Thursday, January 29, 2009

Why Science Matters: a Year of the Science 2009 question

COPUS has been celebrating the Year Of Science 2009 and on the their main page their is a link to Why Science Matters that links to Alom Shaha's site Why is Science Important.

Now we all know that EDGE asks an annual question to leading figures in academia/ intelligentsia and compiles their answers together and publishes as a book. That to me has always provided a rich perspective on contemporary matters. Alom and COPUS, in a similar vein, have asked a very topical question for the Year of Science 2009, which is as to Why Science Matters. This question they have put to prominent people in science education, research, writing, teaching and journalism (bloggers included). People who have answered include scientists  like Dr Susan Blackmore, and there are a variety of perspectives from scientists steeped in diverse fields ranging theoretical physics to molecular biology.

I have been honored to participate in the same and you can read my full response here. Below, I am just providing a small teaser so that you indeed go to the main site to read my and others opinions as to why science matters.


Consider the problem posed by some people whose behavior is crazy or erratic as compared to the rest of the ‘normal’ and ‘sane’ individuals. These might have been labeled heretics or witches in the dark ages and deemed to be possessed by demons / spirits. Lacking a scientific insight into what really haunts and ails this ‘mad’ condition, the cure advised for the treatment / containment of the problem (insanity) would also be similarly non-scientific and irrational. Thus the burning at stakes in the middle ages of those who were perhaps suffering from some form of a mental illness, but were nevertheless characterized as being possessed by ‘spirits’ and thus in need of exorcism. If insanity is seen form this dualistic lens of an alien spirit having possessed the body, then one can easily see how witch-burning might have been a legitimate solution to the problem of insanity.
.......

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Thursday, January 22, 2009

Perosnality and Neurotransmitters

Although all introductory Psychology textbooks warn against any simplistic correlations between neurotransmitters and complex behavioral and cognitive measures like Personality traits, I am going to do exactly that in this post. In an earlier post , I had related personality traits to neurotransmitter systems and operant learning paradigm and here I present some corroborating evidence for the personality- neurotransmitter system linkage.

First to recap:

  1. Nueroticism/ Harm Avoidance: Serotonin system
  2. Conscentiousness/ novelty seeking: Dopamine system
  3. Extarversion/ Reward Dependence:  Norepinephrine system 
  4. Agreeableness/ Persistance: Epinepherine system
  5. Openesses/ Rebeliious-conformity/self-directedness: Histamine system
 First off to bat consider the following- Neuroticism is manifested as anxiety and if serotonin system is implicated , then genes affecting the serotonin system should affect the neuroticism levels of individuals . This is exactly what was found by Lesh et al.

Transporter-facilitated uptake of serotonin (5-hydroxytryptamine or 5-HT) has been implicated in anxiety in humans and animal models and is the site of action of widely used uptake-inhibiting antidepressant and antianxiety drugs. Human 5-HT transporter (5-HTT) gene transcription is modulated by a common polymorphism in its upstream regulatory region. The short variant of the polymorphism reduces the transcriptional efficiency of the 5-HTT gene promoter, resulting in decreased 5-HTT expression and 5-HT uptake in lymphoblasts. Association studies in two independent samples totaling 505 individuals revealed that the 5-HTT polymorphism accounts for 3 to 4 percent of total variation and 7 to 9 percent of inherited variance in anxiety-related personality traits in individuals as well as sibships.

Next comes a recent study finding that a gene variant related to NO (a neurotrasmitter) is related to Impulsiveness. Now One of the defining traits of NS/ C is Impulsiveness. This has been found related to NOS1 gene. Here is the original study.

Context Human personality is characterized by substantial heritability but few functional gene variants have been identified. Although rodent data suggest that the neuronal isoform of nitric oxide synthase (NOS-I) modifies diverse behaviors including aggression, this has not been translated to human studies.

Objectives To investigate the functionality of an NOS1 promoter repeat length variation (NOS1 Ex1f variable number tandem repeat [VNTR]) and to test whether it is associated with phenotypes relevant to impulsivity.

Design Molecular biological studies assessed the cellular consequences of NOS1 Ex1f VNTR; association studies were conducted to investigate the impact of this genetic variant on impulsivity; imaging genetics was applied to determine whether the polymorphism is functional on a neurobiological level.

Setting Three psychiatric university clinics in Germany.

Participants More than 3200 subjects were included in the association study: 1954 controls, 403 patients with personality disorder, 383 patients with adult attention-deficit/hyperactivity disorder (ADHD), 151 with familial ADHD, 189 suicide attempters, and 182 criminal offenders.

Main Outcome Measures For the association studies, the major outcome criteria were phenotypes relevant to impulsivity, namely, the dimensional phenotype conscientiousness and the categorical phenotypes adult ADHD, aggression, and cluster B personality disorder.

Results A novel functional promoter polymorphism in NOS1 was associated with traits related to impulsivity, including hyperactive and aggressive behaviors. Specifically, the short repeat variant was more frequent in adult ADHD, cluster B personality disorder, and autoaggressive and heteroaggressive behavior. This short variant came along with decreased transcriptional activity of the NOS1 exon 1f promoter and alterations in the neuronal transcriptome including RGS4 and GRIN1. On a systems level, it was associated with hypoactivation of the anterior cingulate cortex, which is involved in the processing of emotion and reward in behavioral control.

Conclusion These findings implicate deficits in neuronal signaling via nitric oxide in moderation of prefrontal circuits underlying impulsivity-related behavior in humans.

Now there does exist a relationship between NO and dopamine (but then which two neurotransmitter systems are not related) and that way I can still save my face by claiming that it is the dopamine that is finally mediating the impulsivity and not NO.

There is evidence suggesting that nitric oxide (NO) may play an important role in dopamine (DA) cell death. NO may act as a neuroprotector or neurotoxic agent in dopamine neurons, depending on cell redox status. Glutathione (GSH) depletion is the earliest biochemical alteration shown to date in brains of Parkinson's disease (PD) patients. However, data from animal models show that GSH depletion by itself is not sufficient to induce nigral degeneration. Low NO concentrations have neurotrophic effects on DA cells via a cGMP-independent mechanism that may implicate up-regulation of GSH. On the other hand, higher levels of NO induce cell death in both DA neurons and mature oligodendrocytes that is totally reverted by soluble factors released from glia. Alterations in GSH levels change the neurotrophic effects of NO in dopamine function into neurotoxic, under these conditions, NO triggers a programmed cell death with markers of both apoptosis and necrosis characterised by an early production of free radicals followed by late activation of the sGC/cGMP/PKG pathway. Arachidonic acid metabolism through the 12-lipoxygenase (12-LOX) pathway is also central for this GSH-NO interaction. Neurotrophism of NO switches into neurotoxicity after GSH depletion, due to persistent activation of the ERK-1/2 signaling pathway in glial cells. The implication of these cell death signaling pathways in pathological conditions like Parkinson's disease, where GSH depletion, glial dysfunction and NO overproduction have been documented, are discussed.

Next we move to the sociability factor underlying Extraversion/ Reward dependence. Here studies show that Noardrenaline is related to sociability/ dependence etc. Here is a study showing effects of NA on sociability.
Rationale: Treatment with antidepressants has been shown to affect social functioning, but drugs with actions on different neurotransmitters may have a different profile of effects. Objective: To study the effects of acute manipulation of two neurotransmitters, serotonin and noradrenaline, on social behaviour in healthy volunteers. Methods: Sixty volunteers were randomly assigned to a single dose of a selective noradrenaline reuptake inhibitor, reboxetine (4 mg), a selective serotonin reuptake inhibitor, citalopram (10 mg), or placebo. They socially interacted with a confederate behaving in a non-sociable manner in a stranger-dyadic social interaction paradigm 1.5 h postdrug. Social behaviour during the interaction was video recorded by a hidden camera and subsequently analysed. After the interaction, volunteers played the mixed-motive game with the confederate. This game has been shown to measure cooperative behaviour and communication. Volunteers read a short story and rated their mood predrug and before and after the interaction. Results: Subjects on reboxetine showed reduced hand fiddling during the interaction and gave significantly more cooperative communications during the mixed-motive game. More volunteers on reboxetine were classified as cooperative players. On the reading task, the speech of subjects on citalopram showed less reduction of energy variation after the social interaction. Conclusion: Reboxetine had clear effects on social behaviour. Noradrenaline was related to increased social engagement and cooperation and a reduction in self-focus. Citalopram had less effect on cooperative behaviour but serotonin may be associated with protection of the self from the negative consequences of social interaction.

