Looking Back on Bipolar / Seasonal Transitions and Disruptions

See also related Circadian Rhythm posts –

I used to be bipolar; diagnosed long ago, before Asperger’s was a recognized “thing” (1994) and not considered applicable to females. Looking back, I think this was a mistake – the “bipolar” symptoms I experienced can logically be seen as evidence for “Asperger-ness” as a brain type that processes the environment in a distinct and even radically different way than the overwhelming majority of Modern Social Humans – neurotypicals. One notable problem for me, was and is, a response to seasonal change; lack of sunlight and outdoor activity in winter produce a direct physical effect: extreme restlessness (anxiety) and a longing for the world to “come back” – to revive, to be washed in sunlight and present a landscape wide open to movement. This is not an uncommon condition for many people! The experience can be grossly represented as  claustrophobia. Winter is a time, that once adjusted to, can be very productive; a time of internal focus, mental activity and concentration.

The transition into summer, while eagerly embraced, can be disruptive, unsettling, and “mind-blowing” – Where I live, it’s a long process; inter-leaving of days of increasing sunlight that fool fragile plant life into attempts to emerge, but which are discouraged by snow storms and overnight freezes. The energy gained by extended sunlight at high altitude (6,000-7,000 feet) hits a certain point – and suddenly, our tan and brown,  heavily dissected desert is GREEN. It’s “shocking” to the eye; strange and brief. The sagebrush steppe is covered in prickly shrubs and myriad bunch grasses, which  must reproduce in the short window of mid May through June, and then pack away their chlorophyll for another year, leaving only yellow leaves and seeds to be dispersed by the famous Wyoming wind.  A palette of rich yellows, pale earth, and dusty gray green returns; a much more interesting landscape for sunlight to change in appearance, from moment to moment, throughout the day and evening. A “light show” transforms our two-part landscape of land and sky – a daily cycle of color and shadow that passes into cool night.

I don’t know if this experience of reality is common to Asperger individuals; that is  – the direct influence of the environment on mood, emotion and energy. This responsiveness to the land is not exclusive to Asperger’s types.

This desert has no “social” uses; agriculture is futile. Few people can live here, and without resource extraction for “dollars” and importation of food, even fewer could, or would stay. There is something extremely luxurious about a landscape that can’t be “socialized” – unitized, divided, owned and exploited by human agriculture, trade, commerce – made useful or productive. There’s something extremely luxurious about a life that grows to fit this type of land. I was made for this place: finding it meant “letting go of things not meant for me.” The Bhudda.

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Original post about transitioning from summer into winter:

This is my 65th transition from summer into fall. Of course I don’t remember most of these changes. Fall is a bit of a drive-through season; the way we get to winter. It says so on the calendar: First Day of Fall, but for me it’s a long drawn out state of confusion, instability, moodiness: doom. What has disrupted my normal, careful, mostly peaceful days? Normal for me: my “writer’s routine” of coffee, computer and coming awake. Sometimes writing is easier while I’m still a bit stupefied by sleep.

Anticipation: that’s my experience of Fall, as if something momentous is about to happen, but it never does. One morning the garden plants have frozen, cells bursting; really physically dead; mush with frost rimming the remains. Light snow that melts quickly, the rocks damp and shiny, their colors deep and revealing.

It’s not that I don’t like winter, but some innocent intuitive organ believes that the earth is dying, and me with it. These experiences are so strong and consistent year after year, that I’m sure that being bipolar has something to do with ancient humans -tropical creatures who pushed too far north for their mental health. People whose brains and bodies were extensions of the seasons: work like mad in Spring and Summer and semi-hibernate in winter. Expend the least energy possible obtaining food and water; curl up like most of nature and sleep and dream an alternate existence filled with giants, heroes and mortal powers.

 

 

 

Circadian Rhythm Disturbances / Bipolar – Asperger Syndrome

Bipolar Disorder is thought to be co-morbid to Asperger Syndrome. I want to introduce material from Circadian Rhythm studies.

Circadian Rhythm

Social cues help set sleep patterns

Social cues help set sleep patterns

© 2002 Psychiatric Times. All rights reserved. Circadian Rhythms Factor in Rapid-Cycling Bipolar Disorder by Ellen Leibenluft, M.D. Psychiatric Times May 1996 Vol. XIII Issue 5

The nervous systems of people with bipolar disorder frequently make specific types of regulatory errors. Many of those errors involve the body’s internal clock, which controls the phenomena known as circadian rhythms. These are the regular rhythmic changes in waking and sleeping, activity levels, and sensations of hunger and thirst.

