title: Why is IIT "unmotivated"?

text:
# Question
Title: Why is IIT "unmotivated"?
I'm trying to understand Searle's reply to Tononi and Koch's objections to Searle's characterization of their Intergrated Information Theory (IIT) of consciousness.

Although I do understand why IIT is problematic, both from Searle's original review and from Thagard's alternative proposal, I don't understand his reply.

Specifically, what does Searle mean by IIT being "unmotivated"?

# Answer
I suspect that the reason he considers it unmotivated is that he would like to see a theory that can explain the hard problem(s) of consciousness. In that final paragraph where he argues that the theory is unmotivated, he points out that (in his opinion) IIT seems to do nothing to explain why there is something *it is like* to be conscious from a subjective viewpoint (i.e., qualia).

My two cents is that I can see Searle's point; it is not clear how IIT would explain these aspects even if it is otherwise completely successful. On the other hand, calling it "unmotivated" seems a bit unfair; perhaps it would still be useful for other purposes, for example judging whether patients in a hospital are (likely to be) conscious. A more reasonable claim would be that it is not well motivated by trying to resolve the hard problems of consciousness, but may be well motivated by other goals.
> 2 votes

---
Tags: consciousness, philosophy-of-mind, theory-of-mind
---


# Question
Title: Are emotions local or purely global? Can there be two inconsistent emotions in different parts of the brain?
I am NOT asking whether people can experience two inconsistent emotions "at the same time". Clearly this can happen, e.g. when people have "mixed feelings" about something.

What I'm interested in, is whether emotions are strictly and purely a "global" phenomenon, or a "local" one.

* **hypothesis 1**: emotions are global. Whenever any single brain experiences a set of emotions $X$ at time $t$, then for every region of the brain, that region is influenced by all emotions in $X$ (insofar as that region can be influenced by that emotion at all).
* **hypothesis 2:** emotions can be local. Whenever any single brain experiences a set of emotions $X$ at time $t$, then it may sometimes be that one brain region is only influenced by a subset of emotions in $X$, and another region only influenced by a different subset.

A very extreme example would be that the left hemisphere experiences fear and grief, while the right hemisphere experiences joy and relief.

This particular example seems way too extreme to me, but I am wondering whether a far less extreme version of this might be possible. **Can two different brain regions receive two different emotional signals at any point in time?**

ps. I am obviously not a neuroscientist and I probably am making conceptual and terminological errors. Please be charitable, and address the question I intended to ask.

# Answer
There are two assumptions in this question it may be useful to make explicit. First, there's an assumption that words like "emotion" or "motivation" have meaning at different levels of analysis like organs, neurons, atoms, etc. If when we say emotion we mean the subjective experience, it's not at all clear that meaning exists at the neuronal level. This is related to a grand paradox (below), but even if we backed off from that, connecting subjective with objective creates thorny problems.

> https://en.wikipedia.org/wiki/Hard\_problem\_of\_consciousness

Second, the question sort of implies that cognitive functions are carried out by limited areas. This is looking less and less true; there is some evidence for specialized functions, but in general most complex operations (including emotion) are influenced from a complex forward-and-backward activation-and-inhibition cascades in multiple areas.

> https://en.wikipedia.org/wiki/Functional\_specialization\_(brain)

The experience of emotions appear caused by / related to / influenced by complex cascades of activity across the brain. It's not clear that the words we use to describe the feelings map onto such neuronal activation/inhibition patterns, but even if they did, there's no reason to assume that such patterns of neuronal activation wouldn't co-occur.

tl;dr: Yes.
> 1 votes

---
Tags: neuroscience, emotion
---


# Question
Title: Where can I find recent research on the role of context effect in perception of similarity?
BACKGROUND. I’m writing a paper on the role of similarity in the theories of concept empiricism developed by the British Empiricists Locke, Berkeley, and Hume, and how the idea of context effect from modern cognitive psychology could be used to better understand these theories. The basic idea I’d like to develop in my paper is that similarity is contextual, relative to a frame of reference, and this can explain how a general abstract idea (on Locke’s theory of abstraction) or a set of similar ideas held together in the mind that are called up by awareness of an exemplar (on Berkeley and Hume’s theory of general ideas) can be formed from particular instances none of which are identical: while not identical, they are similar to each other in a certain context, relative to a certain frame of reference, and thus can be classified together by the mind (e.g. scarlet and crimson are not identical but are similar to each other, in context, relative to aquamarine; or mammals are all different from each other but similar to each other relative to birds; or birds and mammals are different but relative to plants are similar. Etc.)

QUESTION. I am unfamiliar with cognitive psychology and the literature on context effect. Where can I find recent papers on context effect? What is the best way to go about finding references, especially with experimental data, on context effect? I am aware of a paper which discusses context effect very well (Tversky, A. (1977). Features of similarity. Psychological review, 84, 327-352 doi: 10.1037/0033-295X.84.4.327). However, I’d appreciate any help I could get on finding more recent work on this phenomenon, preferably (but not necessarily) which further develops or supports Tversky.

# Answer
A classic reference in this space is Goodman (1972) "Problems and projects", which develops exactly this idea that similarity is poorly defined unless you specify in what respect. From your description, you might also enjoy Barsalou's (1983) "Ad-hoc categories", which emphasizes how much coherent groupings depend on context. These are not exactly recent, but you should turn up some relevant stuff by looking for recent papers that cite these.

There are a few different lines of work building on Tversky's results. The most prominent problem with that account is the combinatorial explosion you get out of conjunctive features. The relations between features are also important to people, but considering relations as just another kind of feature explodes the number of features you have to consider in an utterly horrifying way.

Probably the most direct solution is to consider structured representations that assign roles to features and judge similarity by the goodness-of-fit of a mapping between these structured representations. If you had to pick one entry-point to this literature, it'd probably be Gentner & Markman (1997). "Structure mapping in analogy and similarity", but again, if you look for work citing this you'll get stuff up to this year, it's an ongoing project. Goldstone has also done a bunch of work in this area, check out Goldstone & Son (2005). "Similarity" in the Oxford handbook of thinking and reasoning for a nice review.

That's probably the most popular/well known approach, but these folks are not the only game in town. There's a more or less independent angle of attack from people interested in Bayesian property induction. Try Tenenbaum, J. B., & Griffiths, T. L. (2001). "Generalization, similarity, and Bayesian inference." This is a BBS paper, so you'll see commentary from all kinds of positions there. Again, search-citing-articles is your friend for the most recent work in this line.

Getting more out into the fringes (where the really fun stuff happens) you could also consider things like transformational similarity (Hahn, U., Chater, N., & Richardson, L. B. (2003). "Similarity as transformation") or the quantum cognition account (Pothos, E. M., Busemeyer, J. R., & Trueblood, J. S. (2013). "A quantum geometric model of similarity"). Don't be turned off by the word 'quantum', the math is quantum but these folks have their feet firmly on the ground. I think you'll enjoy the intro section to this paper, it's the most recent and engages most directly with the idea of context and frames of reference.

Hope this is the kind of thing you were after!

Full refs:

Goodman, N. (1972). Problems and projects.

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

Gentner, D., & Markman, A. B. (1997). Structure mapping in analogy and similarity. American psychologist, 52(1), 45.

Goldstone, R. L., & Son, J. Y. (2005). Similarity. In The Oxford handbook of thinking and reasoning.

Tenenbaum, J. B., & Griffiths, T. L. (2001). Generalization, similarity, and Bayesian inference. Behavioral and brain sciences, 24(4), 629-640.

Hahn, U., Chater, N., & Richardson, L. B. (2003). Similarity as transformation. Cognition, 87(1), 1-32.

Pothos, E. M., Busemeyer, J. R., & Trueblood, J. S. (2013). A quantum geometric model of similarity. Psychological Review, 120(3), 679.
> 5 votes

---
Tags: cognitive-psychology
---


# Question
Title: Math understanding: intuitions and proofs
I think that cogsci can help me to study a problem in philosophy of math. Consider this case (adapted from M. Detlefsen, *Brouwerian intuitionism*):

Lucy has the kind of understanding of a given math subject S that we typically associate with the master mathematician. John has a superb ability to manipulate the axioms for S according to logical means.

Problem: is there a significant difference between Lucy's knowledge of S and John's knowledge of S? Is it true that the second kind of knowledge does not imply the first? Is it true that Lucy *understands* S to a certain significant degree), John does not understand S to a certain significant degree.

Are there works in cogsci that can help me to study this problem?

I have found a relatively old article (Arbib, *A piagetian perspective on mathematical constructions*), but nothing else.

Thanks very much.

# Answer
> 2 votes
I think it is important here to be clear about what John is really capable of doing. If all he is able to do is manipulate the axioms of S *correctly*, this actually does not get him very far, for at least two reasons. (This is also why theorem proving computer programs have significant limitations.)

1) Suppose we give John a specific theorem P of S and ask him to prove P. Can he do it? Not necessarily. There is a set of logical steps based on the axioms that proves P, so it seems within John's reach. But one problem here is that of *computational complexity*. If John proceeds by just, in an undirected fashion, trying to derive new facts of S from the axioms in the hope of eventually arriving at P, the number of paths that he can go down will increase exponentially and it may take longer than the lifetime of the universe for him to arrive at the result. Master mathematicians in the field of S, on the other hand, have sharp intuitions about what is likely to be an *effective* path to a proof of P.

2) Mathematicians do more than resolving previously specified open problems. They also try to generate important new problems. A mathematician who is not very good at formal proofs may nevertheless make a significant contribution by correctly conjecturing a very interesting result (even if someone else needs to prove it).

1) and 2) overlap somewhat; for example, a master mathematician may conjecture a lemma L in S that is extremely useful for proving P.

If John is not able to do 1) and 2), then it's not clear he is really very skilled at S. If he is, then it seems that maybe he isn't so different from Lucy after all; somewhere he has the right intuitions. Maybe Lucy is more consciously aware of her intuitions, perhaps leading into a discussion about what it is like to experience those intuitions. But many of the intuitions of master mathematicians don't come from conscious processing; certain ways of proceeding just *feel right* to them but they can't necessarily explain why.