Also, Zuckerman has clearly related NA to sociability and dependence.As per him:

Ellison studies the effects of chemical lesions of either dopamine or noradrenaline system in rats. ...Norepeinepherine-lesioned rats spent more time in their burrows and less time in a behavioral arena in which spontaneous social interactions could occur....


That takes us to the fourth trait of agreeableness and the related Empathy system . Here the famous Scacter- singer experiment of administering Adrenaline and then finding that the mood became congruent with that of other people has to be reinterpreted in terms of empathy at work rather than james-lange two-step appraisal of emotion. Do read the expermine in more detail at the above link.
The Experiment in a nut shell.
Independent Variables

1. Injected Adrenaline or Saline solution
2. The subjects were given a description of side-effects, misinformed about the side-effects, or told nothing.
3. The subjects were placed in a 'Euphoric' (Happy) or 'Angry' situation.

Dependent Variables

1. Observed signs of happiness
2. Observed signs of anger
3. Self-report of happiness or anger
Results:
Euphoria: As expected, the adrenaline misinformed group, and the adrenaline ignorant group, reported being happiest
Anger:  This didn't work. Most subjects were positive about their feelings. Schachter and Singer attribute this to the fact that they were students eager to please their tutors

It is important that those people who were placed with confederates exhibiting happy states felt happy and the same was felt by those who received adrenaline; a more valid interpretation is that adrenaline increased the empathetic feelings and lead to transmission or contagion of mood. the situational variable where one tried to induce anger by being irritable did not lead to to anger; perhaps if the confederate was irritated, they might have become irritated too due to empathy; but no anger is expected as per my interpretation that it is empathy that is primary and not the cognitive appraisal of emotional physiological state.

Finally I agree that I have not been able to find much about histamine system and how it may be affect the openness/ rebellious/conformity trait. As an exercise to reader here are some low histamine condition links.

That is it for now. would love if somebody points to some other studies that corroborate the case.
ResearchBlogging.org
K.-P. Lesch, D. Bengel, A. Heils, S. Z. Sabol, B. D. Greenberg, S. Petri, J. Benjamin, C. R. Muller, D. H. Hamer, D. L. Murphy (1996). Association of Anxiety-Related Traits with a Polymorphism in the Serotonin Transporter Gene Regulatory Region Science, 274 (5292), 1527-1531 DOI: 10.1126/science.274.5292.1527
Wai Tse, Alyson Bond (2002). Difference in serotonergic and noradrenergic regulation of human social behaviours Psychopharmacology, 159 (2), 216-221 DOI: 10.1007/s00213-001-0926-9

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Wednesday, January 21, 2009

The Default Brain Network: implications for Autism and Schizophrenia

This blog post has been triggered by a recent news article that found that the default network in schizophrenics was both hyperactive and hyperconnected during rest, and it remained so as they performed demanding cognitive tasks. To quote:

The researchers were especially interested in the default system, a network of brain regions whose activity is suppressed when people perform demanding mental tasks. This network includes the medial prefrontal cortex and the posterior cingulate cortex, regions that are associated with self-reflection and autobiographical memories and which become connected into a synchronously active network when the mind is allowed to wander.

Whitfield-Gabrieli found that in the schizophrenia patients, the default system was both hyperactive and hyperconnected during rest, and it remained so as they performed the memory tasks. In other words, the patients were less able than healthy control subjects to suppress the activity of this network during the task. Interestingly, the less the suppression and the greater the connectivity, the worse they performed on the hard memory task, and the more severe their clinical symptoms.

“We think this may reflect an inability of people with schizophrenia to direct mental resources away from internal thoughts and feelings and toward the external world in order to perform difficult tasks,” Whitfield-Gabrieli explained.

The hyperactive default system could also help to explain hallucinations and paranoia by making neutral external stimuli seem inappropriately self-relevant. For instance, if brain regions whose activity normally signifies self-focus are active while listening to a voice on television, the person may perceive that the voice is speaking directly to them.

The default system is also overactive, though to a lesser extent, in first-degree relatives of schizophrenia patients who did not themselves have the disease. This suggests that overactivation of the default system may be linked to the genetic cause of the disease rather than its consequences.

The study on which this report is based , is supposedly published in advanced online PNAS edition of 19 jan, but I am unable to locate it. However, my readers know my obsession with Autism and Schizophrenia as diametrically opposed disorders theory and so I was seen reading all the other relevant studies related to default Network and especially how it may be differentially and oppositely activated in Autism and Schizophrenia.

First I would like to refer you to an extremely good overview of Default Network by Buckner, Schacter et al which is freely available. I'll now present some quotes from the paper that are relevant to my thesis. I start with the abstract:

Thirty years of brain imaging research has converged to define the brain's default network—a novel and only recently appreciated brain system that participates in internal modes of cognition. Here we synthesize past observations to provide strong evidence that the default network is a specific, anatomically defined brain system preferentially active when individuals are not focused on the external environment. Analysis of connectional anatomy in the monkey supports the presence of an interconnected brain system. Providing insight into function, the default network is active when individuals are engaged in internally focused tasks including autobiographical memory retrieval, envisioning the future, and conceiving the perspectives of others. Probing the functional anatomy of the network in detail reveals that it is best understood as multiple interacting subsystems. The medial temporal lobe subsystem provides information from prior experiences in the form of memories and associations that are the building blocks of mental simulation. The medial prefrontal subsystem facilitates the flexible use of this information during the construction of self-relevant mental simulations. These two subsystems converge on important nodes of integration including the posterior cingulate cortex. The implications of these functional and anatomical observations are discussed in relation to possible adaptive roles of the default network for using past experiences to plan for the future, navigate social interactions, and maximize the utility of moments when we are not otherwise engaged by the external world. We conclude by discussing the relevance of the default network for understanding mental disorders including autism, schizophrenia, and Alzheimer's disease.

Some snippets from the introduction:

A common observation in brain imaging research is that a specific set of brain regions—referred to as the default network—is engaged when individuals are left to think to themselves undisturbed . Probing this phenomenon further reveals that other kinds of situations, beyond freethinking, engage the default network. For example, remembering the past, envisioning future events, and considering the thoughts and perspectives of other people all activate multiple regions within the default network . These observations prompt one to ask such questions as: What do these tasks and spontaneous cognition share in common? and what is the significance of this network to adaptive function? The default network is also disrupted in autism, schizophrenia, and Alzheimer's disease, further encouraging one to consider how the functions of the default network might be important to understanding diseases of the mind. (emphasis mine)

Then they review some history including how default brain activity was recognized when it was found that metabolic demands and blood glucose consumption of brain as a whole remained the same even when the brain was at 'rest' viv-a-vis involved in an active task. They also review how when baseline PET/fMRI rest activity was compared to many disparate tasks related fMRI/ PET activity , then while some task-relevant areas showed activations related to baseline, many correlated areas of brain, the default network, showed deactivation in the task-related conditions as compared to baseline. The modern interpretation is that the default network is active at rest and places metabolic demands on the brain. They then reference the seminal work of Rachile et al and how that made the default network as a study area in itself.

