Primate evolutionary tree: a case of eight stage evolution leading to humans?

I have been looking at primate evolution and taxonomic tress for quite some time and am aware that different scholars parse the same tree in different ways, specifically people try to avoid being anthropocentric. I , on the other hand , will focus exclusively on the primate tree as it relates to humans and try to to show that it might be a living proof of the eight stage theory of evolution/ development.

First let me show you a popular way of portraying the primate tree from Philadelphia Inquirer's Going Ape website.

Now, let me show you an alternative classification (just slightly different from this, but based on cladistics) . It is hard to see the figure (I've lost the original full -kleght versions), but the idea is that the first level branching happens at the level of suborder, then infraorder, then family etc within the order of primates.

Here is a similar diagram from the The Third Chimpanzee by Jared Diamond.

It is instructive to note that here barnching within primate tree is as follows:

1. Suborder branching: Prosimians: I hypothesize that prosimian evolution be driven by first adaptive problem that of hiding from / avoiding predators. (lemurs etc)
   
2. Infraorder branching: Platyrrhine (flatnosed) or New World Monkeys: I hypothesize that these would be most adventurous of all and would be focussed on finding food and resources, having mastered the predation problem. Maybe the main factor here would be their range size etc. This family is as opposed to Catarrhine (down-nosed) or Old World primate to which humans belong.
3. Superfamily branching: Cercopithecoidea: Old World Monkeys. Lets say we focus on old world monkeys here. The hypothesis is that they would be specialized for forming alliances and territorial hierarchical behaviors. This superfmaily is as opposed to hominoidea superfamily.
4. Family branching: Hylobatidae or Gibbons: the hypothesis is that Gibbon evolution may be driven by parental investment conflicts. this family is as opposed to Hominidae to which humans belong.
5.  Subfamily branching: Ponginae or Orangutans :  Orangutan evolution may be driven by kin selection concerns.
6. Tribe branching: Panini or gorillas: Gorilla evolution may be driven by theory of mind considerations. Maybe the driving force behind gorilla evolution is reading others mind and we would find good evidence for the same in gorillas. 
7. Species branching: pan of chimpanzees and bonobos and humans: may be driven by communication or language concerns. Of course language or communication in Humans is phenomenal; but may be of equal importance for the other two also.
8.   This species may be a branching of humans later on along sexual selection lines or assortative mating considerations along the lines of Elois and Morlocks.

I am not a primatologists and the above appears too simplistic and fishy to me; but is there evidence for any of the  hypothesis presented above; if so do let me know! Meanwhile I will be on the lookout for any confirmatory evidence!!

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Intentionality: autism research and implications for schizophrenia

Edouard Machery at the Experiments in Philosophy blog writes about a study he conducted with Zalla that found that people with Aspergers syndrome were deficient when it came to identifying purely instrumental desires and the actions resulting from them as intentional actions.  but to understand all that we have to understand the concept of purely instrumental desire. This is best done with the free-cup and extra-dollar cases that Machery has constructed to illustrate this phenomenon:

The Free-Cup Case

Joe was feeling quite dehydrated, so he stopped by the local smoothie shop to buy the largest sized drink available. Before ordering, the cashier told him that if he bought a Mega-Sized Smoothie he would get it in a special commemorative cup. Joe replied, ‘I don't care about a commemorative cup, I just want the biggest smoothie you have.' Sure enough, Joe received the Mega-Sized Smoothie in a commemorative cup. Did Joe intentionally obtain the commemorative cup?

The Extra-Dollar Case

Joe was feeling quite dehydrated, so he stopped by the local smoothie shop to buy the largest sized drink available. Before ordering, the cashier told him that the Mega-Sized Smoothies were now one dollar more than they used to be. Joe replied, ‘I don't care if I have to pay one dollar more, I just want the biggest smoothie you have.' Sure enough, Joe received the Mega-Sized Smoothie and paid one dollar more for it. Did Joe intentionally pay one dollar more?

You surely think that paying an extra dollar was intentional, while getting the commemorative cup was not. So do most people.

