Research directions | LSM Research – Neurology of empathy, transmission of language, theism, etc.

The primary purpose of this website was:

a) to extensively characterise the social mindset (and its neurological mechanisms) that humans have (and everyone around us has to a much higher degree than us), and
b) to extensively characterise our condition as it stands in comparison to other conditions classed under autism spectrum disorder (ASD) or schizoid personality disorder (SPD).

The research has led to several new research directions, which are listed below.

Social mindset

Neurology

The social mindset is the result of an active link between brainstem responses and episodic memories.

This site documents the neurology of the social mindset and proposes a model for its mechanism in line with the neurology and its features.

The site suggests that research on the social mindset follow the direction set forth by this model.

The social mindset is facilitated by von Economo neurons in the anterior insular cortex and anterior cingulate cortex.

The site documents the role of von Economo neurons in the social mindset and their presence in humans and non-human animals with some social-mindset features, such as other primates, elephants and cetaceans.

Features

The social mindset gives rise to virtually all characteristically human behavioural and psychological features.

The site documents how the social mindset gives rise to virtually all psychological and behavioural features known to be characteristically human.

The site suggests that research into the features of the social mindset factor in the necessary nature of the social mindset in the features and the precise way in which it brings them about.

The social mindset brought about ‘language’, ‘science’ and ‘music’ in the traditional sense but directed transmission of any information (whether spoken, written, signed, embossed, played on an instrument, etc.) to another individual in an actual sense.

The social-mindset feature that gave rise to language, science or music, as traditionally conceived, is the expectation that another individual will understand and benefit from it as you do and the impetus to transmit it to that person. Learning or repeating language (or any information) to the self is not the social-mindset feature.

The shaping of language over time from onomatopoeia (as seen in mimicking birds) to arbitrary words and pictograms to alphabets is an effect resulting from repeated transmission among the social group but is not a social-mindset feature itself.

The site suggests research take into account the distinction between the non-social-mindset semantic aspects of language, knowledge or music and the social-mindset impetus to transmit it to others.

Anti-social personality disorder, psychopathy, borderline personality disorder, etc. are a result of the social mindset interacting with a spontaneous-threat-perception pathology.

The site documents the mechanism by which the threat-proxy features of the social mindset give rise to disorders such as antisocial personality disorder, psychopathy or borderline personality disorder in extreme forms.

The site suggests research into these disorders follow the direction set forth by this mechanism.

Additionally, due to the human-evolved mechanism commonly ascribed to empathy being responsible for multiple other features, including pleasure from witnessed harm, the site suggests that the use of the term ’empathy’ as a substitute for the social mindset be discouraged.

The sexual dimorphism in crime, sadism, zoosadism, psychogenic self-harm, anorexia nervosa, antisocial personality disorder, borderline personality disorder, cosmetics and fashion are a result of the social mindset interacting with the sexual dimorphism in the hypothalamic aggression centres.

The site documents the mechanism by which the sexual dimorphism in the hypothalamic aggression centres interacts with the social mindset to give rise to the sexual dimorphism in outward aggression against threat proxies in several spontaneous-threat-perception pathologies as well as cosmetics and fashion.

The site suggests research into these phenomena factor in the role of this interaction.

Much of human sexuality is governed by sexual social-mindset associations.

The site documents the mechanism by which episodic memories can come to serve as triggers of sexual arousal after experiencing sexual arousal as a result of a visual sexual imprint.

The site also documents the mechanism by which spontaneous-threat-perception pathologies and the sexual dimorphism in the hypothalamic aggression centres interact with sexual social-mindset associations to create sexual tendencies such as sexual sadism and sexual masochism.

Sexual arousal by any social-mindset feature or any other act or scenario is the result of a sexual social-mindset association, however sexual social-mindset associations are often seen as inextricable parts of visual sexual imprints such as partialisms (such as the shoe or nail paint for the foot), and some of them (such as smoking attraction) have sometimes mistakenly been attributed to sexual imprinting.^[1]

The site suggests research make the distinction between sexual social-mindset associations and sexual imprinting when researching human sexuality.

