dual-process distinction because it is too vague and fails to define the key central properties of dual processing (Evans & Stanovich 2013). I should also point out that in spite of defending the validity of much of the research that N&S criticise here, I have in common with them critiqued unconscious thinking theory and other strong assertions of the powers of intuition (see Evans 2010, Ch. 4). This is because dual-process theory confines powers of reflective reasoning – and with it the ability to deal with novel and difficult problems – to Type 2 processing. The case for dual process is in fact based not on the conscious/ unconscious distinction but on the claim that there are two forms of cognitive processing which have distinctive properties and which reflect the operation of distinct cognitive and neural systems. Most of these properties are merely typical correlates, and few are defining features (Evans & Stanovich 2013). I agree with Stanovich that Type 2 processing is distinguished both by its cognitive resources (central working memory, correlation with measures of cognitive capacity) and by its ability to engage in cognitive decoupling and hypothetical thinking. The apparent link of dual-process theory with consciousness comes only from the fact that some of the items attended in working memory are available to verbal report. But using broader definitions of consciousness, I have argued in detail that both Type 1 and Type 2 thinking have aspects that are conscious as well as unconscious (Evans 2010, Ch. 7). In conclusion, not only do I reject the authors’ presumption of conscious decision making, which I believe to be shakily founded on folk psychology, but I also contest their implication that the conscious/unconscious distinction is the basis for contemporary theories of dual processing in higher cognition.

# Answer
> 1 votes
Another classic distinction was given by Bargh in 1997 that helps show muddling (lack of clear overlap) between the dual-systems concept and how the unconscious is defined by psychologists:

> Unconscious cognition is more likely to be one or more: outside awareness, not intended, relatively fast, and difficult to control.
>
> http://psycnet.apa.org/record/1994-97751-001

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Tags: cognitive-psychology, unconscious, thought, analysis, intuition
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