Machery likes to analyze the different actions involved in getting a smoothie in terms of their causal structure as well as their valence for the subject (positive valence means actively desired; while negatively or neutrally valanced meaning that one would not like that action to take place normally, but might indulge in if it is instrumental and an intermediate step towards archiving of an ultimate desire.

Thus, in the extra dollar case  quenching thirst is the ultimate desire, buying a smoothie an instrumental desire, while shelling an extra dollar though negatively valued is still a purely instrumental desire as it is requisite for fulfilling the ultimate desire. Thus, normal people would consider paying the extra-dollar as intentional as it was due to an action due to a (purely) instrumental desire.

In the free-cup case, again the ultimate desire is to quench the thirst, the instrumental desire is to buy a smoothie, and the free cup that one gets is neither desired ultimately or as (purely) instrumentally as a menas towards an end. In simple words it is not desired at all and I would like to name it as co-incidental desire as opposed to instrumental desire (because having a special edition cup may still have some valence for joe, though he doesn't actively desire it. Normal as well as Aspergers people deemed getting the free cup as non-intentional.

Where the Aspergics differed was in the extra dollar case. They still thought that paying the extra dollar was non-intentional and Eduoard theorizes that this may be due to inability of those with ASD to consider acts which are merely means towards an end  as having an intentional quality.

I might not agree with the specific theorizing of Machery, but I agree that people with ASD have deficits in intentionality and I have been shouting this from rooftops for quite some time now. I also assert that Schizophrenics have too much concept of intentionality. I would not be surprised if a schizotypal, schizophrenic population was given these above two scenarios and it was found that a co-incidental desire like getting a free-cup was also deemed to be an intentional actions. One could come up with strange rationalizations and explanations and believe that though he just wanted to quench his thirst he went to this vendor only because he also wanted a free cup.  This would be an extreme case of Magical Thinking, but I wont be surprised to see schizophrenics attributing more intentionality than is done by normal people.  I hope someone does the experiment and lets me know! Edouard are you listening?



EDOUARD MACHERY (2008). The Folk Concept of Intentional Action: Philosophical and Experimental Issues Mind & Language, 23 (2), 165-189 DOI: 10.1111/j.1468-0017.2007.00336.x

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Badcock on Edge: the imprinted gene theory of ASD/ PSD

This edition of Edge features an article by Christopher Badcock, about the imprinted gene theory of Autism Spectrum disorders and the psychotic spectrum disorders that he has been developing with Crespi.  It is a must read and has been very nicely done.

He goes on to list the differences between autism and psychosis in a tabular form and then extends this to list the differences between mentalistic and mechansitic cognitions.

Autism/Asperger's syndrome	Psychosis/Paranoid schizophrenia
gaze-monitoring deficits	delusions of being watched/spied on
apparent deafness/insensitivity to voices	hallucination of and hyper-sensitivity to voices
deficits in interpreting others' intentions	erotomania/delusions of persecution
deficits in appreciating shared-attention/groups	delusions of conspiracy
theory of mind deficits	magical ideation/delusions of reference
deficit in sense of personal agency/episodic memory	megalomania/delusions of grandeur
literalness/inability to deceive	delusional self-deception
pathological single-mindedness	pathological ambivalence
early onset	late onset

Mentalistic Cognition	Mechanistic Cognition
psychological interaction with self and others	physical interaction with nature and objects
uses social, psychological, and political skills	uses mechanical, spatial, and engineering skills
deficits in autism, augmented in women	accentuated in autism, augmented in men
voluntaristic, subjective, particularistic	deterministic, objective, universal
abstract, general, ambivalent	concrete, specific, single-minded
verbal, metaphoric, conformist	visual, literal, eccentric
top-down, holistic, centrally-coherent	bottom-up, reductionistic, field-independent
epitomized in literature, politics, and religion	epitomized in science, engineering, and technology
‘pseudo-science': astrology, alchemy, creationism	‘hard science': astronomy, chemistry, Darwinism
nurtured: culturally- and personally-determined	natural: factually- and genetically-determined
belief-based therapies: placebos, faith-healing, psychotherapy etc.	physical effect-based therapies: drugs, surgery, physiotherapy, etc.

