Emotions: What a Mess! / Physiology, Supernatural Mental State, Words

This drives me “nuts” – emotions ARE physiological responses to the environment; and yet, psychologists (and other sinners) continue to conceive of emotions as “mental or psychological states” and “word objects” that exist somewhere “inside” humans, like colored jelly beans in jar, waiting to be “called on” by their “names”. Worse, other “scientists hah-hah” also continue to confuse “physiology” as arising from some abstract construct or supernatural domain (NT thingie) called emotion.

Physiological Changes Associated with Emotion

https://www.ncbi.nlm.nih.gov/books/NBK10829/

The most obvious signs of emotional arousal involve changes in the activity of the visceral motor (autonomic) system (see Chapter 21). Thus, increases or decreases in heart rate, cutaneous blood flow (blushing or turning pale), piloerection, sweating, and gastrointestinal motility can all accompany various emotions. These responses are brought about by changes in activity in the sympathetic, parasympathetic, and enteric components of the visceral motor system, which govern smooth muscle, cardiac muscle, and glands throughout the body. (This is obviously real physical activity of the body, and not a magical, psychological or mental “state”) As discussed in Chapter 21, Walter Cannon argued that intense activity of the sympathetic division of the visceral motor system prepares the animal to fully utilize metabolic and other resources in challenging or threatening situations.

Honestly? I think in the above we have a working description of the ASD / Asperger “emotional” system: NO WORDS. So-called “emotions” are a SOCIALLY GENERATED SYSTEM that utilizes language to EXTERNALLY REGULATE human “reactivity” – that is, the child learns to IDENTIFY it’s physiological response with the vocabulary supplied to it by parents, teachers, other adults and by overhearing human conversation, in which it is immersed from birth.

Conversely, activity of the parasympathetic division (and the enteric division) promotes a building up of metabolic reserves. Cannon further suggested that the natural opposition of the expenditure and storage of resources is reflected in a parallel opposition of the emotions associated with these different physiological states. As Cannon pointed out, “The desire for food and drink, the relish of taking them, all the pleasures of the table are naught in the presence of anger or great anxiety.” (This is the physiological state that ASD / Asperger children “exist in” when having to negotiate the “world of social typicals” The social environment is confusing, frustrating, and alien. Asking us “how we feel” in such a circumstance will produce a “pure” physiological response: anxiety, fear, and the overwhelming desire to escape.)

Activation of the visceral motor system, particularly the sympathetic division, was long considered an all-or-nothing process. Once effective stimuli engaged the system, it was argued, a widespread discharge of all of its components ensued. More recent studies have shown that the responses of the autonomic nervous system are actually quite specific, with different patterns of activation characterizing different situations and their associated emotional states. (What is an emotional state? Emotion words are not emotions: they are language used to parse, identify and “name” the physiologic arousal AS SOCIETY  DICTATES TO BE ACCEPTABLE) Indeed, emotion-specific expressions produced voluntarily can elicit distinct patterns of autonomic activity. For example, if subjects are given muscle-by-muscle instructions that result in facial expressions recognizable as anger, disgust, fear, happiness, sadness, or surprise without being told which emotion they are simulating, each pattern of facial muscle activity is accompanied by specific and reproducible differences in visceral motor activity (as measured by indices such as heart rate, skin conductance, and skin temperature). Moreover, autonomic responses are strongest when the facial expressions are judged to most closely resemble actual emotional expression and are often accompanied by the subjective experience of that emotion! One interpretation of these findings is that when voluntary facial expressions are produced, signals in the brain engage not only the motor cortex but also some of the circuits that produce emotional states. Perhaps this relationship helps explain how good actors can be so convincing. Nevertheless, we are quite adept at recognizing the difference between a contrived facial expression and the spontaneous smile that accompanies a pleasant emotional state. (Since modern humans are notoriously “gullible” to the false words, body language and manipulations of “con men” of all types, how can this claim be extended outside a controlled “experiment” in THE LAB? Having worked in advertising for 15 years, I can assure the reader that finding models and actors who could act, speak and use body language that was “fake but natural” was a constant challenge. In other words, what was needed was a person who could “fake” natural behavior. Fooling the consumer was the GOAL!)

This evidence, along with many other observations, indicates that one source of emotion is sensory drive from muscles and internal organs. This input forms the sensory limb of reflex circuitry that allows rapid physiological changes in response to altered conditions. However, physiological responses can also be elicited by complex and idiosyncratic stimuli mediated by the forebrain. For example, an anticipated tryst with a lover, a suspenseful episode in a novel or film, stirring patriotic or religious music, or dishonest accusations can all lead to autonomicactivation and strongly felt emotions. (Are these “events, anticipated or actualized”, not social constructs that are learned? Would any child grow up to “behave patriotically” if he or she had not been taught do this by immersion in the total social environment, which “indoctrinates” children in the “proper emotions” of the culture?) The neural activity evoked by such complex stimuli is relayed from the forebrain to autonomic and somatic motor nuclei via the hypothalamus and brainstem reticular formation, the major structures that coordinate the expression of emotional behavior (see next section). (Is exploitation of this “neural activity” not the “pathway” to training social humans to “obey” the social rules?) 

In summary, emotion and motor behavior are inextricably linked. (Why would any one think that they are not? Emotion is merely the language used to manipulate, interpret and communicate the physiology) As William James put it more than a century ago:

What kind of an emotion of fear would be left if the feeling neither of quickened heart-beats nor of shallow breathing, neither of trembling lips nor of weakened limbs, neither of goose-flesh nor of visceral stirrings, were present, it is quite impossible for me to think … I say that for us emotion dissociated from all bodily feeling is inconceivable.

William James, 1893 (Psychology: p. 379.)

NEXT: The representation of “emotions” as “thingies” that can be experienced and eaten! Are we to believe that 34,000 distinct “emotion objects” exist “in nature / in humans” or are these “inventions” of social language? 

Plutchik’s Wheel of Emotions: What is it and How to Use it in Counseling?

Can you guess how many emotions a human can experience?

The answer might shock you – it’s around 34,000.

With so many, how can one navigate the turbulent waters of emotions, its different intensities, and compositions, without getting lost?

The answer – an emotion wheel.

Through years of studying emotions, Dr. Robert Plutchik, an American psychologist, proposed that there are eight primary emotions that serve as the foundation for all others: joy, sadness, acceptance, disgust, fear, anger, surprise and anticipation. (Pollack, 2016)

This means that, while it’s impossible to fully understand all 34,000 distinguishable emotions, (what is referred to is merely “vocabulary” that humans have come up with, and not emotion thingies that exist “somewhere” -) learning how to accurately identify how each of the primary emotions is expressed within you can be empowering. It’s especially useful for moments of intense feelings when the mind is unable to remain objective as it operates from its older compartments that deal with the fight or flight response. (Watkins, 2014) (This refers to the “pop-science” theory of the additive brain, (lizard, etc) which is utter fantasy) 

This article contains:

NEXT: Some Definitions of Emotions / Rather confusing, conflicting, unsatisfying, nonspecific descriptions: – indication that we’ve entered the supernatural realm of word concepts. Aye, yai, yai!

From introductory psychology texts

Sternberg, R. In Search of the Human Mind, 2nd Ed.Harcourt, Brace, 1998 p 542 “An emotion is a feeling comprising physiological and behavioral (and possibly cognitive) reactions to internal and external events.”

Nairne, J. S. Psychology: The Adaptive Mind. 2nd Ed. Wadsworth, 2000. p. 444 ” . . . an emotion is a complex psychological event that involves a mixture of reactions: (1) a physiological response (usually arousal), (2) an expressive reaction (distinctive facial expression, body posture, or vocalization), and (3) some kind of subjective experience (internal thoughts and feelings).”

From a book in which many researchers in the field of emotion discuss their views of some basic issues in the study of emotion. (Ekman, P., & Davidson, R. J. The Nature of Emotions: Fundamental Questions. Oxford, 1994)

Panksepp, Jaak p 86. .Compared to moods, “emotions reflect the intense arousal of brain systems that strongly encourage the organism to act impulsively.”

Clore, Jerald L p 184. “. . . emotion tems refer to internal mental states that are primarily focused on affect (where “affect” simply refers to the perceived goodness or badness of something). [see Clore & Ortony (1988) in V. Hamilton et al. Cognitive Science Perspectives on Emotion and Motivation. 367-398]

Clore, Jerald L p 285-6. “If there are necessary features of emotions, feeling is a good candidate. Of all the features that emotions have in common, feeling seems the least dispensable. It is perfectly reasonable to say about ones anger, for example,’I was angry, but I didn’t do anything,’ but it would be odd to say ‘I was angry, but I didn’t feel anything.’ ”

Ellsworth, Phoebe p 192. “. . . the process of emotion . . . is initiated when one’s attention is captured by some discrepancy or change. When this happens , one’s state is different, physiologically and psychologically, from what it was before. This might be called a “state of preparedness” for an emotion . . . The process almost always begins before the name [of the emotion is known] and almost always continues after it.