# Answer
> 2 votes
Some master mathematicians have written on the process of mathematical invention and on some methods of plausible reasoning in mathematics. Here are some references:

Jacques Hadamard. An Essay on the Psychology of Invention in the Mathematical Field.

George Polya. Mathematics and Plausible Reasoning Volume I: Induction and Analogy in Mathematics. Princeton University Press, 1954.

George Polya. Mathematics and Plausible Reasoning Volume II: Patterns of Plausible Inference. Princeton University Press, 1954.

Henri Poincaré. “Intuition and Logic in Mathematics”. In: La valeur de la science. Available here: http://www-history.mcs.st-andrews.ac.uk/Extras/Poincare\_Intuition.html.

You might also find some interesting papers by David Tall, whose field of research is mathematical thinking: http://homepages.warwick.ac.uk/staff/David.Tall/

As suggested by present, in these paper you can find little on symbolic manipulation and a lot on how to approach new and complex mathematical problems with analogy, intuition, and other similar cognitive tools.

---
Tags: cognitive-psychology, learning, philosophy-of-mind, mathematical-ability, creativity
---


# Question
Title: Why is a cross-dominant/ambidextrous brain more susceptible to mental illness?
The left and right hemispheres of the brain are connected by a bundle of fibers called the corpus callosum. Ambidextrous, left handers and cross-dominant people have symmetrical brains as opposed to right handers, who have larger left hemispheres. Cross-dominant, lefties and ambidextrous people also have a stronger corpus callosum which lends itself to better communication between the two hemispheres. It seems like better communication between hemispheres would be an evolutionary benefit.

So, I am curious as to why a symmetrical brain would have a higher rate of mental illness than a right handed/left brained person, as reported in this news release by Imperial College London: Mixed-handed children more likely to have mental health, language and scholastic problems, say researchers

# Answer
This question is still a little broad...

On the issue of corpus callosum (CC) and mental illness, it's not clear that this follows the same pattern as ambidexterity. Highley et al. (1999) found that there *fewer* fibers in CC of women with schizophrenia:

> A reduction in the total number of fibres in all regions of the corpus callosum except the rostrum was observed in female schizophrenic patients (P = 0.006; when controlling for brain weight, P = 0.053). \[...\] With age, all subregions of the corpus callosum except the rostrum showed a significant reduction in cross-sectional area (P = 0.018) and total fibre number (P = 0.002).

They also found "little change in the males".

In fact the press release you linked does *not* mention corpus callosum.

So whatever common factor drives ambidexterity and mental illness, it doesn't seem a simple as the (higher) number of fibers in CC.

---

Also, cross-dominance is a broader concept when it comes to the brain; the press release doesn't mention this term either. Even though Wikipedia considers it synonymous with mixed-handedness, one can have a cross-dominant vision but not cross-dominant handedness, for example. And in fact some of the more recent research has pointed out to different correlations with mental illness of these various types dominance, e.g.:

> The rate of left or mixed-footedness, eye dominance, and any anomalous lateralization, but not handedness, discriminated between those who developed schizophrenia spectrum disorders and those who did not.

Of course they might not have had enough statistical power to detect it (for handedness.) But also a mini-review of prior work on this in the same paper points to somewhat contradictory conclusions, even for handedness, but still says that

> The preponderance of evidence, however, supports the hypothesis that schizophrenia patients are more often left or mixedhanded compared to controls. Left or mixed-handedness in schizophrenia may indicate abnormalities in neurological structure or functioning.

Interestingly this issue of failing to detect the effects of dominance in handedness has been encountered before:

> Several cohort studies have measured childhood laterality as it relates to later risk for schizophrenia (e.g., Crow et al., 1996; Cannon et al., 1997). Crow et al. investigated handedness in the National Child Development Survey, a study assessing all individuals born in the United Kingdom during a single week in 1958. Mothers of children who later developed schizophrenia were more likely to rate their children as ambidextrous at age 7 as compared to mothers of children who did not develop schizophrenia. Additionally, children who eventually developed schizophrenia were less strongly right-handed than controls at age 11.
>
> Cannon et al. (1997) studied laterality in a total population of 5362 children born in England, Scotland, and Wales during one week in March 1946. Results indicated that at age 11, children who later developed schizophrenia showed a significant excess of mixed-eye dominance as compared to the remainder of the cohort. The authors failed, however, to detect a significant difference in hand preference between children who later developed schizophrenia and children who did not. Nevertheless, Cannon et al. interpreted their eye dominance findings as an indication that lateralization might play a role in the pathogenesis of schizophrenia.

And in the genomic age, some genetic candidates correlating with both lateralization and some mental illnesses have been identified...

> Common polymorphisms in the gene PCSK6, whose protein product mediates the development of brain and body asymmetry through the NODAL pathway, have recently been associated with handedness in three studies, making it a key candidate gene for understanding the developmental and expression of human lateralization. We tested the hypothesis that the PCSK6 VNTR polymorphism rs1053972 influences the expression of handedness and aspects of dimensional schizotypy and autism. For a sample of 709 healthy individuals, rs1053972 genotype was significantly associated with categorical measures of handedness, and with dimensional handedness in subsets of the population with high schizotypy and magical ideation or a lack of strong right-handedness. Both findings showed evidence of stronger or exclusive effects among females, compared to males. Genotypes of PCSK6 also showed significant sex-limited associations with magical ideation, a component of positive schizotypal cognition measured using the Schizotypal Personality Questionnaire, and total autism score, measured using the Autism Spectrum Quotient. These results partially replicate previous studies on effects of PCSK6 rs1053972 genetic variation on handedness phenotypes, link the PCSK6 gene with the dimensional expression of neurodevelopmental conditions in healthy individuals, and show that associations of this gene with handedness and psychological phenotypes exhibit evidence of sex-limited effects.

Although the mechanisms by which PCSK6 causes lateralization are somewhat understood, the paper says nothing about how it might cause any of the mental illnesses mentioned. So it looks like researchers don't have any clue beyond the observation that \[lack of\] lateralization is a risk factor for mental illness... except for...

One theory that's been advanced (prior to any genomic knowledge):

> T. J. Crow suggested that the genetic variance associated with the evolution in Homo sapiens of hemispheric dominance for language carries with it the hazard of the symptoms of schizophrenia. Individuals lacking the typical left hemisphere advantage for language, in particular for phonological components, would be at increased risk of the typical symptoms such as auditory hallucinations and delusions.

And a 2009 paper that has Crow among its authors claims to

> show for the first time how the deficit of lateralization in the schizophrenic brain is specific for the phonological component of language. This loss of hemispheric dominance would explain typical symptoms, e.g. when an individual's own thoughts are perceived as an external intruding voice. The change can be interpreted as a consequence of “hemispheric indecision”, a failure to segregate phonological engrams in one hemisphere.

This study wasn't cited much, so I'm not sure how conclusive its evidence was considered by others.

A year later, a paper (in a more prestigous journal) concluded:

> As language lateralization was not significantly reduced in the non-psychotic individuals with auditory verbal hallucinations, a direct relationship between auditory verbal hallucinations and decreased language lateralization can not be established at present.
> 2 votes

---
Tags: neuroscience
---


# Question
Title: Does psychology have a name for the "click" experienced in mathematics?
To understand what I mean, for three days I stared at a formula that looked Greek. Its semantics of relationship was unknown. The mathematics was just one long blur without logic and making no sense. I came back and forth to it. Then one day it was like a veil was lifted over my head and everything "clicked" and made sense.

I remember some of the best mathematics advice I received was "sometimes things click with repeated exposure and this happens a lot in mathematics." I never paid attention to this until I learned to appreciate this "click" phenomenon which I would like study in a more scientific manner but don't know the term(s) I should be looking for.

Thus why I'm here:

**is there even a name for this "click" experience in mathematics?**

There is a name for Déjà vu which even is studied, but what about the "click"?

# Answer
There are concepts like *insight* and the *Aha moment* which are similar to what you describe.

However, the aha moment is more aligned to flashes of insight to discrete problems. While this could be relevant to the experience you are describing of learning mathematics, perhaps you are also describing a more gradual process of learning. Mathematics can be quite complicated. With each iteration of practice, reflection and consolidation, an you typically learn more. At first you made need to go through the material just to get an organising framework. Then on a second read, you can start to apply the organising framework to your interpretation. The meaning of the text and symbols begin to be stored in long term memory, so you can start to focus on the broader meaning rather than spending substantial cognitive resources on the components.

So in general, what you are describing sounds a lot like the process of cognitive skill acquisition. If you want to learn more you could read something like Anderson (1982). Basically, this is a movement from effortful and error prone performance to fluent and relatively error free performance. Thus, at a certain point, you reflect on your performance and you realise that you have acquired the skill.

### References

* Anderson, J. R. (1982). Acquisition of cognitive skill. Psychological review, 89(4), 369-406. PDF
> 4 votes

# Answer
A similar feeling is described by Poincaré and Hadamard about the mathematical invention. For instance, Poincaré recounts: "*I turned my attention to the study of some arithmetical questions apparently without much success \[...\]. Disgusted with my failure, I went to spend a few days at the seaside, and thought of something else. One morning, walking on the bluff, the idea came to me, with \[...\] the \[...\] characteristics of brevity, suddenness, and immediate certainty.*"

You can find their studies in the book and the paper mentioned below:

Jacques Hadamard. An Essay on the Psychology of Invention in the Mathematical Field, https://press.princeton.edu/titles/5896.html

Henri Poincaré. “Mathematical creation”. The Monist, Volume 20, Issue 3, 1 July 1910, Pages 321–335, https://doi.org/10.1093/monist/20.3.321
> 0 votes

---
Tags: cognitive-psychology
---


# Question
Title: Why is the distribution of mean firing rates assumed to be Gaussian?
I'm reading "Principles of Neural Information Theory" by James V Stone and in section 3.5 he says that the distribution of firing rates (of a single neuron) is generally assumed to be approximately Gaussian. He proceeds to give a mathematical argument for this.