He lists down some of the other arguments that I have made viz the fact that Valproic acid exposure in childhood/ pregnancy causes Autism, while valproic acid is used for treating psychosis. Overall it is a very interesting read and a must read.

He also tries to address the mCDD (or simultaneous occurence of Autism and Schizophrenia) in his article, though I find that part the least convincing. Here is what he has to say:

The model appears to rule out anyone suffering from an ASD and a PSD simultaneously, and such co-morbidity does appear to be rare—but is not unknown. However, I know of cases of individuals diagnosed with bipolar disorder who also show unmistakable signs of ASD during their non-manic phases. Indeed, I have research on one individual who suffers from severe gaze-aversion, autistic deficits in a sense of self and social anxiety most of the time, but who becomes comfortable with other people during manic episodes when his sense of self hypertrophies into megalomania with the feeling that he is the returned Jesus Christ! Furthermore, there is evidence of both ASD and PSD in Newton and Beethoven, and incontrovertibly so in the Nobel-prize winning mathematician John Nash. Here the theory predicts that the ASD must come first (typically in childhood) and leave a permanent savant-like basis later built on by hyper-mentalistic tendencies to produce an unusually broadened and dynamically-balanced cognitive configuration: that of true genius.

I find this fascinating and agree with Badcock that the theory leads to many predictions and all these are testable; so we are witnessing a new paradigmatic shift in our understanding of these neurodevelopmental disorders and further experiments would definitely lend more credence to this theory in my view.

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The eight major evolutionary transitions

Regular readers of this blog can vouch for my fascination with the eight stage  theories and would no doubt be sympathetic when I report my exhilaration of finding that none other than Maynard Smith himself has proposed that there are eight major evolutionary transitions till date in the evolution of life. Maynard Smith and  Szathmary in their book The Major Transitions in Evolution had proposed for the following eight transitions :

More details are available at this wikipedia page . now I , independent of any knowledge that this has already been proposed by Maynard Smith as back as in 1995, a few days ago had come up with similar eight transitions in evolution of life forms . Of course there are some differences, but the important thing to note is the similarities(great minds think alike) and of course my model is far more accurate and realistic than Maynard smiths who I believe leap from multi-cellular organisms to humans quite arbitrarily leaving all the phylum in between un addressed.

I'll now briefly note the similarities and also highlight the dissimilarities in our approaches:

The first three stages are identical (first description of Maynard Smith stage and that is followed by my description in a few days ago post) :

1. Transition from Replicating molecules to "Populations" of molecules in compartments
1. Co-Evolution of genes and proteins/ amino-acids

2. Transition from Independent replicators (probably RNA) to Chromosomes
2. Evolution of the chromosome or two strands of DNA

3. Transitions from RNA as both genes and enzymes to DNA as genes; proteins as enzymes (Prokaryotes)
3. Evolution of a simple unicellular prokaryotic-bacteria-like cells

In the fourth stage I differ a bit from Maynard Smith, in that I propose for an intermediate archea type life-feom evolution while they jump straight to prokaroyotes)
4. Trasition from Prokaryotes to Eaukaryotes
4. Evolution of simple unicellular Archea-like cells

In the fifth stage they stress the importance of sex. I stress the importance of organalles, mitochondria and nucleus (specialized cell structures) instead.
5.Transition from Asexual clones to Sexual populations
5.Evolution of simple uni-cellular Eukaryotic like cells

In the sixth stage they move directly to multi-cellular organisms while I introduce intermediate colonies. I believe their fifth stage sexual populations are a substitute for my colonies (both map to protists)
6. Transition from Protists to Multicellular organisms — animals, plants, fungi
6.Evolution of simple colonies of cells (first animal phylum: the porifera or sponges)

