Infant Synesthesia / A Developmental Stage

No, synesthesia is not a symptom of disorder, but it is a developmental phenomenon. In fact, several researchers have shown that synesthetes can perform better on certain tests of memory and intelligence. Synesthetes as a group are not mentally ill. They test negative on scales that check for schizophrenia, psychosis, delusions, and other disorders.

Synesthesia Project | FAQ – Boston University


What if some symptoms “assigned” by psychologists to Asperger’s Disorder and autism are merely manifestations of synesthesia?

“A friend of mine recently wrote, ‘My daughter just explained to me that she is a picky eater because foods (and other things) taste like colors and sometimes she doesn’t want to eat that color. Is this a form of synesthesia?’ Yes, it is.” – Karen Wang

We see in this graphic how synesthesia is labeled a “defect” that is “eradicated” by normal development (literally “pruned out”). People who retain types of integrated sensory experience are often artists, musicians, and other sensory innovators (like chefs, interior designers, architects, writers and other artists) So, those who characterize “synthesia” as a developmental defect are labeling those individuals who greatly enrich millions of human lives as “defectives”. – Psychology pathologizes the most admired and treasured creative human behavior.

No touching allowed! Once “sensory” categories have been labeled and isolated to locations in the brain, no “talking to” each other is allowed. The fact that this is a totally “unreal” scheme is ignored. Without smell, there IS NO taste…


Infants Possess Intermingled Senses

Babies are born with their senses linked in synesthesia

originally published as “Infant Kandinskys”

What if every visit to the museum was the equivalent of spending time at the philharmonic? For painter Wassily Kandinsky, that was the experience of painting: colors triggered sounds. Now a study from the University of California, San Diego, suggests that we are all born synesthetes like Kandinsky, with senses so joined that stimulating one reliably stimulates another.

The work, published in the August issue of Psychological Science, has become the first experimental confir­mation of the infant-synesthesia hy­pothesis—which has existed, unproved, for almost 20 years.

Researchers presented infantsand adults with images of repeating shapes (either circles or triangles) on a split-color background: one side was red or blue, and the other side was yellow or green. If the infants had shape-color asso­ciations, the scientists hypoth­esized, the shapes would affect their color preferences. For in­stance, some infants might look significantly longer at a green back­ground with circles than at the same green background with triangles. Absent synesthesia, no such dif­ference would be visible.

The study confirmed this hunch. Infants who were two and three months old showed significant shape-color associations. By eight months the preference was no longer pronounced, and in adults it was gone altogether.

The more important implications of this work may lie beyond synesthesia, says lead author Katie Wagner, a psychologist at U.C.S.D. The finding provides insight into how babies learn about the world more generally. “In­fants may perceive the world in a way that’s fundamentally different from adults,” Wagner says. As we age, she adds, we narrow our focus, perhaps gaining an edge in cognitive speed as the sensory symphony quiets down. (Sensory “thinking” is replaced by social-verbal thinking)

(Note: The switch to word-concept language dominance means that modern social humans LOOSE the appreciation of “connectedness” in the environment – connectedness becomes limited to human-human social “reality” The practice of chopping up of reality into isolated categories (word concepts) diminishes detail and erases the connections that link detail into patterns. Hyper-social thinking is a “diminished” state of perception characteristic of neurotypicals)

This article was originally published with the title “Infant Kandinskys”


The Brain from Top to Bottom

McGill University
Explore topics such as emotion, language, and the senses at five levels of organization (from molecular to social) and three levels of explanation (from beginner … advanced)

Debunking Left Brain, Right Brain Myth / Paper – U. Utah Neuroscience

An Evaluation of the Left-Brain vs. Right-Brain Hypothesis with Resting State Functional Connectivity Magnetic Resonance Imaging

Jared A. Nielsen , et al, Affiliation Interdepartmental Program in Neuroscience, University of Utah, Salt Lake City, Utah, United States of America (See original for authors and affiliations)

Published: August 14, 2013 (Extensive paper with loads of supporting graphics, etc.) (Heavy going technical paper)


Lateralized brain regions subserve functions such as language and visuospatial processing. It has been conjectured that individuals may be left-brain dominant or right-brain dominant based on personality and cognitive style, but neuroimaging data has not provided clear evidence whether such phenotypic differences in the strength of left-dominant or right-dominant networks exist. We evaluated whether strongly lateralized connections covaried within the same individuals. Data were analyzed from publicly available resting state scans for 1011 individuals between the ages of 7 and 29. For each subject, functional lateralization was measured for each pair of 7266 regions covering the gray matter at 5-mm resolution as a difference in correlation before and after inverting images across the midsagittal plane. The difference in gray matter density between homotopic coordinates was used as a regressor to reduce the effect of structural asymmetries on functional lateralization. Nine left- and 11 right-lateralized hubs were identified as peaks in the degree map from the graph of significantly lateralized connections. The left-lateralized hubs included regions from the default mode network (medial prefrontal cortex, posterior cingulate cortex, and temporoparietal junction) and language regions (e.g., Broca Area and Wernicke Area), whereas the right-lateralized hubs included regions from the attention control network (e.g., lateral intraparietal sulcus, anterior insula, area MT, and frontal eye fields). Left- and right-lateralized hubs formed two separable networks of mutually lateralized regions. Connections involving only left- or only right-lateralized hubs showed positive correlation across subjects, but only for connections sharing a node. Lateralization of brain connections appears to be a local rather than global property of brain networks, and our data are not consistent with a whole-brain phenotype of greater “left-brained” or greater “right-brained” network strength across individuals. Small increases in lateralization with age were seen, but no differences in gender were observed.

From Discussion

In popular reports, “left-brained” and “right-brained” have become terms associated with both personality traits and cognitive strategies, with a “left-brained” individual or cognitive style typically associated with a logical, methodical approach and “right-brained” with a more creative, fluid, and intuitive approach. Based on the brain regions we identified as hubs in the broader left-dominant and right-dominant connectivity networks, a more consistent schema might include left-dominant connections associated with language and perception of internal stimuli, and right-dominant connections associated with attention to external stimuli.