Phototherapy and melatonin, two interventions that manipulate the circadian system, are being used widely for seasonal affective disorder, jet lag and some forms of insomnia. Scientists continue to make tremendous strides in understanding the regulation of the circadian system in humans and animals. We now know that the body’s clock is located in the suprachiasmatic nucleus (SCN) of the hypothalamus, and that the SCN regulates the pineal gland’s secretion of the hormone melatonin (Klein and colleagues). In humans as well as animals, light suppresses melatonin secretion; recent evidence shows that even ordinary room light can have this effect. Because light suppresses melatonin secretion, the hormone is typically secreted at night. Furthermore, the SCN can “remember” the day-length to which it has been recently exposed, so the timing of nocturnal melatonin secretion is determined by the “lights on” and “lights off” times of the preceding days. In 1994, scientists cloned genes regulating circadian rhythms in mice, making the circadian system the first complex behavioral system whose genetic underpinnings could begin to be unraveled in mammals (Vitaterna and coworkers).

In mood disorder research, interest in circadian rhythms is not new. For at least 50 years, investigators have questioned whether abnormalities in circadian rhythm regulation might be involved in the pathogenesis of mood disorders, including rapid-cycling bipolar disorder. These questions were motivated by three clinical observations. The first of these was that the sleep duration of patients often changes dramatically as they cycle between mania and depression; bipolar depression is typically associated with hypersomnia, while mania is characterized by extreme and sometimes total insomnia.

The second observation was that approximately 60 percent of depressed patients experience remission after a night of total or partial sleep deprivation (SD). In bipolar patients, sleep deprivation (SD) may actually cause a switch into hypomania or mania. However, this “upward” switch usually lasts only until the patient undergoes recovery sleep, leading to the formulation that SD, or extended wakefulness, is antidepressant, (or manicogenic), while sleep is depressogenic, (Wehr). The antidepressant effects of SD are conceptually important because they show that changes in sleep duration are more than just symptoms of the illness, and also play a pathogenic role.

Using a longitudinal analysis of mood and sleep in a sample of patients with rapid-cycling bipolar disorder, we recently demonstrated that decreased sleep duration precedes, rather than simply follows, a switch into hypomania or mania (Leibenluft and coworkers, in press). Furthermore, in this sample, decreased sleep duration was more consistently associated with a shift to an earlier wake-up time than it was with a shift to a later bedtime. Pharmacologically, it is easier to manipulate the time a patient goes to sleep than to change the time he or she wakes up; perhaps for this reason, clinicians have generally attended less to wake-up time than to sleep-onset time. However, these data indicate that interventions designed to shift patients’ wake-up time may deserve further study.

The third observation implicating abnormal circadian rhythms in the pathogenesis of mood disorders concerns diurnal variation. In its classic, typical form, diurnal variation is defined as a gradual improvement in the patient’s depressed mood as the day wears on. Like sleep deprivation, typical diurnal variation demonstrates that extended wakefulness is associated with an antidepressant response. We recently extended the concept of diurnal variation to bipolar patients with data demonstrating that rapid-cycling patients are more likely to switch “up” (i.e., from depression or euthymia into hypomania) during the day, and to switch “down” (from hypomania or euthymia into depression) overnight, while they sleep (Susana Feldman-Naim, M.D., and coworkers, unpublished data). Thus, once again, extended wakefulness is associated with an antidepressant response, while sleep appears to be depressogenic.

Specific theories have been advanced as to how circadian rhythm dysfunction might lead to rapid-cycling bipolar disorder. In 1968, Halberg suggested that some, but not all, circadian rhythms in such patients were not synchronized with the 24-hour day-night cycle (Halberg). According to Halberg’s hypothesis, the interaction between the unsynchronized, “free-running” rhythms and the normally synchronized (entrained) rhythms causes switches back and forth between mania and depression.

Kripke and colleagues then presented data demonstrating what appeared to be a free-running temperature rhythm in five of seven rapid-cycling patients. In these patients, the period (time taken to complete one cycle) was abnormally short, in essence showing that patients with rapid mood cycles had rapid physiological cycles. However, subsequent investigators have not generally found either free-running or unusually fast circadian rhythms in patients with rapid-cycling bipolar disorder.