In the seventh stage they make a leap and go directly to full-fledged solitary individuals (animals, plants fungi) while I take a more conservative approach and introduce multi-cellular organisms now from colonies.
7. Transition from Solitary individuals to Colonies with non-reproductive castes
7. Evolution of multi-cellular organisms with digestive tracts (second animal phyla coelenterate)

In the eighth and final stage they leap from primates to humans while I stay with multi-cellular organisms but introduce a CNS for the first time.
8.Transition from Primate societies to Human societies with language, enabling memes
8. Evolution of multi-cellular organisms moving towards a CNS( bilaterality) (third animal phyla :Ctenophora (Comb Jellies)):

I believe that after multi-cellular organisms they have made big leaps (which may be justified in some contexts), but I have worked more on micro level and believe that we can gain much more by studying the intermediate phyla too. The important thing to note is the common evolutionary and taxonomic approach and the guiding principles as outlined below for each transition:

Maynard Smith and Szathmary identified several properties common to the transitions:

1. Smaller entities have often come about together to form larger entities. e.g. Chromosomes, eukaryotes, sex multicellular colonies.
   
2. Smaller entities often become differentiated as part of a larger entity. e.g. DNA & protein, organelles, anisogamy, tissues, castes
   
3. The smaller entities are often unable to replicate in the absence of the larger entity. e.g. Organelles, tissues, castes
   
4. The smaller entities can sometimes disrupt the development of the larger entity e.g. Meiotic drive (selfish non-Mendelian genes), parthenogenesis, cancers, coup d’état
   
5. New ways of transmitting information have arisen.e.g. DNA-protein, cell heredity, epigenesis, universal grammar.
   

Hat Tip: Shared Symbolic Storage blog

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Support for the Broken Window

Ed at Not Exactly Rocket Science has an important post  on research by Keizer and colleagues, which found support for the broken windows theory of crime spread. He dos a very good job of describing the broken window theory, the experiments of Keizer et al and how they show that disorder spreads like a virus, so I won't repeat all that here but urge you to go to his blog to get the complete lowdown.  

What I would like to highlight instead is that fact that this Broken window theory was brought to public focus by Malcolm Gladwell in The Tipping Point and subsequently the same theory was thrashed in Frekonomics by Dunbar and surprisingly Malcolm Gladwell had promoted and written an encouraging blurb for Freakonomics. You can read more on the controversy here . I obviously had disliked almost all the explanations in Freakonomics and believe that the book was more on trying to be controversial rather than offering new insights. I , on the other hand, have been sympathetic to Gladwell's writings and it is heartening to note that new research supports the old position that lawlessness spreads via small acts and it may be more important to take care of small, everyday acts of lawlessness than to focus on a few big problems like the cocaine addicts. I would just end with a brief note on Gladwell's new book Outliers, which is on my immediate reading list and I am pleased that he shares some of my thoughts about how SES affects outcomes in life (like IQ) and how we are creatures of circumstances.

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The Science Blog Meme

A meme, that started in Nature Networks  , has slowly gained momentum and as many science bloggers have participated, I think I might as well jump in.

1. What is your blog about?
It is definitely not about catching mice, though I sometimes regret why I chose this particular name from the available zillions. My blog is solely focussed and devoted to psychology and neurosceince; within them some pet themes keep emerging; it started with a focus on cognitive maps; another is the focus on stage theories; then still another is focus on Autism and Schizophrenia as diametrically opposed on a continuum.but I take pride in the fact that most reviewers of this blog have determined this blog to be focussed diffusely on disparate subjects.

2. What will you never write about?
about my day-to-day humdrum existence as I lack the capacity to make that sound interesting. Also I like to keep the personal separate from professional as far as possible.

3. Have you ever considered leaving science?
The question is a bit odd, as I am not a working scientist and my science focus is part-time; but leaving science as a hobby/ part-time vocation seems unthinkable - perhaps if all the applied uses of science have been exhausted I may think of leaving sceince; but till the time there is much to be discovered and applied in the real world; there is no parting company.