Averill, James R. p 265-6. “The concept of emotion . . . refer[s] to (1) emotional syndromes, (2) emotional states, and (3) emotional reactions. An emotional syndrome is what we mean when we speak of anger, grief, fear, love and so on in the abstract. . . . For example, the syndrome of anger both describes and prescribes what a person may (or should) do when angry. An emotional state is a relatively short term, reversible (episodic) disposition to respond in a manner representative of the corresponding emotional syndrome. . . . Finally, and emotional reaction is the actual (and highly variable) set of responses manifested by an individual when in an emotional state: . . . facial expressions, physiological changes, overt behavior and subjective experience.”

LeDoux, Joseph E. p 291. “In my view, “emotions” are affectively charged, sujectively experienced states of awareness.”

 

A Plea for Visual Thinking / Rudolf Arnheim

Click to access A-Plea-for-Visual-Thinking.pdf

A Plea for Visual Thinking

see also an interview with RA:  http://www.cabinetmagazine.org/issues/2/rudolfarnheim.php

Rudolf Arnheim Reviewed work(s): Source: Critical Inquiry, Vol. 6, No. 3 (Spring, 1980), pp. 489-497 Published by: The University of Chicago Press Stable URL: http://www.jstor.org/stable/1343105 . Accessed: 31/01/2013 13:04

Perception and thinking are treated by textbooks of psychology in separate chapters. The senses are said to gather information about the outer world; thinking is said to process that information. Thinking emerges from this approach as the “higher,” more respectable function, to which consequently education assigns most of the school hours and most of the credit. The exercise of the senses is a mere recreation, relegated to spare time.

It is left to the playful practice of the arts and music and is readily dispensed with when a tight budget calls for economy. The habit of separating the intuitive from the abstractive functions, as they were called in the Middle Ages, goes far back in our tradition. Descartes, in the sixth Meditation, defined man as “a thing that thinks,” to which reasoning came naturally (it obviously doesn’t!); whereas imagining, the activity of the senses, required a special effort and was in no way necessary to the human nature or essence. (The arts and technology are vital to human health and happiness -)

Note: We see the “elevation” of these narrow ideas about “a hierarchy of thinking” (that damn pyramid obsession again) in the denigration of ASD / Asperger abilities: (formal, old-fashioned use of language if language is present; echoing or copying (parroting) of language with an extensive “memorized” vocabulary, but without a “clue” to the “deeper meaning”  of language; an indictment of ASD / AS individuals as robots that are utterly lacking in imagination or creativity; as enthralled by boring subject matter (to social types) and above all, the failure to accomplish what has recently been elevated to the “highest level of cognition attainable, socio-emotional language, exemplified by: Have a nice day!

For “verbally deficient” autistics, this means an immediate judgement of low intelligence.  

So far, we have a very clear historical explanation as to why “visual-sensory thinking” got trashed, demoted and eventually designated as a “developmental disability” by American psychologists. This vital and creative cognitive process has vanished from the “acceptable human social repertoire” of “brain activity” in puritanical” American culture.  

The passive ability to receive images of sensory things, said Descartes, would be useless if there did not exist in the mind a further and higher active faculty capable of shaping these images and of correcting the errors that derive from sensory experience. (Exactly backwards to how thinking works) A century later Leibniz spoke of two levels of clear cognition.’ Reasoning was cognition of the higher degree: it was distinct, that is, it could analyze things into their components. Sensory experience, on the other hand, was cognition of the lower order: it also could be clear but it was confused, in the original Latin sense of the term; that is, all elements fused and mingled together in an indivisible whole. Thus artists, who rely on this inferior faculty (as do many top inventors and scientists), are good judges of works of art but when asked what is wrong with a particular piece that displeases them can only reply that it lacks nescio quid, a certain “I don’t know what.” (Intuitively, you “get it” or you don’t)

Yes, the Descartes – thing is nonsense. Just because a man is a genius is one field, doesn’t mean that he is an expert on everything; but NTs love authority and will believe without question what “great men” say. Our present predicament of relying on a “false pyramid of thinking” based on “dumb” (not reasonable) value judgements from (European white male) heroes of the past, has devastated the power of thinking “outside the box of verbal abstraction and generalities” in entire societies.

In our own time, language has been designated as the place of refuge from the problems incurred in direct perceptual experience; this in spite of the fact that language, although a powerful help to our thinking, does not offer in and by itself an arena in which thinking can take place. Thus the very title of a recent collection of articles by Jerome S. Bruner suggests that in order to arrive at knowledge the human mind must go “beyond the information given” by direct sensory experience. Bruner adopts the belief that the cognitive development of a child passes through three stages. The child explores the world first through action, then through imagery, and finally through language. 

The implication is, unfortunately, that with the arrival at a next level the earlier one falls by the wayside.

This is obviously untrue: adults retain modes of “thinking” from childhood stages. Magical thinking is the default mode of thinking for neotenic social typicals. Magic  “fills in” the gaps left by inferior sensory data and perception, supplying “fantastical” explanations for phenomena. Reasoning, critical analysis, and effective understanding of “how the universe works” (math-science) may be native to a few individuals, but must be taught and cultivated in the majority of children. This is a taboo in highly religious American culture. Reality-based thinking has been abandoned, even demonized, in American education – and for several generations – in favor of socially-promoted emotional narcissism that contributes to a very distorted social reality and description of “being human.” That is, a supernatural orientation is the result of developmental stagnation, and furnishes the status quo in religious, psychological and social engineering regimes. Neoteny is a fact of life for the modern social human. 

Thus when the child learns to go beyond a particular constellation directly given to his eyes, the ability to restructure the situation in a more suitable way is not credited by Bruner to the maturing of perceptual capacity but to the switch toward a new processing medium, namely, language. Thus language is praised as the indispensable instrument for essential refinements of the mind, toward which in fact, language is little more than a reflector.

To claim that “cognition” suddenly appeared out of nowhere, only with the “arrival of human verbal language” is idiotic and unbelievably arrogant! 550 million years of “arms race” evolution, but “sensory thinking” is inferior…

We are told by psychologists that “autistic” children are defective (low intelligence) due to two outrageous prejudices:

1. Lack of verbal language use, and/or failure to use language as prescribed (social scripts) is automatically a “sign” of defective development. (This overturns and discards 550 millions of years of evolution)

2. Superior sensory perception and processing, which are autistic strengths, are denigrated as ‘low-level’ cognition.

Since experts insist that perception offers nothing better than the fairly mechanical recording of the stimuli arriving at the sensory receptors, it is useful to respond with a few examples which show that perception transcends constantly and routinely the mere mechanical recording of sensory raw material. (I am limiting myself in the following to visual perception.) At a fairly simple level, the psychologist Roger N. Shepard and his coworkers have shown that visual imagination can rotate the spatial position of a given object when a different view is needed to solve a problem, for example, in order to identify the object with, or distinguish it from, a similar one. (I have noted previously that this type of “test” is a very limited and rule-based conception of what visual thinking can and does accomplish) This is worth knowing. But reports by artists and scientists indicate that visual imagination is capable of much more spectacular exploits. Indeed, the imagination of the average person demands our respect.

Let me use an example cited in an article by Lewis E. Walkup. The solution of the puzzle should be attempted without the help of an illustration. Imagine a large cube made up of twenty-seven smaller cubes, that is, three layers of nine cubes each. Imagine further that the entire outer surface of the large cube is painted red and ask yourself how many of the smaller cubes will be red on three sides, two sides, one side, or no side at all.

SEE Skipped TEXT

Far from abandoning our image, we discovered it to be a beautiful, composition, in which each element was defined by its place in the whole. Did we need language to perform this operation? Not at all; although language could help us to codify our results. Did we need intelligence, inventiveness, creative discovery? Yes, some. In a modest way, the operation we performed is of the stuff that good science and good art are made of.

Was it seeing or was it thinking that solved the problem? Obviously, the distinction is absurd.