Yet our analyses suggest that an individual brain is not “left-brained” or “right-brained” as a global property, but that asymmetric lateralization is a property of individual nodes or local subnetworks, and that different aspects of the left-dominant network and right-dominant network may show relatively greater or lesser lateralization within an individual. If a connection involving one of the left hubs is strongly left-lateralized in an individual, then other connections in the left-dominant network also involving this hub may also be more strongly left lateralized, but this did not translate to a significantly generalized lateralization of the left-dominant network or right-dominant network. Similarly, if a left-dominant network connection was strongly left lateralized, this had no significant effect on the degree of lateralization within connections in the right-dominant network, except for those connections where a left-lateralized connection included a hub that was overlapping or close to a homotopic right-lateralized hub.

It is also possible that the relationship between structural lateralization and functional lateralization is more than an artifact. Brain regions with more gray matter in one hemisphere may develop lateralization of brain functions ascribed to those regions. Alternately, if a functional asymmetry develops in a brain region, it is possible that there may be hypertrophy of gray matter in that region. The extent to which structural and functional asymmetries co-evolve in development will require further study, including imaging at earlier points in development and with longitudinal imaging metrics, and whether asymmetric white matter projections [52], [53] contribute to lateralization of functional connectivity.

We observed a weak generalized trend toward greater lateralization of connectivity with age between the 20 hubs included in the analysis, but most individual connections did not show significant age-related changes in lateralization. The weak changes in lateralization with age should be interpreted with caution because the correlations included >1000 data points, so very subtle differences may be observed that are not associated with behavioral or cognitive differences. Prior reports with smaller sample sizes have reported differences in lateralization during adolescence in prefrontal cortex [54] as well as decreased structural asymmetry with age over a similar age range [55].

Similarly, we saw no differences in functional lateralization with gender. These results differ from prior studies in which significant gender differences in functional connectivity lateralization were reported [16], [17]. This may be due to differing methods between the two studies, including the use of short-range connectivity in one of the former reports and correction for structural asymmetries in this report. A prior study performing graph-theoretical analysis of resting state functional connectivity data using a predefined parcellation of the brain also found no significant effects of hemispheric asymmetry with gender, but reported that males tended to be more locally efficient in their right hemispheres and females tended to be more locally efficient in their left hemispheres [56].

It is intriguing that two hubs of both the left-lateralized and right-lateralized network are nearly homotopic. Maximal left-lateralization in Broca Area corresponds to a similar right-lateralized homotopic cluster extending to include the anterior insula in the salience network. Although both networks have bilateral homologues in the inferior frontal gyrus/anterior insular region, it is possible that the relative boundaries of Broca Homologue on the right and the frontoinsular salience region may “compete” for adjacent brain cortical function. Future studies in populations characterized for personality traits [57] or language function may be informative as to whether local connectivity differences in these regions are reflected in behavioral traits or abilities. The study is limited by the lack of behavioral data and subject ascertainment available in the subject sample. In particular, source data regarding handedness is lacking. However, none of the hubs in our left- and right- lateralized networks involve primary motor or sensory cortices and none of the lateralized connections showed significant correlation with metrics of handedness in subjects for whom data was available.

Despite the need for further study of the relationship between behavior and lateralized connectivity, we demonstrate that left- and right-lateralized networks are homogeneously stronger among a constellation of hubs in the left and right hemispheres, but that such connections do not result in a subject-specific global brain lateralization difference that favors one network over the other (i.e. left-brained or right-brained). Rather, lateralized brain networks appear to show local correlation across subjects with only weak changes from childhood into early adulthood and very small if any differences with gender.



Debunking Left Brain, Right Brain Myth / Plos Paper – Corbalis

Left Brain, Right Brain: Facts and Fantasies

Michael C. Corballis, Affiliation School of Psychology, University of Auckland, Auckland, New Zealand

Published: January 21, 2014 )open access. See original for more.


Handedness and brain asymmetry are widely regarded as unique to humans, and associated with complementary functions such as a left-brain specialization for language and logic and a right-brain specialization for creativity and intuition. In fact, asymmetries are widespread among animals, and support the gradual evolution of asymmetrical functions such as language and tool use. Handedness and brain asymmetry are inborn and under partial genetic control, although the gene or genes responsible are not well established. Cognitive and emotional difficulties are sometimes associated with departures from the “norm” of right-handedness and left-brain language dominance, more often with the absence of these asymmetries than their reversal.

Evolution of Brain Asymmetries, with Implications for Language

One myth that persists even in some scientific circles is that asymmetry is uniquely human [3]. Left–right asymmetries of brain and behavior are now known to be widespread among both vertebrates and invertebrates [11], and can arise through a number of genetic, epigenetic, or neural mechanisms [12]. Many of these asymmetries parallel those in humans, or can be seen as evolutionary precursors. A strong left-hemispheric bias for action dynamics in marine mammals and in some primates and the left-hemisphere action biases in humans, perhaps including gesture, speech, and tool use, may derive from a common precursor [13]. A right-hemisphere dominance for emotion seems to be present in all primates so far investigated, suggesting an evolutionary continuity going back at least 30 to 40 million years [14]. A left-hemisphere dominance for vocalization has been shown in mice [15] and frogs [16], and may well relate to the leftward dominance for speech—although language itself is unique to humans and is not necessarily vocal, as sign languages remind us. Around two-thirds of chimpanzees are right-handed, especially in gesturing [17] and throwing [18], and also show left-sided enlargement in two cortical areas homologous to the main language areas in humans—namely, Broca’s area [19] and Wernicke’s area [20] (see Figure 1). These observations have been taken as evidence that language did not appear de novo in humans, as argued by Chomsky [21] and others, but evolved gradually through our primate lineage [22]. They have also been interpreted as evidence that language evolved not from primate calls, but from manual gestures [23][25].