Taboos and laws arise from a three-step process involving a) an initial, innate scenario involving defensive aggression in an individual, b) often, schadenfreude for the defensive aggression by those with the social mindset and differences in the amygdala–hypothalamus network and c) empathy for the individual by others with the social mindset.

The site details the origin of taboos and laws in line with the neurology and mechanism of the social mindset.

The site suggests research into taboos and laws follow the direction set forward by this model.

The social-mindset mechanism results in a form of unconscious thought appropriation that cannot be subjectively felt or rationalised, and this is why it is missing from scientific literature.

The site demonstrates the mechanism by which externally witnessed episodic memories can come to serve as direct triggers of reward/aversion and become the basis of one’s perspective rather than one’s perspective, hence the term ‘social mindset‘.

This has led the social-mindset mechanism to be unduly avoided in almost all research into social-mindset features.

This aspect of the social mindset is elaborated on the Social mindset as a whole and Unconscious thought appropriation sections of Presentation and progression of our lack of the social mindset.

The site suggests research into the social mindset strongly bear this aspect of the social mindset in mind.

The creation of the concepts of ‘consciousness’, ‘self-awareness’, ‘mind’, ‘agency’, ‘free will’, ‘intent’, ‘god’, ‘soul’ and ‘multiple realities’ is an effect resulting from the characterisation of one’s own behaviours, one’s reflection’s behaviours, other people’s behaviours, other animals’ behaviours or the behaviours of natural events by brainstem responses attached to episodic memories that they resemble.

The site documents the mechanism by which the characterisation of other phenomena by brainstem responses attached to episodic memories that they resemble leads to the creation of these concepts, as opposed to their characterisation based only on the external sensory input that they provide (with no second reference).

The mechanism behind the creation of each concept is described in detail in the corresponding links.

Genetics

The Olduvai domains brought about the social mindset.

The site documents the hyperamplification of the HLS triplet of the Olduvai domain after a pericentric inversion on chromosome 1 roughly 3.5 million years ago and its correlation with the evolution of social-mindset features in early humans and the severity of social deficits in high-functioning autism as well as the correlation between the CON subtypes of the Olduvai domain × brain size and the presence of social-mindset features in some non-human animals, such as other primates, elephants and cetaceans.

The Olduvai domains brought about von Economo neurons, likely as a result of their inhibitory role affecting the development of early regions of the cortex over later regions and the development of single, large neurons, axons and dendrites over multiple smaller neurons, axons, dendrites and cortical layers.

The site suggests that this hypothesis as described, including whether the domains bind to PDE4DIP, be investigated when researching the Olduvai domains and how they formed the von Economo neurons of the anterior insula and anterior cingulate cortex.

Our lack of the social mindset

Neurology

Our condition is the result of an overdeveloped cerebral cortex in combination with a comparatively underdeveloped and underlateralised anterior insula and anterior cingulate cortex (ACC). This also appears to manifest with hyperactivity of the dorsal ACC, resulting in obsessive–compulsive disorder–like behaviours, and hyperactivity of the posterior insula, resulting in sensory hypersensitivities.

The site documents the neurology of our condition in line with the neurology of the social mindset, MRIs of myself and published literature on our diagnoses.

Presentation and progression

Our condition presents with a significant relative deficiency in the formation of associations between brainstem-response signals from the anterior insula and episodic memories in the medial prefrontal cortex in comparison to the formation of episodic memories that regulate innate survival mechanisms. This manifests with suppressed social-mindset features that appear in childhood, which are then undone in adolescence as one literally ‘learns their way out of’ the social mindset.

This site documents the presentation and progression of our condition in line with its neurology.

