Defining Autism / The Unicorn Problem

Fantastically Wrong: The Weird, Kinda Perverted History of the Unicorn (Substitute Autism for Unicorn Myth in the following:)

If you’re looking to figure out how an ancient myth started to get out of hand, a good place to start is with the great Roman naturalist Pliny the Elder, whose epic encyclopedia Natural History stood largely as fact for some 1,600 years. Problem was, Pliny wasn’t the most incredulous of writers, and crammed his encyclopedia with pretty much any account he could get his hands on. Autism is born – Autism as we know it…1980- Autism was added to the Diagnostic and Statistical Manual of Mental Disorders- Third Edition (DSM-III) as “infantile autism”. This addition made it possible for doctors to accurately diagnose Autism and gave the ability to easily differentiate Autism from schizophrenia. 1987- “Autistic Disorder” replaced “Infantile Autism” in the manual and gave a more expansive explanation of the diagnosis. 1991- Schools begin to identity and serve students with Autism following the federal government decision to make Autism a special education category. ($$$$$)

The unicorn,” Pliny wrote, “is the fiercest animal, and it is said that it is impossible to capture one alive. It has the body of a horse, the head of a stag, the feet of an elephant, the tail of a boar, and a single black horn three feet long in the middle of its forehead. Its cry is a deep bellow.”

Note the ever-increasing list of Autism “symptoms” (behaviors) without any logical coherence, just like the growing fantasy around the unicorn. The list grows and grows more fabulous with each recounting of the mythical beast called Autism. 

‘Unicorns huh? You look more like a couple of party animals to me.’

The unicorn then shows up in various places in the Bible, at least according to some translations (it’s sometimes instead referred to as the oryx, a kind of antelope whose antlers were indeed sold as unicorn horns in medieval times, or as the auroch, a massive type of cattle that went extinct in the 17th century). Here, its fierceness is affirmed. In Numbers 24:8, for instance: “God brought him forth out of Egypt; he hath as it were the strength of an unicorn: he shall eat up the nations his enemies, and shall break their bones, and pierce them through with his arrows.”

In the 7th century, the scholar Isidore of Seville chimed in, noting that the unicorn “is very strong and pierces anything it attacks. It fights with elephants and kills them by wounding them in the belly.” He also helped popularize the myth that would serve as a hallmark in European folklore for centuries to come: Catching a unicorn is impossible…unless you have access to a virgin woman. “The unicorn is too strong to be caught by hunters,” he writes, “except by a trick: If a virgin girl is placed in front of a unicorn and she bares her breast to it, all of its fierceness will cease and it will lay its head on her bosom, and thus quieted is easily caught.” It’ll suckle until it’s lulled to sleep. So…yeah.

Note the “behavior-based” description of the unicorn – subjective, imaginary, wildly illogical, supernatural – not a “real” animal at all.  

…Not only was the natural history of the animal given, but each was then compared to a biblical figure. And the unicorn stood for Christ, since he was captured and put to death like the unicorn is done in by the virgin (though pretty much every other animal was also compared to Christ, even the pelican, which was said to peck at its own breast to revive its young with blood, like Jesus shed his own blood for us).

Thus the unicorn became firmly implanted in  European lore. And Autism in American Psychology lore. What followed was a full-blown mania for their horns, which were said to detect poison if you stirred them around in your food or drink. They went for tens of thousands of dollars in today’s money, and were particularly popular among paranoid royalty. More industrious users who didn’t want to wait around to have their food poisoned would grind up the horns—usually those of the oryx or narwal (whose horn is actually a giant tooth)—to gain immunity from toxins.

Over in the East, royalty had a rather more complicated relationship with their version of the unicorn, the aforementioned kirin, or qilin. Its appearance was said to foretell the birth of a royal baby, which is nice of it, but can also predict an imminent death, which is not so nice. In the 15th century, a giraffe was brought to China for the first time and presented to the emperor as a kirin, which was a gutsy move considering its proclivities for letting royalty know they’re going to die soon. The emperor, though, dismissed it as a fraud and went on to live another 10 years. Does a giraffe look anything like the mythical unicorn? And yet … maybe it does! Who knows? But unicorns must surely exist? 