Some accounts of language evolution (e.g., [25]) have focused on mirror neurons, first identified in the monkey brain in area F5 [26], a region homologous to Broca’s area in humans, but now considered part of an extensive network more widely homologous to the language network [27]. Mirror neurons are so called because they respond when the monkey performs an action, and also when they see another individual performing the same action. This “mirroring” of what the monkey sees onto what it does seems to provide a natural platform for the evolution of language, which likewise can be seen to involve a mapping of perception onto production. The motor theory of speech perception, for example, holds that we perceive speech sounds according to how we produce them, rather than through acoustic analysis [28]. Mirror neurons in monkeys also respond to the sounds of such physical actions as ripping paper or dropping a stick onto the floor, but they remain silent to animal calls [29]. This suggests an evolutionary trajectory in which mirror neurons emerged as a system for producing and understanding manual actions, but in the course of evolution became increasingly lateralized to the left brain, incorporating vocalization and gaining grammar-like complexity [30]. The left hemisphere is dominant for sign language as for spoken language [31].

Mirror neurons themselves have been victims of hyperbole and myth [32], with the neuroscientist Vilayanur Ramachandran once predicting that “mirror neurons will do for psychology what DNA did for biology” [33]. As the very name suggests, mirror neurons are often taken to be the basis of imitation, yet nonhuman primates are poor imitators. Further, the motor theory of speech perception does not account for the fact that speech can be understood by those deprived of the ability to speak, such as those with damage to Broca’s area. Even chimpanzees [34] and dogs [35] can learn to respond to simple spoken instructions, but cannot produce anything resembling human speech. An alternative is that mirror neurons are part of a system for calibrating movements to conform to perception, as a process of learning rather than direct imitation. A monkey repeatedly observes its hand movements to learn to reach accurately, and the babbling infant calibrates the production of sounds to match what she hears. Babies raised in households where sign language is used “babble” by making repetitive movements of the hands [36]. Moreover, it is this productive aspect of language, rather than the mechanisms of understanding, that shows the more pronounced bias to the left hemisphere [37].

Inborn Asymmetries

Handedness and cerebral asymmetries are detectable in the fetus. Ultrasound recording has shown that by the tenth week of gestation, the majority of fetuses move the right arm more than the left [38], and from the 15th week most suck the right thumb rather than the left [39]—an asymmetry strongly predictive of later handedness [40] (see Figure 2). In the first trimester, a majority of fetuses show a leftward enlargement of the choroid plexus [41], a structure within the ventricles known to synthesize peptides, growth factors, and cytokines that play a role in neurocortical development [42]. This asymmetry may be related to the leftward enlargement of the temporal planum (part of Wernicke’s area), evident at 31 weeks [43].

 In these prenatal brain asymmetries, around two-thirds of cases show the leftward bias. The same ratio applies to the asymmetry of the temporal planum in both infants and adults [44]. The incidence of right-handedness in the chimpanzee is also around 65–70 percent, as is a clockwise torque, in which the right hemisphere protrudes forwards and the left hemisphere rearwards, in both humans and great apes [45]. These and other asymmetries have led to the suggestion that a “default” asymmetry of around 65–70 percent, in great apes as well as humans, is inborn, with the asymmetry of human handedness and cerebral asymmetry for language increased to around 90 percent by “cultural literacy” [46].

Variations in Asymmetry

Whatever their “true” incidence, variations in handedness and cerebral asymmetry raise doubts as to the significance of the “standard” condition of right-handedness and left-cerebral specialization for language, along with other qualities associated with the left and right brains that so often feature in popular discourse. Handedness and cerebral asymmetry are not only variable, they are also imperfectly related. Some 95–99 percent of right-handed individuals are left-brained for language, but so are about 70 percent of left-handed individuals. Brain asymmetry for language may actually correlate more highly with brain asymmetry for skilled manual action, such as using tools [47],[48], which again supports the idea that language itself grew out of manual skill—perhaps initially through pantomime.

Even when the brain is at rest, brain imaging shows that there are asymmetries of activity in a number of regions. A factor analysis of these asymmetries revealed four different dimensions, each mutually uncorrelated. Only one of these dimensions corresponded to the language regions of the brain; the other three had to do with vision, internal thought, and attention [49]—vision and attention were biased toward the right hemisphere, language and internal thought to the left. This multidimensional aspect throws further doubt on the idea that cerebral asymmetry has some unitary and universal import.

Handedness, at least, is partly influenced by parental handedness, suggesting a genetic component [50], but genes can’t tell the whole story. For instance some 23 percent of monozygotic twins, who share the same genes, are of opposite handedness [51]. These so-called “mirror twins” have themselves fallen prey to a Through the Looking Glass myth; according to Martin Gardner [52], Lewis Carroll intended the twins Tweedledum and Tweedledee in that book to be enantiomers, or perfect three-dimensional mirror images in bodily form as well as in hand and brain function. Although some have argued that mirroring arises in the process of twinning itself [53],[54], large-scale studies suggest that handedness [55],[56] and cerebral asymmetry [57] in mirror twins are not subject to special mirroring effects. In the majority of twins of opposite handedness the left hemisphere is dominant for language in both twins, consistent with the finding that the majority of single-born left-handed individuals are also left-hemisphere dominant for language. In twins, as in the singly born, it is estimated that only about a quarter of the variation in handedness is due to genetic influences [56].

The manner in which handedness is inherited has been most successfully modeled by supposing that a gene or genes influence not whether the individual is right- or left-handed, but whether a bias to right-handedness will be expressed or not. In those lacking the “right shift” bias, the direction of handedness is a matter of chance; that is, left-handedness arises from the lack of a bias toward the right hand, and not from a “left-hand gene.” Such models can account reasonably well for the parental influence [58][60], and even for the relation between handedness and cerebral asymmetry if it is supposed that the same gene or genes bias the brain toward a left-sided dominance for speech [60],[61]. It now seems likely that a number of such genes are involved, but the basic insight that genes influence whether or not a given directional bias is expressed, rather than whether or not it can be reversed, remains plausible (see Box 1).