They further elaborate on how the default network may be identified as an interconnected and functional brain system and list various approaches like spontaneous correlations at rest, seeding from a RoI and determining the areas correlated to activity in seed region etc, to determine the components of the default network. While dMPFC and PCC are implicated in all analysis, the case for vMPFC, IPL, HF+ and LTC is also strong.

I'll skip most of this stuff , including comparative analysis. Suffice it to note here that the default brain regions are up to 30% more metabolically demanding then the rest of the brain and are recently evolved/ selected for. this becomes significant in view of recent studies showing that schizophrenia may be a result of selection for metabolism related genes.

The interesting part begins when trying to determine the behavioral/cognitive correlates of this default brain activity. The consensus seems to be that it is used for daydreaming, reconstructing the past, simulating the future, taking other peoples perspective, self-referential processes and in general stimulus independent thought.

A shared human experience is our active internal mental life. Left without an immediate task that demands full attention, our minds wander jumping from one passing thought to next—what William James (1890) called the "stream of consciousness." We muse about past happenings, envision possible future events, and lapse into ideations about worlds that are far from our immediate surroundings. In lay terms, these are the mental processes that make up fantasy, imagination, daydreams, and thought. A central issue for our present purposes is to understand to what degree, if any, the default network mediates these forms of spontaneous cognition. The observation that the default network is most active during passive cognitive states, when thought is directed toward internal channels, encourages serious consideration of the possibility that the default network is the core brain system associated with spontaneous cognition, and further that people have a strong tendency to engage the default network during moments when they are not otherwise occupied by external tasks.

Support for the same is then provided. The next task the authors undertake is that of determining the function, usefulness and evolutionary rationale for this default brain activity. Two ,in my opinion not mutually exclusive, theories are offered. One is simulation of something that is not tied to current reality (whether it be past memories, future expectations and scenarios or other peoples intentions, beliefs, perspectives). The other theory is that the default mode is a diffused attentional/ exploration state and is suppressed by foveal attention/task focus. The over activity of default network in Schizophrenia can be related to both theories equally well.

In this section, we explore two possible functions of the network, while recognizing that it is too soon to rule out various alternatives. One possibility is that the default network directly supports internal mentation that is largely detached from the external world. Within this possibility, the default network plays a role in constructing dynamic mental simulations based on personal past experiences such as used during remembering, thinking about the future, and generally when imagining alternative perspectives and scenarios to the present. This possibility is consistent with a growing number of studies that activate components of the default network during diverse forms of self-relevant mentalizing as well as with the anatomic observation that the default network is coupled to memory systems and not sensory systems. Another possibility is that the default network functions to support exploratory monitoring of the external environment when focused attention is relaxed. This alternative possibility is consistent with more traditional ideas of posterior parietal function but does not explain other aspects of the data such as the default network's association with memory structures. It is important to recognize that the correlational nature of available data makes it difficult to differentiate between possibilities, especially because focus on internal channels of thought is almost always correlated with a change in external attention . We also explore in this section an intriguing functional property of the default network: the default network operates in opposition to other brain systems that are used for focused external attention and sensory processing. When the default network is most active, the external attention system is attenuated and vice versa.

To me both the Sentinel and the Internal Mentation hypothesis appear to be somewhat valid and relevant to Schizophrenia. One can attribute Psychosis to both increased 'watchfulness' and and increased internal mentation or mentalizing and I have written about the second hypothesis in detail previously.

The most relevant part of the paper is their discussion of Autism, Schizophrenia and Alzheimer's. I reproduce the entire autism and Schizophrenia section , highlighting a few points:

Autism Spectrum Disorders

The autism spectrum disorders (ASD) are developmental disorders characterized by impaired social interactions and communication. Symptoms emerge by early childhood and include stereotyped (repetitive) behaviors. Baron-Cohen and colleagues (1985) proposed that a core deficit in many children with ASD is the failure to represent the mental states of others, as needed to solve theory-of-mind tasks. Based on an extensive review of the functional anatomy that supports theory-of-mind and social interaction skills, Mundy (2003) proposed that the MPFC may be central for understanding the disturbances in ASD. Given the convergent evidence presented here that suggests the default network contributes to such functions, it is natural to explore whether the default network is disrupted in ASD.

Developmental disruption of the default network, in particular disruption linked to the MPFC, might result in a mind that is environmentally focused and absent a conception of other people's thoughts. The inability to interact with others in social contexts would be an expected behavioral consequence. It is important to also note that such disruptions, if identified, may not be linked to the originating developmental events that cause ASD but rather reflect a developmental endpoint. That is, dysfunction of the default network and associated symptoms may emerge as an indirect consequence of early developmental events that begin outside the network.

Many studies have explored whether ASD is associated with morphological differences in brain structure. The general conclusion from this literature is that the brain changes are complex, reflecting differences in growth rates and attenuation of growth (see Brambilla et al. 2003 for review). At certain developmental stages these differences are manifest as overgrowth and at later stages as undergrowth. Early observations have implicated the cerebellum. A further consistent observation has been that the amygdala is increased in volume in children with ASD (e.g., Abell et al. 1999, Schumann et al. 2004), perhaps as a reflection of abnormal regulation of brain growth (Courchesne et al. 2001). While not discussed earlier because of our focus on cortical regions, the amygdala is known to contribute to social cognition (Brothers 1990, Adolphs 2001, Phelps 2006) and interacts with regions within the default network. The amygdala has extensive projections to orbital frontal cortex (OFC) and vMPFC (Carmichael & Price 1995).

Of perhaps more direct relevance to the default network, dMPFC has shown volume reduction in several studies of ASD that used survey methods to explore regional differences in brain volume (Abell et al. 1999, McAlonan et al. 2005). The effects are subtle and will require further exploration, but it is noteworthy that, of those studies that have looked, several have noted dMPFC volume reductions in ASD. Of interest, a study using voxel-based morphometry to investigate grey matter differences in male adolescents with ASD noted that several regions within the default network exhibited a relative increase in grey matter volume compared to the control population (Waiter et al. 2004). Because this observation has generally not been replicated in adult ASD groups, future studies should investigate whether complex patterns of overgrowth and undergrowth of the regions within the default network exist in ASD and, if so, whether they track behavioral improvement on tests of social function (see also Carper & Courchesne 2005).

Kennedy and colleagues (2006) recently used fMRI to directly explore the functional integrity of the default network in ASD. In their study, young adults with ASD and age-matched individuals without ASD were imaged during passive tasks and demanding active tasks that elicit strong activity differences in the default network. While the control participants showed the typical pattern of activity in the default network during the passive tasks, such activity was absent in the individuals with ASD. Direct comparison between the groups revealed differences in vMPFC and PCC. Moreover, in an exploratory analysis of individual differences within the ASD group, those individuals with the greatest social impairment (measured using a standardized diagnostic inventory) were those with the most atypical vMPFC activity levels (Fig. 16). An intriguing possibility suggested by the authors of the study and extended by Iacoboni (2006) is that the failure to modulate the default network in ASD is driven by differential cognitive mentation during rest, specifically a lack of self-referential processing.

Another recent study using analysis of intrinsic functional correlations showed that the default network correlations were weaker in ASD (Cherkassky et al. 2006).Of note, the individuals with ASD showed differences in a fronto-parietal network that has been recently hypothesized to control interactions between the default network and brain systems linked to external attention (Vincent et al. 2007b). These data in ASD suggest an interesting possibility: the default network may be largely intact in ASD but under utilized perhaps because of a dysfunction in control systems that regulate its use.