If we measure the activity during a period of $T$ seconds over intervals $\Delta t$, there are $N=T/\Delta t$ possible positions for spikes to occur. The probability of $n$ spikes occurring this period is $$p(n)=\frac{N!}{n!(N-n)!}P^nQ^{N-n}$$ Where $P$ is the probability fo a spike occurring and $Q$ is the probability of a spike not occuring. If $N$ and $T$ increase while firing rate $r$ stays constant, $p(n)$ approaches the Poisson distribution. If $T$ is held constant then a simple change of variables can be used to obtain a distribution for firing rate. If $N$ is large and $P$ is small, apparently this distribution is approximated by a Gaussian distribution.

I don't really understand this derivation. It would be nice if someone could provide an in-depth version of the argument with all steps full fleshed-out. I'm particularly confused about how one goes from p(n) to a Poisson distribution.

# Answer
The distribution is not Gaussian, it's Poisson, as noted in your question. However, outside of certain edge cases (e.g. when there are very few spikes, or very few trials), a Poisson Distribution with rate parameter $\lambda$ looks very like a Gaussian with both mean and variance equal to $\lambda$ (standard deviation $= \sqrt{\lambda}$). This is useful, because if you treat the distribution as a Gaussian, you can apply methods such as the t-test or linear regression, without being too far wrong.

Here's some R code that shows the correspondance between the Poisson and the Gaussian.

```
library(tidyverse)
x = seq(0, 30, 1) # Possible spike counts
poisson.density = dopois(x, 10)
gaussian.density = dnorm(x, 10, sqrt(10))
d = data.frame(x = x, Poisson=poisson.density, Gaussian=gaussian.density) %>%
  gather(Distribution, Density, -x)
ggplot(d, aes(x, Density, color=Distribution, linetype=Distribution)) +
  geom_path() +
  theme(legend.position=c(1,1), legend.justification=c(1,1)) +
  labs(x='Spike count')

```
> 3 votes

---
Tags: neuroscience
---


# Question
Title: Why isn't high functioning autism recognized by the DSM-5 or the ICD-10?
I was looking at this https://en.m.wikipedia.org/wiki/High-functioning\_autism and it said that. Aspergers is also closely related to high functioning autism but it is also not recognized anymore. Does this mean that neither of them are a "thing" anymore? Would diagnosing someone with either of these labels be inaccurate?

# Answer
Asperger's being "subsumed" in DSM-5 is not the whole story. There's indeed a new DSM-5 coding for the severity of the disorder. But applying the DSM-5 actual clinical criteria results in fewer people being diagnosed with autistic spectrum disorders, and the reduction is more significant for the mild versions (such as Asperger's):

A 2014 mini-review looking at 12 papers concluded:

> The application of DSM-5 diagnostic criteria resulted in an approximately one third reduction in Autism Spectrum Disorders. The reduction was approximately two thirds for mild forms of Autism.

So yeah, the DSM-5 take (intentional or not) is that a lot of "Aspies" don't have a level of dysfunction that raises to the (DSM-5) bar of a mental \*disorder \*.

However in an astute form of politicking, people with an existing Asperger's diagnosis were "grandfathered in" by the DSM-5. From the same review:

> The American Psychiatric Association partially acknowledged the exclusion of mild forms of ASD when the added rider to the diagnostic criteria was that “Individuals with a well-established DSM-IV diagnosis of autistic disorder, Asperger’s disorder, or pervasive developmental disorder not otherwise specified should be given the diagnosis of autism spectrum disorder”, but this approach to diagnosis of autismis strange. It enables individuals who previously were diagnosed with ASD to continue to be eligible for services, but results in two odd consequences. First, consider two individuals with identical symptoms who meet DSM-IV criteria for ASD, one of whom was diagnosed before the publication of DSM5 and one diagnosed after: The first will be diagnosed with ASD and eligible for services, but the second will not. The second consequence is that the meaning of the DSM5 term ASD is obfuscated as it refers to different entities using the same term.

And a 2016 meta-analysis confirms the effect of stricter criteria (using twice as many studies as the 2014 review):

> Our meta-analysis measured the percentage of people with an ASD diagnosis from the DSM-IV or DSM-IV-TR obtaining an ASD diagnosis from the DSM-5. All 24 studies identified indicated a reduction in the number of people with a DSM-IV or DSM-IV-TR ASD diagnosis being eligible for a DSM-5 ASD diagnosis, a 35 and 37 % reduction respectfully. Our meta-analysis also showed that those with a DSM-IV-TR or DSM-IV diagnosis of PDD-NOS were the least likely to qualify for a DSM-5 ASD diagnosis at 26 and 47 % followed by 55 and 19 %, respectfully of people with Asperger syndrome, and 80 and 87 %, respectfully of people with an autism diagnosis.

A more recent (2017) study on Australian children (where the use of DSM is mandated by certain government programs) found that DSM-5 did seem to stop to the previously increasing trend in rising autism diagnoses:

> De-identified data for 32,199 children aged under 7 years between 2010 and 2015 was utilised. \[...\] The incidence of autism increased from 2010 to 2013, and then plateaued to 2015. A significant trend-relative reduction in the number of children registered to receive autism-specific funding was evident post 2013, suggesting the more stringent DSM-5 criteria may have curbed the trend of increasing diagnoses over time.

---

As for why the DSM-5 removed the separate criteria (including Asperger's), quoting from the last paper:

> These previously distinct diagnostic categories were removed in light of empirical data that questioned the reliability and validity of these subtypes (Daniels et al. 2011; Lord 2012; Macintosh and Dissanayake 2004; Mahjouri and Lord 2012).

Whether this was the right thing to do or not... it depends who you ask. Asperger's diagnosis definitely has its supporters, at least one of whom even predicted its return in the next version of the DSM.
> 4 votes

# Answer
High-functioning autism along with Asperger's syndrome were both subsumed by Autism Spectrum Disorder in the DSM-5 in 2013. The Autism Society has a good page on the distinctions and history of these various diagnoses.
> 2 votes

---
Tags: autism
---


# Question
Title: Is there a non-interactive alternative to the concept of SuperMemo/spaced repetition?
I recently wrote an open-source application that lets you practice Chinese writing and the decisions I made about its inner workings were related to my theories of how human memory works. I'm not sure which facts specifically are relevant, so I'll explain it all in context (scroll down to the the "question" section if you don't believe it's relevant):

The goal of the application is to help user remember the writing of Chinese characters and their pronunciation. The assumption is that the user would input a set of Chinese characters, most of which are non-trivial to write with aid, let alone from memory. Moreover, there is the concept of stroke order which is useful to remember: each character is made of strokes which should be written in a specific shape, position and order. This makes it pretty complex. I heard that the way Chinese people cope with learning this is that they repeat writing of each character 1000 times, but I believe this is not the best use of time, given the number of characters.

The way my program works is that for each input character, user is taught each stroke four times - 1) alone, 2) with all strokes introduced so far, 3) in context and 4) in context but with no aid -- like in this example:

In this example, user is exposed to first four digits in Chinese and should fill in the highlighted strokes, as well as ones already introduced. In each fourth tile, user is expected to fill in all already introduced strokes with no aid, forcing them to focus on geometry.

As you can see, tiles are split into groups that have thicker borders. After introducing the first two characters, there is a special group of tiles at the end of second and beginning of third line: it is blank and contains a pronunciation hint. The user is expected to try to recall the character and write it in its entirety in those tiles.

# Question

This is the part I have a question about: the goal of those specific tiles is to try to get the user to try to recall the characters hoping they eventually land in long-term memory, which should already not be in the working memory because it usually takes more than five minutes to write two characters. Then user is expected to practice next two characters and the drill repeats. Then, user is expected to recall all four characters introduced so far, as shown in the graphic above. This pattern repeats and for characters ABCDEFGH would look like following - hopefully you can deduce how it works:

```
A
B
AB
C
D
CD
ABCD
E
F
EF
G
H
EFGH
ABCDEFGH

```

I showed it to a person interested in psychology and she immediately said: "this reminds me of spaced repetition"! I read about this and also found SuperMemo, and a program that implements it: Anki flashcards.

The problem is that both those programs are based on a formula that prognosticates if the user has already memorized a certain item; with that, they assign relative importance to review this item.

Is there another statistical model of human memory I could use for my application that doesn't have this requirement, but - for example - assumes an "average person" and a certain expected probability that this character will be at a given time remembered?

# Answer
Spaced repetition is based off the forgetting curve. Each review per day strengthens the memory:

Both Anki flashcards and SuperMemo also utilize the Leitner (box) system:

(Animation by Zirguezi \- CC0.)

Other freeware, such as Cram or Quizlet, do not have these enhanced features. They're more for the quick and dirty academic game. The material is only meant to linger for a semester or two. Then it essentially becomes lost in the abyss.

Yet, that's not quite the same breakdown for learning how to *write* Chinese characters correctly. Using the metaphor that the brain is a muscle: It flexes more when writing. See *Writing Strengthens Orthography and Alphabetic-Coding Strengthens Phonology in Learning to Read Chinese*. Writing is more active than reading. The more senses engaged the better. SuperMemo and Anki have algorithms based primarily from *seeing* the information. (Granted, Anki does have the feature where you can write directly on the application.)

At the end of the day there still is a hierarchy based on the user's "history" with the each item. (Also, easier material or material with less chunks will strengthen, therefore lengthen the time until subsequent review.) **Memory has a natural atrophy. There is no avoiding this** (aside from abnormal exceptions). Think of normal brains as having a half-life, a natural rate of decay.

To answer you directly: There are only a few ways: brute repetition, spaced repetition, chunking and the Leitner system. Your app involves repetition with chunking. You could improve from there with different combinations of the current design with spaced repetition and the Leitner system. EDIT: You can approximate a rough spaced-repetition interval, but this will depend on if the user actually completes the worksheet in one sitting and how serious they keep up a consistent practice.