Genetic considerations aside, departures from right-handedness or left-cerebral dominance have sometimes been linked to disabilities. In the 1920s and 1930s, the American physician Samuel Torrey Orton attributed both reading disability and stuttering to a failure to establish cerebral dominance [62]. Orton’s views declined in influence, perhaps in part because he held eccentric ideas about interhemispheric reversals giving rise to left–right confusions [63], and in part because learning-theory explanations came to be preferred to neurological ones. In a recent article, Dorothy Bishop reverses Orton’s argument, suggesting that weak cerebral lateralization may itself result from impaired language learning [64]. Either way, the idea of an association between disability and failure of cerebral dominance may be due for revival, as recent studies have suggested that ambidexterity, or a lack of clear handedness or cerebral asymmetry, is indeed associated with stuttering [65] and deficits in academic skills [66], as well as mental health difficulties [67] and schizophrenia (see Box 1).

Although it may be the absence of asymmetry rather than its reversal that can be linked to problems of social or educational adjustment, left-handed individuals have often been regarded as deficient or contrarian, but this may be based more on prejudice than on the facts. Left-handers have excelled in all walks of life. They include five of the past seven US presidents, sports stars such as Rafael Nadal in tennis and Babe Ruth in baseball, and Renaissance man Leonardo da Vinci, perhaps the greatest genius of all time.





Unraveling Asperger’s and Pain / “Normalizing” Chronic Misery

I don’t like to rely solely on my experiences to unravel what might be going on with Asperger types, but sometimes it’s all you have to go on. One reads that Asperger individuals either over react to pain and discomfort, or will not notice pain at all. Another of those “gotcha” symptoms in which we are either “over or under” the “normal” human behavior or experience, but in the case of pain, which is a subjective experience, what is “normal”?

Now is a good time to think about this, since I have a toothache (not another root canal!) and severe allergies. I’m a mess. I hate being sick, mostly because I’m very active and have trouble staying in bed or on the couch, resting as one should.

Questions arise. What was I like as a kid whenever some illness like the flu was going around? The plot thickens: how did my parents behave toward us (I had an older brother) when the inevitable sick days that kids have, came round?

Not good! My brother was six years older and from my observations was babied. He always had something “mysterious or nebulous” going on that meant staying home from school or being spared from regular tasks and chores that he didn’t want to do. This was very bad; by the time I arrived, a triad of dysfunctional relationships was already in place.

You say you're sick? PROVE IT

You say you’re sick? PROVE IT

The short story is that my brother received gifts, toys and attention if ill, but I was punished. If I said I didn’t feel well, I had to prove it: have a measurable fever, be vomiting or be possessed of some obvious bug going around school, and parents had been asked to keep symptomatic kids at home. I wasn’t allowed out of bed, or to have books or toys. Although my mother was merely peeved or angry with me, when my Asperger father came home, he  would state how he never became ill (it was true) and that illness was a sign of weakness and failure; why wasn’t I like him?  This message came through loud and clear and has been a negative influence – absolutely. When unwell, I have to fight feelings of inadequacy and failure, and a residue of abandonment. It’s ridiculous.

Here’s the question: Is this cruel message served up by my father a product of Asperger’s, or is it something else? Although his attitude was obviously hurtful, I also knew my father’s story: he had been a premature twin and his brother died at birth. He  was not expected to live, but he pulled through.  My father’s childhood had been a living Hell of beatings and hard work on the farm, dished out as tough love by his father in order to make him strong. In one of those “tragic” outcomes, my father ended up being a highly fit and muscular adult; tragic, because he believed his father’s cruelty was responsible for his good health.

I attribute my father’s survival to having good care as an infant, and good genes, not magic or cruelty. If a premature baby survived in the 1910s, long before the elaborate interventions of today’s medical devices and drugs, he or she had to have had a package of healthy provisions on board, just to survive the first year. I was stuck with a mystery; was my father a product of nature, or “severe” nurturing?

It just wasn’t my father’s nature to be cruel; his weak – strong theory of life descended like a dark curtain when issues of vulnerability appeared. Otherwise he was generous with his time and attention and I remember that father also. Unfortunately, he had no insight into the brutal treatment he endured as a child, and let’s face it, American males are subject to the irrational fear of being labeled as “weak” or soft; a “girl” – a fear intensively cultivated by American culture, then and now. And, the outcome was that “spoiling” my brother left him entirely dependent on my parents, but some “ill-treatment” did prepare me for an  independent life; the challenges were great, but made me an adult – slowly, but at least I made it.

It is my view, after two years of reading and thinking about Asperger’s, especially the bizarre dogma of psychology, medical information, and anecdotal references, that Asperger’s is a personality or temperament type, characterized by an intellectual “state” that is simply not socially-oriented, but attuned to the physical world: sensory attention, logic based, not word-supernatural based.

Conformity institutions (like psychology, corporations, religions and schools) simply cannot tolerate people who think for themselves. It’s the old story of domestication: dogs are useful to humans because they “work for food” and “adjust to” cruelty from humans, because – mostly they have no choice, and have been bred to various “addictions” – behaviors like extreme herding behavior or tracking of drugs, criminals or lost people; exploitation of their more accurate and extensive sensory abilities. abilities,drugs and criminals or lost people. A lucky few (?) become family, and are classified as “pets” – literally, we stroke and hug them, overfeed them bad food, and lock them in tiny apartments, basements or porches, abandoning them for long hours. Many breeds have been literally deformed to physically fulfill the awful constraints of being substitute infants for infantile people: purposely deformed, as if we were acceptable to “create” humans with severe physical distortions and disabilities, because it satisfies some warped idea of “cuteness”.