In order to see we had to think; and we had nothing to think about if we were not looking. But our claim goes farther. We assert not only that perceptual problems can be solved by perceptual operations but that productive thinking solves any kind of problem in the perceptual realm because there exists no other arena in which true thinking can take place. Therefore it is now necessary to show, at least sketchily, how one goes about solving a highly “abstract” problem. For the sake of an example, let me ask the old question of whether free will is compatible with determinism. Instead of looking up the answer in Saint Augustine or Spinoza, I watch what happens when I begin to think. In what medium does the thinking take place? Images start to form. Motivational forces, in order to become manipulable, take the shape of arrows. These arrows line up in a sequence, each pushing the next-a deterministic chain that does not seem to leave room for any freedom (fig. la). Next I ask What is freedom? and I see a sheaf of vectors issuing from a base (fig. lb). Each arrow is free, within the limits of the constellation, to move in any direction it pleases and to reach as far as it can and will. But there is something incomplete about this image of freedom. It operates in empty space, and there is no sense to freedom without the context of the world to which it applies. My next image adds an external system of a world minding its own business and thereby frustrating the arrows that issue from my freedom-seeking creature (fig. ic). I must ask: Are the two systems incompatible in principle? In my … GO TO: 

Click to access A-Plea-for-Visual-Thinking.pdf

 

Every Asperger Needs to Read this Paper! / Symptoms of entrapment and captivity

Research that supports my challenge to contemporary (American) psychology that Asperger symptoms are the result of “captivity” and not “defective brains” 

From: Depression Research and Treatment

Depress Res Treat. 2010; 2010: 501782. Published online 2010 Nov 4. doi:  10.1155/2010/501782 PMCID: PMC2989705

Full Article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989705/

Testing a German Adaption of the Entrapment Scale and Assessing the Relation to Depression

Manuel Trachsel, 1 ,* Tobias Krieger, 2 Paul Gilbert, 3 and Martin Grosse Holtforth 2 :

Abstract

The construct of entrapment is used in evolutionary theory to explain the etiology of depression. The perception of entrapment can emerge when defeated individuals want to escape but are incapable. Studies have shown relationships of entrapment to depression, and suicidal tendencies. The aim of this study was a psychometric evaluation and validation of the Entrapment Scale in German (ES-D). 540 normal subjects completed the ES-D along with other measures of depressive symptoms, hopelessness, and distress. Good reliability and validity of the ES-D was demonstrated. Further, whereas entrapment originally has been regarded as a two-dimensional construct, our analyses supported a single-factor model. Entrapment explained variance in depressive symptoms beyond that explained by stress and hopelessness supporting the relevance of the construct for depression research. These findings are discussed with regard to their theoretical implications as well as to the future use of the entrapment scale in clinical research and practice.

Being outnumbered by social humans, 99% to 1%, is de facto defeat and captivity

1. Introduction

Assuming a certain degree of adaptivity of behavior and emotion, evolutionary theorists have suggested various functions of moodiness and depression. Whereas adaptive mechanisms may become functionally maladaptive [1, 2], there have been many attempts to explain potentially adaptive functions of depression. For example, Price [3] suggested that depression evolved from the strategic importance of having a de-escalating or losing strategy. Social rank theory [4, 5] built on this and suggests that some aspects of depression, such as mood and drive variations, may have evolved as mechanisms for regulating behavior in contexts of conflicts and competition for resources and mates. Hence, subordinates are sensitive to down rank threats and are less confident than dominants, while those who are defeated will seek to avoid those who defeated them. Depression may also serve the function to help individuals disengage from unattainable goals and deal with losses [6]. 

Social rank theory (e.g., [4]) links defeat states to depression. Drawing on Dixon’s arrested defences model of mood variation [7, 8], this theory suggests that especially when stresses associated with social defeats and social threats arise, individuals are automatically orientated to fight, flight or both. Usually, either of those defensive behaviors will work. So, flight and escape remove the individual from the conditions in which stress is arising (e.g., threats from a dominant), or anger/aggression curtails the threat. These defensive behaviors typically work for nonhuman animals. However, for humans, such basic fight and flight strategies may be less effective facing the relatively novel problems of living in modern societies, perhaps explaining the prevalence of disorders such as depression [8]. Dixon suggested that in depression, defensive behaviors can be highly aroused but also blocked and arrested and in this situation depression ensues. Dixon et al. [8] called this arrested flight. For example, in lizards, being defeated but able to escape has proven to be less problematic than being defeated and being trapped. Those who are in caged conditions, where escape is impossible, are at risk of depression and even death [9]. Gilbert [4, 10] and Gilbert and Allan [5] noted that depressed individuals commonly verbalize strong escape wishes and that feelings of entrapment and desires to escape have also been strongly linked to suicide, according to O’Connor [11]. In addition they may also have strong feelings of anger or resentment that they find difficult to express or become frightening to them. (Or are NOT ALLOWED to express, without being punished) 

Gilbert [4] and Gilbert and Allan [5] proposed that a variety of situations (not just interpersonal conflicts) that produce feeling of defeat, or uncontrollable stress, which stimulate strong escape desires but also makes it impossible for an individual to escape, lead the individual to a perception of entrapment. They defined entrapment as a desire to escape from the current situation in combination with the perception that all possibilities to overcome a given situation are blocked. Thus, theoretically entrapment follows defeat if the individual is not able to escape. This inability may be due to a dominant subject who does not offer propitiatory gestures following antagonistic competition, or if the individual keeps being attacked. (Relentless social bullying) 

In contrast to individuals who feel helpless (cf. the concept of learned helplessness [12]), which focus on perceptions of control, the entrapped model focuses on the outputs of the threat system emanating from areas such as the amygdala [13]. In addition, depressed people are still highly motivated and would like to change their situation or mood state. It was also argued that, unlike helplessness, entrapment takes into account the social forces that lead to depressive symptoms, which is important for group-living species with dominance hierarchies such as human beings [14]. Empirical findings by Holden and Fekken [15] support this assumption. Gilbert [4] argued that the construct of entrapment may explain the etiology of depression better than learned helplessness, because according to the theory of learned helplessness, helpless individuals have already lost their flight motivation whereas entrapped individuals have not.

According to Gilbert [4], the perception of entrapment can be triggered, increased, and maintained by external factors but also internal processes such as intrusive, unwanted thoughts and ruminations can play an important role (e.g., [16, 17]). For example, ruminating on the sense of defeat or inferiority may act as an internal signal of down-rank attack that makes an individual feel increasingly inferior and defeated. Such rumination may occur despite the fact that an individual successfully escaped from an entrapping external situation because of feelings of failure, which may cause a feeling of internal entrapment. For example, Sturman and Mongrain [18] found that internal entrapment increased following an athletic defeat. Moreover, thoughts and feelings like “internal dominants” in self-critics may exist that can also activate defensive behaviors.

For the empirical assessment of entrapment, Gilbert and Allan [5] developed the self-report Entrapment Scale (ES) and demonstrated its reliability. Using the ES, several studies have shown that the perception of entrapment is strongly related to low mood, anhedonia, and depression [5, 1921]. Sturman and Mongrain [22] found that entrapment was a significant predictor of recurrence of major depression. Further, Allan and Gilbert [23] found that entrapment relates to increased feelings of anger and to a lower expression of these feelings. In a study by Martin et al. [24], the perception of entrapment was associated with feelings of shame, but not with feelings of guilt. Investigating the temporal connection between depression and entrapment, Goldstein and Willner [25, 26] concluded that the relation between depression and entrapment is equivocal and might be bilateral; that is, entrapment may lead to depression and vice versa.

Entrapment was further used as a construct explaining suicidal tendency. In their cry-of pain-model, Williams and Pollock [27, 28] argued that suicidal behavior should be seen as a cry of pain rather than as a cry for help. Consistent with the concept of arrested flight, they proposed that suicidal behavior is reactive. In their model, the response (the cry) to a situation is supposed to have the following three components: defeat, no escape potential, and no rescue. O’Connor [11] provided empirical support in a case control study by comparing suicidal patients and matched hospital controls on measures of affect, stress, and posttraumatic stress. The authors hypothesized that the copresence of all three cry-of-pain variables primes an individual for suicidal behavior. The suicidal patients, with respect to a recent stressful event, reported significantly higher levels of defeat, lower levels of escape potential, and lower levels of rescue than the controls. Furthermore, Rasmussen et al. [21] showed that entrapment strongly mediated the relationship between defeat and suicidal ideation in a sample of first-time and repeated self-harming patients. Nevertheless, there has also been some criticism of the concept of entrapment as it is derived from animal literature [29].

To our knowledge so far, there is no data on the retest reliability or the temporal stability of the Entrapment Scale. Because entrapment is seen as a state-like rather than a trait-like construct, its stability is likely dependent on the stability of its causes. (Remove the social terrorism, or remove yourself) Therefore, if the causes of entrapment are stable (e.g., a long-lasting abusive relationship), then also entrapment will remain stable over time. In contrast, for the Beck Hopelessness Scale (BHS), there are studies assessing temporal stability that have yielded stable trait-like components of hopelessness [30]. Young and coworkers [30] stated that the high stability of hopelessness is a crucial predictor of depressive relapses and suicidal attempts. For the Perceived Stress Questionnaire (PSQ), there are studies examining retest reliability. The PSQ has shown high retest reliability over 13 days (r = .80) in a Spanish sample [31]. It is to be expected that with longer retest intervals as in the present study (3 months), the stability of perceived stress will be substantially lower. We, therefore, expect the stability of entrapment to be higher than that of perceived stress as a state-like construct, but lower than that of hopelessness, which has been shown to be more trait-like [32].

Previous research is equivocal regarding the dimensionality of the entrapment construct. Internal and external entrapment were originally conceived as two separate constructs (cf. [5]) and were widely assessed using two subscales measuring entrapment caused by situations and other people (e.g., “I feel trapped by other people”) or by one’s own limitations (e.g., “I want to get away from myself”). The scores of the two subscales were averaged to result in a total entrapment score in many studies. However as Taylor et al. [33] have shown, entrapment may be best conceptualized as a unidimensional construct. This reasoning is supported by the observation that some of the items of the ES cannot easily be classified either as internal or external entrapment and because the corresponding subscales lack face validity (e.g., “I am in a situation I feel trapped in” or “I can see no way out of my current situation”).