Furthermore, different users will have different obligations and habit forming tendencies. Having added functions, will improve user's experience. For example, a tag feature in Anki allows users to study only cards with the same tag. This is useful for, say, having an exam come up involving a large deck. I recommend sifting though Anki's user manual for more ideas.

---

*Bonus*

I actually was developing my own Android app based on using spaced repetition to remember larger bodies of information (opposed to simple flashcards). The spacing effect for memory is **roughly triple the time** (immediately again, 3 min, 9 min, 30 min, 90 min, etc). Needless to say, I put that project on the backburner. However, there is a similar app for memorizing music pieces. (I am not involved, no kickbacks.)
> 2 votes

# Answer
So basically \[for me\] this question is whether there exists a learning model informed by the structure and usage of the Chinese writing.

The answer is yes, see for example Loach & Wang (2016):

> The question we address is the optimum order in which Chinese characters should be learned.
>
> There are two orders that make intuitive sense: in order of usage frequency, from high to low, and in order of network hierarchy, starting with primitives and building up compound characters using components that have already been learned. The first of these follows directly from the goal of the learner but the second merits further discussion. In general terms, the desirability of learning characters in hierarchal order follows from a broad principle of human cognition, that mastery of a complex system rests on mastery of the relevant features of its sub-components \[14, 15\]. This applies to Chinese characters if one assumes that it is productive to treat them as a complex system rather than as a set of unrelated symbols to be learned by rote. A number of experimental studies indicate that this assumption is valid. They show that orthographic awareness is of critical importance to skilled native readers and in learning to read by both Chinese children and second language learners \[16–22\]. These also show that orthographic awareness is present whether or not it is taught explicitly and, among learners, that the extent of the awareness is correlated with performance \[23\]. We consider learning characters in order of hierarchy to be desirable because we infer that a learning order that explicitly reflects orthographic principles is more likely to generate accurate and productive orthographic awareness in students.
>
> There is, however, necessarily a tension between learning by usage frequency and learning by hierarchy, because frequency is only weakly correlated with character complexity. \[...\] Learning characters in order of frequency would therefore often mean learning characters before their components had been learned, whereas learning them in order of hierarchy would often mean learning rarer characters in advance of more common ones.
>
> When devising a learning order one can choose either of the extremes, of frequency or hierarchy, or attempt to find a balance between them in which some common characters are learned in advance of their components. One previous approach that searched for such a balance was a network theory-based approach by Yan et al. \[24\]. They demonstrated that an algorithmically-optimized, balanced order can be substantially more efficient than one that follows frequency. \[...\]
>
> The tension between frequency and hierarchy is a dominant consideration in determining the learning order but it is not the only one. Small-scale character-to-character patterns are also known to be important, especially for encouraging orthographic awareness \[25–27\]. Patterns can be chosen to emphasize the logic of character construction, by introducing components directly before their compounds, or to emphasize the functional role of components, by presenting their compounds in sets. These patterns are often found in human-curated orders, and especially in books on learning Chinese characters (for example, those of Heisig and Richardson \[28, 29\]). They embody sound educational principles, which can be understood in terms of Marton’s variation theory \[30–33\]. \[...\]
>
> Our algorithm is built on the fundamental assumption that hierarchal orders are the pedagogically desirable way to accumulate usage frequency and we search among this subset of orders for the one that is most efficient. The algorithm is implemented using the conceptual framework of network theory, within which we conceive the network of Chinese characters as a directed analytic graph \[34\]. The nodes in the graph represent characters and the edges represent the structural relationships between them. We devise a measure of node centrality that relates each character’s usage frequency to the effort required to learn it, and order the characters by this measure to provide a first approximation to the optimal learning order. We then sort this list into topological (hierarchal) order using an algorithm designed to minimally disturb the starting order. The algorithm can be applied to any scheduling task where nodes have intrinsic differences in importance and must be visited in topological order.

Looking at the quantitative evaluation section of this paper though, the prior work of Yan et. al seems "good enough" though, and it might less work to implement. I don't know if either of that is suitable for your application or not, as it might require you to redesign it from the ground up. (Also, beware that I can't write in Chinese myself.)
> 2 votes

---
Tags: cognitive-psychology, learning, long-term-memory, writing
---


# Question
Title: What can be the causes of the difference in performance?
The box-plot above represents the number of programming tasks performed correctly in 30 minutes during an experiment by me. Each box represents an age group:

* p1 = 6 - 7 years old
* p2 = 7 - 8 years old
* ...
* p6 = 11 - 12 years old
* s1 = 12 - 13 years old
* s2 = 13 - 14 years old
* ...
* b1 = 16 - 17 years old
* b2 = 17 - 18 years old

When I see the results, I am surprised by the difference between p4, p5 and p6. The set of tasks was almost identical by age. The only difference is that by increasing the age they have some less start tasks. I think it may be due to the ability of reading comprehension and motor development ...

Are there more factors that can influence?

UPDATE

# Answer
Are those reliable differences? Without knowing what confidence intervals you plotted it's difficult to estimate visually (95%? ±1 SD?), but I wouldn't be surprised that there are no statistically significant performance differences between those levels. Keep in mind that if this test emerged only after seeing the data, rather than a priori based on theory, then that changes how to interpret the significance of such tests and makes them less trustworthy:

> HARKing: Hypothesizing After the Results are Known http://journals.sagepub.com/doi/abs/10.1207/s15327957pspr0203\_4

The main finding seems to be an increase with age, possibly non-linear. Thresholding could be due to the task complexity.
> 2 votes

---
Tags: cognitive-neuroscience, learning, metacognition
---


# Question
Title: Why are we so possessive of our significant others?
Something about falling in love seems to make people very possessive about their significant other. This happens even though sharing is almost universally acknowledged as an act of kindness and regarded positively.

For example suppose Alice is married to Bob, and Charlie is their friend (genders don't matter; I'm only using these names because they correspond to A, B and C in the alphabet). If Charlie wants to borrow from Bob:

* a vacuum cleaner, Bob will likely say "sure".
* Alice for a one-night stand (and Alice is willing), Bob will likely say "no way", and might even get violent with Charlie and / or threaten divorce if Alice goes ahead.

Oddly, if Bob refuses to share the vacuum cleaner, outsiders will generally perceive his behavior negatively, but the reverse applies to Bob not agreeing to share Alice. Most outsiders will approve of Bob's stand, which sounds contradictory.

Why do we encourage sharing but discourage infidelity? The only thing I can think of is sexually transmitted diseases - if Bob allows Alice to have a tryst with Charlie, she could become infected with something that she later passes to Bob. But there're many ways to have protected sex these days, so this doesn't seem like a valid reason.

I've not been able to find anything on Google about this - all the results treat different issues.

# Answer
The big hot potato here is the evolutionary hypothesis that men are more sexually jealous whereas women are more emotionally jealous.

Contrast Harris (2003) totally dissing it (but also giving a nice summary of it, which is why I'm quoting it first):

> The specific innate modular theory of jealousy hypothesizes that natural selection shaped sexual jealousy as a mechanism to prevent cuckoldry, and emotional jealousy as a mechanism to prevent resource loss. Therefore, men should be primarily jealous over a mate's sexual infidelity and women over a mate's emotional infidelity. Five lines of evidence have been offered as support: self report responses, psychophysiological data, domestic violence (including spousal abuse and homicide), and morbid jealousy cases. This article reviews each line of evidence and finds only one hypothetical measure consistent with the hypothesis. This, however, is contradicted by a variety of other measures (including reported reactions to real infidelity). A meta-analysis of jealousy-inspired homicides, taking into account base rates for murder, found no evidence that jealousy disproportionately motivates men to kill. The findings are discussed from a social-cognitive theoretical perspective.

Harris (of course) has her preferred counter-theory (as the last quoted sentence suggests; more on that in a moment). The contrast I want to make on the evolutionary issue is with Frederick and Fales (2016):

> One hypothesis derived from evolutionary perspectives is that men are more upset than women by sexual infidelity and women are more upset than men by emotional infidelity. The proposed explanation is that men, in contrast to women, face the risk of unwittingly investing in genetically unrelated offspring. Most studies, however, have relied on small college or community samples of heterosexual participants. We examined upset over sexual versus emotional jealousy among 63,894 gay, lesbian, bisexual, and heterosexual participants. Participants imagined which would upset them more: their partners having sex with someone else (but not falling in love with them) or their partners falling in love with someone else (but not having sex with them). Consistent with this evolutionary perspective, heterosexual men were more likely than heterosexual women to be upset by sexual infidelity (54 vs. 35 %) and less likely than heterosexual women to be upset by emotional infidelity (46 vs. 65 %). This gender difference emerged across age groups, income levels, history of being cheated on, history of being unfaithful, relationship type, and length. The gender difference, however, was limited to heterosexual participants. Bisexual men and women did not differ significantly from each other in upset over sexual infidelity (30 vs. 27 %), regardless of whether they were currently dating a man (35 vs. 29 %) or woman (28 vs. 20 %). Gay men and lesbian women also did not differ (32 vs. 34 %). The findings present strong evidence that a gender difference exists in a broad sample of U.S. adults, but only among heterosexuals.

And what's the (alternative) social-cognitive theoretical perspective? Based on Wikipedia's summary (since Harris' own is waaay too long):

> The social-cognitive perspective proposes the transactional model of jealousy, which can be used to explain why there may be differences in the degree to which individuals experience sexual jealousy within genders, as well as between genders. This model examines how three variables – (1) arousability, (2) commitment and, (3) insecurity – moderate jealousy.
>
> 1. Individual differences in sexual jealousy are determined by the difference in levels of physiological arousal: individuals who are easily aroused have more intense jealous reactions, than those with lower physiological arousal.
> 2. Commitment refers to the degree of dedication a person has in the relationship: the more committed a person is to a relationship, the greater the threat of loss, which leads to greater feelings of jealousy
> 3. Insecurity refers to the perceived level of commitment of the partner: if we perceive our partner to be uninvolved or disinterested in the relationship, we feel more insecure.
>
> The degree to which these factors are experienced together determine the intensity of sexual jealousy felt by an individual.