The desire for lifeforms to be either enslaved by work or to be enslaved as “cute social objects – status symbols” is domestication.

Wolves are despised and exterminated because they can’t be tamed; they remain free to be competing predators. Myth, fairytales and fabrications place wolves close to the devil. It’s not true; like any competing predator species, they have been hunted by human predators to near extinction.

There is no doubt that humans have domesticated humans: slavery is “forced ” domestication followed by sexual selection from the “survivors”. The designation of an individual, or group, or class of humans as having “potential” to be tamed – that is, be forced to work without resistance, as dogs and horses and other animal laborers do,   has always been paramount. Humans were selected just as animals were, to be reshaped into “useful” tame forms. Over thousands of years of this “civilizing” process, the “owners” of grand cities and the agricultural and manufacturing systems necessary to their existence, simply exterminated all things wild and increasingly cultivated submissive behavior, just as we continue to do today.

The relentless selection of human form and abilities “useful” to the predatory hierarchy changed humans into “specialized” organisms; varieties of people that have become “natural” to us – the class system as it exists today, in which domestic types – peasants, wage slaves; the middle and low classes; immigrants, and others who do the “shit work” for the upper and ruling classes, are fed scraps from the “dinner table” because like dogs, they have been bred to this condition, which no “wild human” could or would, tolerate.

Pain and its subjective experience by individuals is a tricky subject when you look into it. We are amazed and frightened by the “dangers” that wild animals live with 24 / 7 – but we forget that “pain” in nature is usually swift and brief: a few seconds to a few hours – and the animal has either recovered, been “finished off” or has died of stress – lack of water, blood loss and shock.

The human “domestic” condition may be seen as far worse. Someone said, “The problem with humans is that they will put up with anything.” One of the most obvious “changes” to the human animal has been the development of tolerance of very bad treatment by other humans, not unlike the dog that is chained to a post or fence, day after day, with little or no food, a dirty bucket of water (if that) and is expected to demonstrate “wild affection” at the appearance of its tormentor.

Human empathy, compassion or kindness? The system provides relief, but not freedom, and an “easy” new form of slavery – to religion, to drugs, to alcohol, to violent punishment and sadistic entertainment; to hopelessness and lies. Pain in humans is not swift; it is chronic and lifelong. Pain is stretched out over decades, and declared to be “progress” when medical intervention patches people up, so that they can return to fulfilling their role in the social machinery. Pain does not go away; it is a protracted state of dependency cultivated by the hierarchy. “Modern pain” is a result of domestication, which has become panhuman, and is “considered” to be normal – pain and slavery have been socialized.

The “idea” of pain, despite the knowledge that this is a highly subjective and variable physical experience, is so controlled, that Asperger types are classified as defective, because “supposedly” our experience of pain is “abnormal” – that is, we do not “behave” like domesticated animals; we do not respond with compliance to pain applied as punishment and control: our “reactivity” falls outside the imposed parameters of “being suitable for use as a slave.” We “leave” – physically if possible, and we suffer greatly if we can’t. Withdrawal into a “better world that exists in nature and in satisfying our curiosity and need to acquire knowledge” (labeled as “obsessions”) is a healthy reaction – too healthy for society to tolerate.







What is the experiential phenomenon that is called EMOTION?

Emotion in animals is pretty simple: a subjective physiological reaction to “something” in the environment. What we call “emotion” is activation of the familiar “fight, flight or freeze response” that results from sensory stimulation, and is usually attuned to “danger”.

Emotion is a word: a noun, which designates an object that can be “named” – but the physical phenomenon is not an object: the naming of “emotions” is a socio-cultural activity. Nature never created an “emotion thing” that resides somewhere inside a human or animal; like other animals, we have a brain and nervous system which interacts with the environment, ostensibly for our benefit – to promote survival. Humans created the social “idea monstrosity” that claims to be “the truth” about how Homo sapiens works. Emotions are presented as parts “inside of you” – their location has been argued over forever! The heart, brain, gut, mysterious fluids, etc. have been given the attribution as the “seat” of emotion. Most “social” views of emotion are negative: weird and destructive animal inheritances that must be controlled, not surprisingly, by society!

Peculiar dogma plagues our concepts and application of “emotion rules” –  notions which are purely cultural and do not “transfer” from Western psychology to “all humans”. Psychology demands the conceit that ALL HUMANS are mere replicas of “normal humans” who happen to be white males; underneath all the obvious  “human diversity” of size, form, skin color, hair types, skull dimensions, manners, behaviors and individual preferences is a “white male” prototype. “Evolution” is deemed to be a “mistake” – all humans were meant to be white males in thought, behavior and belief; inferior mistakes ought to at least “mimic” their superiors.

This promotion of a bizarre “evolutionary” fantasy sounds ridiculous when plainly stated; a farce, a narrative born of childish arrogance, a sociopathic “plan” for world domination, and yet this Western psychological addiction to imaginary superiority is supported, promoted and fed by American Psychology – in theory, policy and practice.

As usual, we must go back to basics to untangle the mess surrounding “emotions” and the “off-topic” arguments over good and evil, positive and negative, male and female, race and class, biology and religion, authority and expertise and supernatural origins, which are indulged as serious consequences of human beliefs (not facts) of what we call “emotions” – fact, myth and propaganda.

Example 1.

From Gerrig, Richard J. & Philip G. Zimbardo (a self-diagnosed psychopath, BTW) . Psychology And Life, 16th ed.  Published by Allyn and Bacon, Boston, MA. Copyright (c) 2002 by Pearson Education.

