The Psychological & Neuroscientific musings of sandygautam
neuroscience
Perceived age as a bio-marker of ageing
Dec 15th
Do you look younger than your age? If so you have reasons to cheer! According to a new study as per Kaare et al, the perceived age is directly related to the actual ageing and inversely related to your telomere length.
It is well established that telomere length is a good indicator of ageing and also plays a crucial role in diseases like cancer, and when it becomes too small hastens cell apostasies. in this study, what Kaare et al found that of the twins, the one who had more perceived age also had a shorter telomere length on average and thus was more aged.
They also found a long -term effect of perceived age on mortality and thus more corroborating proof about this association. They used a cohort study of twins to reach their conclusions. I’ll quote from their abstract and discussion:
Results: For all three groups of assessors, perceived age was significantly associated with survival, even after adjustment for chronological age, sex, and rearing environment. Perceived age was still significantly associated with survival after further adjustment for physical and cognitive functioning. The likelihood that the older looking twin of the pair died first increased with increasing discordance in perceived age within the twin pair—that is, the bigger the difference in perceived age within the pair, the more likely that the older looking twin died first. Twin analyses suggested that common genetic factors influence both perceived age and survival. Perceived age, controlled for chronological age and sex, also correlated significantly with physical and cognitive functioning as well as with leucocyte telomere length.
Conclusion: Perceived age—which is widely used by clinicians as a general indication of a patient’s health—is a robust biomarker of ageing that predicts survival among those aged 70 and correlates with important functional and molecular ageing phenotypes.
Perceived age predicts survival among people aged 70, even after adjustment for chronological age, sex, and other readily measurable biomarkers of ageing. Perceived age also correlates with age related phenotypes such as physical and cognitive functioning and leucocyte telomere length. Clinicians use perceived age as part of their assessment of patients, but research on the validity of the approach has been sparse.1 13 14 We have shown that perceived age based on facial photographs is a robust biomarker of ageing that does not depend on the sex, age, and professional background of the assessors. In our analysis, the comparison within pairs of dizygotic twins controlled for rearing environment and, on average, half the genetic factor variants present in a population, while the comparison within pairs of monozygotic twins controlled for all genetic factors and rearing environment. We found indication of common genetic factors influencing both perceived age and survival because controlling for genetic factors (the comparison within monozygotic pairs) removed the association between perceived age and survival (fig 3). This was in contrast with the results for the overall twin sample and for the dizygotic twins, where comparison within pairs showed a clear “dose response” association between perceived age and survival (fig 2). Hence, the comparison within pairs suggests that there are genetic factors influencing both survival and perceived age (for example, genetic factors that influence the condition of cardiovascular tissue could affect the risk of myocardial infarction as well as the appearance of skin). Full details of this study design can be found elsewhere.
it is important to note that they found the association only in dizygotic twins and not in monozygotic twins, so apparently genetic factors determine both perceived age and actual mortality/ageing. If the effect had been also found in monozygotic twins perhaps epigenetic /non-shared environmental factors would be the deciding factor, but in their absence it is wise to conclude that genes are the third factor that has led to perceived age and ageing correlation and neither is causative of the other. Alternately , underlying tissue ageing might directly affect perceived age and might be evolutionary coded for m, especially in females, so that males could determine the youth and fecundity accurately. In that way the direction would be causal but in the other direction.
What it means is that if you have young looks as per your age, there is reason to rejoice; if not you can not do much by looking young even if you indulge all your money in face lifts etc. Of course there are other benefits of looking young artificially, but increased actual age might not be one of them.
Christensen, K., Thinggaard, M., McGue, M., Rexbye, H., Hjelmborg, J., Aviv, A., Gunn, D., van der Ouderaa, F., & Vaupel, J. (2009). Perceived age as clinically useful biomarker of ageing: cohort study BMJ, 339 (dec11 2) DOI: 10.1136/bmj.b5262
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Nov 20th
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I recently came across this article by Rosengren and Hickling about how children explain seemingly impossible or extraordinary transformations in terms of magic or trickery or natural/physical explanations based on their ages and developmental level.