Wikipedia's summary seems mostly based on Erber, R., & Erber, M. W. (2016). Intimate relationships: Issues, theories, and research. New York, NY: Routledge.

The latter book actually has a chapter (TLDR) and the cheat-sheet at the end lists more theories:

> • Prototype model defines jealousy as a subtype of anger
> • Cognitive appraisal approaches contend that jealousy is a bona fide emotion
> • Bringle’s (1991) transactional theory of jealousy proposes that it arises from the interplay between the individual and the situation
> • Cognitive motivational approaches emphasize attributions and how we think about jealousy-provoking situations
> • The SEM \[self-evaluation maintenance\] approach focuses on the interaction between rival characteristics and the jealous person’s self-evaluation
> • Attachment model of jealousy predicts the intensity and frequency of jealous reactions based on attachment type
> 6 votes

---
Tags: social-psychology, sexuality, love
---


title: Why do errors such as typos happen?

text:
# Question
Title: Why do errors such as typos happen?
Why do typos happen? Why do we sometimes type the same word right, and sometimes wrong?

For the same reason, why does a player of Flappy Bird for instance crash at pipe 138? Why not any of the 137 other pipes, and why not any later?

# Answer
**Short answer**
Multiple factors are in play that affect error making. Cognitive load is an important element that increases the chance of making errors. Other factors are the presence of distraction, levels of stress or level of vigilance.

**Background**
It's a matter of chance. In psychophysics, the field of research I'm spending most of my time in at the time of this writing, models subject responses with psychometric curves. These curves represent the correct rates as a function of the level of the physical stimulus presented (Fig. 1).

Basically, it shows that at high enough stimulus levels the %correct score increases steadily, up to the point where the response is correct for all the trials. In the figure % seen is plotted, for example in a test where image brightness (gamma correction) is varied on a computer screen and the subject is asked if a stimulus is seen yes or no. The characteristic that is mostly reported in such an experiment is the 50% correct point, *i.e.*, the steepest point in the curve. This means that the subject was correct in 50% of the trials.

Now, back to your question - if one not plots intensity, but task difficulty on the x-axis, a similar plot is obtained. Think, for example, speech recognition in noise - when the signal-to-noise ratio increases, %correct will increase. Or, consider a task where cognitive load is slowly decreased, *i.e.*, the task is made easier and easier - then at a certain point the %correct response will also approach 100% (time constraints). Thus, when you are typing, you're typing a lot of characters per minute as you're in a hurry to meet that deadline. And you're thinking about the problem and the solution of the assignment you're working on behind your laptop (cognitive load), your roommates are talking (distraction), and all the while the cat keeps on nestling herself on top of your keyboard (distraction). You might have been working all-nighters, which increases sleepiness that reduces your cognitive abilities overall. These conditions increase mental load and promote incorrect responses (incorrect key strokes) and hence increase the number of typos you make.

If your assignment's deadline was only 3 months from now, and you were already well on your way and you've set yourself the goal of writing one sentence per hour, you wouldn't make any typos at all, because you can look at the keyboard and find every single individual key before pressing it.

It's a matter of cognitive load. Which responses go wrong is all a matter of chance. As Fig. 1 shows, it's a matter of chance that overall results, after many repeats, in a nice psychometric curve.

Fig.1. Psychometric curve. source: Kalloniatis & Luu C (2005)

**Reference**
**-** Kalloniatis & Luu Principles of Vision. In: Kolb H, Fernandez E, Nelson R, editors. Webvision: The Organization of the Retina and Visual System \[2005\]. Salt Lake City (UT): University of Utah Health Sciences Center
> 3 votes

---
Tags: cognitive-psychology, psychophysics, human-error, typing
---


# Question
Title: What are the effects of the "blue eyes/brown eyes" racism exercise?
In the "blue eyes/brown eyes" exercise created by Jane Elliott in the 1960s, she divided a group of schoolchildren by eye color and characterized one of them (e.g., the blue eyed group) as an inferior group. The aim of the exercise is to show how racism works and how it feels to be discriminated against.

Is the exercise effective? What are the psychological consequences of it? Does the exercise still "work" today? What are the ethics when this exercise is done with adults or children?

# Answer
In addition to the descriptions of these particular students, at the site mentioned above by Kate Gladstone and also shown a bit in the documentary (see https://en.wikipedia.org/wiki/Jane\_Elliott)

You might consider what's known from the broader set of studies using this type of manipulation. This rich literature is valuable for your question because the Blue eyes/Brown eyes study was more a demonstration than a study and has not been repeated much (see https://en.wikipedia.org/wiki/Minimal\_group\_paradigm)
> 1 votes

---
Tags: social-psychology, attitudes, racism
---


# Question
Title: Moral Foundations Theory and trigger word combinations
Moral foundations theory splits morality into six categories. In his book, *The Righteous Mind*, Haidt mentioned that looking at church sermons of southern baptist vs less conservative christian Church sermons showed strong moral splits into "Conservative" and "Liberal" mindsets, defined by subsets of the six foundations, in particular those that triggered more often in the texts. Specifically, this was done using a predefined list such as this one and then doing a word count for each category, thereby binning the sermon into one of the two mindsets. Lets call such words "trigger words."

My question is the following: has there been any work done on looking at combinations of these trigger words from different categories? Let me be more specific. Lets take the sentence:

"Hurting a dog is one of the worst things a person can do."

One such trigger word here is "hurting" which is a vice of the Care foundation. This is something that appeals to the Care foundation and will, statistically speaking, be highly agreed with by the Liberal mindset. Also there will generally be less agreement with this from the Conservative mindset. Now, what if we write the sentence as:

"We must respect dogs."

Here, "respect" is a trigger word for the Conservative mindset. Moreover, consider the sentence:

"Hurting dogs is one of the worst things a person can do. We must respect all animals and those who harm them are evil, wicked and sick."

I've purposely overloaded the last sentence with Sanctity and Respect trigger words.

**Question 1**: If one overloads sentences as done above, will it trigger more positive reactions from the Conservative mindset?

**Question 2**: When asked to explain the above overloaded sentences, will both Liberal and Conservative mindsets agree on a similar meaning ("don't hurt dogs")?

**Question 3**: In other words, is there evidence for the ability to trigger low-priority foundations by invoking high-priority ones for a given mindset? I'm am relying here on the notion that words are generally *ambiguous* and *context-dependent*. As well, I am assuming reactions and parsing of meaning is instantaneous and the subject is not given time to reflect and analyze, i.e. intuition.

I'm grossly oversimplifying things here but I hope the general theme of these questions will lead to a nice discussion.

# Answer
I am a research psychologist working with moral foundations theory and messaging and I haven't seen these particular questions addressed. But you maybe interested to see work that uses different framed messages with these 'trigger words' in different populations (e.g., by political orientation) and measures outcomes, e.g.,

> The Moral Roots of Environmental Attitudes - Feinberg & Willer journals.sagepub.com/doi/abs/10.1177/0956797612449177
> 1 votes

---
Tags: social-psychology, reference-request, moral-psychology
---


# Question
Title: What is the name of the effect or concept behind getting along better with people after time apart?
I notice this happens ubiquitously. When siblings are apart in college, or kids away from parents due to college, or even long distance relationships - during a reunion (like over the holidays) only the positives tend to be highlighted, there is generally less fighting and more harmony and the overall relationship feels much better than it would be on average if the separation was not there.

What is the name of this effect, if it has one? Or are there any results/studies about this?

# Answer
In general, I would have said the opposite: there's a robust literature on familiarity driving liking, even with non-social stimuli like shapes:

> https://en.wikipedia.org/wiki/Mere-exposure\_effect

This is also true with people. There may be some kind of an effect whereby people who are familiar and then separated bicker less after the break than before, but I haven't seen this studied. I'd suggest you look at terms like conflict in close relationships for psychological research, e.g.:

> Simpson, J. A., Rholes, W. S., & Phillips, D. (1996). Conflict in close relationships: An attachment perspective. Journal of Personality and Social Psychology, 71(5), 899-914. http://dx.doi.org/10.1037/0022-3514.71.5.899
> 1 votes

---
Tags: social-psychology, perception
---


# Question
Title: How has psychology categorised different types of love?
How has psychological theory categorised the different types of love? What taxonomies of love are most accepted or useful in psychology?

**EDIT:** I went through Triangular theory of love. Are there any other theories like this out there?

# Answer
Sternberg's Triangular theory is certainly well-known. The field you want to dig into more is called 'close relationships'. Here's an accessible treatment of other common theories:

> Summary of psychological theories of love https://www.psychologytoday.com/us/blog/in-love-and-war/201208/love-decoded

This gives a good theoretical overview using many different approaches:

> More abstract positioning of theories of relationships and attachment with relation to other fields http://www.wwnorton.com/college/psych/intimate-relationships/ch/03/summary.aspx

Here's another I learned about in grad school:

> Bem - Exotic Becomes Erotic: Interpreting the Biological Correlates of Sexual Orientation http://doi.org/10.1023/A:1002050303320
> 1 votes

---
Tags: social-psychology, emotion, physical-attraction, love
---


# Question
Title: Why do we see shadows in the following black-and-white optical illusion?
How does neuroscience explain the following optical illusion? Look at tiles. You will see spots of shadow near all corners. The shadow will be missing from some corners very near the center of your attention.

So, the brain has ganglia that detect horizontal and vertical edges as well as more complex edges. They work best with high contrast edges. That's all I know right now that might be relevant. Thanks in advance.

# Answer
> 2 votes
Looks like these are variations on the Hermann grid illusion, wiki page here: https://en.wikipedia.org/wiki/Grid\_illusion

As the wiki page notes, the first-pass explanation of this was lateral inhibition, but this is not really 100% satisfactory. There's a nice quick walk-through of the old explanation and the problems with it here: http://web.mit.edu/bcs/schillerlab/research/A-Vision/A15-2.htm A journal paper version of this stuff from the same lab is: Schiller, P. H., & Carvey, C. E. (2005). The Hermann grid illusion revisited. Perception, 34(11), 1375-1397.