Emotion:  A complex pattern of changes, including physiological arousal, feelings, cognitive processes, and behavioral reactions, made in response to a situation perceived to be personally significant. (Wow! Considerable “mumbo-jumbo” ahead)

Emotional intelligence: Type of intelligence defined as the abilities to perceive, appraise, and express emotions accurately and appropriately, to use emotions to facilitate thinking, to understand and analyze emotions, to use emotional knowledge effectively, and to regulate one’s emotions to promote both emotional and intellectual growth. (See? Mumbo-jumbo of the ‘throw in every Psych-concept cliché you can think of’ type)

Example 2.

Paul Thagard Ph.D./ What Are Emotions? / April 15, 2010

Happiness is a brain process 

Philosophers and psychologists have long debated the nature of emotions such as happiness. Are they states of supernatural souls, cognitive judgments about goal satisfaction, or perceptions of physiological changes? Advances in neuroscience suggest how brains generate emotions through a combination of cognitive appraisal and bodily perception.

Suppose that something really good happens to you today: you win the lottery, your child gets admitted to Harvard, or someone you’ve been interested in asks you out. Naturally, you feel happy, but what does this happiness amount to? On the traditional dualist view of a person, you consist of both a body and a soul, and it is the soul that experiences mental states such as happiness. This view has the appealing implication that you can even feel happiness after your body is gone, if your soul continues to exist in a pleasant location such as heaven. Unfortunately, there is no good evidence for the existence of the soul and immortality, so the dualist view of emotions and the mind in general can be dismissed as wishful thinking or motivated inference. (Not so fast: this “duality” remains the hard-core belief of the “majority” of people in the U.S. And, as we shall see, in American Psychology.)

There are currently two main scientific ways of explaining the nature of emotions. According to the cognitive appraisal theory emotions are judgments about the extent that the current situation meets your goals. Happiness is the evaluation that your goals are being satisfied, as when winning the lottery solves your financial problems and being asked out holds the promise of satisfying your romantic needs. Similarly, sadness is the evaluation that your goals are not being satisfied, and anger is the judgment aimed at whatever is blocking the accomplishment of your goals. (BTW, this is not a scientific theory – it is a social narrative)

Alternatively, William James and others have argued that emotions are perceptions of changes in your body such as heart rate, breathing rate, perspiration, and hormone levels. (A reasonable proposition based in physiology) On this view, happiness is a kind of physiological perception, not a judgment, and other emotions such as sadness and anger are mental reactions (why is “mental” used here? That “ghostly” duality again!) to different kinds of physiological stages. The problem with this account is that bodily states do not seem to be nearly as finely tuned as the many different kinds of emotional states.Yet there is undoubtedly some connection between emotions and physiological changes. (OMG! This is a rambling misconception of a “supernatural origin of emotions” and refutation of physical reality as the foundation for valid hypotheses about thought and behavior in humans. This brilliantly demonstrates the serious mistake of believing that words are “actual objects” that precede and supersede physical reality. This is word magic – the belief that words have the power to create reality – Abracadabra!)

Understanding how the brain works shows that these theories of emotion – cognitive appraisal and physiological perception – can be combined into a unified account of emotions. (are you ready for some fabulous psych nonsense?) The brain is a parallel processor, doing many things at once. Visual and other kinds of perception are the result of both inputs from the senses and top-down interpretations based on past knowledge. Similarly, the brain can perform emotions by interactively combining both high-level judgments about goal satisfactions and low-level perceptions of bodily changes. The judgments are performed by the prefrontal cortex which interacts with the amygdala and insula that process information about physiological states. Hence happiness can be a brain process that simultaneously makes appraisals and perceives the body. For details about how this might work, see the EMOCON model of emotional consciousness (link is external).

Before we proceed to, Major Theories of Emotion,

(I desperately need a break)

let’s peruse a few “general” definitions of emotion.

Word origin of ’emotion’: from old French esmovoir to excite, from Latin ēmovēre to disturb, from movēre to move (this is the same, regardless of the specific definition)

Note how many “non-physical” reference words are included

Thanks to FARLEX ONLINE, which collects stuff for you, in one place.


a state of arousal characterized by alteration of feeling tone and by physiologic behavioral changes. The external manifestation of emotion is called affect; a pervasive and sustained emotional state, mood. adj., adj emo´tional. The physical form of emotion may be outward and evident to others, as in crying, laughing, blushing, or a variety of facial expressions. However, emotion is not always reflected in one’s appearance and actions even though psychic changes (duality again) are taking place. Joy, grief, fear, and anger are examples of emotions.

Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.


A strong feeling, aroused mental state, or intense state of drive or unrest, which may be directed toward a definite object and is evidenced in both behavior and in psychological changes, with accompanying autonomic nervous system manifestations.

Farlex Partner Medical Dictionary © Farlex 2012


a strong feeling state, arising subjectively and directed toward a specific object, with physiological, somatic, and behavioral components.

Dorland’s Medical Dictionary for Health Consumers. © 2007 by Saunders, an imprint of Elsevier, Inc. All rights reserved.


1. A mental state that arises spontaneously rather than through conscious effort and is often accompanied by physiological changes; a feeling: the emotions of joy, sorrow, and anger.

2. Such mental states or the qualities that are associated with them, especially in contrast to reason: a decision based on emotion rather than logic. (That duality again, when “reason” and emotion are not opposed in human behavior, but work together)!

The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.


1 the outward expression or display of mood or feeling states.

2 the affective aspect of consciousness as compared with volition and cognition. Physiological alterations often occur with a marked change of emotion regardless of whether the feelings are conscious or unconscious, expressed or unexpressed. See also emotional need, emotional response. (“Conceptual clichés” again)

Mosby’s Medical Dictionary, 9th edition. © 2009, Elsevier.


Psychology A mood, affect or feeling of any kind–eg, anger, excitement, fear, grief, joy, hatred, love. See Negative emotion, Positive emotion, Toxic emotion. (Yeah, a list of emotion words is not a definition; neither is a social “judgement” about “good and evil”) 

Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.