To summarize the study , I’m presenting the abstract:
Children’s magical explanations and beliefs were investigated in 2 studies. In Study 1, we first asked 4- and 5-year-old children to judge the possibility of certain object transformations and to suggest mechanisms that might accomplish them. We then presented several commonplace transformations (e.g., cutting a string) and impossible events (magic tricks). Prior to viewing these transformations, children suggested predominantly physical mechanisms for the events and judged the magical ones to be impossible. After seeing the impossible events, many 4-year-olds explained them as “magic,” whereas 5- year-olds explained them as “tricks.” In Study 2, we replaced the magic tricks with “extraordinary” events brought about by physical or chemical reactions (e.g., heat causing paint on a toy car to change color). Prior to viewing the “extraordinary” transformations, children judged them to be impossible. After viewing these events, 4-yearolds gave more magical and fewer physical explanations than did 5-year-olds. Follow-up interviews revealed that most 4-year-olds viewed magic as possible under the control of an agent (magician) with special powers, whereas most 5-year-olds viewed magic as tricks that anyone can learn. In a third study, we surveyed parents to assess their perceptions and conceptions of children’s beliefs in magic and fantasy flgures. Parents perceived their children as believing in a number of magic and fantasy flgures and reported encouraging such beliefs to some degree. Taken together, these findings suggest that many 4-year-olds view magic as a plausible mechanism, yet reserve magical explanations for certain real world events which violate their causal expectations.
In effect, the children were shown some impossible transformations like making color appear on the pages of a blank coloring book; at the same time they were also shown some commonplace transformations like a piece of Play-Doh changing shape. They were asked to provide causal reasons for these transformations both a priori and after the transformations were demonstrated. Important form my point of view was the finding that all children showed this effect that for impossible transformations though before the vent they provided physical/natural explanations, after seeing the event, they changed their stance and labeled them as ‘magic’ or ‘trick’ as per their development level. To quote:
Children of both ages gave more physical/natural explanations prior to seeing the transformations than after seeing the events, F(l, 46) = 36, p < .001, but gave more trick and magic responses after seeing the transformations than before seeing them, Fs(l, 46) > 50, p < .001. Very few magic explanations were provided for the commonplace events before or after the viewing of the events; however, both groups of children provided significantly more magic explanations following the magic events than prior to these events. There was no difference between the two age groups in the number of magic explanations given prior to seeing the magic events; however, after viewing the magic events the 4-ye£ir-oIds gave significantly more magic responses (M = 2.96) than the 5-year-oIds did (M = 1.09). Similar to the results for the magic explanations, few trick responses were provided for the commonplace events before or after the viewing of the commonplace events.
To me this is a significant result, that after seeing something impossible we classify it as either magic or trickery, but prior to that we believe we could have provided a natural and causal explanation. To take an example, we all know statistics and would agree that there is a statistical probability that we are thinking of someone and the person phones at the same time. However, when we do think of someone and he calls at the same time and this happens say once or twice in a row, we will not tend to resort to statistical reasoning; we’ll either think in magical terms (magical thinking- my intention to remember/talk to them caused them to phone me; or psychic ability- that there is a deep connection between us) or we will try to think this a as a trickery played on us (perhaps they or someone is secretly watching me and my intentions and as soon as I reach to make a phone call, they call me instead juts to make fun/play a silly trick). Both types of thinking are fertile ground for psychosis and delusions.
It is now known that many people prone to psychosis suffer from an unusual amounts of anomalous experiences and also have magical ideation. To those of us who do not have those unusual experiences, it is very easy to dismiss what the effects having such anomalous experiences would have on our causal thinking abilities. We in our blue-pill Matrix where things are ordered and in their place following known causal relations, believe everything is fine with the world. to someone who has taken the red pill and is having anomalous experiences, it is difficult to believe that there isn’t a world apart from the matrix where magical rules may apply! (OK, the matrix analogy is not good, but it does make a point that it is difficult to comprehend the reality that someone delusional may be living in).
To return to my example of thinking of calling someone and picking the phone and at the same time receibving a callfor that perosn, such coincidences may be marked as causal by psychosis prone minds beacue again they have been hypothesized to have high and sensitive coincidence detectors and a ‘jump to conclusions’ bias. Given these facts they may be more prone to attribute magical causality instead of normal causality and get freaked out. Magical thinking and delusions may follow naturally from these. Anomalous experience may not just be important to explain hallucinations, but may be important for explaining delusions too.
Rosengren, K., & Hickling, A. (1994). Seeing Is Believing: Children’s Explanations of Commonplace, Magical, and Extraordinary Transformations Child Development, 65 (6) DOI: 10.1111/j.1467-8624.1994.tb00838.x
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Oct 31st
I have just started a new blog called My 2 Brains and you can read more about that blog and what topics and themes it will cover over here.