---
Tags: neuroscience, perception, vision, optical-illusion
---


# Question
Title: Converting human's memory into digital data
I am wondering whether converting someone's memory into digital data is possible or not. It may sound ridiculous. However, if chance is not 0 then what kind of studies might be used? What kind of theories and facts can be used to make convert someone's memory into digital data?

I just watched these two videos and now I am even more excited thinking about it. https://www.youtube.com/watch?v=eqKTdIZIBfU

https://www.youtube.com/watch?v=Te6VFZeaADY&index=2&list=PLzCrlK3-4PXyOs4nuDpYSTScUYFJt3L4l (Second video starts at 7:56)

Thank you very much

# Answer
> I am wondering whether converting someone's memory into digital data is possible or not.

Not today, but it is an active area of research.

One non-profit foundation, headed by computational neuroscientist Dr. Randal A. Koene (see also his personal website), that is working in this field is Carbon Copies.

Dr. Koene, in collaboration dozens of others and the Center for Neurogenomics and Cognitive Research (CNCR) (2nd link) has developed simulation software called Netmorph:

> "NETMORPH is a simulation environment for the developmental generation of 3D large-scale neuronal networks with realistic neuron morphologies. In NETMORPH, neuronal morphogenesis is simulated from the perspective of the individual growth cone. For each growth cone in a growing axonal or dendritic tree, its actions of elongation, branching and turning are described in a stochastic, phenomenological manner. In this way, neurons with realistic axonal and dendritic morphologies, including neurite curvature, can be generated. Synapses are formed as neurons grow out and axonal and dendritic branches come in close proximity of each other.".

Also, Wikipedia has a webpage on Mind Uploading and Extracellular Recording.

The ability to make direct electrophysiological recordings from populations of neurons requires multiple parallel recording channels and high sampling rates (\>10KHz) in order to properly characterize action potentials.

Electrodes can be placed on the scalp to record electroencephalograms (EEGs), but that is only the summation of the synchronous activity of thousands or millions of neurons that have similar spatial orientation. There are 64 channel neural probes available to record the action potentials (APs) of individual neurons, but the human brain has around a hundred billion of them:

> "The human brain has a huge number of synapses. Each of the 10$^{11}$ (one hundred billion) neurons has on average 7,000 synaptic connections to other neurons. It has been estimated that the brain of a three-year-old child has about 10$^{15}$ synapses (1 quadrillion). This number declines with age, stabilizing by adulthood. Estimates vary for an adult, ranging from 10$^{14}$ to 5 x 10$^{14}$ synapses (100 to 500 trillion). \[Source: "Do we have brain to spare?" (Jun 27 2005), by David A. Drachman\].

> It may sound ridiculous. However, if chance is not 0 then what kind of studies might be used?

Less than "ridiculous", less than possible too. You would need to install a trillion probes or find a means to externally measure with sufficient resolution, and make low error and low noise measurements. Still it's possible to measure very tiny portions of the human brain, or much smaller brains.

Perhaps neurophotonics can be combined with magnetoencephalography (MEG) to derive a means to obtain high resolution measurements simultaneously over a much larger area.

> What kind of theories and facts can be used to make convert someone's memory into digital data?

You can make digital and analog recording of a small section of the brain today, *playing it back* into another brain or interpreting the information is another matter entirely.

Even identical twins do not have identical genetics (due to copy error or copy number variation (CNV)) or identical brains, see Psychology Today's article: "Identical Twins Are Not Genetically Identical. In addition to recording the information you would need to remap from where it was read to where it was written, much like creating an .ISO file from a CD and burning it to a new disk; a procedure some people find challenging.

National Geographic's YouTube channel has a video titled: "National Geographic Live! - Mapping the Brain | Nat Geo Live" which provides a more in-depth yet accessable explanation, as does the TEDx Talk's channel video titled: "Human brain mapping and brain decoding. | Jack Gallant | TEDxSanFrancisco".

More advanced than the EEG and the functional magnetic resonance imaging or functional MRI (fMRI), which measures brain activity by detecting changes associated with blood flow, is the magnetoencephalography (MEG) functional neuroimaging technique. Even state of the art equipment has limited resolution.

See the Scientific America article about Nature's publication: "A Massive Global Effort Maps How the Brain Is Wired" (Oct 2 2015) which discusses the Human Connectome Project where by the end of the project they will have amassed a petabyte's (10$^{15}$) worth of pictures.

> "HCP collaborators worked with Siemens Healthcare in Erlangen, Germany, to soup up a standard MRI scanner. It generates a 3-tesla magnetic field—comparable to that in standard machines—but can control the field more precisely. MRI scanners use gradients of magnetic fields to aim at parts of the brain, and the stronger gradient of the HCP machine offers faster imaging and better resolution. That creates more-detailed images of axon bundles. A version of their machine is now available commercially, known as the MAGNETOM Prisma (an MRI).".

$$\text{CFT CMEG 275}$$
> 4 votes

# Answer
Rob's answer is good: lots of detail on current research.

What is meant by memory? Nearly all of the operations of the brain are based on or involve retrieving previous states of physiology or activity.

There's a more fundamental problem that remains unresolved: if the exact pattern of activation of your neurons were instantiated in another form, silicon or otherwise, would there be a conscious experience?

> https://en.wikipedia.org/wiki/Hard\_problem\_of\_consciousness https://en.wikipedia.org/wiki/Brain\_in\_a\_vat

I suppose some future technology might be able to operate a non-conscious memory store to retrieve data, but that's much less interesting... to me, at least.
> 1 votes

---
Tags: neuroscience, brain, artificial-intelligence, brain-computer-interface, experimental-neuroscience
---


# Question
Title: What are the differences between Orch OR and Hartley's vibratiuncles?
Roger Penrose and Stuart Hameroff have a theory called ***Orgastrated Objective Reduction*** or Orch OR, and they claim this has been confirmed. The article says:

> "The origin of consciousness reflects our place in the universe, the nature of our existence. Did consciousness evolve from complex computations among brain neurons, as most scientists assert? Or has consciousness, in some sense, been here all along, as spiritual approaches maintain?' ask Hameroff and Penrose in the current review. 'This opens a potential Pandora's Box, but our theory accommodates both these views, **suggesting consciousness derives from quantum vibrations in microtubules**, protein polymers inside brain neurons, which both govern neuronal and synaptic function, and connect brain processes to self-organizing processes in the fine scale, 'proto-conscious' quantum structure of reality."

In the 18th century, **David Hartley** proposed in his book ***Observations of Man*** that counciousness arises when particles of matter vibrate in our brain. Wikipedia says:

> Hartley's physical theory gave birth to the modern study of the intimate connection of physiological and psychical facts. He believed that **sensation is the result of a vibration of the minute particles of the medullary substance of the nerves**, to account for which he postulated, with Newton, a subtle elastic ether, rare in the interstices of solid bodies and in their close neighbourhood, and denser as it recedes from them. Pleasure is the result of moderate vibrations, pain of vibrations so violent as to break the continuity of the nerves. **These vibrations leave behind them in the brain a tendency to fainter vibrations or "vibratiuncles" of a similar kind, which correspond to "ideas of sensation."** This accounts for memory.

**Joseph Priestley** expanded on this idea in his essay ***Disquisitions Relating to Matter and Spirit***. Priestley believed that all matter had the power of attraction and repulsion (fundamental interactions?) and that perception and thought arises from this phenomena in our brain through ***association***. Priestley says:

> **Nothing but a precise and definite knowledge of the nature of perception and thought can authorize any person to affirm, whether they may not belong to an extended substance, which has also the properties of attraction and repulsion.** Seeing, therefore, no sort of reason to imagine that these different properties are really inconsistent any more than the different properties of resistance and extension, I am, of course, under the necessity of being guided by the phenomena in my conclusions concerning the proper feat of the powers of perception and thought.

Giving Hartley and Priestley a little latitude because they lived 300 years ago, is Orch OR basically a reworking of their theories?

# Answer
As far as I can tell, the common theme is that "vibration" is involved in both of them. But that's where the similarities seem to stop.

Hartley formulated specific hypotheses such as

> Pleasure is the result of moderate vibrations, pain of vibrations so violent as to break the continuity of the nerves.

which we now know it's not exactly how these sensations are differentiated, but actually wasn't a bad prediction given the scientific knowledge at the time.

On the other hand Hartley postulated these vibrations to be transmitted by ether, which of course we now know does not exist.

Microtubules are real, but whether quantum vibrations in them have anything to do with consciousness is another matter. As far as I know there's no convincing evidence for it. The Orch OR article on Wikipedia discusses some theoretical criticism as well.
> 1 votes

---
Tags: philosophy-of-mind, neurophysiology, history-of-psychology
---


# Question
Title: Do we understand the non-subjective mechanisms behind pleasure and pain?
If we are to view pleasure and pain as being essentially synonymous with the more mechanistic concept of reward and punishment (i.e. as a part of learning and motivation system) then do we understand how this actually occurs at a neurobiological level? At least in "lower" animals, pain seems to simply cause an aversion response. Pain motivates the animal to stop whatever it was doing (possibly stopping the pain), and to avoid in the future repeating similar responses to those that preceded (and therefore were possibly causal toward) the incident that caused pain.

This sort of thing is not that hard to replicate in computational models, so it is clearly nothing magical. Obviously, the subjective "experience" of pleasure and pain gets more into philosophy of mind and that's not what I am asking about. I am only concerned about the mechanism which can explain outwardly observable behavior -- especially in simpler animals -- such as the basic stimulus-response-reward/punishment learning that a mouse or bird can do.

**Do we understand the mechanism by which a pain signal causes the brain to suppress recently followed decision paths, and a pleasure signal causes the brain to reinforce them?** Or is this still completely mysterious at this time?