5. Discussion

The entrapment construct embeds depressiveness theoretically into an evolutionary context. The situation of arrested flight or blocked escape, in which a defeated individual is incapable of escaping despite a maintained motivation to escape, may lead to the perception of entrapment in affected individuals [8]. In this study, the Entrapment Scale (ES) was translated to German (ES-D), tested psychometrically, and validated by associations with other measures. This study provides evidence that the ES-D is a reliable self-report measure of entrapment demonstrating high internal consistency. The study also shows that the ES-D is a valid measure that relates to other similar constructs like hopelessness, depressive symptoms or perceived stress. Levels of entrapment as measured with the ES-D were associated with depressiveness, perceived stress, and hopelessness, showing moderate to high correlations. Results were consistent with those obtained by Gilbert and Allan [5]. Entrapment explained additional variance in depressiveness beyond that explained by stress and hopelessness. Taken together, the present data support the conception of entrapment as a relevant and distinct construct in the explanation of depression. (And much of Asperger behavior)

The results of our study confirm the findings of Taylor et al. [33], thereby showing that entrapment is only theoretically, but not empirically, separable into internal and external sources of entrapment. The authors even went further by showing that entrapment and defeat could represent a single construct. Although in this study the defeat scale [5] was not included, the results are in line with the assumption of Taylor et al. [33] and support other studies using entrapment a priori as a single construct. However, although this study supports the general idea that escape motivation affects both internal and external events and depression, clinically it can be very important to distinguish between them. For example, in studies of psychosis entrapment can be very focused on internal stimuli, particularly voices [47].

The state conceptualization of entrapment implies that the perception of entrapment may change over time. Therefore, we did not expect retest correlations as high as retest correlations for more trait-like constructs like hopelessness [32]. Since the correlation over time is generally a function of both the reliability of the measure and the stability of the construct, high reliability is a necessary condition for high stability [48]. In this study, we showed that the ES-D is a reliable scale, and we considered retest correlations as an indicator for stability. The intraclass correlation of .67 suggests that entrapment is more sensitive to change than hopelessness (r = .82). Furthermore, the state of entrapment seems to be more stable than perceived stress, which may be influenced to a greater extent by external factors. Given the confirmed reliability and validity of the ES-D in this study, we therefore cautiously conclude that entrapment lies between hopelessness and perceived stress regarding stability.

Whereas the high correlation between entrapment and depressive symptoms in this study may be interpreted as evidence of conceptual equivalence, an examination of the item wordings of two scales clearly suggest that these questionnaires assess distinct constructs. However, the causal direction of this bivariate relation is not clear. Theoretically, both directions are plausible. Entrapment may be a cause or a consequence of depressive symptoms, or even both. Unfortunately, studies examining the temporal precedence so far have yielded equivocal results and have methodological shortcomings (e.g., no clinical samples, only mild and transitory depression and entrapment scores with musical mood induction) in order to answer this question conclusively [25, 26]. It remains unclear whether entrapment only is depression specific. Entrapment might not only be associated with depression, but also with other psychological symptoms, or even psychopathology in general. This interpretation is supported by research showing a relation between distress arising from voices and entrapment in psychotic patients [49, 50]. Furthermore, other studies show the relation between entrapment and depressive symptoms [5153] and social anxiety and shame [54] in psychosis. The usefulness of entrapment as a construct for explaining psychopathologies in humans has been questioned [29]. Due to the present study, it is now possible to investigate entrapment in psychopathology in the German speaking area.

Modern social humans and the social hierarchy: Driving Asperger types crazy for thousands of years!

 

Does Self-Awareness Require a Complex Brain?

Aye, yai, yai. Here we go again…which definitions of consciousness and self-awareness are being discussed?

(SciAm Article after sample definitions) NOTE: The media function on my page is screwed up… can’t size or delete some images – you’ll have to search out “brain parts images” for yourself. 

From: Home » Positive Psychology Articles » What is Self-Awareness and Why Does it Matter? 

So What is Self-Awareness Exactly? / The psychological study of self-awareness can be first traced back to 1972 when Psychologists Shelley Duval and Robert Wicklund developed the theory of self-awareness.

They proposed that: “when we focus our attention on ourselves, we evaluate and compare our current behavior to our internal standards and values. We become self-conscious as objective evaluators of ourselves.”

In essence, they consider self-awareness as a major mechanism of self-control.

Sounds pretty good; a state of “owning” one’s thoughts and intentions and the recognition that one’s behavior is often not congruent with these “values”. NOT the simple act of “mirror recognition” which belongs to the brain’s “visual system”. 

Basic physical def: When you are awake and aware of your surroundings, that’s consciousness. (That “jives with” mirror recognition -type awareness as a property of an active sensory system). 

The most influential modern physical theories of consciousness (there are supernatural theories, of course) are based on psychology and neuroscience. Theories proposed by neuroscientists such as Gerald Edelman and Antonio Damasio, and by philosophers such as Daniel Dennett, seek to explain consciousness in terms of neural events occurring within the brain. Consciousness – Wikipedia

It’s impossible here to present the long-standing and ever-growing confusion over the modern “concepts” of consciousness. It’s a word that is used for the most part, without any meaning whatsoever. Technology also has entered the arena. 

My own idea is this… What we commonly refer to as “being consciousness” is a social interaction, an act of Co-consciousness; the product of language : “In Western cultures verbal language is inseparable from the process of creating a conscious human being.” see previous post: https://aspergerhuman.wordpress.com/?p=9198&preview=true

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Article: https://blogs.scientificamerican.com/brainwaves/does-self-awareness-require-a-complex-brain/

By Ferris Jabr on August 22, 2012

The computer, smartphone or other electronic device on which you are reading this article has a rudimentary brain—kind of.* (uh-oh. Pop-Sci) It has highly organized electrical circuits that store information and behave in specific, predictable ways, just like the interconnected cells in your brain. (No) On the most fundamental level, electrical circuits and neurons are made of the same stuff—atoms and their constituent elementary particles—but whereas the human brain is conscious, manmade gadgets do not know they exist. (WOW! NT nonsense!) Consciousness, most scientists argue, (made up assertion) is not a universal property of all matter in the universe. Rather, consciousness is restricted to a subset of animals with relatively complex brains. The more scientists study animal behavior and brain anatomy, however, the more universal consciousness seems to be. (Confused yet?) (Mirror awareness is a VISUAL phenomenon)

A brain as complex as the human brain is definitely not necessary for consciousness. (!!!)

On July 7 this year, a group of neuroscientists convening at Cambridge University signed a document officially declaring that non-human animals, “including all mammals and birds, and many other creatures, including octopuses” are conscious. (Well, that’s certainly proof that some poorly-defined experiential state in humans is a “thingy” also “in mammals and birds, and many other creatures, including octopuses” !!)

Humans are more than just conscious—they are also self-aware. Scientists differ on the difference between consciousness and self-awareness, (those imaginary Science Elves again, messing us up with “tricky” non specific definitions of “consciousness and self-awareness”) but here is one common explanation: Consciousness is awareness of one’s body and one’s environment; self-awareness is recognition of that consciousness—not only understanding that one exists, but further understanding that one is aware of one’s existence. Another way of thinking about it: To be conscious is to think; to be self-aware is to realize that you are a thinking being and to think about your thoughts. Presumably, human infants are conscious—they perceive and respond to people and things around them—but they are not yet self-aware. In their first years of life, infants develop a sense of self, learn to recognize themselves in the mirror (a phenomenon of the SENSORY SYSTEM) and to distinguish their own point of view from other people’s perspectives.

Notice how a lack of distinction / definition of terms leads to the inevitable “linear-causal-but-hierarchical arrangement of “notions” assumed to be correct (that is, how the brain works as an “isolated” command center, but which are “phrases” merely strung together by “social habit”.

Numerous neuroimaging studies have suggested that thinking about ourselves, recognizing images of ourselves and reflecting on our thoughts and feelings—that is, different forms self-awareness—all involve the cerebral cortex, the outermost, intricately wrinkled part of the brain. The fact that humans have a particularly large and wrinkly cerebral cortex relative to body size supposedly explains why we seem to be more self-aware than most other animals. (This pop-sci blah, blah is unforgivable in a “science” article. 

One would expect, then, that a man missing huge portions of his cerebral cortex would lose at least some of his self-awareness. Patient R, also known as Roger, defies that expectation. Roger is a 57-year-old man who suffered extensive brain damage in 1980 after a severe bout of herpes simplex encephalitis—inflammation of the brain caused by the herpes virus. The disease destroyed most of Roger’s insular cortex, anterior cingulate cortex (ACC), and medial prefrontal cortex (mPFC), all brain regions thought to be essential for self-awareness. About 10 percent of his insula remains and only one percent of his ACC.

Note that “self-awareness” in this article is the “you are awake and aware of your surroundings” definition, and not the Duval, Wickland definition.