Schizophrenia

Schizophrenia is a mental illness characterized by altered perceptions of reality. Auditory hallucinations, paranoid and bizarre delusions, and disorganized speech are common positive clinical symptoms (Liddle 1987). Cognitive tests also reveal negative symptoms, including impaired memory and attention (Kuperberg & Heckers 2000). These symptoms lead to questions about their relationship to the default network for a few reasons. The first reason surrounds the association of the default network with internal mentation. Many symptoms of schizophrenia stem from misattributions of thought and therefore raise the question of an association with the default network because of its functional connection with mental simulation. A second related reason has to do with the broader context of control of the default network. While still poorly understood, there appears to be dynamic competition between the default network and brain systems supporting focused external attention (Fransson 2005, Fox et al. 2005, Golland et al. 2007, Tian et al. 2007, see also Williamson 2007). Frontal-parietal systems are candidates for controlling these interactions (Vincent et al. 2007b). The complex symptoms of schizophrenia could arise from a disruption in this control system resulting in an overactive (or inappropriately active) default network. The normally strongly defined boundary between perceptions arising from imagined scenarios and those from the external world might become blurry, including the boundary between self and other (similar to that proposed by Frith 1996).

Three studies have provided preliminary data supporting the possibility that the default network is functionally overactive. Garrity and colleagues (2007) recently reported an analysis of correlations among default network regions in patients with schizophrenia. Studying a sizable data sample (21 patients and 22 controls), they explored task-associated activity modulations within the default network and identified largely similar correlations among default network regions in patients and controls. Differences were noted in specific subregions, as were differences in the dynamics of activity as measured from the timecourses of the fMRI signal. Of particular interest, they noted that within the patient group, the positive symptoms of the disease (e.g., hallucinations, delusions, and thought confusions) were correlated with increased default network activity during the passive epochs, including MPFC and PCC/Rsp. In a related analysis, Harrison et al. (2007) noted accentuated default network activity during passive task epochs in patients with schizophrenia as contrasted to controls, again suggesting an overactive default network. Moreover, within the patient group, poor performance was again correlated with MPFC activation during the passive as compared to the active tasks. Finally, Zhou and colleagues (2007) found that regions constituting the default network were functionally correlated with each other to a significantly higher degree in patients than in control participants. Thus, while the data are limited, these studies converge to suggest that patients with schizophrenia have an overactive default network, as would be expected if the boundary between imagination and reality were disrupted. Overactivity within the network correlates with task performance (Harrison et al. 2007) and clinical symptoms (Garrity et al. 2007).


I now link to two abstracts form Autism and default network research by Kennedy et al:

Several regions of the brain (including medial prefrontal cortex, rostral anterior cingulate, posterior cingulate, and precuneus) are known to have high metabolic activity during rest, which is suppressed during cognitively demanding tasks. With functional magnetic resonance imaging (fMRI), this suppression of activity is observed as “deactivations,” which are thought to be indicative of an interruption of the mental activity that persists during rest. Thus, measuring deactivation provides a means by which rest-associated functional activity can be quantitatively examined. Applying this approach to autism, we found that the autism group failed to demonstrate this deactivation effect. Furthermore, there was a strong correlation between a clinical measure of social impairment and functional activity within the ventral medial prefrontal cortex. We speculate that the lack of deactivation in the autism group is indicative of abnormal internally directed processes at rest, which may be an important contribution to the social and emotional deficits of autism.

In their discussion they make explicit the fact that in Autism, the default Netwrok may be under active.

There are two possible reasons why the ASD group failed to show the typical deactivation effect. One possibility is that midline resting network activity during both rest and task performance is high, and, thus, a subtraction between these conditions would reveal no difference in activity levels. We believe, however, that it is unlikely that high midline network activity was maintained during the cognitively demanding number task in autism for several reasons. First, as mentioned previously, behavioral performance was similar between control and ASD groups. This result, however, would be unexpected if the ASD group were carrying out additional mental processing that control subjects inhibit during cognitively demanding conditions. Second, positron-emission tomography studies of autism, which provide an absolute measure of brain metabolism, have found reduced, as opposed to increased, glucose metabolism in rACC and PCC (36) during task performance, as compared with controls. Furthermore, one positron-emission tomography study found that lower blood flow in MPFC and rACC at rest was correlated with more severe social and communicative impairments in subjects with autism (37), a finding similar to our correlational results. Third, reduced anatomical volumes and neurochemical deficiencies have consistently been observed in MPFC∕rACC in adults with autism (reviewed in ref. 26), likely indicative of a reduced functioning of these regions. Therefore, an alternative explanation, the one to which we attribute the lack of deactivation, is that midline activity is low during rest. We suggest, then, that the absence of deactivation in this network indicates that the mental processes that normally occur at rest are absent or abnormal in autism.

What are these mental processes that dominate during rest? Evidence in the literature to date seems to suggest that tasks that induce certain types of internal processing activate this resting network. Examples of such tasks are self- and other-person judgments (4, 6, 7, 19–22, 38–45), person familiarity judgments (24, 25), emotion processing (15–17, 46), perspective-taking (22, 47), passive observation of social interactions vs. nonsocial interactions (18), relaxation based on interoceptive biofeedback (48, 49), conceptual judgments (based on internal knowledge stores) vs. perceptual judgments (50), and episodic memory tasks (51), among others [moral decision making (52), joint attention experience (23), and pleasantness judgments (53)]. Therefore, the activity in these regions at rest might simply reflect the extent to which these types of internally directed thoughts are engaged at rest. In fact, a particularly intriguing behavioral study found that individuals with ASD report very different internal thoughts than control subjects (54, 55), lending support to our interpretation that an absence of this resting activity in autism may be directly related to abnormal internal thought. Admittedly, this is a speculative hypothesis but one that can be explicitly tested.

Another of their recent papers comes to the same conclusion.

Recent studies of autism have identified functional abnormalities of the default network during a passive resting state. Since the default network is also typically engaged during social, emotional and introspective processing, dysfunction of this network may underlie some of the difficulties individuals with autism exhibit in these broad domains. In the present experiment, we attempted to further delineate the nature of default network abnormality in autism using experimentally constrained social and introspective tasks. Thirteen autism and 12 control participants were scanned while making true/false judgments for various statements about themselves (SELF condition) or a close other person (OTHER), and pertaining to either psychological personality traits (INTERNAL) or observable characteristics and behaviors (EXTERNAL). In the ventral medial prefrontal cortex/ventral anterior cingulate cortex, activity was reduced in the autism group across all judgment conditions and also during a resting condition, suggestive of task-independent dysfunction of this region. In other default network regions, overall levels of activity were not different between groups. Furthermore, in several of these regions, we found group by condition interactions only for INTERNAL/EXTERNAL judgments, and not SELF/OTHER judgments, suggestive of task-specific dysfunction. Overall, these results provide a more detailed view of default network functionality and abnormality in autism.

If you want to read more about Schizophrenia - default network linkage , read here. If you want to read about Default Network in general , read here ( a very good blog I have recently discovered).

I think the case is settled that at least in the case of Default Network activations, Schizophrenia and Autism are on opposite poles. One has too much default brain activity, the other too little. Also, the function of default network suggests that it is primarily the focus on self and the ability to imagine that is disrupted in autism and heightend to dramatic effects in Schizophrenics.
ResearchBlogging.org

R. L. BUCKNER, J. R. ANDREWS-HANNA, D. L. SCHACTER (2008). The Brain's Default Network: Anatomy, Function, and Relevance to Disease Annals of the New York Academy of Sciences, 1124 (1), 1-38 DOI: 10.1196/annals.1440.011
D. P. Kennedy, E. Courchesne (2008). Functional abnormalities of the default network during self- and other-reflection in autism Social Cognitive and Affective Neuroscience, 3 (2), 177-190 DOI: 10.1093/scan/nsn011
D. P. Kennedy (2006). Failing to deactivate: Resting functional abnormalities in autism Proceedings of the National Academy of Sciences, 103 (21), 8275-8280 DOI: 10.1073/pnas.0600674103

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Monday, January 19, 2009

Get High on Encephalon #62

Welcome to the 62nd brain-dope edition of the brain carnival Encephalon.