# Answer
> 16 votes
I think part of the answer to your question is going to include the dopamine "reward" pathway in the basal ganglia. In particular, a leading theory of dopaminergic function is the **predictive reward error** or **reinforcement learning** hypothesis. In this theory, dopamine neurons signal expectations about the outcome of particular stimuli.

Some key experiments are outlined in Schultz, 1998 (PDF). First, an unexpected reward elicits a short activity increase in dopamine neurons. Second, if a conditioned stimulus (CS) precedes the reward, the dopamine neuron fires in response to the CS but not the reward. That is, the dopamine signal is now a predictive reward signal. Third, if the CS is presented and then the reward does not occur, the response to the CS occurs but the dopamine neuron depresses activity immediately after the reward *should have happened*.

So the theory goes that dopamine neurons are not simply saying whether a reward has occurred, but rather as a learning signal that adjusts predictions about rewards. If an unpredicted reward occurs, the neuron signals a positive error ("Oops, that was a reward I should know about!"). If a predicted reward occurs, the neuron signals no error at the time of the reward ("shrug, I knew that was going to happen"). If a predicted reward does not occur, the neuron signals a negative error ("Aw shucks, guess that bell doesn't mean food after all.").

A somewhat updated revision of the theory is outlined in a review by Redgrave and Gurney, 2006 (PDF). Importantly, they note that dopamine neurons suppress their activity in response to noxious stimuli (the **pain** aspect of your question). They also raise some tough questions about how exactly this dopamine signal interacts with other parts of the brain to mediate the learning suggested in the theory.

As with basically all neurobiology theory, a full understanding of how this signal that we detect in individual neurons translates into a coherent behavioral response program is a long ways away. But the basal ganglia, in general, are sometimes thought of as an action selection system (or "decision path" selection to use your words), so the ability of dopamine neurons to signal expectations is relevant.

# Answer
> 6 votes
Neurobiology is not my field of expertise, but this paper seems relevant:

Kent C. Berridge, Chao-Yi Ho, Jocelyn M. Richard, Alexandra G. DiFeliceantonio (2010) The tempted brain eats: Pleasure and desire circuits in obesity and eating disorders. *Brain Research*, 1350, 43-64.

> What we eat, when and how much, all are influenced by brain reward mechanisms that generate “liking” and “wanting” for foods. As a corollary, dysfunction in reward circuits might contribute to the recent rise of obesity and eating disorders. Here we assess brain mechanisms known to generate “liking” and “wanting” for foods and evaluate their interaction with regulatory mechanisms of hunger and satiety, relevant to clinical issues. “Liking” mechanisms include hedonic circuits that connect together cubic-millimeter hotspots in forebrain limbic structures such as nucleus accumbens and ventral pallidum (where opioid/endocannabinoid/orexin signals can amplify sensory pleasure). “Wanting” mechanisms include larger opioid networks in nucleus accumbens, striatum, and amygdala that extend beyond the hedonic hotspots, as well as mesolimbic dopamine systems, and corticolimbic glutamate signals that interact with those systems. We focus on ways in which these brain reward circuits might participate in obesity or in eating disorders.

You may also be interested in these two book chapters:

Smith, Kyle, Stephen V. Mahler, Susana Pecina, and Kent C. Berridge. “Hedonic Hotspots: Generating Sensory Pleasure in the Brain.” In *Pleasures of the Brain*, edited by Morten L. Kringelbach and Kent C. Berridge, 27–49. New York: Oxford University Press, 2009.

> A vital question concerning sensory pleasure is how brain mechanisms cause stimuli to become pleasurable and liked. Pleasure is not an intrinsic feature of any stimulus, but instead refl ects an affective evaluation added to the stimulus by the brain. That is, as Frijda expresses it (Frijda, this volume; Frijda, 2006), a pleasure gloss or hedonic value must be actively ‘painted’ on sweet or other sensations to make them pleasant. Brain mechanisms of pleasure, whatever they are, must take a mere sensory signal and transform it into a hedonic and ‘liked’ reward.
>
> Finding the brain mechanisms responsible for painting a pleasure gloss is a major challenge for affective neuroscience (Barrett and Wager, 2006; Berridge, 2003b; Damasio, 1999; Davidson, this volume; Davidson and Irwin, 1999; Kringelbach, 2005; Kringelbach, this volume; LeDoux, 1996; Panksepp, 1991; Peciña et al., 2006). Fortunately, progress on fi nding hedonic generators in the brain is being made. In this chapter we focus specifi cally on the neuroanatomical hedonic hotspots in the brain where neurochemical signals actually contribute causally to the generation of pleasure.

Aldridge, J. Wayne, and Kent C. Berridge. “Neural Coding of Pleasure: ‘Rose-tinted Glasses’ of the Ventral Pallidum.” In *Pleasures of the Brain*, edited by Morten L. Kringelbach and Kent C. Berridge, 62–72. New York: Oxford University Press, 2009.

> Pleasure is not a sensation. What is it then? Nico Frijda's answer in the "pleasure questions" section of this book (which he suggested a number of years ago) epitomizes an emerging consensus among many psychologists and neuroscientists (Frijda, Chapter 6, this book). He notes that pleasure "is a 'pleasantness gloss' added to whatever is pleasant". \[...\]
>
> Here we ask: how is a "pleasure gloss" encoded in brain activity? Where in the brain is this glossing operation performed and how does it work? Is it possible for neuroscientists to recognize the signature patterns of neural activity that represent a pleasure gloss? These are difficult questions that are only beginning to be addressed. The "pleasure gloss" metaphor, applied to the transformation of neural signals for a stimulus, is like a varnish that is applied on top of a dull object to transform it into a shiny one. Adding hedonic tone to the signal passed on to downstream structures, the neural gloss effectively gives the entire brain a "rose-tinted" hedonic perception of the stimulus as pleasant.
>
> In the context of neural firing signals, our idea is that a particular pattern of neuronal spikes or action potentials in crucial neurons may apply a glaze of pleasure on what might otherwise be an ordinary sensation or action signal.

# Answer
> 0 votes
To add to yamad's answer (which is pretty good), for about a decade, the way pain was thought to lower the effect of rewards is by tonic release of dopamine; in contrast, pleasure/reward triggers phasic release of dopamine. If you want an (imperfect) electrical analogy, the tonic release is the "DC" level and phasic are transients or spikes on top of that. More correctly:

> Tonic dopamine activity refers to the level of extrasynaptic dopamine that is present at a steady-state concentration in the extracellular space. \[...\]
>
> Importantly, tonic dopamine levels regulate the responsiveness of the phasic dopamine system to salient environmental cues: high tonic dopamine attenuates phasic dopamine release whereas low tonic dopamine facilitates phasic dopamine firing. The level of tonic dopamine in the limbic striatum is in turn modulated by corticostriatal and hippocampal afferents and homeostasis
>
> Increased tonic dopamine is known to result from prolonged stress or pain, a mechanism that might have evolved to ensure rest and low activity levels during injury.

And among the refs cited in support of that is a (pretty highly cited) experiment of Floresco et al. (2003):

> we report dissociable regulation of dopamine neuron discharge by two separate afferent systems in rats; inhibition of pallidal afferents selectively increased the population activity of dopamine neurons, whereas activation of pedunculopontine inputs increased burst firing. Only the increase in population activity increased ventral striatal dopamine efflux. After blockade of dopamine reuptake, however, enhanced bursting increased dopamine efflux three times more than did enhanced population activity. These results provide insight into multiple regulatory systems that modulate dopamine system function: burst firing induces massive synaptic dopamine release, which is rapidly removed by reuptake before escaping the synaptic cleft, whereas increased population activity modulates tonic extrasynaptic dopamine levels that are less influenced by reuptake.

---

That was the view circa 2008. A 2016 review paints a fairly different picture (citing only post-2009 primary studies for this update):

> Recent studies suggest that dopamine neurons in the VTA \[ventral tegmental area\] and SN \[substantia nigra\] form a heterogeneous population tuned to either (or both) aversive or rewarding stimuli.
>
> The heterogeneity of dopamine neurons in response to aversive and rewarding stimuli suggests that they serve unique functional roles. Cells activated by reward and inhibited by punishment are well suited to code motivational valence, whereas neurons activated by both rewarding and punishing stimuli are likely to code motivational salience \[stimulus awareness\]. Neurons coding motivational valence \[whether the stimulus is positive or negative in value\] would provide a signal for reward seeking, evaluation, and value learning, in line with current theories on the role of dopamine in reward processing. In contrast, neurons coding motivational salience would provide a signal for detection and prediction of highly important events independent of valence, pursuant to dopamine's role in salience processing. These distinct aspects of dopamine neurotransmission might be neuroanatomically separate: dopaminergic neurons coding motivational valence have been found more commonly in the ventromedial SN and lateral VTA with projections to nucleus accumbens \[NAc\] shell, whereas neurons coding motivational salience are more often reported in the dorsolateral SN with projections to the nucleus accumbens core.

It's anybody's guess if this is the correct/complete picture. Time will tell.

The primary evidence for this updated view seems mostly based (in order of the number of citations) on 3 papers:

One open problem remains though: how are pain and pleasure balanced by the brain? For example, we expect that an organism could tolerate mild pain in order to reap a reward. Where is this balancing decision made? A tentative answer comes from the authors of the aforementioned review, who in a newer (2017) empirical study found that the decision area in this case is the medial orbitofrontal cortex:

>

Alas this latter study used monetary rewards, so it's not terribly clear how well its result applies to lower species.

---

And on a really interesting \[for me\] research side, in some species dopmamine signaling not only alters behavior but induces morphological changes in response to the environment; examples include both predator (e.g. Echinoid larvae) and prey (e.g. Daphnia) changing their morphology in reaction to prey/predators via dompamine-mediated pathways. Although not obviously related to predator/prey behavior, but to the wider environment; dopamine mediates myopia (eye growth) in humans and other species.

Finally, I only focused on the highlighted question at the end of the questotion-body. Your title question is actually substantially broader.