4. What would you do instead?
Social Work (though for some reasons I don't like the word..juts like the concept of working for the disadvantaged)/ Education and guidance---of course the assumption is that I have all the resources to enjoy my present lifestyle and only then in my free time instead of science do these things.

5. What do you think will science blogging be like in 5 years?
It should replace scince journalism even before that and might perhaps be replaced by somemore disruptive technologies. It would be more actual science and less reporting. The science would be prominent over the blogging part and both will happen collaboratively.

6. What is the most extraordinary thing that happened to you because of blogging?
In the real world, not much! In the online world, I met and befreinded many interesting, prominent and like-minded people. Overall, blogging provided me a much needed outlet for sharing all the knowledge/information that I was accumulating but finding no outlet for.

7. Did you write a blog post or comment you later regretted?
Yes, one or two blog posts I regret to have written. even today, I feel embarrassed when someone comments on them.


8. When did you first learn about science blogging?
I believe it must have been 3 years back; as soon as I learnt about that I started my own blog!!


9. What do your colleagues at work say about your blogging?
Not many at my work place read my blog or are aware of its existence; for those who are aware its more of a personal eccentricity and a freaky thing - though I have received some very positive feedback too from some; but most say it is incomprehensible and too technical for them (my workplace is not in a scientific setting/ concerned with psychology/ neuroscience)

10.Extra credit: are you able to write an entry to your blog that takes the form of a poem about your research?
I believe I am able, for I pride myself as the next big thing- an undiscovered poet/ creative writer that is just waiting for the right break; the bad part is that I maintain a dedicated creative writing blog , that is separate from my scientific blog, so have never mixed the too, so am not quite sure!!

Thats it folks! I love these memes, especially those that come without any tagging requirements!!

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Autism and Schizophrenia co-occurence

Socrates has raised an important point in one of the recent comments that if Autism and Schizophrenia are opposite poles , how do you explain their (rare) simultaneous co-occurrence?  This same question has been raised by other commentators (like Julia)  before and though I have responded in the comments, I'll like to highlight the earlier response here for the benefit of all readers. Here is one of my earlier responses to the prevalance of mCDD and I hope to stimulate some discussion on this:

One way to look at this (mCDD) would be to treat this as similar to mixed episodes in bipolar disorder. Here both symptoms of Mania and depression are present in the same individual though traditionally Mania and depression are thought of as opposite poles on a continuum. In effect though Autism and Schizophrenia/psychosis are opposite extremes, in some individuals both may be present. However, also note the differences form mixed episodes in bipolar; there the mixed state as well as mania and depression happen in the same individual over time; here the disorders itself are simultaneously present in the individual.

Another example I can think of is of recessive alleles for both disorder at the same gene locus. (lets for example consider that eye color is due to recessive alleles at the eye-color locus). Now suppose that recessive allele S confers risk of schizophrenia and N is the normal variant. so SS is schizophrenic; SN is on the continuum toward schizophrenia and normality, perhaps a schizotypal individual. Suppose also that recessive allele A at the same locus makes one susceptible to Autism (they are opposite poles so evidently should work on same locus / loci). Thus AA is autistic and AN is asperper's; now consider the rare scenario where one gets AS genotype ; in this case one might be asperger's and schizotypal; in rare scenario this may develop into full-blown child-onset schizophrenia and classified as PDD_NOS or McDD.

To test my theory one can see the frequencies of Autistic and Schizophrenics and also the McDD iondividuals. If there was no interaction, Autism and schizophrenia should be independently inherited and P(mcDD) = P(Autism) * p(schizophrenia) where P is probability of an individual in a population belonging to that disorder. As my theory predicts there should be some interaction (the gene locus is same), so P(mcDD) should be different from that calculated from above (though I lack the requisite math knowledge to come up with a good formula!)