Other features

Obsessive–compulsive disorder (OCD), as clinically defined, requires the involvement of the social mindset (brainstem signals in the medial prefrontal cortex), leading to distress or unwanted, illogical behaviours, but when it does not involve the social mindset, it leads to no such distress.

The site describes how the social mindset and its contamination of the medial prefrontal cortex with brainstem signals fundamentally alters the way in which hyperactivity of the dorsal anterior cingulate cortex (ACC) presents, so much so that diagnostic literature is only familiar with this presentation, which is described as obsessive–compulsive disorder and involves significant distress or unwanted, illogical behaviours.

However, without the social mindset, such distress does not result from hyperactivity of the dorsal ACC, and this manifests in our condition.

The site suggests that our presentation of OCD-like behaviours with a lack of distress be diagnostically recognised as an independent result of hyperactivity of the dorsal ACC (when there is a lack of the social mindset).

Swallowing difficulties related to hyperactivity of the dorsal ACC are a significant part of our condition, and when tic disorder is present with our lack of the social mindset, it is especially or exclusively prominent when swallowing food.

The site suggests that research recognise the presence of swallowing difficulties and the prominence of tics when swallowing food as an aspect of our lack of the social mindset, in line with our hyperactivity of the dorsal ACC but with the reduced contamination of the medial prefrontal cortex by brainstem signals.

Differences between us

Visually imprinted partner preference and partialisms are established by laughter/smiling in early childhood.

The site theorises a mechanism for visually imprinted partner preference and partialisms in line with the evidence on Differences between us.

It suggests that broadly, quality of relationship with a parent, as reported in several studies, should indeed be a factor in parental imprinting, but not this specifically; specifically, laughter/smiling should have been permitted more often while witnessing the parent, which does not necessarily equate to quality of relationship and in fact would more equate to mere close presence of the parent, due to the existence of the visually imprinted separation anxiety mechanism in children.

In line with the evidence, imprinted partialisms should be more common in children from families in which tickling occurred more often, or more members are known to have tickled the child.

The site suggests research be carried out to confirm these theories.

Arachnid and snake phobias likely arise from exposure to sharp pinpricks and faeces, respectively, in early childhood (in those with high temporal-lobe synaptic consolidation).

The site theorises a mechanism for imprinted specific phobias in line with the evidence on Differences between us.

The site suggests research be carried out to confirm these theories.

Genetics

The genetics of our condition likely involve a genetic background involving microtubule-related genes (most significantly, those of the NBPF family) combined with a probable causative mutation in a gene related to the RAS/MAPK pathway.

The site documents the role of microtubule-related genes, especially those of the NBPF family, in autism spectrum disorder with megalencephaly and/or above-average intelligence and the role of gain-of-function mutations in genes related to the RAS/MAPK pathway in autism spectrum disorder with megalencephaly, the paternal age effect and several physiological features that I have.

Prevalence

The prevalence of our severity and presentation of our condition is likely to be somewhere around 1 in 7,500 in males and potentially absent in females.

The site suggests two main prevalence estimates for our condition and suggests that it likely does not exist at our severity in females.

The site suggests that if one is to systematically establish a prevalence figure and sex ratio for our condition, to use our criteria.

Criteria

Asperger syndrome is not necessarily a ‘mild’ form of autism, and Asperger syndrome and schizoid personality disorder are not mutually exclusive. In fact, when combined, they genetically, neurologically and phenotypically represent the most severe form of Asperger syndrome and one of the most severe forms of autism spectrum disorder as a whole.

Asperger syndrome has traditionally been conceived as a ‘mild’ form of autism, in contrast to autism with language delay or intellectual disability, which is considered ‘severe’.^[2]

Additionally, current diagnostic criteria require that either Asperger syndrome or schizoid personality disorder (SPD) only be diagnosed to the exclusion of each other.