In the 1970s and ’80s Wehr and collaborators, working at the National Institute of Mental Health, continued to study biological rhythms in this patient population. Using both cross-sectional and longitudinal designs, they showed that the phase (timing) of patients’ sleep, temperature and motor activity rhythms varied systematically as they cycled between hypomania or mania and depression. Specifically, the timing of these rhythms appeared to be earlier in manic than in depressed patients, and earlier in depressed patients than in controls (Wehr and colleagues 1980). We now have preliminary data indicating a similar pattern in the time of onset of nocturnal melatonin secretion. These new data show that, in rapid-cycling bipolar patients, the time of nocturnal melatonin onset may be approximately 90 minutes earlier when they are hypomanic, compared to when they are depressed (Leibenluft and colleagues 1993). It is as if rapid-cycling patients might have an endogenous form of jet lag, internally traveling back and forth over one or two time zones as they cycle between hypomania and depression. Indeed, several studies show that bipolar patients are at risk to develop an affective episode when they travel across time zones (Young).

What might cause these shifts in the phase (time) of onset of nocturnal melatonin secretion? It is possible that phase shifts.i.phase shifts; in nocturnal melatonin secretion precede the patients’ mood switches and play a pathogenic role in mood cycling. However, it is also possible that the phase shifts are epiphenomena caused by the patient’s symptoms. Specifically, the phase shifts may be secondary to the changes in the sleep-wake cycle.i.sleep-wake cycle; that occur with mood cycling. The phase of circadian rhythms is determined by zeitgebers (“time-givers”).

While light is the most potent zeitgeber, physical activity, eating and social routines can probably also affect the timing of circadian rhythms. The timing of all these zeitgebers is often different when a patient is hypomanic, compared to when he or she is depressed, and shifts in the timing of zeitgebers would cause phase shifts in circadian rhythms.

However, a third possibility also exists. We suggest that phase shifts in melatonin secretion and other circadian rhythms are not the primary cause of mood cycling, but they are also not irrelevant epiphenomena. We hypothesize that phase shifts in melatonin secretion are secondary to the patient’s symptoms or to more fundamental causes of bipolar illness, but they nonetheless have pathogenic significance and contribute to the development of a full-blown affective episode.

This formulation is analogous to that of Wehr and coworkers (1987) in describing the contribution of sleep deprivation to the development of manic episodes. These authors suggested that insomnia, which is itself a symptom of mania, contributes to the development of a manic episode because it causes sleep deprivation. In other words, insomnia is both a symptom and a cause of mania. If one treats the insomnia early and aggressively, one can truncate an episode, or prevent mild or moderate symptoms from snowballing into a severe and destructive episode. Similarly, it is possible that the shifts in circadian rhythms, while not the initial cause of a mood switch, contribute to the severity and duration of an episode, and thus play a role in determining the course of illness.

We are currently testing this hypothesis by determining whether interventions designed to prevent phase shifts in nocturnal melatonin secretion have therapeutic effects in rapid-cycling bipolar patients. One such experimental treatment involves the use of phototherapy. Data indicate that midday bright light may increase the amplitude of nocturnal melatonin secretion. Since increasing the amplitude of a rhythm makes it more resistant to phase shifts, midday light might be expected to stabilize the time of nocturnal melatonin secretion. In other words, midday phototherapy administered to these patients might prevent the shifts in timing of nocturnal melatonin secretion that we believe have pathogenic significance. After encouraging results with a small number of patients, we are now conducting a formal, controlled trial of this intervention. Interestingly, morning bright light, which shifts patients’ circadian rhythms, may have caused several of our rapid-cycling bipolar patients to cycle more dramatically.

Thus, even if circadian abnormalities are neither the sole nor the primary cause of bipolar illness, it is possible that circadian interventions can have therapeutic utility. Compared to psychotropic medications, circadian interventions are relatively flexible therapeutic modalities; they have a rapid onset and offset of action, and their clinical effects may be altered by changing the time that they are administered. This flexibility may be particularly useful in rapid-cycling bipolar patients, whose frequent mood cycles may require rapid alterations in their therapeutic regimen. Further research will indicate what, if any, role circadian dysfunction plays in the pathogenesis of rapid-cycling bipolar disorder, and whether circadian interventions can be helpful to these often treatment-resistant patients.