 I believe I owe a bigger response to the questions raised, but I am hoping this to turn out as more of a conversation, then a one -sided defense of my pet theory,  and would encourage more and more readers to get involved and propose new and radical solutions to this conundrum that has been highlighted!  Also any statistics on the co-occurrence and individual occurrence and prevalence of Autism and schizophrenia would be more than welcome

 

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Decision-making research in autism and schizophrenia: Implications for each other

Today I would like to review two recent articles on decision-making: one concerned with autism or ASD and the other with Schizophrenia individuals. I would like to demonstrate how some of the findings fit in, in the larger context of Autism and Schizophrenia as diametrical poles on a continuum.

The first article is by Martino et al, and discusses a finding that those with ASD display more consistent and logical decision-making that is immune to framing effects.  Here is the abstract of the study:

The emotional responses elicited by the way options are framed often results in lack of logical consistency in human decision making. In this study, we investigated subjects with autism spectrum disorder (ASD) using a financial task in which the monetary prospects were presented as either loss or gain. We report both behavioral evidence that ASD subjects show a reduced susceptibility to the framing effect and psycho-physiological evidence that they fail to incorporate emotional context into the decision-making process. On this basis, we suggest that this insensitivity to contextual frame, although enhancing choice consistency in ASD, may also underpin core deficits in this disorder. These data highlight both benefits and costs arising from multiple decision processes in human cognition.

Here is the introduction:

Logical consistency across decisions, regardless of how choices are presented, is a central tenet of rational choice theory and the cornerstone of modern economic and political science. Empirical data challenge this perspective by showing that humans are highly susceptible to the manner or context in which options are cast, resulting in a decision bias termed the "framing effect". We have previously shown that the amygdala mediates this framing bias, a finding that highlights the importance of incorporating emotional processes within models of human decision making. An ability to integrate emotional contextual information into the decision process provides a useful heuristic in decision making under uncertainty. This is a factor that is likely to assume considerable importance during social interactions in which information about others is often incomplete, ambiguous, and not easily amenable to standard inferential reasoning processes.

In this study, we investigated the effect of contextual frame on choice behavior of individuals with autistic spectrum disorder (ASD). Autism is a neurodevelopmental disorder characterized by deficits in social interaction, qualitative impairments in communication, and repetitive and stereotyped patterns of behavior, interests, and activities. From Kanner's earliest description, it has been recognized that individuals with ASD have a strong tendency to focus on parts rather than global aspects of objects of interest and are unable to integrate disparate information into a meaningful whole (weak central coherence theory).

We previously proposed that susceptibility to a framing bias reflects the operation of an affect heuristic. Here, we show that individuals with ASD, a condition characterized by marked behavioral inflexibility, demonstrate a decreased susceptibility to framing resulting in an unusual enhancement in logical consistency that is paradoxically more in line with the normative prescriptions of rationality at the core of the current economics theory. Furthermore, insensitivity in these subjects to a contextual framing bias was associated with a failure to express a differential autonomic response to contextual cues as indexed in skin conductance responses (SCRs), a standard measure of emotional processing. Our findings suggest that a more consistent pattern of choice in the ASD group reflects a failure to incorporate emotional cues into the decision process, an enhanced economic "rationality" that may come at a cost of reduced behavioral flexibility.

The experimental procedure used framing of gambles in terms of loss and gain and it is a well established paradigm that shows that normal people are risk-averse when the same gamble is framed in gain terms and risk-prone when the same gamble is framed in loss terms. Autistcis were not only more risk-averse in general , but their responses did not differ in relation to whether the frame was of loss or of gain. Thus, they were consistent in both the framing conditions. also , a measure fo their skin conductance did not show differential activation in the two frames of loss and gain; while the SCR of controls differed significantly. thus, teh authors conclude that it is the inability to take into account emotional information, that results in the consistent response of the autistics.Here is the discussion:

These findings suggest the ASD group fail to integrate emotional contextual cues into the decision-making process. This is evident both in a reduced behavioral susceptibility of a framing effect and an absence of a differential SCR response to our contextual manipulation. The concept that ASD individuals fail to integrate information across cognitive domains also informs the suggestion that an uneven profile of abilities and deficiencies in autistic individuals may reveal an imbalance in empathizing and systemizing behaviors (Baron-Cohen and Belmonte, 2005)