No one seems to notice throughout this sad charade, that just like the unicorn, the mythical beast called Autism, does not require proof of its existence. No such animal called the unicorn was ever shown to be real; nothing more than a barrage of  anecdotal reports, subjective opinions and imaginary conclusions have ever been  presented by psychologists.   

A Myth Is Born / “Autism, 1994”

The myth of the unicorn may have come from sightings of antelope and such ungulates with only one horn, having either been born with the defect or lost the horn when scrapping with a predator or one of its own kind. Less likely still is seeing a normal antelope from afar in profile, since that would only last as long as the animal didn’t move.

Reality is of no importance; social typical inattentional blindness conveniently “denies” any physical evidence that is contrary to social dogma.  

A far more likely culprit is the Indian rhinoceros, and clues for this are sprinkled throughout the early accounts—indeed, the unicorn is sometimes referred to as the Indian ass. Pliny, for instance, mentions that the unicorn has “the feet of an elephant,” a rhino’s feet in fact being not hooved like a horse’s, but fleshy like an elephant’s. He also notes that it has “the tail of a boar,” much like a rhino’s, “and a single black horn three feet long in the middle of its forehead.” Writers would only later describe the horn as white. Evidence? What evidence? Neurotypicals can look a rhinoceros in the face and call it a moose. If authorities say it is a duck, they will then call it a duck – or an Autistic duck.   

The ancient Greeks and Romans, you see, had been making forays into India and bringing back tales of the strange beasts there, and the facts tended to get a bit…lost. Cotton, for instance, was said to grow in India as an actual lamb that sprouted from the ground, just hanging there patiently producing cotton. And while Pliny actually did a pretty good job of describing the rhino, his popularization of the “unicorn” picked up more and more improbabilities as the centuries wore on. We also know that the ancient Chinese had contact with rhinos from art made out of their horns, so the animal could well have also inspired the kirin.



The tragedy of this story is that people who ought to know better – medical doctors, geneticists, and neuroscientists, have “bought” the myth of Autism as a “thing” in itself, when it is merely a collection of symptoms due to real and specific and different causes.

Symptoms can be as “supernatural” as a brain that “lights up wrong” – or social difficulties judged to “be annoying” by self-centered adults; parents, teachers and Puritanical psychologists who demand obedience. Who enforce an unsuccessful social behavior regime specific to “certain Americans” but which is alien to many “diverse” groups, cultures and child-raising traditions. Kids are being declared “defective” by opinionated psychologists and miscellaneous imperious adults on the basis of utterly subjective criteria.

Autism is not a “disease, mental illness, or even a MEDICAL DIAGNOSIS. It is a grab bag of social behavior that is rejected by psychologists and proclaimed to be “defective”. It has become fear-induced hysteria in the U.S. 

Autism Spectrum Disorder  / DSM 5 299.00 (F84.0)

Diagnostic Criteria (What a joke!)

A.      Persistent deficits in social communication and social interaction across multiple contexts, as manifested by the following, currently or by history (examples are illustrative, not exhaustive, see text): This is utterly subjective; depends on the “opinion” of the person doing the “reporting” – hearsay evidence; not admissible in a court of law, but “good enough” for labeling a child as defective. No standards for comparison are provided: “behaviors” are not-quantifiable; those listed vary wildly from family to family and culture to culture. 

1.       Deficits in social-emotional reciprocity, ranging, for example, from abnormal social approach and failure of normal back-and-forth conversation; to reduced sharing of interests, emotions, or affect; to failure to initiate or respond to social interactions.Abnormal and reduced compared to what “standard”? There are no objective criteria in these judgements. None of these blah, blah, blah criteria are even testable!

2.       Deficits in nonverbal communicative behaviors used for social interaction, ranging, for example, from poorly integrated verbal and nonverbal communication; to abnormalities in eye contact and body language or deficits in understanding and use of gestures; to a total lack of facial expressions and nonverbal communication. So vague, arbitrary and subjective as to be ridiculous. Where are the objective standards and “proof” that the vast majority of human children conform to these “undefined but absolutist” subjective interpretations of behavior? Where is the proof that any two people observing a child, will even agree with each other that these observations are factual? No “facts” are allowed!