Ellen Leibenluft, M.D., is chief, Unit on Rapid-Cycling Bipolar Disorder, Clinical Psychobiology Branch, National Institute of Mental Health.

Graphic Novels for Visual Thinkers / Educating Aspergers

Support a new Middle School project in New York! (from a site offering funding for teacher proposals)

Graphic Novels Motivate Readers With Asperger Syndrome

My students need a library of graphic novels to motivate readers because these books provide the visual cues kids with Asperger and autism need to truly understand characters.

 

My ten students are middle-schoolers who have Asperger Syndrome.

Students in my classroom have difficulty understanding people, so it’s not surprising that they also struggle to infer characters’ motives and purpose in books. Nonfiction, full of facts? No problem! But fiction? The majority of my students with Asperger Syndrome could leave it completely.

Vintage “graphic novels” were aimed at boys who didn’t like to read.

They like to follow rules – but they make a lot of their own. They like to be right, so they hate to admit when they don’t know something, and they avoid things that are difficult. Tough concepts, like characterization, theme and tone in a novel, make them feel uncomfortable – so they’d rather not read fiction. And, as educators know, the only thing that really improves reading once the school day ends, is more reading. Then I found the novel, The Inventions of Hugo Cabret. We only have one copy – I borrowed it from our library, and they want it back! But the students were riveted. Not only were they fascinated by the format of the book – half graphic novel, half traditional – but they understood Hugo’s emotions, portrayed as they were with matching drawings, moving incrementally forward! Experiments with other graphic novels are also proving successful, but we don’t have a lot of them to go around.

I am requesting class sets of popular graphic novels for my self-contained English class of students with Asperger Syndrome (and High-Functioning Autism.) The novels I request will be taught in the same manner as traditional literature, and I will compare each work with a traditional novel, which we will also read. This will help my students be on equal footing with their peers, because they will have more insight into concepts about characterization (as well as plot, theme, tone, etc.) when they rejoin their peers in high school reading more traditional works. I hope that, ultimately, these graphic novels lead them to enjoy literature in a way that many people without autism do – for the love of the story and the characters we would otherwise not know.

I was a MAD Magazine addict and a sucker for cats and rabbits dressed in charming clothing.

Please help me bridge the “understanding gap” for my students, who are so smart and fun and have so much potential. Help them understand literature by opening the door, using pictures with the text, and engendering a level of understanding that their disability would otherwise prevents them from obtaining. Thank you so much for reading my proposal.

Remember when all childhood schoolbooks had plenty of beautiful illustrations – stylized but realistic (not infantilized and deformed neotenic blobs) FOR ALL CHILDREN? Maybe our “old-fashioned” predecessors in publishing and education knew a lot more than we do about visual thinking being basic to the human ability to learn…

What “The World” Sounds like to (Many) Asperger People

The woman who made this audio track is correct! I could not bear to listen longer than a few seconds. If you can listen to this COMFORTABLY, you will likely not be able to understand what an Asperger person goes through daily, when trapped in social typical environments.

One particular point: It’s nearly impossible to pay attention to and to understand what a person is saying when “background noise” is not in the background! It’s competing with the person speaking; the impulse is to get away from the discordant “sounds” – the effect is like being tortured. Truly!

 

Neurotypical Perception Defects / Inferred Images, Social Filters

Humans rely more on ‘inferred’ visual objects than ‘real’ ones

May 16, 2017
Summary:
Humans treat ‘inferred’ visual objects generated by the brain as more reliable than external images from the real world, according to new research.
“In such situations with the blind spot, the brain ‘fills in’ the missing information from its surroundings, resulting in no apparent difference in what we see,” says senior author Professor Peter König, from the University of Osnabrück’s Institute of Cognitive Science. “While this fill-in is normally accurate enough, it is mostly unreliable because no actual information from the real world ever reaches the brain. We wanted to find out if we typically handle this filled-in information differently to real, direct sensory information, or whether we treat it as equal.”

Visual thinkers are all too aware of this reality deficit in the “typical” perception of reality; I can’t say that the mechanism described here is the “cause” of discrepancies between “typical” perception and the greatly enhanced perception of visually-oriented brains, but it does point out that the typical human brain has evolved “short cuts” that result in varying accuracy in the  perception of the environment. This deficit, combined with de facto “magical-social” thinking has dire consequences for survival.