One of the first posts is about the real-time stream and analyzes it from a psychological perspective focusing on the virtual self one can associate with one’s stream. I am planning to write the other posts too in a similar format, though the topics covered would range from sociology, culture and politics to current affairs.
Please do visit the My 2 Brains blog and give me some feedback as to how you like the concept and what topics/ themes you would like me to cover there.
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Oct 31st
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Autism is a hard disorder to nail down genetically- single nucleotide polymorphisms (SNPs) or even multiple locus genetic effects are not able to account for the large genetic component to the disorder. In recent times, Copy number variations (CNVs) has come to the forefront of Autism research , suggesting that microdeletions, duplications etc may account for some cases. Another new , till now unsuspected mechanism that has recently been implicated in autism is epigenetic mechanism of increased methylation in promoter regions that has the effect of silencing/reducing the expression of genes involved to a certain extent. The recent study by Gregory et al, is just such a step in the right direction, which will hopefully bring us closer to the truth.
The study is available in full at BMC Medicine site and is accompanied by a must read commentary that explains a lot of things and puts the finding in context.
In a nutshell, the study authors used CNV determining methods to discover that a deletion of OXTR (oxytocin receptor) gene was presnet in an autistic subject and was not de novo , but the deletion was inherited from his mother. One of the affected siblings of the autistic subject, who too was autistic, on the other hand did not have a deletion, but had increased methylation of the OXTR. this led the study authors to revisit their genomics data and look at adta across all autistic subjects and controls and discover that indeed, in other autistics too the OXTR had increased methylation. Then they looked for expression of OXTR in peripheral blood cells and temporal cortex and found that indedd in autistics, as compared to controls, there was reduced expression of OXTR. This strongly suggest that the epigentic changes that lead to autism (the efffect of OXTR suppression) happen quite early in the devlopmenet and might happen in utero.
Before I elaborate on my take home from the study, there are some excerpts (as I know you didn’t read the originals)
Classic autism comprises a spectrum of behavioral and cognitive disturbances of childhood development. The core autism phenotype includes deficits in social interaction, language development and patterns of repetitive behaviors and/or restricted interests. The population prevalence of the spectrum of autism disorders is estimated to range between 1/300 [1] to 1/100 (http://www.nschdata.org/), with a male: female ratio of 4:1 [2,3]. The disorder has been shown to be highly heritable with the relative risk for siblings being approximately 2% to 8%, much higher than that of the general population [4]. To date, only a small percentage of autism cases (<10%) have been ascribed to single gene disorders such as fragile X syndrome, tuberous sclerosis [5] and Rett syndrome [6]. Numerous approaches including genetic linkage, genome-wide association, candidate gene association and gene expression analysis have been used to identify the additional genes implicated in the development of autism [7,8]. However, the heterogeneous nature of autism and autism spectrum disorders has limited their success.
An additional approach to identify genes involved in autism is to characterize copy number variants (CNVs), that is, chromosomal deletions and duplications, that are known to be present within at least 5% of individuals with idiopathic autism [9]. Autism CNVs have been shown to involve almost all chromosomes [10,11], with the most frequently observed alteration localizing to chromosome 15q11-13 [12-23]. A number of different methods have been used to characterize autism related CNVs, including but not limited to, cytogenetic Gbanding [14,23,24], metaphase fluorescence in situ hybridization (FISH) [22], Southern blotting [18], loss of heterozygosity (LOH) analysis [15-17,19], quantitative polymerase chain reaction (PCR) [25] and, more recently, genotyping and representational oligonucleotide microarray analysis (ROMA) [26]. Here we describe the use of genome-wide tilepath microarrays and array comparative genomic hybridization (CGH) to identify CNVs in a dataset of 119 unrelated probands from multiplex autism families [27]. The genomic profiles of our autism dataset were compared to the array CGH profiles of 54 phenotypically normal individuals, to previously published CNVs present within the database of genomic variants [28] and to the Autism Chromosome Rearrangement Database (http://projects.tcag.ca/autism/). The most significant finding thus far from our analysis is a heterozygous deletion of the oxytocin receptor gene (OXTR) (MIM accession no.: 167055) in an individual with autism and his mother with putative obsessive-compulsive disorder (OCD). We further investigated the relationship between OXTR and autism by carrying out epigenetic analysis of the promoter region of OXTR. We show that the gene is hypermethylated in independent cohorts with autism as compared to controls, in both peripheral blood mononuclear cells (PBMCs) and the temporal cortex. Additionally, our analysis of expression levels of OXTR in the temporal cortex shows decreased levels of expression in individuals with autism as compared to controls matched for age and sex.