Roger cannot remember much of what happened to him between 1970 and 1980 and he has great difficulty forming new memories. He cannot taste or smell either. But he still knows who he is—he has a sense of self. He recognizes himself in the mirror and in photographs. (This would indicate that his VISUAL system / memory is intact) To most people, Roger seems like a relatively typical man who does not act out of the ordinary. (That’s NTs for you; minimal evidence, inattentional blindness, social convention = “must be a normal person”) LOL

Carissa Philippi and David Rudrauf of the University of Iowa and their colleagues investigated the extent of Roger’s self-awareness in a series of tests. In a mirror recognition task, for example, a researcher pretended to brush something off of Roger’s nose with a tissue that concealed black eye shadow. 15 minutes later, the researcher asked Roger to look at himself in the mirror. Roger immediately rubbed away the black smudge on his nose and wondered aloud how it got there in the first place.

Philippi and Rudrauf also showed Roger photographs of himself, of people he knew and of strangers. He almost always recognized himself and never mistook someone else for himself, but he sometimes had difficulty recognizing a photo of his face when it appeared by itself on a black background, absent of hair and clothing. (Visual system)

Roger also distinguished the sensation of tickling himself from the feeling of someone else tickling him and consistently found the latter more stimulating. When one researcher asked for permission to tickler Roger’s armpits, he replied, “Got a towel?” As Philippi and Rudrauf note, Roger’s quick wit indicates that in addition to maintaining a sense of self, he adopts the perspective of others—a talent known as theory of mind. (Hmmm… a man without an insular cortex, anterior cingulate cortex (ACC), and medial prefrontal cortex is capable of “mind-reading” and subtle social thinking and interaction. BUT, ASD Asperger people who have these “parts” intact, are not capable of “mind-reading” and social communication) He anticipated that the researcher would notice his sweaty armpits and used humor to preempt any awkwardness.

Just where is the “mythic social brain” located? In a textbook perhaps?

In another task, Roger had to use a computer mouse to drag a blue box from the center of a computer screen towards a green box in one of the corners of the screen. In some cases, the program gave him complete control over the blue box; in other cases, the program restricted his control. Roger easily discriminated between sessions in which he had full control and times when some other force was at work. In other words, he understood when he was and was not responsible for certain actions. (Aye, yai, yai. What a “stretchy” conclusion!) The results appear online August 22 in PLOS One.

Given the evidence of Roger’s largely intact self-awareness (visual recognition)despite his ravaged brain, Philippi, Rudrauf and their colleagues argue that the insular cortex, anterior cingulate cortex (ACC), and medial prefrontal cortex (mPFC) cannot by themselves account for conscious recognition of oneself as a thinking being. (Well, congratulations!) Instead, they propose that self-awareness is a far more diffuse cognitive process, relying on many parts of the brain, including regions not located in the cerebral cortex. (Why no recognition of VISUAL processing??)

In their new study, Philippi and Rudrauf point to a fascinating review of children with hydranencephaly—a rare disorder in which fluid-filled sacs replace the brain’s cerebral hemispheres. Children with hydranencphaly are essentially missing every part of their brain except the brainstem and cerebellum and a few other structures. Holding a light near such a child’s head illuminates the skull like a jack-o-lantern. Although many children with hydranencephaly appear relatively normal at birth, they often quickly develop growth problems, seizures and impaired vision. Most die within their first year of life. In some cases, however, children with hydranencephaly live for years or even decades. Such children lack a cerebral cortex—the part of the brain thought to be most important for consciousness and self-awareness—but, as the review paper makes clear, at least some hydranencephalic children give every appearance of genuine consciousness. They respond to people and things in their environment. When someone calls, they perk up. The children smile, laugh and cry. They know the difference between familiar people and strangers. They move themselves towards objects they desire. And they prefer some kinds of music over others. If some children with hydranencephaly are conscious, then the brain does not require an intact cerebral cortex to produce consciousness. (Which “consciousness” are we discussing?)

Hydranencephaly: “conscious” by definition “awake and aware of its surroundings” – there seems to be a consistent error in equating this definition (which is true of any animal that is not “asleep, dormant, anesthetized, or comatose” and includes automatic reflexes) and being aware that one is aware, or self-awareness). 

Whether such children are truly self-aware, however, is more difficult to answer, especially as they cannot communicate with language. In D. Alan Shewmon‘s review, one child showed intense fascination with his reflection in a mirror (visual system), but it’s not clear whether he recognized his reflection as his own. Still, research on hydranencephaly and Roger’s case study indicate that self-awareness—this ostensibly sophisticated and unique cognitive process layered upon consciousness—might be more universal than we realized. (Totally ridiculous statement. Mixing simple visual recognition with Duval, Wickland definition. Still no clue as to what “consciousness” is. 

References

Merker B (2007) Consciousness without a cerebral cortex: A challenge for neuroscience and medicine. Behavioral and Brain Sciences 30: 63-81.

Philippi C., Feinstein J.S., Khalsa S.S., Damasio A., Tranel D., Landini G., Williford K.5, Rudrauf D. Preserved self-awareness following extensive bilateral brain damage to the insula, anterior cingulate, and medial prefrontal cortices. PLOS ONE. Aug 22.

Shewmon DA, Holmes GL, Byrne PA. Consciousness in congenitally decorticate children: developmental vegetative state as self-fulfilling prophecy. Dev Med Child Neurol. 1999 Jun;41(6):364-74.

Why Asperger Types Exist / Videos LOL

No, I’m not “diagnosing” these lecturers as Asperger, but the topics discussed are an important part of the Asperger “realm of” (supposedly) bizarre, annoying, antisocial and dangerous “obsessions.”

What would mankind do without these people?

Hey, Neurotypicals: GROW UP. It’s called SCIENCE.

Environmental Influences on Gene Expression / Social Human Denial

One of the most mind-boggling aspects of Autism research is the insistence that ASD /Asperger types have “defective sensory systems” because they “react negatively” to “toxic” modern social environments: This is so backwards! “Autism experts” expect human fetuses, infants and children to develop “normally” in what are ANTI-LIFE artificial environments. This is simply ignorant “social blindness” to the fact that “toxic environments” are wreaking havoc on human physiology, which evolved over millions of years in Nature, and not in polluted, unhealthy and high stress “concentration camps” of millions of people, denied clean air and water, nutritious food, privacy and autonomy and self-preservation. Attempts are made to “drug” and medically intervene in the catastrophic so-called “mental illness” epidemic and the failing health of millions; drastic medical intervention is resorted to, in order to “artificially adapt” Homo sapiens to killer environments. Not even the cascade of species extinctions caused by modern human degradation of the environment can “penetrate” the ignorance of   social humans. 

Internal and external environmental factors, like gender and temperature, influence gene expression.

https://www.nature.com/scitable/topicpage/environmental-influences-on-gene-expression-536

By: Ingrid Lobo, Ph.D. (Write Science Right) © 2008 Nature Education

The expression of genes in an organism can be influenced by the environment, including the external world in which the organism is located or develops, as well as the organism’s internal world, which includes such factors as its hormones and metabolism. One major internal environmental influence that affects gene expression is gender, as is the case with sex-influenced and sex-limited traits. Similarly, drugs, chemicals, temperature, and light are among the external environmental factors that can determine which genes are turned on and off, thereby influencing the way an organism develops and functions.

Sex-Influenced and Sex-Limited Traits

 Sex-influenced traits are those that are expressed differently in the two sexes. Such traits are autosomal, which means that the genes responsible for their expression are not carried on the sex chromosomes. An example of a sex-influenced trait is male-pattern baldness. The baldness allele, which causes hair loss, is influenced by the hormones testosterone and dihydrotestosterone, but only when levels of the two hormones are high. In general, males have much higher levels of these hormones than females, so the baldness allele has a stronger effect in males than in females. However, high levels of stress can lead to expression of the gene in women. In stressful situations, women’s adrenal glands can produce testosterone and convert it into dihydrotestosterone, which can result in hair loss.

Sex-limited traits are also autosomal. Unlike sex-influenced traits, whose expression differs according to sex, sex-limited traits are expressed in individuals of only one sex. An example of a sex-limited trait is lactation, or milk production. Although the genes for producing milk are carried by both males and females, only lactating females express these genes.

Drugs and Chemicals

The presence of drugs or chemicals in an organism’s environment can also influence gene expression in the organism. Cyclops fish are a dramatic example of the way in which an environmental chemical can affect development. In 1907, researcher C. R. Stockard created cyclopean fish embryos by placing fertilized Fundulus heteroclitus eggs in 100 mL of seawater mixed with approximately 6 g of magnesium chloride. Normally, F. heteroclitus embryos feature two eyes; however, in this experiment, half of the eggs placed in the magnesium chloride mixture gave rise to one-eyed embryos (Stockard, 1907).

A second example of how chemical environments affect gene expression is the case of supplemental oxygen administration causing blindness in premature infants (Silverman, 2004). In the 1940s, supplemental oxygen administration became a popular practice when doctors noticed that increasing oxygen levels converted the breathing pattern of premature infants to a “normal” rhythm. Unfortunately, there is a causal relationship between oxygen administration and retinopathy of prematurity (ROP), although this relationship was unknown at the time; thus, by 1953, ROP had blinded approximately 10,000 infants worldwide. Finally, in 1954, a randomized clinical trial identified supplemental oxygen as the factor causing blindness. Complicating the issue is the fact that too little oxygen results in a higher rate of brain damage and mortality in premature infants. Unfortunately, even today, the optimal amount of oxygenation necessary to treat premature infants while completely avoiding these complications is still not clear.