3.       Deficits in developing, maintaining, and understanding relationships, ranging, for example, from difficulties adjusting behavior to suit various social contexts; to difficulties in sharing imaginative play or in making friends; to absence of interest in peers. WOW! This paragraph is so general that it could apply to any generic human being alive on planet earth.

Specify current severity:

Severity is based on social communication impairments and restricted repetitive patterns of behavior (see Table 2).

B.      Restricted, repetitive patterns of behavior, interests, or activities, as manifested by at least two of the following, currently or by history (examples are illustrative, not exhaustive; see text):

Any child could be diagnosed as autistic using this “potpourri” of “socially objectionable” activities!

1.       Stereotyped or repetitive motor movements, use of objects, or speech (e.g., simple motor stereotypies, lining up toys or flipping objects, echolalia, idiosyncratic phrases). If you throw enough non-related behaviors at a wall, and this is quite a mix of motor, language, organizational, speech and cognitive behaviors!, then one will likely “stick”. 

2.       Insistence on sameness, inflexible adherence to routines, or ritualized patterns or verbal nonverbal behavior (e.g., extreme distress at small changes, difficulties with transitions, rigid thinking patterns, greeting rituals, need to take same route or eat food every day). Describes half the people in any office environment every day; and 100% of humans at some point, depending on “what kind of day” they are experiencing. 

3.       Highly restricted, fixated interests that are abnormal in intensity or focus (e.g, strong attachment to or preoccupation with unusual objects, excessively circumscribed or perseverative interest). Such as obsessions that “normal kids” display: playing video games, constant social media monitoring, texting, uploading selfies, extremely limited self-image conformity, incessant talking, cruelty to other children, foul language, and mutual verbal abuse – but these are “not unusual” and therefore acceptable. But that child who likes to arrange toys by size and color? A threat to the social order…

4.       Hyper- or hyporeactivity to sensory input or unusual interests in sensory aspects of the environment (e.g., apparent indifference to pain/temperature, adverse response to specific sounds or textures, excessive smelling or touching of objects, visual fascination with lights or movement). Any reactions to the environment other than those displayed by a “perfect child” (a being as mythical as the Unicorn), are pathological. The perfect child notices nothing in the environment, even if it is dangerous, toxic or extraordinarily beautiful. No personal preferences are allowed. 

Specify current severity:

Severity is based on social communication impairments and restricted, repetitive patterns of behavior (see Table 2).

C.      Symptoms must be present in the early developmental period (but may not become fully manifest until social demands exceed limited capacities, or may be masked by learned strategies in later life). How non-specific! Anywhere, anytime, any behavior, observable or not – pathological. 

D.      Symptoms cause clinically significant impairment in social, occupational, or other important areas of current functioning. What constitutes clinically significant? Your clinic, or mine? The gym teacher’s or school counselor’s office? The BA in psychology who “does” therapy? Anyone and everyone is “diagnosing” Autism today. 

E.       These disturbances are not better explained by intellectual disability (intellectual developmental disorder) or global developmental delay. Intellectual disability and autism spectrum disorder frequently co-occur WOW! How lame: Autism “symptoms” are the RESULT of specific disabilities due to birth defects, premature birth, emotional and physical trauma, injury or disease, rare genetic conditions and myriad unknown “causes” – including the fact that human beings are not identical “clones” of imaginary supernatural “templates” but individuals with a range of personalities and temperaments AND BRAIN ORGANIZATION; to make comorbid diagnoses of autism spectrum disorder and intellectual disability, social communication should be below that expected for general developmental level. Who sets the standards and parameters for “judging” and “rating” childhood behavior? Just who are these people? No one asks; neurotypicals accept social authority as being reliable in the same way that the Laws of Physics are reliable.  

Note: Individuals with a well-established DSM-IV diagnosis of autistic disorder, Asperger’s disorder, or pervasive developmental disorder not otherwise specified should be given the diagnosis of autism spectrum disorder. Individuals who have marked deficits in social communication, but whose symptoms do not otherwise meet criteria for autism spectrum disorder, should be evaluated for social (pragmatic) communication disorder. Wow! Nothing like throwing you own previous diagnostic criteria under the bus! Why should anyone trust the existence of Autism to start with?