Sci@Neurotopia, sets the stage by asking the question whether Prozac and other anti-depressants can be called addictive. While we all know that drugs like cocaine and heroin can be addictive, yet can other benign drugs that we take to relive symptoms that are problematic in the first place, can also be classified as being addictive based on the fact that these drugs show at least two of the DSM criteria for addiction- tolerance and withdrawal? What about their non-high nature or non-craving properties? An interesting discussion ensues, but Sci also seemingly puts her-foot-in-her-mouth by trying to argue that there are two types of addictions- physical and psychological! She makes amend for the same by writing a subsequent post that clarifies that she is not a Dualist who believes that psychological symptoms of addiction like craving are not a result of brain chemistry but indeed does believe that they are as physical in origins as the 'physical' withdrawal symptoms such as constipation. An undertone of the post and comments was that perhaps we need different categories for addiction - one based solely on substance abuse and other more general addiction based on craving and other psychological components included too. DrugMonkey however, seemed to think that this opens a Pandora box for other spurious addictions like net or video-games addiction.

Daniel@Neuroanthropology however is not afraid of rocking the boat, and clearly and persuasively argues for recogintion of psychological as well as physical aspects of addiction. He argues that the fact that we use two systems of inferring causality- the intention based model applied to human interactions and the billiard-ball model of physical causality applied to non-animate interactions; is relevant to addiction and how that is viewed in terms of a disease model or a morality model.Based on his interaction with his class students, he is inclined to believe that we apply intentional model and subjectivity when referring to our own obsessions and to substance dependence, but a disease model when applied to substance abuse. Dependence, involving psychological components , he believes to be more critical.

Although Daniel mentions facebook and related obsession and dependence and not in terms of addiction per se, we all know too well Vaughan's view on the matters of internet and related addictions. This time however, Vaughan@MindHacks is in not a critical mood, but laughing all the way  with the recent discovery that laughing gas (N2O), not to be confused with the brain neuro transmitter nitric oxide, has some hitherto unknown effects on those inhaling it. Laughing gas is a popular anesthetic and it has been found that it increases imagination and suggestibility.It can be safely concluded that suggesting that the surgery will not cause pain, would just enhance the anesthetic effects of N2O by using its suggestibility effects too to the fullest. All that remains to be seen is is N2O addictive and if so would people line up for repetitive surgeries or dental procedures given the ability-to-make-one laugh (and thus imaginably get oneself 'high':-)  effects of the gas!

While inhaling the N20 may not really present an addictive conundrum, what about Deep Brain Stimulation for Pleasure? Sajid@BrainBlogger reports that some studies at Oxford are being carried to ascertain the DBS effects in orbital PFC and how that may affect reward/ pleasure/ Libido. The benefits are to be found in female sexual dysfunction, but bypassing the normal brain circuitry and directly stimulating the brain for pleasure may be more akin to the way the addictive drugs act. what about tolerance and increasing DBS to get the same quantity of reward? What if someone removes the implant , would there be withdrawal effects?

A different type of conundrum is posed by Maria@BrianBlogger as she reports on the face transplant follow-up studies that found that the woman who received face transplant was pleased with the effects though she ostensibly sees a different face in the mirror daily.   She concludes that one should not just screen for organ compatibility, but also psychological coping mechanisms in the case of face transplant as psychological issues are involved here.

When one talks of Psychological coping, who else needs more support than the one being stalked? In the national stalking awareness month swivelchair@NeurologicalCorrelates focuses on stalking and highlights research that found that stalking involved many components of OCD like cognitive inflexibility (being obsessed and feeling compelled) and source-monitoring issues with memory (inability to recall the source of memory) apart from other deficits like lacking an ability to take others' perspective. while we treat stalking as related to OCD, should we also extend and relate it to addiction in general? Is craving for a non-responding beloved the same as craving for a substance as the beloved has been 'objectified' and is worth only as a an object and not as a person? should the same environmental sensitivity and cue based approaches to addiction recovery be applied to stalkers too? Does it make sense to restrict the stalkers from any access to the 'drug' or any environment that reminds them of the 'drug'?

Swivelchair@NeurologicalCorrelates also sends in a post regarding  a hypothesis that aggression may be a result of excessive pruning of white matter tracts. He arrives at this by putting the fact that an ErbB4 gene variant leads  to demyelenation/ less connectivity of left frontotemporal brain region. This region, is also implicated in aggression/hostility and thus his deduction. I have doubts as he mentions the same gene and brain region also implicated in schizophrenia/Psychosis and I disagree that psychotics are in general more aggressive than the normal human population. (although, to be fair, this is not explicitly claimed by Swivelchair anywhere).

Talking of Schizophrrenia, how did such a disease evolve and get fixed in the human population at such a high level of incidence? Walter@HighlightHealth writes about a study that found that genes in the human lineage that were under recent selection pressure and diverged from the chimpanzees , were also related to energy metabolism in the brain and on the same locus are present some of the schizophrenia genes. Thus, he concludes that Schizophrenia is a direct costly byproduct  to the cognitive demands placed during human evolution especially the demands of brain metabolism and maintaining a big brain for greater cognitive work and thus the need to increase efficiency of metabolisms etc. Thus, the assertion that Schizophrenia is a direct result of  changes in metabolism during human brain evolution.

Talking about evolution and comparative methods, did you know how manual dexterity evolved in humans? Mo@Neurophilosophy illustrates how manual dexterity evolved in humans giving us the ability of fine motor control. He notes that we have a direct (synapsing directly on motor neurons)  as well as indirect (involving inter neurons) path from the primary motor coretx to the motor neurons. Also, their appear to be two distinct sub regions of M1- one involving neurons synapsing directly onto the motor neurons and the other synpasing via inter neurons in the spinal chord. Also doing a comparative analysis on Capuchin (who have a prominenet direct as well as indirect pathway like humans)  and Squirrel monkey (who only have the weak direct path) reveals that Capuchins are manually dexterous while Squirrels are not, thus confirming that it is the direct pathway which is anatomically recent and used in fine motor control. Now this is called cutting edge science reporting.   

DoctorSpurt@EffortlessIncitement reports on a study that found correlation between physicological traits like EMG and skin conductance and political attitudes like high support for preserving the social structure form internal/ external threats. In brief, and in a crude reading it found that 'conservatives are cowards'. Put other way, using a variety of measure sit was found that threatening stimuli caused more physiological reaction in those who were of a conservative bent of mind. Now that is some correlation between political attitudes, personality and fearfulness.  

We have talked about aggression and fearfulness and we have talked about evolution. And we know that people differ from each other in their baseline aggressive and fearfulness rates. How does this difference come about. I@TheMouseTrap present evolutionary perspectives on personality traits and I owe a post that would  link the evolution of personality traits to evolution of co-operation/ altruism.

Now, if you have read the Mouse Trap posts, you may wonder if some of the correlations I see between different personality traits and evolutionary adaptive tasks are not spurious and voodoo like? A different kind of voodoo correlation is examined by Neurocrtic , this time referring to the exaggerated and spurious correlation found between fMRI brain regions identified in social cognitive neuroscience and behavioral and personality measures. I haven't read the Vul et al paper, but Neurocritc presents a good summary and details the points-counterpoints that are raised. One thing that caught my attention, off-the-bat,  was the confusion of state personality variables with trait variables (anxiety or empathy can be measured as both trait and state variables). While the trait variable correlations in personality psychology may be low (~ 0.7); I'm not sure the measures that measure state variables (like anxiety at the present moment ) suffer from same level of reliability concerns (but how can we test-retest a state...isn't the state bound to change with each experiment). Anyway the discussion is very enlightening and Neurocritic rejoices in seeing the others slither in pain as their studies are put to question . Oh Schadenfreude.!   