Just with respect to the rewarding side: liking and wanting are thought to have substantially different neurobiological circuitry, cf. the \[highly cited\] review of Berridge et al. (2009) (whose closely related work Kaj's answer indicated).

A similarly extensive line of work exists with respect to pain (i.e., the aversive side), e.g. see Baliki and Apkarian (2015) "Nociception, Pain, Negative Moods, and Behavior Selection".

---
Tags: neuroscience, behaviorism, sensation
---


# Question
Title: Are Pareto charts identified in the cognitive sciences (and for willpower in particular)?
I'm a layman when it comes to the cognitive sciences. I've read some number of popular self-help books, but not any academic journals. I've noticed that many times a book suggests some techniques for willpower, anxiety management etc., but will never list them out in a prioritized fashion.

While there might be some variation based on the circumstances and the individuals involved, I feel like a one or a few techniques should always dominate the list. The effectiveness of techniques that deal with different cognitive issues is most likely somwhat geometrically distributed (all else being equal), i.e., most of the time they obey the power law (most techniques are moderately effective, but a few are *really* effective).

In particular I'm currently interested in effective techniques for willpower. I'm aware of which techniques are recommended (split a task into subtasks, positive self-talk and many more), but what are their relative effectiveness? Are there some well-executed studies out there that determined which techniques work comparatively better?

**What are effective and generalizable self-regulatory skills and strategies?**

**How do their relative efficacy compare?**

# Answer
Regarding reducing one's anxiety, a "meta-analytic review" by Cheng et al. (2014) published in a fairly high-impact venue suggests that coping flexibility is the stuff that matters... when it comes to coping outcomes, of course. (As the joke goes, madness is doing the same thing and expecting different results.) What exactly coping flexibility is isn't so easy to pin down, but apparently some conceptions of that notion are better than others:

> Researchers have conceptualized coping flexibility in diverse ways: as a broad coping repertoire, a well-balanced coping profile, cross-situational variability in strategy deployment, a good strategy–situation fit, or the perceived ability to cope with environmental changes. \[...\] Studies adopting the perceived ability or strategy–situation fit conceptualization yielded moderate effect sizes, whereas those adopting the broad repertoire, balanced profile, or cross-situational variability conceptualization yielded small effect sizes.

The notion of strategy–situation fit seems largely derived from the CAPS theory. For a more recent (quantitative) work of that kind see e.g. Kato (2012).

The meta-analysis by Cheng et al. also identified a small role played by individualism (and age):

> In addition, the positive link between coping flexibility and psychological adjustment was stronger in samples from countries lower (vs. higher) in individualism and samples with higher (vs. lower) average ages. Individualism and age explained 10% and 13% of the variance, respectively.

(Cheng et al. also conducted a quantitative analysis of publication bias for the set of studies they considered and concluded that "publication bias is not a concern".)

Having said that coping is basically reducing your own stress, which is not the same thing as achieving some externally set goal (e.g. meeting society's expectation in some regard). I'm not sure what research has to say with respect to "willpower" strategies for the latter. Clearly if one considers unreasonable goals in some societies (e.g. eliminating homosexuality) probably no such "willpower" strategy is going to work. It would be more interesting how less incongruent goals fare; from Koestner et al. (2014)

> research has begun to show that support for autonomy facilitates goal progress, whereas more directive forms of support appear to be less consistently helpful, or even unhelpful.

There's a substantial body of work on the effects of goal setting. I'm not incredibly familiar with it, but one highly cited line of work by Locke and Latham (see 2006 update or the Wikipedia page on it) finds that setting high bars is better than "best effort" approaches as far as achievements go.

There's also a substantial body of work on conflicting goals, e.g. see Fishbach and Dhar (2005), but such research doesn't seem to involve ranking strategies. Note that reducing your own anxiety and achieving some externally imposed goal may well be conflicting goals.
> 1 votes

---
Tags: motivation, positive-psychology
---


# Question
Title: Does consumption of amino acid supplements improve human executive function and self-regulation in ADHD cases?
Based on my understanding, executive function primarily takes place in the frontal lobes. Inzlicht and Gutsell found that exhaustion in mental tasks shows itself in decreased activity in the anterior cingulate cortex. The main neurotransmitter in that region, and in the frontal lobes in general, seems to be glutamate. L-Theanine inhibits reuptake of glutamate via EAAT2. However, when a person consumes a L-Theanine supplement, it might not be necessarily the case that the human body will update the neurotransmitter distribution beyond the blood-brain barrier in a tantamount fashion.

L-tyrosine, like amphetamines (prescribed for ADHD), seems to increase dopamine by reuptake inhibition. I have similar concerns to the above (i.e., it might not be necessarily the case that the human body will update the neurotransmitter distribution beyond the blood-brain barrier in a tantamount fashion).

In general, there tends to be a lot of quackery and a lot of p-hacking with small samples when it comes to uses of L-Theanine supplements and natural remedies on health. This might be especially the case in neuroscience, where a lot of treatment effects are hard to trace.

# Answer
> 1 votes
There's a recent negative study: Bergwerff et al. (2016) "No Tryptophan, Tyrosine and Phenylalanine Abnormalities in Children with Attention-Deficit/Hyperactivity Disorder":

> This study is the first to explore AAA metabolism in children with ADHD using a well-defined and relatively large sample. We found that AAA deficiencies are not related to ADHD. The results do not support treatment with AAA supplements in children with ADHD.

Also reviews prior work on defficiency:

> Thus far, five case-control studies have been published on AAA blood concentrations in individuals with ADHD \[21–25\]. Three studies, of which two describing the same sample \[21, 22\], reported lower plasma concentrations of tryptophan, tyrosine and phenylalanine in ADHD \[21–23\]. The other two studies, however, showed increased concentrations of free tryptophan in ADHD \[24\] and a trend towards increased serum concentrations of tryptophan in children with ADHD \[25\]. All five studies are limited by non-standardized assessments of ADHD and small sample sizes (ranging from N = 12 to N = 48), and therefore further research into the availability of AAAs in ADHD is warranted. \[thus their own study.\]

After their negative finding Bergwerff et al. do mention however that:

> We found a relatively high odds ratio of 2.2 for being diagnosed with ADHD when having low phenylalanine concentrations, but this result just escaped conventional levels of significance. Therefore, our study does not definitively rule out that low phenylalanine concentrations are present in (a subgroup of) children with ADHD. For instance, it might be that only children with severe deficiencies in executive functioning have decreased phenylalanine concentrations, as an altered dopamine functioning in the prefrontal cortex and the striatum is thought to impair executive functions, including sustained attention and interference control in ADHD \[8, 67\]

And they also reviewed treatments with supplementation:

> The hypothesis that AAA concentrations are related to ADHD symptoms is the basis for a number of depletion and supplementation studies. Depletion of dietary tryptophan was found to impair sustained attention in adults with ADHD \[30\], and to weaken behavioural inhibition in hostile children with ADHD \[31\]. Supplementation with tryptophan, on the other hand, resulted in a decrease of ADHD symptoms in children with ADHD \[32\]. Tyrosine supplementation decreased ADHD symptoms in adults with ADHD \[33\], but showed no effects on behavioural functioning in children with ADHD \[32\]. Phenylalanine supplementation in adults with ADHD caused a decrease of restlessness and an increase on the ability to concentrate at trend level \[34\], but in children no effects were reported for phenylalanine supplementation on ADHD symptoms \[35\]. However, also these depletion and supplementation studies are limited by non-standardized assessments of ADHD and small sample sizes (ranging from N = 10 to N = 20), as well as the lack of control groups, hampering conclusions regarding the relation between AAAs and ADHD. Therefore, there is a need of further research to support the hypothesis that AAA concentrations may contribute to the expression of ADHD symptoms.

So evidence for AAA supplementation effectiveness for treating ADHD is insofar of low quality; and there are contradictory findings (to put it mildly) on the actual AAA deficiencies in ADHD.

And regarding L-theanine, there's a study, Lyon et al. (2011) on sleep quality in ADHD. Which is probably the way they "salvaged" not observing much else in terms of improvements. The (2006) registration info for that trial had loftier goals to "examine the effects of L-theanine (an amino acid found in green tea) on the behavior, cognitive performance and sleep quality of boys with ADHD."

I tried to find a more systematic (or even meta-analytic) review of supplements in ADHD, but not much with that. It looks like most research on ADHD and diet is on restrictions (i.e. what not to eat), and even that area is full of controversy.

---
Tags: adhd, self-control, neuro-transmitters, drugs, frontal-lobes
---


# Question
Title: Is Dr. Russo’s “endocannabinoid deficiency” a valid theory?
There was a study published in *Neuro Endocrinology Letters* by Dr. Ethan Russo in 2004 that says many diseases being treated with cannabis correlate with an “endocannabinoid deficiency”, but I cannot read the study or find any more information about this.

Are there other studies that can confirm or deny this? Or are there strong or weak arguments in Russo’s study that can help us understand whether it’s a valid theory?

# Answer
I'd say it is a low-impact theory. The original (2004) paper in which this was proposed has around 60 citations in Google Scholar. That's pretty low for a paper like this (if the theory were influential). For contrast a 2000 paper on the monoamine hypothesis for depression (which is far from being the first paper proposing it) has around 460 citations and another one on the same topic from the same year \[probably a theme issue in that journal\] has 440, again according to Google Scholar.

There have been some reappraisals of endocannabinoid deficiency theory, e.g. in 2014 by different authors but in the same low-impact publication (IF \< 1) as the original proposal.

The initial propomotor of this theory has published his own reappraisal in 2016, but I can't even find the impact factor of this latter venue.

In general, deficiency in a given neurotransmitter has failed to satisfactorily explain any single widespread psychiatric disorder. For depression and the monoamines (serotonin etc.) at least here are experimental protocols to test the hypotheses (e.g. ATD), but the results are fairly mixed. Briefly looking at the 2016 paper on endocannabinoid deficiency theory, I'm not even seeing an experimental way to test it like that. So it looks like the evidence is more circumstantial.
> 2 votes

---
Tags: neurophysiology, neuro-transmitters, medication
---