Specify if:
With or without accompanying intellectual impairment
With or without accompanying language impairment
Associated with a known medical or genetic condition (which is the ACTUAL PROBLEM) or environmental factor
(Coding note: Use additional code to identify the associated medical or genetic condition.)
Associated with another neurodevelopmental, mental, or behavioral disorder
(Coding note: Use additional code[s] to identify the associated neurodevelopmental, mental, or behavioral disorder[s].)
With catatonia (refer to the criteria for catatonia associated with another mental disorder, pp. 119-120, for definition) (Coding note: Use additional code 293.89 [F06.1] catatonia associated with autism spectrum disorder to indicate the presence of the comorbid catatonia.)

Codes – this Autism Diagnosis charade is driven by insurance reimbursement: it the CODE that matters, not the accuracy of the diagnosis.  

“Autism” is a selective symptom-based system for socially pathologizing and isolating children who suffer from a range of effects previously known as “mental retardation” – conditions caused by real physical impairments.
Today, Autism has grown to be a highly profitable industry, by sweeping inclusion of non-medical, non-scientific labeling of children who are not “retarded” but “socially unacceptable” using vague and subjective opinions dictated by overblown psychological dogma, which is “prescriptive” in origin and structure. It is a “super-fraud” that destroys families and dooms children to a lifetime of social “subhuman” status. And prevents effective provisions for real treatment for real problems experienced by real people.   

Table 2  Severity levels for autism spectrum disorder “The Table of Social Doom”

Severity level Restricted, repetitive behaviors
Level 3
“Requiring very substantial support”
Severe deficits in verbal and nonverbal social communication skills cause severe impairments in functioning, very limited initiation of social interactions, and minimal response to social overtures from others. For example, a person with few words of intelligible speech who rarely initiates interaction and, when he or she does, makes unusual approaches to meet needs only and responds to only very direct social approaches
Inflexibility of behavior, extreme difficulty coping with change, or other restricted/repetitive behaviors markedly interfere with functioning in all spheres. Great distress/difficulty changing focus or action.
Level 2
“Requiring substantial support”
Marked deficits in verbal and nonverbal social communication skills; social impairments apparent even with supports in place; limited initiation of social interactions; and reduced or  abnormal responses to social overtures from others. For example, a person who speaks simple sentences, whose interaction is limited  to narrow special interests, and how has markedly odd nonverbal communication.
Inflexibility of behavior, difficulty coping with change, or other restricted/repetitive behaviors appear frequently enough to be obvious to the casual observer and interfere with functioning in  a variety of contexts. Distress and/or difficulty changing focus or action.
Level 1
“Requiring support”
Without supports in place, deficits in social communication cause noticeable impairments. Difficulty initiating social interactions, and clear examples of atypical or unsuccessful response to social overtures of others. May appear to have decreased interest in social interactions. For example, a person who is able to speak in full sentences and engages in communication but whose to- and-fro conversation with others fails, and whose attempts to make friends are odd and typically unsuccessful.
Inflexibility of behavior causes significant interference with functioning in one or more contexts. Difficulty switching between activities. Problems of organization and planning hamper independence.

John Hawks on Y chromosome genes / Human Chimp Surprise!

john hawks weblog

Unbelievable Y chromosome differences between humans and chimpanzees

Holy crap!

Indeed, at 6 million years of separation, the difference in MSY gene content in chimpanzee and human is more comparable to the difference in autosomal gene content in chicken and human, at 310 million years of separation.

So much for 98 percent. Let me just repeat part of that: humans and chimpanzees, “comparable to the difference … in chicken and human”.

This is from a new paper that’s just shown up in the Nature advance publication zone. The authors are Jennifer Hughes and colleagues, and the subject is the first complete sequencing of the chimpanzee Y chromosome. “MSY” stands for “male-specific region of the Y chromosome” – it’s most of the Y, aside from a small fraction that recombines with the X chromosome.