However, the evidence on the site demonstrates that severe forms of Asperger syndrome without language delay or intellectual disability exist (e.g., our own). My scores on the Autism Diagnostic Interview-Revised at age 14 approached the maximums, despite the fact that scores in the bottom third were sufficient for diagnosis.

Additionally, several studies have pointed out how those with Asperger syndrome who also meet criteria for SPD have more severe social-interaction impairments, stereotyped behaviours and specific interests, and genetic evidence, such as an increase in copy number of the CON1 subtype of the Olduvai domain, correlates with both an increase in severity of the primary symptoms of autism and an increase in severity of the symptoms of schizoid personality disorder (negative symptoms of schizophrenia) without language delay or intellectual disability – instead, an increase in brain size and, in our case, precocious language and increased mental ability.

As such, Asperger syndrome can no longer be seen as a ‘mild’ form of autism simply due to lacking language delay or intellectual disability, and the site suggests that this conception of Asperger syndrome be discouraged.

Additionally, Asperger syndrome to our severity and schizoid personality disorder can no longer be seen as distinct diagnoses. They represent one condition with one genetic, neurological and phenotypic basis.

Instead, it appears that our form of Asperger syndrome/SPD is the most severe form possible, given the lack of virtually all human social-mindset features that arrived after the split from chimpanzees.

In short, ‘severity’ of autism is currently used to refer to language delay and global impairment not restricted to the social mindset (which is due to other effects of diffuse brain underdevelopment and is found in the most common, low-functioning forms of autism).

To be most accurate, ‘severity’ of autism should only refer to the severity of the primary symptoms of autism (those related to the social mindset), which do not include language ‘delay’, only the impetus to transmit language to others, and are severe in our condition.

Schizophrenia and autism

Positive symptoms of schizophrenia are the result of a relatively overlateralised anterior insula and anterior cingulate cortex within the context of comparatively less development in the rest of the cerebral cortex.

The site documents the neurology of the positive symptoms of psychotic spectrum disorders such as schizophrenia in line with the neurology of the social mindset, which is inverse to that of autism spectrum disorder with megalencephaly.

Positive symptoms of schizophrenia are heightened forms of social-mindset features with a negative undertone.

The site details how the neurology of the positive symptoms of psychotic spectrum disorders explains the persecutory and paranoid nature of positive symptoms, given that the right anterior insula and right anterior cingulate cortex respond more to sympathetic-nervous-system (‘fight-or-flight’) signals.

The site suggests that research into the positive symptoms of psychotic spectrum disorders follow the direction set forth by this evidence.

Bipolar disorder is likely the result of a pattern of episodic memories, linked to an abnormally strong social mindset, that oscillates due to behaviours instigated by those memories and the resulting response by others around.

The site hypothesises a model of bipolar disorder that factors in the heightened social mindset.

The site suggests that the hypothesis as described be considered as a model for the progression of bipolar disorder.

The predominance of depressive symptoms in mood disorders is due to the response of the overlateralised anterior insula and anterior cingulate cortex to sympathetic-nervous-system signals.

The site states how the overlateralised social-mindset brain regions explain the predominance of depressive symptoms over manic symptoms in mood disorders.

The typical onset of psychotic spectrum disorders in adolescence is a result of the increasing disparity in episodic memories attached to brainstem responses vs. those that regulate innate survival mechanisms.

The site explains how the progressive disparity in episodic memories linked to brainstem responses vs. those not gives rise to the typical time of onset of psychotic spectrum disorders in adolescence, similar to that of our loss of the social mindset.

Psychotic spectrum disorders are associated with loss-of-function mutations in microtubule-related genes and genes related to the RAS/MAPK pathway.

The site documents the genetics of psychotic spectrum disorders with positive symptoms, which is inverse to that associated with autism spectrum disorder with megalencephaly (but not low-functioning autism with microcephaly).

Negative symptoms of schizophrenia are associated with underlateralisation of the anterior insula and anterior cingulate cortex and less underdevelopment in the rest of the cerebral cortex than that of schizophrenia with predominantly positive symptoms.