One thing however that Neurocritic does put into question is the allure of fMRI brain scans and how having a brain scan in a study can lead to credibility.Dr Deb at her blog links to a provocative study that found that more brain areas lit up when net surfing than when reading. So do we conclude that net surfing, is good for your health? If so, as its effects are largely beneficial, can we still consider it as an addiction? We seem to have come a full circle.

Before I conclude, just a brief note to let all of you know that you can now subscribe to the encephalon feed here and to many other health and medicine related carnivals here.

That is all for this edition. hope you got your kicks and are dependent on the fortnightly dose of enecpehalon to maintain your sanity. BTW, did anyone miss the 5 Jan edition of encepahlon....did someone suffer from withdrawal symptoms? do let us know via comments!

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Tuesday, January 13, 2009

The Varieties of Altruistic Experiences

Altruism is a very heavily loaded word  in evolutionary psychology/ biology and I would not add to the confusion by defining the term myself. Suffice it to say , that I will use it in all of its various intuitive and theoretical usages.

The evolution of biological Altruism is generally considered as a challenge to Darwinian evolution and there are thought to be two main theories of how Altruism is possible or has evolved. These are Hamilton's Kin-selection and inclusive fitness theory and Trivers' Reciprocal Altruism theory, though some prominent people disagree that there are indeed two separate phenomenon at work and try to argue that they are one and the same phenomenon

I would argue instead that there are more varieties of Altruism than the above two- and that it may also be beneficial to decompose the phenomenon of kin selection and reciprocal altruism into their sub components and to to derive/ elucidate the proximate mechanisms that are involved in these phenomenon as opposed to a single-minded focus on the ultimate explanations of why and how such models can give rise to altruism.

To that effect I would like to separate the parental-investment and parent-child 'kid-selection' effects from other genetic relatives or 'kin-selection' effects. The reason I believe they are separate is because having a child or Kid involves bringing in a new relative with 0.5 relatedness in this world , so the cost to bring in to the parent can be very high as post facto (childbirth) the inclusive fitness becomes 1.5 +0.5b-c (cost) while earlier it was only 1.  Thus, the act can be undertaken if 0.5 +0.5b>c.  In the kin selection case however the inclusive fitness is 1-c +0.5+ 0.5*b after the altruistic act vis-a-vis 1.5 before the act ; so  the act can only be undertaken if 0.5b>c . the addition of a constant 0.5 to the first equation changes the dynamics to a large extent and thus my idea to keep the two phenomenon separate.

Also, reciprocal altruism can itself be broken into some differing phenomenons. The first phenomenon is generalized reciprocity (which is even found in rats , see also this) and others are direct, indirect and strong reciprocity. To summarize form an earlier post:

As per what is know about the evolution of Altruism, it is surmised that co-operation in groups emerges based on four types of reciprocity- direct, indirect, strong and generalized.

In direct reciprocity, one helps another person/animal because the other animal has helped oneself in the past. This requires cognitive capacities to recognize different individuals and require social memory as to which member of the group had helped and which had defected or free loafed. While some animals like the Elephant have good social memories and the ability to remember and recognize different individuals, most animals fall short on these traits.

In indirect reciprocity, one helps another because one has observed the other guy to have helped someone else. This again requires cognitive capacities to recognize and also to remember This is more so based on a reputation system, wherein you start trusting someone more if you observe him doing good deeds. In return you are likely to help the do-gooder , when he is in time of need.

In strong reciprocity, people punish the defectors or free-loafers or non-cooperators. This requires sophisticated cognitive abilities to recognize the defectors and a willingness to undergo cost to oneself while punishing the defector. This too, along with the above two, has rarely been observed in animals apart from humans.

Finally, generalized reciprocity happens when one indulges in good deeds towards a stranger just based on the fact that one has in the near future received such help from other strangers/ con specifics. There are variations on this theme, whereby if people have been put in a good mood (which is a substitute for having received a good deed) they are more likely to indulge in altruistic acts like picking up books dropped by a confederate. This type of reciprocity does not make very strong cognitive demands as one just has to remember the summary of whether the environment is cooperative or not, to produce the right kind of behavior.

So based on above I would like to differentiate between two clusters of reciprocity: Generalized reciprocity not requiring sophisticated cognitive mechanisms, but requiring global assumptions about the social environment; and strong, direct and indirect reciprocity - all involving sophisticated cognitive mechanisms but not dependent on assumptions about the global social environment.

With this I would now like to move to my main thesis. I argue that altruism is a social and group phenomenon and to understand all the proximal mechanisms that are involved in altruistic acts we have to appreciate the mechanisms and drives that lead to group formation, group cohesion and expansion and finally group thriving or differential success from other similar groups based on selection of members belonging to the group such that their is non-zero sum benefits of being in the group.

I would argue that all of the above can be understood in the eight stage framework, with the first three stages related to group formation; the next two related to investment in group (expanding or making it cohesive) and the last three related to populating the group with better individuals/ creating a suitable group that has maximum payoffs for all.

To start with , let us revisit the eight basic adaptive problems as elaborated here and here.

  1. The first problem to be solved 'foe' is also the first primary driver for the evolution of groups. Groups or herd evolve per se, because a solitary creature is more vulnerable to predation than as part of a group. This is how herding evolved. The proximate mechanism working at this level is that of merging with a group. 
  2. The second problem to be solved 'food' is the secondary driver for evolution of groups. It is envisaged that hunting/ gathering as part of a group leads to better  and bigger catches than are individually possible. this provides the incentive to work with other group members to hunt/ forage. This introduces the problem of who would eat the catch when one of them kills, but others are part of the raid party. The solution to the above problem is achieved using the mechanisms of sharing of the spoils. Thus, the proximate mechanism working at this level is a tendency to share the food / resources when begged for by those who are of the same band/ herd/ raiding party.  
  3. The third problem to be solved is 'friends' or con-specifics themselves. As all the group members  are competitors in the same niche, they have to learn to form alliances and co-operate in non-zero sum games with other partners when such co-operation does not entail a price and leads to mutual benefit.the example here would be that of grooming. A bird cannot remove lice from the top of its own head , but can do so easily if another friend removes the lice for her. This is a nonzero sum game. by co-operating both gain and nobody loses. The grooming can happen simultaneously so there is no reciprocity or memory involved. The proximate mechanism here is that of grooming or befriending (spending time with other just to make the alliance better).
  4. The fourth problem to be solved is that of 'kids' and how to help those vulnerable, but related individuals. The kid-selection and parental investment concerns dominate here and lead to emergence of altruism directed towards ones offspring. Now the proximate mechanism devised to help in kid selection is that of care or empathy and this extends to all those who are sick,  vulnerable, infirm or unable to fend for themselves. The care ethic is born and is most visible in contexts where the mother-child or provider-infirm relationship can be activated. Help in rearing infants by related aunts etc is an example of this mechanisms.
  5. The fifth problem to be solved is that of 'kin' or all the other related individuals in the group. Kin selection comes into picture, but for it to work one has to properly identify 'like' people, who are likely to share genes. It is presumed that selection favored those who can judge likeness of phenotype from likeness of genotype and a a simplistic scenario could be that all the group members are considered as like and one tries to identify with them. This is as opposed to trying to differentiate from them and treating them as not-like. Thus, the proximate mechanism involved could be that of loyalty to the group and identification with the group as opposed to rebelliousness/ unconventionality/ differentiation from the group. The drive to find 'like' and 'related' individuals could easily lead to the ethic of community/ loyalty towards the self identified group. Also, forgiveness instinct towards those considered part of group and hence pertaining to valuable relationships that should be maintained despite small annoyances.
  6. The sixth problem to be solved is that of 'selecting' a partner/ partners with which one could indulge in altruistic games. Here the payoff to another would be at a cost to oneself and hence it is not a simple case of co-operation or mutualism in which both parties would benefit. Ideally, when partners have not been determined a priori and one has to discover the characteristics of the majority of the partners (or the population)  and at the same time not harm oneself by unconditional altruistic costs, the viable strategy would be to play with many diverse individuals and play using a generalized reciprocity scheme. At the end of many iterations, one can look at ones strategy and depending on how much altruistic or selfish it is, determine the characteristics of the population. This requires minimal cognitive demands as in not requiring the ability to remember individual interactions. In simple words this can be dubbed as Trust. You trust other people as you do not really know them, except in so far as they are part of the group and hence likely to have a majority group characteristic.  thus, a typical example would be ultimatum game. though the person with which you may playing may be stranger, you know a few things from your generalized reciprocity interactions with other individuals to know that majority of them are fair (make offers at 50 %) and also punish small splits. Thus, based on how you yourself have been given endowments in the past (and how others have rejected endowments given by you) you can reasonably play an ultimatum game with a stranger with same population wide results. Thus, the proximate mechanism here is that of Trusting others to be like the general population stereotype. thus, in humans, most of us are 'altruistic'/ 'good' and hence we trust well rather than be suspicious.             
  7. The seventh task is that of seducing or attracting the right kind of partners so that the payoff the group, and hence yours, increases. Three separate mechanisms are at work here. Direct reciprocity harnesses our ability to remember individuals to pay them back in the future. Gratitude is the proximal mechanism that ensures that we do indeed pay back when time comes. Strong reciprocity ensures that we pay back, in another sense of the term, to the free-riders / defectors. By having punishment in the system one can ensure that the group is not overtaken by free-riders and defectors. The proximal mechanism active here is that of vengeance and not letting the culprits go off scot free. Indirect reciprocity on the other hand works on third party interactions and is based on respect , that is a generalized reputation of an agent to be 'good'/'bad' and acting towards them based on their reputations rather than their immediate behaviors. The proximate mechanism active here is respect/ authority. 
  8. The eighth task is to secure the group or keep the group well-knit and isolate form other 'corrosive' groups. One problem that poses a hurdle to group securing is unexpected payoffs (like war loot) and how they are handled by the group. They may be distributed to everyone equally, distributed as per a hierarchy or consumed by a few dominant individuals.Here the ethics of fairness and equality is the proximate mechanism that is used to settle matters. Another important factor here is not to let other group members infiltrate the successful group and subvert it from within. This gives rise to the ethic of purity and sanctity : the group is considered pure and sanctimonious and only other pure individual are allowed to join the group. The perverts within the group may be destroyed/ redeemed/ salvaged.                     
Thus, in my view, altruism involves all these proximal mechanisms: merging, sharing, grooming and befriending, caring, loyalty (identifying and forgiving), trusting; justice as in gratitude (positive justice),vengeance (negative justice) and respect (generalized justice); and finally the ethics of fairness/equality and purity /sanctity. Some of these can be easily mapped to Haidt's five basic moral foundations.