These data suggest that OXTR and the oxytocin signaling pathway play an important role in the etiology of autism and autism spectrum disorders and implicate epigenetic misregulation of OXTR in this complex disease. … Epigenetic control of autism susceptibility is a recent concept and most certainly a topic of great interest in the field. Over the past decade, researchers have uncovered suggestive links between epigenetics and autism, for example, autism is associated with duplications of 15q11-13 (especially maternally inherited), an imprinted region in the genome where DNA methylation status has been linked to Prader-Willi syndrome (PWS) and Angelman syndrome (AS) [66]; mutation within a gene that encodes a methyl-DNA-binding protein (MECP2, (MIM accession no.: 300005)) is the causative agent of Rett syndrome [67]; and mutation of this same gene has been associated with both autism and AS populations [55]. Nagarajan et al. have shown that 79% of autism cases have a decrease in MECP2 expression in the frontal cortex and that an increase in aberrant DNA methylation correlates with this decrease in MECP2 expression [68]. These data implicate epigenetic dysregulation as a mechanism for the development of autism and justify the examination of DNA methylation of autism candidate genes, such as OXTR identified in this study.
Now from the accompanying (more accessible) commentary:
The article by Gregory et al. published this month in BMC Medicine, reports on genomic and epigenetic alterations of OXTR, the gene encoding the receptor for oxytocin. The involvement of this gene was suggested by its deletion in an autistic patient. The subsequent analysis of a group of unrelated autistic subjects did not show an OXTR deletion, but rather hypermethylation of the gene promoter, with a reduced mRNA expression.
These findings address two major points of the current debate on the etiology and pathogenesis of autism: the role of oxytocin, known to be involved in modeling human behavior, and the possible involvement of epigenetic mechanisms. The nature of this epigenetic dysregulation is unknown but, if proved to be true, might explain the failure to identify sequence alterations in a host of candidate genes. Practical implications of these findings may be forthcoming, however not before extension and validation on a larger scale have confirmed their value. .. The second issue raised by Gregory et al. deals with the epigenetic inhibition of OXTR expression in ASD. Such epigenetic modification, at least as reported so far, does not seem to be sequence based but rather of a different, as yet unknown nature. This might explain why researchers have been looking for decades for genetic mutations in ASD and yet have found almost none. An epigenetic mechanism would justify the ‘unusual’, non-Mendelian familial aggregations of ASD. In this respect, even the family with OXTR deficiency reported by Gregory et al. shows an unusual genotype-phenotype correlation, in that the same phenotype is caused by alterations of the same gene but due to different molecular defects (deletion versus hypermethylation).
Also, the possibility that in most ASD patients there might be an epigenomic instability is of interest in consideration of the fact that it has been shown that the epigenetic status in early fetal development can be reprogrammed by maternal behavior in a reversible way [34]. Therefore, other environmental factors, yet to be discovered, might also be able to reprogram the epigenotype of the embryo.
I hope the fact that epigenetic changes may happen during pregnancy line of reasoning does not lead to the harmful and without-any-basis vaccination is cause of autism arguments. On the other hand I had covered earlier how Autism is more likely if mother was exposed to valproate during pregnancy or the child soon after birth. What if valproate is instrumental in an epigenetic fashion in leading to more or less methylation and gene expression. It is well known that valproate and valporic acid is given as treatment for psychosis/bipolar. In a similar vein, I am inclined to stick my neck out and claim that in schizophrenics/psychotics , the OXTR should be more expressed : perhaps more methylation, duplications etc . However I am checked in my musings by these studies that claim that negative symptoms of schizophrneia may be associated with reduced oxytocin activity in the brain. Yet, all said and done I would like to see a study that analyzes for epigenetic mechanisms in schizophrneia especially at the OXTR locus. Although the negative symptoms like social withdrawal of schizophrenia may lead to the opposite hypothesis regarding schizophrenia and oxytocin correlation, I am inclined to believe that schizophrenics (at least those suffering from positive symptoms predominantly) are too much oxytocin guided , trusting and socially too much involved in others type of people.