The site documents the neurology of the negative symptoms of schizophrenia, which is similar to that of autism spectrum disorder.

Negative symptoms of schizophrenia are symptoms of a lack of the social mindset.

The site details how the neurology of the negative symptoms of schizophrenia explains their similarity to symptoms of autism spectrum disorder / a lack of the social mindset.

The site suggests that research into the negative symptoms of schizophrenia follow the direction set forth by this evidence.

Schizophrenia with predominantly negative symptoms is associated with a genetic background involving high repeats of the CON1 subtype of the Olduvai domain.

The site documents part of the genetic background of schizophrenia with predominantly negative symptoms, which is in line with that associated with autism spectrum disorder with megalencephaly.

The importance of an ‘exclusively internal fantasy’ in the diagnosis of and psychoanalytic literature on schizoid personality disorder (SPD) is likely an artefact of bias from the social mindset.

In line with the evidence on the mechanism of the social mindset, our high conformity to other symptoms of SPD and the lack of evidence of how such an ‘exclusively internal fantasy’ is being measured, the site suggests that the importance of an ‘exclusively internal fantasy’ in the construct of schizoid personality disorder is likely an artefact of bias from assessors with the social mindset, under the assumption that the person must be generating an internal imaginary world as someone with the social mindset may do if they were depleted of social interaction.

Instead, in line with the social-mindset mechanism and ourselves, the converse is more likely to be true: a reduced internal imagination due to a reduced ability for episodic memories to serve as direct sources of reward/aversion.

Low-functioning autism with microcephaly is the result of more severe loss-of-function mutations in the same genes associated with psychotic spectrum disorders.

The site documents the genetic overlap between low-functioning autism with microcephaly and psychotic spectrum disorders.

The site suggests that research bear this evidence in mind and distinguish low-functioning autism with microcephaly from autism spectrum disorder with megalencephaly.

There is a strong genetic, neurological and phenotypic diametric relationship between schizophrenia with predominantly positive symptoms (typical schizophrenia) and high-functioning autism with megalencephaly.
There is a strong genetic and partial neurological and phenotypic diametric relationship between low-functioning autism with microcephaly and high-functioning autism with megalencephaly.
There is a genetic, neurological and phenotypic diametric relationship between the positive and primary negative symptoms of schizophrenia.

The site concludes the Schizophrenia and autism section with the diametric relationships that are indicated by the genetic, neurological and phenotypic evidence on the site.

The site suggests that research into the two conditions bear these diametric relationships in mind.

Negative symptoms of schizophrenia may involve more importance of the medial prefrontal cortex (so as to include avolition or, in the most extreme cases, catatonia), while symptoms of autism may involve more importance of the anterior insula (so as to include symptoms such as sensory hyper- or hypo-sensitivity).

The site proposes one hypothesis for the few discrepancies between the negative symptoms of schizophrenia and the symptoms of autism spectrum disorder but recognises that the diagnostic literature likely illustrates a more exaggerated distinction between the two classes of symptoms than that reflected in their genetics and neurology.

Nonetheless, this site proposes that research investigate the relative roles of the anterior insula and anterior cingulate/medial prefrontal cortex in the negative symptoms of schizophrenia vs. the symptoms of autism.

References

^ Aronsson, H.; Lind, J.; Ghirlanda, S.; Enquist, M (2011-03-01). "Parental influences on sexual preferences: The case of attraction to smoking". Journal of Evolutionary Psychology. 9 (1): 21–41. doi:10.1556/jep.9.2011.12.1. ISSN 1789-2082, 2060-5587.
^ Frith, Uta (2004). "Emanuel Miller lecture: Confusions and controversies about Asperger syndrome". Journal of Child Psychology and Psychiatry. 45 (4): 672–686. doi:10.1111/j.1469-7610.2004.00262.x. ISSN 1469-7610.