How much devastating and life long damage continues to be suffered by infants due to the “promotion” of premature birth as the new normal? 

Yet another example of the way in which chemicals can alter gene expression involves thalidomide, a sedative, antiemetic, and nonbarbiturate drug that was first manufactured and marketed during the mid-1950s. While thalidomide has no discernable effect on gene expression and development in healthy adults, it has a profoundly detrimental effect on developing fetuses. When the drug was first created, however, its impact on fetuses was not known. Moreover, because of its apparent lack of toxicity in adult human volunteers, thalidomide was marketed as the safest available sedative of its time and rapidly became popular in Europe, Australia, Asia, and South America for countering the effects of morning sickness. (In the United States, the drug failed to receive Food and Drug Administration approval because its side effects included tingling hands and feet after long-term administration, which led to concerns that the drug might be associated with neuropathy.) Not until 1961 did Australian researcher William McBride and German researcher Widukind Lenz independently report that thalidomide was a teratogen, meaning that its use was associated with birth defects. (How many of today’s medical drugs and treatments will be / are being “discovered” to be dangerous, due to ignorance and lack of diligent testing, when “rush to market” profitability is the motivation, not human benefit)  Another study associated thalidomide use with neuropathies. Sadly, the drug was withdrawn too late to prevent severe developmental deformities in approximately 8,000 to 12,000 infants, many of whom were born with stunted limb development. Interestingly, despite the fact that thalidomide is dangerous during embryonic development, the drug continues to be used in certain instances yet today. For example, it has therapeutic potential in treating leprosy, and in recent years, it has also been used to treat cancers and enhance the effectiveness of cancer vaccines (Bartlett et al., 2004; Fraser, 1988).

Nature is packed full with evidence for the wide-ranging and specific effects of environment! Why do “researchers” cling to the socio-religious fantasy that humans, as “special creations” are somehow “exempt” from the consequences of animal reality?

Temperature and Light  A pigment gene is influenced by temperature.

© 2013 Nature Education Adapted from Pierce, Benjamin. Genetics: A Conceptual Approach, 2nd ed. All rights reserved.

In addition to drugs and chemicals, temperature and light are external environmental factors that may influence gene expression in certain organisms. For example, Himalayan rabbits carry the C gene, which is required for the development of pigments in the fur, skin, and eyes, and whose expression is regulated by temperature (Sturtevant, 1913). Specifically, the C gene is inactive above 35°C, and it is maximally active from 15°C to 25°C. This temperature regulation of gene expression produces rabbits with a distinctive coat coloring. In the warm, central parts of the rabbit’s body, the gene is inactive, and no pigments are produced, causing the fur color to be white (Figure 1). Meanwhile, in the rabbit’s extremities (i.e., the ears, tip of the nose, and feet), where the temperature is much lower than 35°C, the C gene actively produces pigment, making these parts of the animal black.

Light can also influence gene expression, as in the case of butterfly wing development and growth. For example, in 1917, biologist Thomas Hunt Morgan conducted studies in which he placed Vanessa urtica and Vanessa io caterpillars under red, green, or blue light, while other caterpillars were kept in the dark. When the caterpillars developed into butterflies, their wings showed dramatic differences. Exposure to red light resulted in intensely colored wings, while exposure to green light resulted in dusky wings. Blue light and darkness led to paler colored wings. In addition, the V. urtica butterflies reared under blue light and V. io butterflies reared in the dark were larger than the other butterflies.

As these examples illustrate, there are many specific instances of environmental influences on gene expression. However, it is important to keep in mind that there is a very complex interaction between our genes and our environment that defines our phenotype and who we are.

And yet “autistic” children are blamed for physical effects that originate in unhealthy human-created and imposed toxic environments. Which, not surprisingly, are also negatively impacting ALL HUMANS. 

Widespread Bias Large Genetic Studies / Implications for ASD Asperger’s

Pleiotropy: This certainly has implications for the endlessly repeated assertion that heritable genetic pathologies account for symptoms that include everything from “being antisocial” to being interested in subjects that bore neurotypicals” to female ASDs “preferring to wear clothing with lots of pockets”. It is acknowledged that ASD / Asperger’s are a highly ‘heterogeneous’ bunch of individuals; no two are alike. Claims for “discovery” of scads of “autism-linked genes” are highly suspicious to begin with, and now this unsurprising report, in which “causal” links are over- and under- estimated, or MISSED COMPLETELY.  

Source of Potential Bias Widespread in Large Genetic Studies

A new statistical method finds that many genetic variants used to determine trait-disease relationships may have additional effects that GWAS analyses don’t pick up.

By Diana Kwon | May 15, 2018

Genome-wide association studies, which scan thousands of genetic variants to identify links to a specific trait, have recently provided epidemiologists with a rich source of data. By applying Mendelian randomization, a technique that leverages an individual’s unique genetic variation to recreate randomized experiments, researchers have been able to infer the causal effect of specific risk factors on health outcomes, such as the link between elevated blood pressure and heart disease. (And all those supposed “links” between ASD / Autism “genes” and a bizarre selection / collection of “manifestations” in ASD / Asperger behavior, brain function and even in apparel choices)

The Mendelian randomization technique has long operated on the key assumption that horizontal pleiotropy, a phenomenon in which a single gene contributes to a disease through more than one pathway, is not happening. However, a new study published last month (April 23) in Nature Genetics finds that when it comes to potentially causal trait-disease relationships identified from genome-wide association studies (GWAS), pleiotropy is widespread—and may bias findings.

The “no pleiotropy” assumption was reasonable when scientists were examining only a few genes and much more was known about their specific biological functions, says Jack Bowden, a biostatistician at the University of Bristol’s MRC Integrative Epidemiology Unit in the U.K., who was not involved in the study. Nowadays, GWAS, which include many more genetic variants, are often conducted with little understanding about the precise mechanisms through which each gene could act on physiological traits, he adds.

Although researchers have suspected that pleiotropy exists in a large number of Mendelian randomization studies using GWAS datasets, “no one has actually tested how much of a problem this was,” says study coauthor Ron Do, a geneticist at the Icahn School of Medicine Mount Sinai.

To address this question, Do and his colleagues developed the so-called MR-PRESSO technique, an algorithm that identifies pleiotropy in Mendelian randomization analyses by searching for outliers in the relationship between the genetic variants’ effects on the trait of interest, say, blood pressure, and the same polymorphisms’ effects on the health outcome, such as heart disease. Outliers suggest that some genetic variants may not only be acting on the outcome through that particular trait—in other words, that pleiotropy exists. 

The team used this method to test all possible trait-disease combinations generated from 82 publicly available GWAS datasets and found that pleiotropy was present in approximately 48 percent of the 191 statistically significant causal relationships they identified. (Yes, statistics are only as good as the quality of the “thinking” of the people manipulating the process) 

When the researchers compared the Mendelian randomization results before and after correcting for pleiotropy, they discovered that pleiotropy could lead to drastic over- or underestimations of the magnitude of a trait’s influence on a disease. (And ASD / Autism is NOT A DISEASE; it’s a collection of symptoms – which have multiple sources including WESTERN socio-cultural prejudice) Approximately 10 percent of the causal associations they found were significantly distorted, and by as much as 200 percent.

For example, the team identified an outlier variant in one of the significant causal relationships they found using Mendelian randomization—a link between body mass index (BMI) and levels of C-reactive protein, a marker for inflammation and heart disease. Further examination revealed that this variant, found in a gene encoding apolipoprotein E—a protein involved in metabolism—was associated with several traits and diseases, including BMI, C-reactive protein, cholesterol levels, and Alzheimer’s disease. After removing this outlier, the effect of BMI on C-reactive protein dropped by 12 percent, still statistically significant, but obviously to a lesser degree.

“There is growing awareness that there’s widespread pleiotropy in the human genome in general, and I think these findings suggest that there needs to be rigorous analysis and careful interpretation of casual relationships when performing Mendelian randomization,” (One would have thought that this was the conservative baseline in “science-based” research) Do says. “I think what’s going to have the biggest impact is not just saying whether causal relationships exist, but actually showing that the magnitude of the causal relationship can be distorted due to pleiotropy.”

Bowden notes that the presence of pleiotropy does not mean that Mendelian randomization is necessarily a flawed technique. “Many research groups around the world are currently developing novel statistical approaches that can detect and adjust for pleiotropy, enabling you to reliability test whether a [gene] has a causal effect on an outcome,” he tells The Scientist. For example, he and his colleagues at the University of Bristol recently reported another method to identify and correct for pleiotropy in large-scale Mendelian randomization analyses. (Are these “novel statistical approaches” proven to correct a problem that has much to do with the “reductive mindset” of those who place prime value on “any positive results” for their research agenda, above scientific discipline?)