They discuss these findings in terms of the two-system theory of decision-making and here is what they have to say:

Recent theoretical accounts of decision making have put forward a "two-systems" model of human judgment (Evans, 2003). This view proposes that human decision making arises through a combination of intuitive and analytic processes. This model proposes that intuitive reasoning is rapid and capable of processing large amounts of information in parallel; however, it is prone to mistakes and strongly influenced by contextual emotional information (Kahneman, 2003). In contrast, analytical reasoning is more accurate but slow and computationally demanding. According to this view, the framing bias reflects an affect heuristic by which normal individuals incorporate a potentially broad range of additional emotional information into the decision process. In evolutionary terms, this mechanism may confer a strong advantage because such contextual cues may carry useful, even critical, information that dictates a rapid response. We propose that this ability is particularly crucial in a social context in that subtle contextual cues communicate knowledge elements (possibly unconscious) that allow optimal decisions to be made in uncertain environments (Stanovich and West, 2002).

In the context of the "two-systems" model of decision making described above, these results suggest that ASD individuals have an increased tendency toward the analytic type of decision making, attributable to impairment within their intuitive reasoning mechanisms. This interpretation would also support the empathizing-systemizing (E-S) theory of autism (Baron-Cohen and Belmonte, 2005). The E-S theory proposes that the imbalance between analytic and empathic behavior underlies both the impairment in social skills in ASD and their enhanced analytical skills. During the framing task, ASD subjects were better able to ignore biasing contextual information and isolate the critical information about the numerical value of the sure and risky options. This result is consistent with other experimental findings showing that ASD have enhanced attention for the task's details but reduced capacity to deal with the global aspect of the task as predicted by weak coherence theory (Frith and Happé, 1994).

Now, I am just overjoyed reading the above. It has always been my contention that Autistics use a more deliberate, rational approach to decisions while schizophrenics are at the opposite end relying on the intuitive part. I elaborated it in the form of Maximisers and Satisficers distinction that Barry Scwatrz has proposed and extended it to include exploration and exploitation in general. In short my thesis was, and remains, that autistics are more analytical while decision-making and schizophrenics more intuitive . the former does not take the context or frames into account while making decisions while the other takes into account too much context and is susceptible to too much framing effects.

If the above thesis is correct it leads to many testable predictions:

• 1) Schizophnrenics/ Schizotypal individuals should be more susceptible to framing effects and should show greater inconsistencies in decision-making under uncertainity as compared to controls.
  
• 2) They may also show more SCR variability when different frames of loss and gain are presented to them as compared to controls.
  
• 3) They may have higher baseline risk-prone behavior than controls in all conditions.
  
• 4) They may have higher activation in amygdala than controls as they use affect heuristic quite frequently while making decisions.
  

Part of this prediction may be satisfied by this decision-making and schizophrenia study by Ludwig et al  that found decision-making dysregulation in first episode Schizophrneia patients. Here is the abstract of the study:

Studies with chronic schizophrenia patients have demonstrated that patients fluctuate between rigid and unpredictable responses in decision-making situations, a phenomenon which has been called dysregulation. The aim of this study was to investigate whether schizophrenia patients already display dysregulated behavior at the beginning of their illness. Thirty-two first-episode schizophrenia or schizophreniform patients and 30 healthy controls performed the two-choice prediction task. The decision-making behavior of first-episode patients was shown to be characterized by a high degree of dysregulation accompanied by low metric entropy and a tendency towards increased mutual information. These results indicate that behavioral abnormalities during the two-choice prediction task are already present during the early stages of the illness.