In a follow-up post I will try to show how these eight altruistic proximate mechanism are reflected in personality traits especially with reference to HEXACO personality model to which one of my readers pointed me to.

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Encephalon: call for submissions.

The next edition of the Encephalon carnival , which also happens to be the first edition in this new year 2009, will be hosted right here at the Mouse Trap on 19th January. Here is requesting you all to send in your psychology/ neuroscience related contributions to encephalon(DOT)host(AT)gmail(DOT)com or directly to me at sandygautam(AT)yahoo(DOT)com.

Please do send in as many quality contributions as possible so that we can kickstart the new year in style! Dont forget that I need the submission by Sunday, the 18th Jan to include in the 19th jan edition.

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Wednesday, January 07, 2009

Perosnality traits: some more evolutionary perspectives

My last post  was about the David Buss chapter in The Handbook of Personality Psychology book by Hogan et al; this post is about the Arnold Buss chapter in the same book.

In this chapter, Buss considers Humans as a primate and lists down 7 personality traits that are found in most primates especially the great apes. These are:

The seven traits listed below have already been mentioned in previous sections. They may be divided into two groups.
The first involves activation, which is defined as involving various kinds of arousal (here defined broadly):
1. Activity, the total energy output as observed in rate of movements and their vigor
2. Fearfulness, wariness, running away, cowering, and the concomitant physiological arousal
3. Impulsivity, acting suddenly and on the spur of the moment; the opposite is the tendency to inhibit behavior
The second set of personality traits are all social:
4. Sociability, preferring being with others (though primates are a highly social group, there are still individual differences in sociability within each species)
5. Nurturance, helping others, especially those who need help, even at a cost to the helper (altruism)
6. Aggressiveness, attacking or threatening others
7. Dominance, seeking and maintaining superior status over others versus the opposite pole, submissiveness

I would like to group them slightly differently ( and in accordance with my eight stage theories) and also introduce another trait that of suspiciousness when we consider humans as other primates have a rudimentary ToM ability.

  1. Fearfulness mapped to Neurtoticsm.
  2. Impulsivity mapped to Conscnetiousness
  3. Sociability mapped to Extraversion
  4. Nurturance mapped to Agreeableness
  5. Dominance mapped to Rebelliousness/ Conformity
  6. Suspiciousness mapped to Trust/Defensiveness
  7. Activity mapped to Activity
  8. Agressivenss mapped to Masculinity/Feminity
He also lays down the framework for how such traits may become evident ; he works within attachment theory paradigm and highlights research on primate attachment studies to lay down the foundation for why such traits may develop in an individual.
The period of attachment in primates has been divided into three phases (H. F. Harlow, Harlow, & Hansen, 1963). At first the mother is solicitous and completely accepting of the infant, and she is a haven of safety and nurturance.
The infant's feeling of security depends in large part on the mother. If she is sufficiently protective and available, the infant will be secure enough to venture out in the wider environment. Primate infants appear to be motivated by two opposing tendencies: the need to seek novelty and stimulation versus the need for security and protection (Mason, 1970). An insecure infant remains close to the mother, too scared to explore the environment. A secure infant tends to be low in fear and can venture away from the mother so long as she is in sight.
In the second phase of attachment, the mother withdraws affection, diminishing attention to the infant, and starts to punish the infant. The latter may react with withdrawal, anger, resistance, or negativism. These first signs of independence are typically met by even more irritabihty and punishment by the mother.
In the third phase, the mother is often occupied with the birth of the next offspring and therefore is even more rejecting of her older child. The presence of this new infant is likely to elicit jealously and temper tantrums by the displaced sibling. If the mother can spare some attention and affection for her older sibling, the latter's jealousy and annoyance should gradually wane.
The events of the attachment period may be expected to affect personality traits. The mother's behavior should be regarded as only one determinant, albeit an important one, of her youngster's personality. If she is not sufficiently protective and a haven of security, her infant may become fearful and inhibited. If she fails to provide enough attention and social stimulation, her infant may become withdrawn and less sociable. And if she cannot share at least some affect with her older offspring after the birth of a new one, the older one may become intensely jealous. In brief, the events of attachment are assumed to affect the personality traits of fearfulness, impulsivity (the opposite of inhibition), sociability, and the anger component of aggressiveness (jealousy).
To me this seems to be valid developmental trajectory of the traits: A non-protecting mother leading to Fearfulness (N); not providing a safe haven leading to lack Impulsivity or Inhibition (C); not providing enough attention leading to less sociability (E); not providing social stimulation and care leading to lack of Nurturnace in child (A) (which Buss doesn't touch upon) and finally not sharing affect leading to Jealousy/ Dominance problems within siblings(Rebelliousness/Conformity).

Before we accept this attachment theory in its entirety it is apt to pause and remeber that many times the behaviour of mother is driven by infant behaviour and that mother and chil may share the sam temperamental quality due to genes and not due to nurturing and this however reflects in a pattern of traits in child and parenting practice in parent.