“I hope that this paper will raise people’s attention to the potential problems in the assumptions behind [these studies],” says Wei Pan, a biostatistician at the University of Minnesota who was not involved in this work. “Large genetic datasets give researchers the opportunity to use a method like this to move the field forward, and as long as they use the method carefully, they can reach meaningful conclusions.” (Is this true, or social blah, blah?)

M. Verbanck et al., “Detection of widespread horizontal pleiotropy in causal relationships inferred from Mendelian randomization between complex traits and diseases,” Nature Genet, doi:10.1038/s41588-018-0099-7, 2018.

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 A chicken with the frizzle gene
© 2004 Richard Blatchford, Dept. of Animal Science UC Davis. All rights reserved. View Terms of Use

Pleiotropy: 

https://www.nature.com/scitable/topicpage/pleiotropy-one-gene-can-affect-multiple-traits-569

The term pleiotropy is derived from the Greek words pleio, which means “many,” and tropic, which means “affecting.” Genes that affect multiple, apparently unrelated, phenotypes are thus called pleiotropic genes Pleiotropy should not be confused with polygenic traits, in which multiple genes converge to result in a single phenotype.

Examples of Pleiotropy

In some instances of pleiotropy, the influence of the single gene may be direct. For example, if a mouse is born blind due to any number of single-gene traits (Chang et al., 2002), it is not surprising that this mouse would also do poorly in visual learning tasks. In other instances, however, a single gene might be involved in multiple pathways. For instance, consider the amino acid tyrosine. This substance is needed for general protein synthesis, and it is also a precursor for several neurotransmitters (e.g., dopamine, norepinephrine), the hormone thyroxine, and the pigment melanin. Thus, mutations in any one of the genes that affect tyrosine synthesis or metabolism may affect multiple body systems. These and other instances in which a single gene affects multiple systems and therefore has widespread phenotypic effects are referred to as indirect or secondary pleiotropy (Grüneberg, 1938; Hodgkin, 1998).

Other examples of both direct and indirect pleiotropy are described in the sections that follow.
Chickens and the Frizzle Trait

In 1936, researchers Walter Landauer and Elizabeth Upham observed that chickens that expressed the dominant frizzle gene produced feathers that curled outward rather than lying flat against their bodies (Figure 2). However, this was not the only phenotypic effect of this gene — along with producing defective feathers, the frizzle gene caused the fowl to have abnormal body temperatures, higher metabolic and blood flow rates, and greater digestive capacity. Furthermore, chickens who had this allele also laid fewer eggs than their wild-type counterparts, further highlighting the pleiotropic nature of the frizzle gene.

See article for Pigmentation and Deafness in Cats, and Antagonistic Pleiotropy and much much more on genetics….  https://www.nature.com/scitable/topicpage/pleiotropy-one-gene-can-affect-multiple-traits-569

Human Pleiotropy

As touched upon earlier in this article, there are many examples of pleiotropic genes in humans, some of which are associated with disease. For instance, Marfan syndrome is a disorder in humans in which one gene is responsible for a constellation of symptoms, including thinness, joint hypermobility, limb elongation, lens dislocation, and increased susceptibility to heart disease. Similarly, mutations in the gene that codes for transcription factor TBX5 cause the cardiac and limb defects of Holt-Oram syndrome, while mutation of the gene that codes for DNA damage repair protein NBS1 leads to microcephaly, immunodeficiency, and cancer predisposition in Nijmegen breakage syndrome.

One of the most widely cited examples of pleiotropy in humans is phenylketonuria (PKU). This disorder is caused by a deficiency of the enzyme phenylalanine hydroxylase, which is necessary to convert the essential amino acid phenylalanine to tyrosine. A defect in the single gene that codes for this enzyme therefore results in the multiple phenotypes associated with PKU, including mental retardation, eczema, and pigment defects that make affected individuals lighter skinned (Paul, 2000).

The phenotypic effects that single genes may impose in multiple systems often give us insight into the biological function of specific genes. Pleiotropic genes can also provide us valuable information regarding the evolution of different genes and gene families, as genes are “co-opted” for new purposes beyond what is believed to be their original function (Hodgkin, 1998). Quite simply, pleiotropy reflects the fact that most proteins have multiple roles in distinct cell types; thus, any genetic change that alters gene expression or function can potentially have wide-ranging effects in a variety of tissues.

Somewhat ironic, that large genetic studies REMOVE PLEIOTROPY, a “fact” in human genetics that may provide real progress in finding genetic links to physical conditions that are at present lumped together under a phony  “autistic pathology” that is based in the “social brain” of neutrotypicals – and not in scientific reality.

 

How does life arise from randomness? / Physics to the rescue…

see also: https://aspergerhuman.wordpress.com/2016/01/21/entropy-thermodynamics-life-and-death/

Why does life exist?

For figures and illustrations go to original. 

Popular hypotheses credit a primordial soup, a bolt of lightning and a colossal stroke of luck. But if a provocative new theory is correct, luck may have little to do with it. Instead, according to the physicist proposing the idea, the origin and subsequent evolution of life follow from the fundamental laws of nature and “should be as unsurprising as rocks rolling downhill.”

From the standpoint of physics, there is one essential difference between living things and inanimate clumps of carbon atoms: The former tend to be much better at capturing energy from their environment and dissipating that energy as heat. Jeremy England, a 31-year-old assistant professor at the Massachusetts Institute of Technology, has derived a mathematical formula that he believes explains this capacity. The formula, based on established physics, indicates that when a group of atoms is driven by an external source of energy (like the sun or chemical fuel) and surrounded by a heat bath (like the ocean or atmosphere), it will often gradually restructure itself in order to dissipate increasingly more energy. This could mean that under certain conditions, matter inexorably acquires the key physical attribute associated with life.

“You start with a random clump of atoms, and if you shine light on it for long enough, it should not be so surprising that you get a plant,” England said.

England’s theory is meant to underlie, rather than replace, Darwin’s theory of evolution by natural selection, which provides a powerful description of life at the level of genes and populations. “I am certainly not saying that Darwinian ideas are wrong,” he explained. “On the contrary, I am just saying that from the perspective of the physics, you might call Darwinian evolution a special case of a more general phenomenon.”

*******

England’s theoretical results are generally considered valid. It is his interpretation — that his formula represents the driving force behind a class of phenomena in nature that includes life — that remains unproven. But already, there are ideas about how to test that interpretation in the lab.

“He’s trying something radically different,” said Mara Prentiss, a professor of physics at Harvard who is contemplating such an experiment after learning about England’s work. “As an organizing lens, I think he has a fabulous idea. Right or wrong, it’s going to be very much worth the investigation.”

At the heart of England’s idea is the second law of thermodynamics, also known as the law of increasing entropy or the “arrow of time.” Hot things cool down, gas diffuses through air, eggs scramble but never spontaneously unscramble; in short, energy tends to disperse or spread out as time progresses. Entropy is a measure of this tendency, quantifying how dispersed the energy is among the particles in a system, and how diffuse those particles are throughout space. It increases as a simple matter of probability: There are more ways for energy to be spread out than for it to be concentrated. Thus, as particles in a system move around and interact, they will, through sheer chance, tend to adopt configurations in which the energy is spread out. Eventually, the system arrives at a state of maximum entropy called “thermodynamic equilibrium,” in which energy is uniformly distributed. A cup of coffee and the room it sits in become the same temperature, for example. As long as the cup and the room are left alone, this process is irreversible. The coffee never spontaneously heats up again because the odds are overwhelmingly stacked against so much of the room’s energy randomly concentrating in its atoms.

Although entropy must increase over time in an isolated or “closed” system, an “open” system can keep its entropy low — that is, divide energy unevenly among its atoms — by greatly increasing the entropy of its surroundings. In his influential 1944 monograph “What Is Life?” the eminent quantum physicist Erwin Schrödinger argued that this is what living things must do. A plant, for example, absorbs extremely energetic sunlight, uses it to build sugars, and ejects infrared light, a much less concentrated form of energy. The overall entropy of the universe increases during photosynthesis as the sunlight dissipates, even as the plant prevents itself from decaying by maintaining an orderly internal structure.

Life does not violate the second law of thermodynamics, but until recently, physicists were unable to use thermodynamics to explain why it should arise in the first place. In Schrödinger’s day, they could solve the equations of thermodynamics only for closed systems in equilibrium. In the 1960s, the Belgian physicist Ilya Prigogine made progress on predicting the behavior of open systems weakly driven by external energy sources (for which he won the 1977 Nobel Prize in chemistry). But the behavior of systems that are far from equilibrium, which are connected to the outside environment and strongly driven by external sources of energy, could not be predicted.

This situation changed in the late 1990s, due primarily to the work of Chris Jarzynski, now at the University of Maryland, and Gavin Crooks, now at Lawrence Berkeley National Laboratory. Jarzynski and Crooks showed that the entropy produced by a thermodynamic process, such as the cooling of a cup of coffee, corresponds to a simple ratio: the probability that the atoms will undergo that process divided by their probability of undergoing the reverse process (that is, spontaneously interacting in such a way that the coffee warms up). As entropy production increases, so does this ratio: A system’s behavior becomes more and more “irreversible.” The simple yet rigorous formula could in principle be applied to any thermodynamic process, no matter how fast or far from equilibrium. “Our understanding of far-from-equilibrium statistical mechanics greatly improved,” Grosberg said. England, who is trained in both biochemistry and physics, started his own lab at MIT two years ago and decided to apply the new knowledge of statistical physics to biology.