The Y chromosome was part of the initial chimpanzee genome draft, and was recognized then as a “clear outlier” in showing low human-chimpanzee sequence similarity (Chimpanzee Genome Consortium 2005). But it wasn’t obvious just how different it was because the relatively short sequencing reads aligned fairly well with the human draft. That comparison also seems not to have included the missing genes (they might have just been missed during sequencing), or duplications. Moreover, the Y chromosome includes a high fraction of repetitive sequence, including long front-to-back, or “palindromic” passages. Only with very long reads with long overlaps is it possible to straighten out the large-scale sequence, and thereby detect sequence reorganizations and large copy number variants. This kind of intensive sequencing has so far been completed only for chromosome 21 and now the Y chromosome.

I can’t believe how sedated the reaction to this paper has been so far. The outcome of the sequencing is really, really weird. More than thirty percent of the chimpanzee Y chromosome has no homolog in humans, and likewise for the human Y in chimpanzees.

I mean, really – here’s a map:

Chimpanzee compared to human Y chromosome

Just glancing at the ideograms, they don’t even look like homologous chromosomes!

Obviously they are; there’s a whole lot of homologous sequence in there including functional genes. But the structure of both human and chimpanzee Y chromosomes has evolved incredibly fast compared to the rest of the genome.

The central question: beyond its interest for Y chromosome structural evolution, what does this result say about the evolution of human (and chimpanzee) phenotypes?

Option 1: Maybe nothing. The main mechanism for the rapid structural evolution was probably autologous recombination. Imagine that the Y chromosome wriggles around and different copies of repetitive sequences get together with each other.

The molecular mechanisms that enabled this wholesale remodelling of ampliconic regions merit consideration. Although the chimpanzee and human MSYs do not normally participate in meiotic exchange with a partner chromosome, the mirroring of sequences in the ampliconic regions provides ample opportunity for ectopic homologous recombination within the MSY. This recombinational proclivity is well documented in the human MSY, where it has repeatedly given rise to large-scale structural polymorphisms during the past 100,000 years of human history as well as to Y-chromosomal anomalies that cause spermatogenic failure and sex reversal in current generations. We suggest that ectopic homologous recombination between MSY amplicons has similarly accelerated structural remodelling of the MSY in the chimpanzee and human lineages during the past 6 million years.

That leads to rapid structural evolution, but not necessarily any functional changes.

Option 2: Massive changes in gene regulation. Then again, widespread relocations of genes have a way of stripping them apart from upstream (or downstream) elements that may regulate their expression. Besides that, chimpanzees have lost several genes entirely, while humans have picked up a few that weren’t in the common ancestor. So there’s a potential for phenotypic evolution from these changes, possibly reverberating through the genome.

In aggregate, the consequence of gene loss and gain in the chimpanzee and human lineages, respectively, is that the chimpanzee MSY contains only two-thirds as many distinct genes or gene families as the human MSY, and only half as many protein-coding transcription units.

That’s pretty amazing. They speculate that the most important phenotypic correlates of these genetic changes may be related to sperm or testicular function, which certainly is a target of rapid evolution elsewhere in the chimpanzee and human genomes.

Option 3: Hitchhiking. OK, this isn’t different or mutually exclusive from the above, but it’s worth remembering that it only takes a single advantageous mutation to fix the entire Y chromosome in the population. That event carries with it whatever strange mutations might be on the same copy as the initial advantageous change. This kind of event may have happened dozens or even hundreds of times on the chimpanzee and human lineages. Indeed, if it was common enough, hitchhiking can drive its own dynamic, since it tends to fix lots of slightly deleterious variations that later have to be repaired or accommodated.

An interesting possibility: Maybe the extreme evolution of the Y chromosome in the emerging human and chimpanzee lineages explains the unusual similarity of their X chromosomes.

I’m thinking back to the story about chumans and the divergence of chimpanzee and human lineages (“The dawn chumans”). Patterson and colleagues (2006) suggested that the two lineages had undergone some kind of hybridization event long after they began to diverge. This surprising hypothesis was meant to explain why the X chromosome shows a substantially lower level of genetic difference between humans and chimpanzees, compared to the average autosomal locus. I don’t think that a late hybridization is necessary to account for X chromosome similarity. A large ancestral effective population size implies a wide variance in coalescence times in the ancestral population; the average on the X will be lower than the autosomes, and if there was any hitchhiking the X would be lower still.