Finally Buss goes on to show how some of the traits in other primates are not well developed as compared to humans and are at the level of human infants and thus cannot lead to much insight about human personality. One exapmle is that of self-awareness; though primates and human infants may have a mirror-test self-awareness, it is limited.
Adult humans are capable of mirror-image recognition, which is absent in infants and develops slowly during the second year of life as part of more general trends in cognitive development. By the age of 2 years most infants possess this capacity (Amsterdam, 1972; Schulman & Kaplowitz, 1977). Does this mean that children of 2 years have a self-concept and the same kind of self-awareness as older children and adults? There are five cognitive attributes present in older children that are absent in 2-year-olds, which suggests that the answer is no.
The first is self-esteem. The basis for later self-esteem may be laid down in 2- year-olds, but children of this age do not show behavior that allows us to infer the general self-evaluation called self-esteem. This diffuse feeling of self-worth develops gradually and can be measured perhaps by the age of 4 years. Nor are infants clearly aware of the difference between their private feelings and public behavior.
It is still too early for the sense of covertness and an awareness that private thoughts and feelings cannot be observed. Infants and primates lack the sense of covertness that can be inferred in children of 4 years. Infants are still egocentric and do not know that others view the world from different perspectives. Even children of several years of age are Umited in social perspective-taking. In one study children were asked to select gifts for their parents, teacher, brother, sister, and self (Flavell, 1968). Most 3-year-olds selected the same gifts for others as for themselves. Some 4-year-olds selected gifts appropriate for others, half the 5-year-olds did, and all the 6-year-olds did. Social perspective-taking evidently emerges during the fifth year of life. Linked to perspective-taking is the abihty to view oneself as a social object. Such public self-awareness, as seen in the reaction of embarrassment, does not occur until the fifth year of life (Buss, Iscoe, & Buss, 1979).
The last facet of the advanced self to develop is identity. It may be a personal identity, the sense of being different from everyone else in appearance, behavior, character, or personal history, or it may be social identity, knowing oneself to be a member of a nation, religion, race, vocation, or any other group that offers a sense of belonging to something larger than oneself. And most of us have a sense of continuity, identifying ourselves as the same person across decades of time or across diverse social roles.
Thus five aspects of the self are absent in 2-year-old human children: selfesteem, a sense of covertness, perspective-taking, public self-awareness, and identity. These may be regarded as evidence for an advanced or cognitive self, which is conspicuously absent in human infants and the great apes. They do appear to have a primitive, sensory self—an awareness of where the body ends and not-me begins, and mirror-image recognition (Buss, 1980). But they lack the advanced cognitive self that is implicit in constructs such as self-concept, self-esteem, selfconsciousness, and identity, constructs easily applied to older human children and adults.

To me this beautifullay sums-up what we can and cannot derive from studies of primates and other mammals about human personality.

References: Buss, H. Arnold. (1997). Evolutionary perspectives on personality traits. In R. Hogan, J. A. Johnson, & S. R. Briggs (Eds.), Handbook of Personality Psychology (pp. 345-366). New York: Academic Press..

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COPUS and the Year of Science 2009

Please find below the fold some information about COPUS and how it plans to celebrate the Year of Science 2009. As a blog partner I'll be looking forward to ways in which I, and The Mouse Trap reader community,  could get involved in the YoS2009.


The Coalition on the Public Understanding of Science (COPUS) kicked off Year of Science 2009 (YoS2009) -- a national, yearlong, grassroots celebration--this week in Boston at the annual meeting of the Society for Integrative and Comparative Biology. COPUS, which represents more than 500 organizations, is celebrating how science works, who scientists are, and why science matters. Ira Flatow, host of Science Friday, broadcast every week on National Public Radio, launched the week’s events with a plenary presentation encouraging scientists to get involved in communicating and sharing the excitement of science at every opportunity.

Flatow said: “If you don’t stand up for science, then no one else is going to do it. We as journalists and scientists have to figure out ways to share science in plain English whenever possible.” This call to action is what drives YoS2009: it is a call for scientists to step out of their laboratories and into the public eye.

COPUS participants—museums, federal agencies, K–12 schools, universities, scientific societies, and nonprofit and for-profit organizations from all 50 states and 13 countries—will host events in celebration of YoS2009. Regionally connected COPUS participants are bringing science to their local communities in innovative ways. Some of the activities taking place in different regions of the country are described below.

Florida
Charlie Crist of Florida was the first governor to issue a statewide proclamation of YoS2009. The proclamation will be formally presented in an event bringing together representatives from the Girl Scouts, local schools, the National Football League’s (NFL) Environmental Program, and Florida’s Division of Forestry, among many other diverse organizations, in a day of celebrating science through hands-on activities showcasing rich and diverse science resources.

Washington, DC
The nation’s capital will be the site of a week-long “Meet the Scientist” effort in which leading scientists will go to schools, community groups, and science festivals to share their science with the general public and explain how they know what they know about science.

Berkeley, California
The University of California (UC) Berkeley maintains the Web site Science@Cal (http://scienceatcal.berkeley.edu) to promote the depth and breadth of science on campus. The site highlights opportunities for the public to meet UC scientists at the East Bay Science Café. Also, scientists can teach people how they do their work by hosting Flat Stanley at their labs and institutions (www.flatstanley.com/yearofscience2009/intro.htm).

Seattle, Washington
At Northwest School, the annual Winterfest celebration will highlight YoS2009 themes with rocket launches, flaming chemistry demonstrations, mousetrap cars, a play based on the Fibonacci number series, Rube Goldberg machines, and more!

Nationally
A special Web site (www.yearofscience2009.org) will help the general public learn more about this yearlong, national event. The site will feature a different scientific theme each month, complemented by blogs from scientists and science communicators about those topics and their fields of expertise. Highlights from the dynamic YoS2009 Web site include the integration of components from the newly launched Understanding Science Web site (www.understandingscience.org), Flat Stanley explorations of science, the opportunity to name a new species of jellyfish or adopt a species for the Encyclopedia of Life, and a contest to build the most scientific pizza.

All of these events and activities foster innovative new partnerships that will bring science and the public closer together locally, regionally, and nationally—all in a growing celebration of science!

Rita Colwell, former director of the National Science Foundation, states: "In this Year of Science 2009, scientists around the globe collectively are shining a spotlight on their work to highlight the achievements of modern science in the public square. This year provides a special opportunity to be optimistic and express hope for a better future. Through their passion and dedication, scientists and nonscientists alike are able to share in the thrill of scientific discovery.”

COPUS, which began with support from the National Science Foundation, has grown to be an inclusive grassroots endeavor spurring communication and collaboration in the scientific community while shining the spotlight on science in 2009. Still growing, the COPUS network of more than 500 organizations includes a broad range of participants from large federal agencies such as the National Oceanic and Atmospheric Administration and the Environmental Protection Agency to local groups such as the Banana Slug String Band from Santa Cruz, California, and TalkingScience, a New York City nonprofit that is organizing a “Rock-it Science” concert in 2009. Major sponsors of the Year of Science 2009 include the American Institute of Biological Sciences, the University of California Museum of Paleontology, the Geological Society of America, and the National Science Teachers Association. To register as a participant or to learn more, visit www.copusproject.org.

For more information about COPUS and the Year of Science 2009, please visit
•    www.copusproject.org 
•    www.yearofscience2009.org 
•    http://blogs.aibs.org/copus/ 

About COPUS  
Support for COPUS planning workshops was provided by the National Science Foundation under grant nos. EAR-0606600, EAR-0628790, and EAR-0814048 to the University of California Museum of Paleontology. The cognizant fiduciary body for COPUS and the Year of Science 2009 project is the American Institute of Biological Sciences Inc., a 501(c)(3) nonprofit organization, which is providing staffing support and IT and other resources. The Geological Society of America, the University of California Museum of Paleontology, and the National Science Teachers Association are also contributing funds for COPUS and Year of Science 2009.

Year of Science sponsorship opportunities are available now! For more information, contact Sheri Potter (e-mail:spotter@copusproject.org).

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