Gregory, S., Connelly, J., Towers, A., Johnson, J., Biscocho, D., Markunas, C., Lintas, C., Abramson, R., Wright, H., Ellis, P., Langford, C., Worley, G., Delong, G., Murphy, S., Cuccaro, M., Persico, A., & Pericak-Vance, M. (2009). Genomic and epigenetic evidence for oxytocin receptor deficiency in autism BMC Medicine, 7 (1) DOI: 10.1186/1741-7015-7-62 Gurrieri, F., & Neri, G. (2009). Defective oxytocin function: a clue to understanding the cause of autism? BMC Medicine, 7 (1) DOI: 10.1186/1741-7015-7-63 Hat tip to @Boraz for tweeting about this study.
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Oct 30th
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I came across this study article today by Farb et al, that talks about two distinct neural networks in the brain that are involved in self-reference. To be fair, the networks are somewhat blurred and overlap in naive people, while in people who practice mindfulness meditation, the networks are more distinct and non-overlapping. My interest was piqued as I am a keen follower of default-brain network , which has been implicated in self-referential thinking and this article seems to at one point argue that the narrative self viz ‘me’ is grounded in default brain network, while the experiencer ‘I” has some other nearby related areas as the neural substrates.
But first let us clarify what we mean by ‘me’ and ‘I’. For this I would like to quote form a Gallagher article:
Ever since William James (1890) provided a catalogue of different senses of the self, philosophers and psychologists have been hard at work refining and expanding the possible variations of this concept. Supplementing James’ inventory of physical self, mental self, spiritual self, and the ego, Neisser (1988), for example, suggested important distinctions between ecological, interpersonal, extended, private, and conceptual aspects of self. More recently, reviewing a contentious collection of essays from various disciplines, Strawson (1999) found an overabundance of delineations between cognitive, embodied, fictional, and narrative selves, among others. It would be impossible to review all of these diverse notions of self in this short paper, so I have focused on several recently developed approaches that promise the best exchange between philosophy of mind and the other cognitive sciences. Because these approaches move in divergent theoretical directions they should help to convey the breadth of philosophical analysis on this topic. They can be divided into two groups that are focused, respectively, on two important aspects of self.
A first approach involves various attempts to account for a ‘minimal’ sense of self. If we strip away all of the unessential features of self, the intuition is that there is a basic, immediate, or primitive something that we are still willing to call a self. This approach leaves aside questions about the degree to which the self is extended beyond the short-term or ’specious’ present to include past thoughts and actions. Although identity over time is a major issue in the philosophical definition of personal identity, the concept of the minimal self is limited to that which is accessible to immediate and present self-consciousness. Non-philosophers have found that certain aspects of the minimal self are relevant to current research in robotics. Furthermore, aspects of the minimal self that involve senses of ownership and agency in the context of both motor action and cognition can be clarified by neurocognitive models (developed to explain pathologies such as schizophrenia) that suggest the involvement of specific brain systems (including prefrontal cortex, SMA, and cerebellum).
A second approach involves conceiving of the self in terms of narrative, a concept imported into the cognitive-science context by Dennett (1991) , but one which may have a more complex significance than indicated in Dennett’s account. The narrative self is extended in time to include memories of the past and intentions toward the future. It is what Neisser refers to as the extended self, and what Dennett calls a ‘nonminimal selfy’ self. Neuropsychological accounts of episodic memory or loss of memory can help to circumscribe the neurological underpinnings of the narrative self.
If you haven’t guessed by now, the minimal self is ‘I’: the doer , experiencer experiencing the immediate present; the narrative self is ‘me’ -an entity stretched in time and living as much in past and future as in the present. The study authors delineate the same as follows (note that they too start with William James reference):(* references removed)
Since William James’ early conceptualization, the ‘self ’ has been characterised as a source of permanence beneath the constantly shifting set of experiences that constitute conscious life. This permanence is often related to the construction of narratives that weave together the threads of temporally disparate experiences into a cohesive fabric. To account for this continuity, William James posited an explanatory ‘me’ to make sense of the ‘I’ acting in the present moment . Recently, progress has been made in characterizing the neural bases of the processes supporting William James’ ‘me’ in the form of ‘narrative’ self-reference , highlighting the role of the medial prefrontal cortices (mPFC) in supporting self awareness by linking subjective experiences across time . The mPFC has been shown to support an array of self-related capacities, including memory for self-traits , traits of similar others , reflected self-knowledge , and aspirations for the future . As such, cortical midline processes may be characterised as supporting narrative self-reference that maintains continuity of identity across time .
