Archive for November, 2008
Badcock on Edge: the imprinted gene theory of ASD/ PSD
Nov 24th
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
Nov 21st
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:
- Smaller entities have often come about together to form larger entities. e.g. Chromosomes, eukaryotes, sex multicellular colonies.
- Smaller entities often become differentiated as part of a larger entity. e.g. DNA & protein, organelles, anisogamy, tissues, castes
- The smaller entities are often unable to replicate in the absence of the larger entity. e.g. Organelles, tissues, castes
- 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
- 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
Nov 21st
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
Nov 17th
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
Nov 17th
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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