Links:

Article in Science Daily: https://sciencedaily.com/releases/2017/05/170516080752.htm

Original Paper with figures, charts: 10.7554/eLife.21761

Posts on inattentional blindness: https://aspergerhuman.wordpress.com/2015/12/04/visual-thinking-inattentional-blindness/

https://aspergerhuman.wordpress.com/2015/12/04/inattentional-blindness-why-the-u-s-gets-sucker-punched-by-terrorists/

Inflammatory Diseases, Deadly Modern Environments / ASD, Depression

quick summation from Torrey Institute for Molecular Studies: 

Inflammatory Disorders (click here for website)

Inflammation is the body’s protective response to injury and infection; it is a complex process involving many cell types, as well as different components of blood.

The inflammatory process works quickly to destroy and eliminate foreign and damaged cells, and to isolate the infected or injured tissues from the rest of the body. Inflammatory disorders arise when inflammation becomes uncontrolled, and causes destruction of healthy tissue. There are dozens of inflammatory disorders. Many occur when the immune system mistakenly triggers inflammation in the absence of infection, such as inflammation of the joints in rheumatoid arthritis. Others result from a response to tissue injury or trauma but affect the entire body.

There are many ways by which normal cells and tissues can be damaged during inflammation. One important mechanism is by assembly of a complex of proteins that forms holes on the surface of a cell, where it causes damage and can potentially kill the cell. This complex is called a Membrane Attack Complex or MAC. Torrey Pines Institute researchers are working to understand how MAC contributes to a number of inflammation-associated disorders, including the complications of diabetes and rheumatoid arthritis. Understanding how MAC assembles will provide insights into the design of drugs to prevent inflammatory damage to cells.

Inflammation is also an important secondary component of many diseases. An example of this is atherosclerosis, or hardening of the arteries, where inflammation can cause more damage to arteries in a failed attempt to heal the artery wall. There is also an important link between obesity and inflammation, because substances that promote inflammation are released from fat cells, as well as from other cells embedded in fat tissue. The Institute’s scientists are leading the way in understanding these new and exciting areas of inflammation research.

The first article below presents the hypothesis that psychological stress and depression may be associated with “inflammatory” diseases.

The second presents the evolutionary “Inflammatory Bias” that has lead to rampant inflammatory disease in modern humans.

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Article 1: Brain Behav Immun. Author manuscript; available in PMC 2014 Jul 1.

 Published in final edited form as: Brain Behav Immun. 2013 Jul; 31: 1–8. Published online 2013 Apr 30. doi:  10.1016/j.bbi.2013.04.009

Malaise, Melancholia and Madness: The Evolutionary Legacy of an Inflammatory Bias

Technical paper, so I’m looking for a credible translation into common language!

Excerpt that may possibly be significant to ASD, Asperger’s and other “social” disorders.  

 5a. Immune Pathways and the Inflammasome

In a paper in this issue, Iwata et al. propose the provocative hypothesis that the recently characterized inflammasome may serve as a critical link between psychological stress and depression, as well as other illnesses related to inflammation (Iwata et al. 2012).

The inflammasome is a protein complex that can detect diverse danger signals including not only pathogen-associated molecules but also molecules associated with cellular damage such as adenosine triphosphate (ATP). Upon activation, the inflammasome can generate an inflammatory response notably through the production of IL-1-beta by activation of a caspase that cleaves the precursor peptide pro-IL-1-beta. Given the capacity of the inflammasome to react to danger signals generated by stimuli other than pathogens, the authors suggest that the inflammasome may be uniquely poised to serve as the molecular mechanism that transduces psychological responses to stress into an inflammatory response in the absence of pathogen challenge.

Thus, the inflammasome may represent an evolutionary adaptation that extends the immune and behavioral response to pathogens and the microbial world to include challenges emanating from predators, people and the social world. Although of significant value in detecting and responding to tissue damage and destruction, by virtue of the inflammasome,

the inflammatory bias may have been given an entrée into the modern world where people, not pathogens or predators represent the primary challenges.