But…that X chromosome similarity might have a different explanation. A fraction of the human Y chromosome continues to recombine with the X. Imagine an initially rapid divergence of Y chromosomes within the chuman population. For a while, there might have been a strong selection pressure on the ancestral X to equip it for the structural diversity of the Y. Possibly an inverse relation would have emerged: the as the Y becomes variable (possibly in partially isolated subpopulations), the X adapts to that variation until reproductive isolation finally occurs.

Could this have been the proximate cause of human-chimpanzee reproductive isolation? The sex chromosomes are often implicated in speciation through Haldane’s rule. It’s a bit of speculation, but not too far from some discussion within the paper, particularly the relation between Y chromosome variations and infertility.


Hughes JF and 16 others. 2010. Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content. Nature (early online) doi:10.1038/nature08700

Evolution of the Y Chromosome


How did the human Y chromosome become so small relative to its X counterpart? 

Animation: To watch a truly fascinating video, click “Launch this resource” in box at top of article.

This animation depicts the 300-million-year odyssey of the sex chromosomes that began when the proto X and Y were an identical pair. Over time, structural changes in the Y chromosome resulted in its current form, which is specialized to trigger male development. The evolutionary timescale is represented by positioning the chromosomal remodeling events along an abbreviated vertebrate cladogram, a chart of evolutionary relationships.

Part 1. Sex chromosomes originated as autosomes

The sex chromosomes began as an ordinary pair of autosomes. During meiosis. chromosomes replicate their DNA, pair, and exchange genes (recombination; red lines). A mutation in the SOX3 gene produced the SRY gene, a critical determinant of maleness, on the proto Y. While the functions of SRY and SOX3 became very different over time, another gene, RPS4, retained a similar function on both the X and Y chromosomes.

Part 2. Inversions restrict recombination between the X and the Y chromosome

Inversions, which are internal recombination events, caused a rearrangement of genes on the Y chromosome. These rearrangements meant that large portions of the X and Y chromosome no longer recombined, which made the Y chromosome susceptible to deletions, and it decreased in size.

Part 3. Comparison of sex-chromosome recombination in males and females

After our lineage diverged from the ancestors of the monotremes, such as the duck-billed platypus, another inversion further scrambled the genes on the proto Y. In males, only the tips of the Y chromosome were left able to recombine with homologous genes on the X chromosome. In contrast, in females, recombination continued to occur across the full length of the two identical X chromosomes.

Part 4. Autosomal expansion of X and Y chromosomes

About 130 million years ago (Ma), an autosome donated a block of genes that extended the length of both the X and the Y chromosome. The X and Y were able to recombine in these expanded regions of the chromosomes. Subsequently, inversions rearranged the order of genes on the Y chromosome. Additional rearrangements occured almost exclusively on the Y. Without recombination to preserve its integrity, the Y continued to lose genes and, over time, shrank.

Part 5. An autosome contributed a copy of the DAZ spermatogenesis gene to the Y chromosome

Sometime after squirrel monkeys diverged from the primates that evolved into humans, an autosome contributed a copy of the DAZ spermatogenesis gene to the Y chromosome. The DAZ gene was copied and copied again and now the modern Y chromosome contains four identical DAZ gene sequences. The modern Y chromosome is about one-third the size of its X-chromosome partner.

Sperm and Healthy Fetus Production / Not just “magic bullets”

How Men’s Sperm Can (Does) Affect Pregnancy

Transcript from: / University of Utah Health Sciences Radio.

My comments in green 

In the past 20 years, we’ve been learning about changes to genes that happen very early in development, very early. As early as the first week after fertilization of the human egg. Before a woman even knows that she’s pregnant, the environment that the developing embryo sees turns genes on, or off, or modifies the way they work. This continues through pregnancy and early childhood development and it’s a process that’s called epigenetic. It means that the genes of the developing baby and child are not changed in their basic DNA, but the way the genes work.