Any state of arousal in response to external events or memories of such events that affect, or threaten to affect, personal advantage. Emotion is never purely mental (emotion is physical, actually) but is always associated with bodily changes such as the secretion of ADRENALINE and cortisol and their effects. The limbic system and the hypothalamus of the brain are the mediators of emotional expression and feeling. The external expression of emotional content is known as ‘affect’. Repressed emotions are associated with psychosomatic disease. The most important, in this context, are anger, a sense of dependency, and fear. (Oh dear, the unscientific social narratives never end – emotions  are the “bringers” of pestilence and punishment.)

Collins Dictionary of Medicine © Robert M. Youngson 2004, 2005


a short-term positive or negative affective state. Typically differentiated from mood in that an emotion is of shorter duration and evoked in response to a specific event, such as anger. (So odd! Anger is  the ’emotion’ – reaction; there seems to be a universal neurotypical inability to discern cause and effect!)

Dictionary of Sport and Exercise Science and Medicine by Churchill Livingstone © 2008 Elsevier Limited. All rights reserved.


a complex feeling or state (affect) accompanied by characteristic motor and glandular activities; feelings; mood.

Mosby’s Dental Dictionary, 2nd edition. © 2008 Elsevier, Inc. All rights reserved.


aroused state involving intense feeling, autonomic activation and related behavior. Animals have emotions insofar as they are motivated to behave by what they perceive and much of the reaction is learned rather than intuitive (instinctive) (Hmm … the categorical division  animal  / human is maintained, but with animal emotion being “lower in status” – a mere reaction – which is true in humans also. The reactions are based on rewarding and adversive properties of stimuli from the external environment. The center for the control of emotional behavior is the limbic system of the brain.

Saunders Comprehensive Veterinary Dictionary, 3 ed. © 2007 Elsevier, Inc. All rights reserved.

Is there any question as to why social  humans cannot communicate with each other?  Without a foundation in physical fact and common meaning, language is gibberish – an extension of confused personal opinion, narcissism and nonsense.; a toy, a sham, a hindrance to understanding.

Steven Pinker on Male-Female Brain Differences / Important

This is an important presentation of the “problem” of differences between the male female brain as characterized in Western Civilization. Yes, I have much to say about specific claims made: Pinker makes the case – a description actually, of the “status quo” as a cultural phenomenon which is “rooted in” biology. But – the biology can be interpreted and “applied” in many ways. Men have traditionally done the interpreting – and mislabel their opinions as “truth” which is the wrong word to begin with in a science context.

The problem is, Pinker, as a speaker for the status quo, does not grasp the essential questions. He does not venture outside the western psychological paradigm that “everything human” can be accounted for by the SYSTEM of psychology that has created the Western status quo regarding male – female status. The “division” of all things human into male and female “camps” IGNORES what males and females SHARE as characteristic of Homo sapiens, the species. This intra-species competition is ridiculous! Why would an “intelligent species” divide its wealth of abilities and capabilities into two parts; value one set of those traits and talents (male) as important, but denigrate “the other” set (female) as unimportant. This in itself is idiotic –

A grand accumulation of “studies” does not sum up to be a anything but that – a body of studies which DO NOT QUESTION the assumption that such studies “are interested in truth” to begin with, or represent any serious investigation of male and female contributions to the species as a whole. Our evolution, which has been the product of a “male-female co-operative team” is cast as an adversarial proposition, in stark contrast to our admiration for a male-female co-operative system for survival that is evident in many species. Male-female “contact” beyond mere reproduction in Homo sapiens is ignored, in favor of a “male brain” obsession – that of dominance. This too, is idiotic –

“Our” view (the male is always assumed to be the species exemplar) of “human truth” is highly unbalanced! And it’s not “our truth as a species”  if women, and our female brains, are not included.

More later…

Genes and Autism / A Look Back to 2004

Pediatrics. 2004 May

The genetics of autism.

Muhle R1, Trentacoste SV, Rapin I. Author information


Autism is a complex, behaviorally defined, static disorder of the immature brain that is of great concern to the practicing pediatrician because of an astonishing 556% reported increase in pediatric prevalence between 1991 and 1997, to a prevalence higher than that of spina bifida, cancer, or Down syndrome. This jump is probably attributable to heightened awareness and changing diagnostic criteria rather than to new environmental influences. Autism is not a disease but a syndrome with multiple non-genetic and genetic causes. By autism (the autistic spectrum disorders [ASDs]), we mean the wide spectrum of developmental disorders characterized by impairments in 3 behavioral domains: 1) social interaction; 2) language, communication, and imaginative play; and 3) range of interests and activities. Autism corresponds in this article to pervasive developmental disorder (PDD) of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition and International Classification of Diseases, Tenth Revision. Except for Rett syndrome–attributable in most affected individuals to mutations of the methyl-CpG-binding protein 2 (MeCP2) gene–the other PDD subtypes (autistic disorder, Asperger disorder, disintegrative disorder, and PDD Not Otherwise Specified [PDD-NOS]) are not linked to any particular genetic or non-genetic cause.

Review of 2 major textbooks on autism and of papers published between 1961 and 2003 yields convincing evidence for multiple interacting genetic factors as the main causative determinants of autism. Epidemiologic studies indicate that environmental factors such as toxic exposures, teratogens, perinatal insults, and prenatal infections such as rubella and cytomegalovirus account for few cases. These studies fail to confirm that immunizations with the measles-mumps-rubella vaccine are responsible for the surge in autism. Epilepsy, the medical condition most highly associated with autism, has equally complex genetic/non-genetic (but mostly unknown) causes. Autism is frequent in tuberous sclerosis complex and fragile X syndrome, but these 2 disorders account for but a small minority of cases. Currently, diagnosable medical conditions, cytogenetic abnormalities, and single-gene defects (eg, tuberous sclerosis complex, fragile X syndrome, and other rare diseases) together account for <10% of cases. There is convincing evidence that “idiopathic” (relating to or denoting any disease or condition that arises spontaneously or for which the cause is unknown )autism is a heritable disorder. Epidemiologic studies report an ASD prevalence of approximately 3 to 6/1000, with a male to female ratio of 3:1. This skewed ratio remains unexplained: despite the contribution of a few well-characterized X-linked disorders, male-to-male transmission in a number of families rules out X-linkage as the prevailing mode of inheritance. The recurrence rate in siblings of affected children is approximately 2% to 8%, much higher than the prevalence rate in the general population but much lower than in single-gene diseases. Twin studies reported 60% concordance for classic autism in monozygotic (MZ) twins versus 0 in dizygotic (DZ) twins, the higher MZ concordance attesting to genetic inheritance as the predominant causative agent. Reevaluation for a broader autistic phenotype  that included communication and social disorders increased concordance remarkably from 60% to 92% in MZ twins and from 0% to 10% in DZ pairs. (Real, or artifact?)