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Article 2:

The role of inflammation in depression: from evolutionary imperative to modern treatment target

Andrew G. Miller and Charles L. Raison

Nature Reviews Immunology Volume:16,Pages:22–34Year published:(2016)DOI:doi:10.1038/nri.2015.5 (click to access article)

Fig. 1 Evolutionary legacy of an inflammatory bias. Early evolutionary pressures derived from human interactions with pathogens, predators and human conspecifics (such as rivals) resulted in an inflammatory bias that included an integrated suite of immunological and behavioural responses that conserved energy for fighting infection and healing wounds, while maintaining vigilance against attack.This inflammatory bias is believed to have been held in check during much of human evolution by exposure to minimally pathogenic, tolerogenic organisms in traditional (that is, rural) environments that engendered immunological responses characterized by the induction of regulatory T (TReg) cells, regulatory B (BReg) cells and immunoregulatory M2 macrophages as well as the production of the anti-inflammatory cytokines interleukin-10 (IL-10) and transforming growth factor-β (TGFβ). In modern times, sanitized urban environments of more developed societies are rife with psychological challenges but generally lacking in the types of infectious challenges that were primary sources of morbidity and mortality across most of human evolution. In the absence of traditional immunological checks and balances, the psychological challenges of the modern world instigate ancestral immunological and behavioural repertoires that represent a decided liability, such as high rates of various inflammation-related disorders including depression.

In proper perspective, modern social environments ARE DEADLY to life; not only to ASD Asperger people, but to ALL HUMANS and to every species that we are driving to extinction – Mass extinction is the likely outcome.

 

Sensory Deprivation Experiment / 48 Hours Isolation BBC Videos

All 5 short episodes will run automatically…

Five part BBC doc. of a 48 hour “sensory deprivation” experiment. I’m looking into “stimming” (self-stimulation) as a NORMAL reaction to finding a “proper” type and level of brain stimulation for individual humans.

Not humorous: I experienced these same “symptoms” when kept in a drug coma (due to a physical brain emergency) in a hospital for nearly two weeks, especially intense hallucinations, which often incorporated the people and activity going on around me in the hospital environment. I had assumed that the hallucinations were induced by the drugs, but after watching this experiment, I’m not sure. Was my intensely traumatic experience due at least in part to sensory deprivation? I was seriously “messed up” for months following the episode. I self-recovered by persistent exposure to – and trust in – everyday sense experience – but, the content of the hallucinations recur as intrusive memories. (There were many scenarios, locations and types of events, each having a specific “theme” – many historical and detailed and intensely lucid. It’s as if I lived several lifetimes within a “timeless” domain.) Is this lingering “recall” a PTSD-type experience? Not sure, because I don’t hallucinate the experiences, I just remember them very clearly and they are really unpleasant.

I actually think that watching the video relieves some of the “mystery” about the experience, and will help to defuse it! Give an Asperger a “concrete” explanation and much “healing” will occur.

The hospital staff did nothing regarding the after-math: refused to answer medical questions; offered no counseling, no explanation as to “what happens” in these circumstances of induced coma. There was no admission or recognition of these events at all! Another “bat-crap-crazy” neurotypical lack of empathy (and responsibility) that is so typical of the American medical industry. It’s the “black box” assumption that human beings have no “interior” reality.

But, it left me with personal insight as to what the brain is capable of doing under critical stress…and the extreme cruelty of subjecting human beings to solitary confinement as “punishment” for a variety of behaviors, whether criminal, political or social.

 

Wolf vs. Dog / Wild vs. Domestic Intelligence

Wolf uses “digging” instinct to “dig” – (displace) water. What’s notable is it’s persistence – dogs “give up” and manipulate a human to do things for them. (As do human children LOL) Which animal is more intelligent? The important observation is that each uses its intelligence in accord with “what works” in its particular environment. This applies also to humans.

Wolves are the wolf’s environment; humans are the domestic dog’s environment.

Fixation and persistence in the wild animal; fascinating contrast with domesticated (tame) behavior in dogs and humans. In humans, there is a range of behavior from wild predator to tame prey, also due to degree of domestication.

Stereotypic repetitive behaviors: Stimming / Environmental Causes

Why do psychologists ignore the facts? We are animals! What are Autistic (and typical) children trying to tell us about modern environments? That these environments are  STRESSFUL for children; humans evolved in stimulating NATURAL environments, not in restrictive, violent, emotionally barren and anxiety-driven social prisons.

If an animal is prevented from performing its “natural behaviors” it will invent abnormal compulsive behaviors to stimulate itself. Modern environments are ABNORMAL.