David Kaplan explains how the law of increasing entropy could drive random bits of matter into the stable, orderly structures of life. Filming by Tom Hurwitz and Richard Fleming. Editing and motion graphics by Tom McNamara. Music by Podington Bear.

Using Jarzynski and Crooks’ formulation, he derived a generalization of the second law of thermodynamics that holds for systems of particles with certain characteristics: The systems are strongly driven by an external energy source such as an electromagnetic wave, and they can dump heat into a surrounding bath. This class of systems includes all living things. England then determined how such systems tend to evolve over time as they increase their irreversibility. “We can show very simply from the formula that the more likely evolutionary outcomes are going to be the ones that absorbed and dissipated more energy from the environment’s external drives on the way to getting there,” he said. The finding makes intuitive sense: Particles tend to dissipate more energy when they resonate with a driving force, or move in the direction it is pushing them, and they are more likely to move in that direction than any other at any given moment.

“This means clumps of atoms surrounded by a bath at some temperature, like the atmosphere or the ocean, should tend over time to arrange themselves to resonate better and better with the sources of mechanical, electromagnetic or chemical work in their environments,” England explained.

Self-replication (or reproduction, in biological terms), the process that drives the evolution of life on Earth, is one such mechanism by which a system might dissipate an increasing amount of energy over time. As England put it, “A great way of dissipating more is to make more copies of yourself.” In a September paper in the Journal of Chemical Physics, he reported the theoretical minimum amount of dissipation that can occur during the self-replication of RNA molecules and bacterial cells, and showed that it is very close to the actual amounts these systems dissipate when replicating. He also showed that RNA, the nucleic acid that many scientists believe served as the precursor to DNA-based life, is a particularly cheap building material. Once RNA arose, he argues, its “Darwinian takeover” was perhaps not surprising.

The chemistry of the primordial soup, random mutations, geography, catastrophic events and countless other factors have contributed to the fine details of Earth’s diverse flora and fauna. But according to England’s theory, the underlying principle driving the whole process is dissipation-driven adaptation of matter.

This principle would apply to inanimate matter as well. “It is very tempting to speculate about what phenomena in nature we can now fit under this big tent of dissipation-driven adaptive organization,” England said. “Many examples could just be right under our nose, but because we haven’t been looking for them we haven’t noticed them.”

Scientists have already observed self-replication in nonliving systems. According to new research led by Philip Marcus of the University of California, Berkeley, and reported in Physical Review Letters in August, vortices in turbulent fluids spontaneously replicate themselves by drawing energy from shear in the surrounding fluid. And in a paper appearing online this week in Proceedings of the National Academy of Sciences, Michael Brenner, a professor of applied mathematics and physics at Harvard, and his collaborators present theoretical models and simulations of microstructures that self-replicate. These clusters of specially coated microspheres dissipate energy by roping nearby spheres into forming identical clusters. “This connects very much to what Jeremy is saying,” Brenner said.

Besides self-replication, greater structural organization is another means by which strongly driven systems ramp up their ability to dissipate energy. A plant, for example, is much better at capturing and routing solar energy through itself than an unstructured heap of carbon atoms. Thus, England argues that under certain conditions, matter will spontaneously self-organize. This tendency could account for the internal order of living things and of many inanimate structures as well. “Snowflakes, sand dunes and turbulent vortices all have in common that they are strikingly patterned structures that emerge in many-particle systems driven by some dissipative process,” he said. Condensation, wind and viscous drag are the relevant processes in these particular cases.

“He is making me think that the distinction between living and nonliving matter is not sharp,” said Carl Franck, a biological physicist at Cornell University, in an email. “I’m particularly impressed by this notion when one considers systems as small as chemical circuits involving a few biomolecules.”

Prentiss, who runs an experimental biophysics lab at Harvard, says England’s theory could be tested by comparing cells with different mutations and looking for a correlation between the amount of energy the cells dissipate and their replication rates. “One has to be careful because any mutation might do many things,” she said. “But if one kept doing many of these experiments on different systems and if [dissipation and replication success] are indeed correlated, that would suggest this is the correct organizing principle.”

Brenner said he hopes to connect England’s theory to his own microsphere constructions and determine whether the theory correctly predicts which self-replication and self-assembly processes can occur — “a fundamental question in science,” he said.

Having an overarching principle of life and evolution would give researchers a broader perspective on the emergence of structure and function in living things, many of the researchers said. “Natural selection doesn’t explain certain characteristics,” said Ard Louis, a biophysicist at Oxford University, in an email. These characteristics include a heritable change to gene expression called methylation, increases in complexity in the absence of natural selection, and certain molecular changes Louis has recently studied.

If England’s approach stands up to more testing, it could further liberate biologists from seeking a Darwinian explanation for every adaptation

and allow them to think more generally in terms of dissipation-driven organization. They might find, for example, that “the reason that an organism shows characteristic X rather than Y may not be because X is more fit than Y, but because physical constraints make it easier for X to evolve than for Y to evolve,” Louis said.

“People often get stuck in thinking about individual problems,” Prentiss said. Whether or not England’s ideas turn out to be exactly right, she said, “thinking more broadly is where many scientific breakthroughs are made.”

Emily Singer contributed reporting. This article was reprinted on ScientificAmerican.com and BusinessInsider.com

Facial Hair / Not just for Humans

Apes: Not so different after all.

Monkey Mustaches Reveal Evolution of Facial Hair

https://www.seeker.com/monkey-mustaches-reveal-evolution-of-facial-hair-1769477454.html

Mustaches and eyebrows help certain monkeys (same species) recognize each other, research finds.

Distinctive facial hair, like mustaches and eyebrows, are not unique to people — those traits also help certain monkeys identify each other. Mustaches, beards, bushy eyebrows and other facial hair might have first evolved in primates to help them easily recognize each other in forest environments, according to new research in the latest issue of the Proceedings of the Royal Society B.

The study shows how much primates rely on vision in their social networks.

“Primates are a visual group that have lots and lots of face-to-face interactions,” co-author James Higham told Discovery News.

“The evolutionary history of primates is one of increasing reliance on vision at the expense of olfaction, which is the sense that is used more ancestrally among mammals.”

For the study, Higham, an assistant professor of anthropology at New York University, and co-author William Allen studied guenon monkeys, which sport all sorts of quirky facial hair, from ear tufts to beards and bushy eyebrows. Both male and female guenon monkeys have these features, to the point that humans looking at them cannot always tell which monkey is a male and which is a female.

The researchers designed a computer algorithm that could assess 500 photographs of 12 species of guenons. The images were collected in various settings, including at U.S. and U.K. zoos and at a wildlife sanctuary in Nigeria. The photos were of both male and female guenons.

“We sought to test a computer’s ability to do something close to what a guenon viewing other guenons’ faces would do,” explained Allen, who is now a post-doctoral researcher at the University of Hull.

___________________________________________________________________________________________

Sexual selection for “tame” females produced neotenic “symptoms”: little to no facial / body hair, baby faces, select fat deposition, monthly instead of yearly fertility, arrested development at juvenile developmental stages.

This selection produced easy visual recognition of females; females became “easy prey” animals – a domesticated animal. Modern Western female ideals include physical features of young males: boys with boobs syndrome. ______________________________________________________________ 

Chimps actually have “patchy” body and facial hair.

The computer succeeded in correctly identifying individuals and their species, but like humans looking at the images, it too was stumped at trying to figure out if the photos were of males or females. It also could not categorize the photos by the age of the monkeys.

There seems to have been selection for a role for facial appearance in species recognition, Higham said. For age and sex, he speculated that “perhaps if you live in a stable social group, and you have individual recognition, then you can just learn those other individuals and whether they are old or young, or male or female, and so do not need this to be encoded in their facial appearance. “This makes sense for guenons, which often live high in rainforest canopies with many closely related species. For breeding and other social purposes, they need to quickly identify their own kind.

The distant ancestors of humans were also tree dwellers that likely lived close to similar species. A growing body of evidence even supports that more recent members of our genus co-existed, such as Neanderthals and early Homo sapiens sharing some of the same territories.

While guenon monkeys, owl monkeys and some other primates have males and females that look nearly identical, it is usually very easy to distinguish a human man from a woman with just a glance. Facial hair in our case takes on a sexier function.

Sexual deception by visual disguise: Ducati ads, etc. 

Are men imitating women, or women imitating men? 

https://www.naukrinama.com/stressbuster/men-copying-womens-pose/

“In humans, mustaches and beards are what we call a ‘sexually dimorphic’ trait, i.e. they are present in one sex and not the other,” Higham said. “This suggests that they are a sexually-selected trait, and perhaps play a role in mate choice or in competition between individuals of the same sex.”

Allen and Higham believe that the computer technique could be used to analyze the facial traits of all sorts of other animals, helping to determine the function of these traits and why and how they evolved in the first place.

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