This suggests that interactions between multiple genes cause “idiopathic” autism but that epigenetic factors and exposure to environmental modifiers may contribute to variable expression of autism-related traits. The identity and number of genes involved remain unknown. The wide phenotypic variability of the ASDs likely reflects the interaction of multiple genes within an individual’s genome and the existence of distinct genes and gene combinations among those affected.

There are 3 main approaches to identifying genetic loci, chromosomal regions likely to contain relevant genes: 1) whole genome screens, searching for linkage of autism to shared genetic markers in populations of multiplex families (families with >1 affected family member; 2) cytogenetic studies that may guide molecular studies by pointing to relevant inherited or de novo chromosomal abnormalities in affected individuals and their families; and 3) evaluation of candidate genes known to affect brain development in these significantly linked regions or, alternatively, linkage of candidate genes selected a priori because of their presumptive contribution to the pathogenesis of autism. Data from whole-genome screens in multiplex families suggest interactions of at least 10 genes in the causation of autism. Thus far, a putative speech and language region at 7q31-q33 seems most strongly linked to autism, with linkages to multiple other loci under investigation. Cytogenetic abnormalities at the 15q11-q13 locus are fairly frequent in people with autism, and a “chromosome 15 phenotype” was described in individuals with chromosome 15 duplications. Among other candidate genes are the FOXP2, RAY1/ST7, IMMP2L, and RELN genes at 7q22-q33 and the GABA(A) receptor subunit and UBE3A genes on chromosome 15q11-q13. Variant alleles of the serotonin transporter gene (5-HTT) on 17q11-q12 are more frequent in individuals with autism than in non-autistic populations. In addition, animal models and linkage data from genome screens implicate the oxytocin receptor at 3p25-p26. Most pediatricians will have 1 or more children with this disorder in their practices. They must diagnose ASD expeditiously because early intervention increases its effectiveness. Children with dysmorphic features, congenital anomalies, mental retardation, or family members with developmental disorders are those most likely to benefit from extensive medical testing and genetic consultation.

The yield of testing is much less in high-functioning children with a normal appearance and IQ and moderate social and language impairments. Genetic counseling justifies testing, but until autism genes are identified and their functions are understood, prenatal diagnosis will exist only for the rare cases ascribable to single-gene defects or overt chromosomal abnormalities. Parents who wish to have more children must be told of their increased statistical risk. It is crucial for pediatricians to try to involve families with multiple affected members in formal research projects, as family studies are key to unraveling the causes and pathogenesis of autism. Parents need to understand that they and their affected children are the only available sources for identifying and studying the elusive genes responsible for autism. Future clinically useful insights and potential medications depend on identifying these genes and elucidating the influences of their products on brain development and physiology.

PMID: 15121991

Again, we have the assumption that Aspergers is a defect in development – a set of vague symptoms that constitute  pathology. People who study pathologies will look for pathologies and may identify a genome as belonging to a “defective” person, therefore, there must be defects in their genome.

I wish for once that someone would set all that aside and compare Asperger individual genomes to other Asperger individuals, without prejudice.

And also look for genetic neoteny in modern social humans, instead of classifying all neurotypicals as “normal”

Visual-Spatial Thinking / Watch Crows “Do it”

The crows do not think verbally. They are “visual thinkers” as are Asperger types.  Humans once primarily “thought like crows” but in modern social humans, word-language dominates communication, and visual thinking ability has atrophied. In fact, the power of visual-spatial processing has been forgotten.

Gene Mutations / Most have ZERO influence on development

Links are all live! Tons of info. Aspergers is often attributed to a group of scattered genes, but there is no proof that even if this occurs, that the genes explain Aspergers. Those “changes” could actually be null, positive or simply characteristic of the Asperger brain and not a defect at all.  

Artist Sandra Yagi

Do all gene mutations affect health and development?

No; only a small percentage of mutations cause genetic disorders—most have no impact on health or development. For example, some mutations alter a gene’s DNA sequence but do not change the function of the protein made by the gene.

Often, gene mutations that could cause a genetic disorder are repaired by certain enzymes before the gene is expressed and an altered protein is produced. Each cell has a number of pathways through which enzymes recognize and repair mistakes in DNA. Because DNA can be damaged or mutated in many ways, DNA repair is an important process by which the body protects itself from disease.

A very small percentage of all mutations actually have a positive effect. These mutations lead to new versions of proteins that help an individual better adapt to changes in his or her environment. For example, a beneficial mutation could result in a protein that protects an individual and future generations from a new strain of bacteria.

Because a person’s genetic code can have a large number of mutations with no effect on health, diagnosing genetic conditions can be difficult. Sometimes, genes thought to be related to a particular genetic condition have mutations, but whether these changes are involved in development of the condition has not been determined; these genetic changes are known as variants of unknown significance (VOUS). Sometimes, no mutations are found in suspected disease-related genes, but mutations are found in other genes whose relationship to a particular genetic condition is unknown. It is difficult to know whether these variants are involved in the disease.

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