Narrative self-reference stands in stark contrast to the immediate, agentic ‘I’ supporting the notion of momentary experience as an expression of selfhood. Most examinations of self-reference ignore mechanisms of momentary consciousness, which may represent core aspects of self-experience achieved earlier in development and may have evolved in earlier animal species. Indeed, little is known about whether the neural substrates underlying momentary self-reference are one and the same, or distinct from, cortical midline structures supporting narrative experience. One hypothesis suggests that awareness of momentary self-reference is neurally distinct from narrative self-reference and is derived from neural markers of transient body states, in particular, right lateralised exteroceptive somatic and interoceptive insular cortices. In the present study, we examined this thesis.
In short using fMRI, they tried to find the different hypothesized neural networks underlying the two senses of self and did find evidence for clear segregation in those practicing mindfulness meditation. Their methodology however, is not fool proof and this they themselves note in their conclusions. Here are their findings:
Consistent with a theory of self-reference as mentalising, linguistically mediated and of higher order executive origin , participants engaged midline prefrontal cortices and a left lateralised linguistic-semantic network (inferior lateral PFC, middle temporal and angular gyri) during NF (narrative focus: ‘me’ condition). Demonstrating a default bias towards NF as previously revealed in ‘resting’ mind wandering states , relatively restricted reductions in the cortical midline network were found when attention was explicitly directed towards a moment-to-moment EF (experiential focus: ‘I’ condition) in novice participants with little training in this form of self-reflection. These individuals revealed increased left lateralised prefrontal-parietal activations during EF likely reflecting greater task-related linguistic processing that has been shown to be associated with decreased medial prefrontal recruitment .
So what they found was that a part of default network was engaged in ‘me’ condition; while task-related areas were recruited in “I” condition and appropriate task-related suppression of some part of default network observed. This effect was with naive subjects, but with those trained in mindfulness meditation, they observed a sort of double dissociation:
Following an intensive 8 week course in mindfulness meditation, during which individuals learn to develop the capacity to monitor moment-to-moment experience, EF resulted in a pronounced shift away from midline cortices towards a right lateralised network comprised of the ventral and dorsolateral PFC, as well as right insula, SII and inferior parietal lobule. Consistent with a dual-mode hypothesis of self-awareness, these results suggest a fundamental neural dissociation in modes of self-representation that support distinct, but habitually integrated, aspects of self-reference: (i) higher order self-reference characterised by neural processes supporting awareness of a self that extends across time and (ii) more basic momentary self-reference characterised by neural changes supporting awareness of the psychological present. The latter, represented by evolutionary older neural regions, may represent a return to the neural origins of identity, in which self-awareness in each moment arises from the integration of basic interoceptive and exteroceptive bodily sensory processes. In contrast, the narrative mode of self-reference may represent an overlearned mode of information processing that has become automatic through practice, consistent with established findings on training-induced automaticity.
To me this sounds interesting: If I had to stretch my neck and relate this to autism and schizophrenia , I would say that based on earlier coverage on this blog: Schizophrenics have a higher default brain activity and perhaps try to spin too much of a narrative. Perhaps they are the ones that would best benefit with mindfulness meditation trainings to calm their default ‘me’ and activate the ‘I’ also at relevant times. On the opposite side, one is all too aware of the here-and-now feeling of self that many autistics have- a direct and immediate perceptual relation with world. Perhaps, they too can benefit from some for of mindfulness meditation by learning to use the default brain network too at times – letting teh mind wander and spinning a tale (however fictional) about themselves.
Farb, N., Segal, Z., Mayberg, H., Bean, J., McKeon, D., Fatima, Z., & Anderson, A. (2007). Attending to the present: mindfulness meditation reveals distinct neural modes of self-reference Social Cognitive and Affective Neuroscience, 2 (4), 313-322 DOI: 10.1093/scan/nsm030 Gallagher, S. (2000). Philosophical conceptions of the self: implications for cognitive science Trends in Cognitive Sciences, 4 (1), 14-21 DOI: 10.1016/S1364-6613(99)01417-5
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