The authors used the CT paradigm and it is important to explain that a bit here:

The purpose of the CT is to quantify decision-making characteristics based on the individuals’ sequential response patterns, which result from repeated selections of different alternatives associated with an uncertain outcome. Each subject received computerized instructions. The subject’s task is to predict on which side a stimulus (a car on the screen) will appear and select a response (to match up one of 2 figures shown on the screen) accordingly. The outcome is shown for 250 milliseconds after the subject has selected as response. A new trial begins immediately after the car has been displayed. The subject is not given any information about the sequence of the stimulus presentations, i.e., whether the stimulus is presented randomly or in any kind of order. Unbeknownst to the subjects, the location of the car shown is based on the subject’s response, i.e., the subject “correctly” predicts the location of the car in 64 trials. The basic measurements consist of the subject’s response, the presentation of the car and the latency of the response selection process, i.e., the time from the beginning of the trial to the pressing of the button. For the behavioral analysis, we used nonlinear methods— described elsewhere in detail (Paulus et al., 2001)—to obtain the following key measures:

Dysregulation: Dysregulation quantifies the range of response sequence entropies during the course of an experiment.A high dysregulation value indicates that the response sequences occurring during the experiment are characterized by botho¨perseverative tendencies“ and highly unpredictable or dynamically ”chaotic” strategies.

Metric entropy: Entropy measures the “sequential order” within sequences of responses. Whereas low entropy indicates that the response sequences are highly predictable, high entropy implies highly unpredictable response sequences. Thus, predictability is a collateral measure for the degree to which sequences of responses are based on a consistent internal strategy. However,this measure does not take into account the dependence of the response sequence on external stimuli, which is measured by the cross-mutual information (see below).

Mutual information: Mutual information quantifies the degree to which the previous response predicted the current response and provides a measure of the immediate influence of the past response on the decision in the current trial.

Cross-mutual information: Cross-mutual information quantifies the degree to which the previous location of the stimulus (presentation of the car on the LEFT or RIGHT hand side) is able to predict the current response. As opposed to entropy and mutual information, this measure quantifies the influence of external stimuli on the response sequences.

Switching probability: the probability of using the simple strategy RIGHT – LEFT.

Reaction time: the time between stimulus and response.

What they observed is summarized below:

As shown above in the results section, first-episode patients performing this decision-making test, irrespective of whether they were unmedicated or recently medicated, can be observed to have (a) more dysregulated behavior, (b) a reduced metric entropy, and (c) a tendency towards increased mutual information. As a specific response behavior (d), the patients used the switching strategy more intensely (switching between pushing the right and the left button). This study has supported our main hypothesis that decision-making dysfunctions are already present in first-episode schizophrenia (or SZ) patients.

I believe the results need some explanation, and I will stick my neck out here. More dysregulated behavior in my view, is due to the schizophrenic either trying too hard to remain consistent (when in self-aware frame of mind) or trying to be unpredictable (when in other-aware and being-watched frame of mind). The reduced metric entropy can be explained similarly . Tendency towards increased mutual information is quite informative in my view. It seems that the schizophenreic is working on the basis of an internal model and is ignoring external feedback: thus his reliance on previous response.I propose that an opposite pattern would be observed in Autistics with Autistics showing no or less mutual information, as they have poor self-models; but greater cross-mutual information , as they would base their decisions more on external stimuli or feedback.

Some other predictions, keeping in mind the autism is opposite of Schizophrenia theory are:

• 1) Autistcis should show lesser dysregulation and more rational behavior than even controls.
  
• 2) autistcis should show greater cross-mutual information than controls.
  
• 3) Autistcis may or may not show lesser mutual information.
  
• 4) Autistcis should use less switching strategy than controls.
  

All these are testable predictions and I hope someone out there tests these and lets me know!

B. De Martino, N. A. Harrison, S. Knafo, G. Bird, R. J. Dolan (2008). Explaining Enhanced Logical Consistency during Decision Making in Autism Journal of Neuroscience, 28 (42), 10746-10750 DOI: 10.1523/JNEUROSCI.2895-08.2008
Cattapan-Ludewig Katja; Ludewig Stephan; Messerli Nadine; Vollenweider Franz X; Seitz Antonia; Feldon Joram; Paulus Martin P (2008). Decision-Making Dysregulation in First-Episode
Schizophrenia The Journal of nervous and mental disease, 196 (2), 157-160

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