How awkward; the embryo doesn’t “see” anything – it’s a part of the woman’s body, not a “separate” living entity. This may seem minor, but all the stressful (idiotic) arguments over the ‘facts’ of human reproduction, that is, the neurotypical version, remain mythological. Basically: babies, or at least their “human substance, content or souls” are “gifts” from God.  

God says to the man, “Good job! You weren’t shooting blanks. You can now leave the room.”

Part of the NT debate is over timing – When exactly does God insert the “magic part of the new human” into the woman’s body? At “conception” (it’s in the sperm and delivered to the egg), or at some other “magical” moment in the pregnancy, and what happens to the “magic part” if the pregnancy fails? Well, it’s the woman’s fault, of course!

transcript cont., How they are transcribed to make proteins, that’s how they’re working, and that’s changed. But we always thought that men just provided genetic material with sperm. A sperm was a sperm, and all it did was deliver a man’s DNA to the egg. Now, in research that has been building up over the past several years, we are beginning to see the genes encoded in sperm can be modified by the environment in which they were developing, meaning, in the guy. And those modifications may affect the developing child.

So let’s start with mice. (Of course) In 2013, in the “Journal of Neuroscience,” researchers reported that stressed mouse dads (this cute label makes it seem that mouse “test results” apply to human males) had changes in their sperm and their offspring had abnormal stress responses when compared to offspring of non-stressed mouse dads. It takes about 42 days to make a mouse sperm. During that time, the researchers exposed the mouse dads to (experience) be in one stressful thing each day. The smell of foxes, wet bedding, restriction in a tube for 15 minutes, new noises, that kind of stressful stuff. The sperm from the stressed mouse dads had the same DNA as the non-stressed dads, but the way the DNA was processed (?) was different. And the mouse babies had abnormal stress responses as adult mice.

Well, what about human dads-to-be? The cord blood of babies (whose fathers were obese) of obese men was studied and they had changes in the way one of the genes that controls growth and calorie use was regulated. These changes were seen less in babies of normal weight men. These changes are associated with a tendency toward obesity in adulthood. Now, here’s the cool part, this year researchers published a study of the sperm of obese men before and after they had weight loss surgery. They found different epigenetic patterns in the sperm in the men before they lost weight, compared to after they lost weight. Losing weight made a difference in the epigenetic programming of the sperm.

This research sounds more than a bit misleading, given the current trend in American “science” for low number of sample subjects in studies (these are not scientific experiments); reliance on non-proven assumptions to “point the way” of study direction – and conclusions; that “beliefs” are a substitute for unbiased hypothesis;  and the “unconscious” intrusion of magical thinking, as evident in the “before-and-after” false advertising so popular in American media, aided and abetted by “weasel words” that purposefully “lead on” non-logical thinkers to false conclusions. The focus on weight-loss surgery, which is a massively profitable industry that benefits directly from the “positive outcome” of the study, is blatant propaganda.

The sad effect is that real concern for “dad’s health and contribution” to healthy babies and children, is as usual, mixed up with unwarranted conclusions presented as “earth-shaking” new information gleaned from minimally productive studies; results that are immediately distorted toward profitable “new arenas” of diagnosis, medical intervention, treatments, drug development, and “solutions” being promoted in the U.S. mass market. “Studies” have become industry-funded staging platforms for “problems that must be solved by profit-seeking entities; corporations and the massive numbers of their “employees” that facilitate profit.

transcript cont., So what do we think we know? We know that we don’t know about how large the effect of stress and obesity in a dad is on the baby and growing child and adult. We do know that there’s evidence (but of what quality in correspondence to reality?) that a man’s environment and behavior can change his sperm, and in the case of the mouse dad, not for the good of the mouse baby.

So what should we do? We should tell men that are thinking of making a baby the same things we tell women. Clean up your act, eat well, maintain a healthy weight, try to manage your stress and response to stress. Consider yourself an equal partner in the health of your future child, literally. It takes 90 days to make a sperm so let’s get cracking, plan ahead, it’ll be good for you anyway, and thanks for joining us on The Scope. (“Puritan-lite” instruction…) You guys can now leave the room. 

Thanks coach, we’ll work on that! (NOT!)

Announcer: is University of Utah Health Sciences Radio. If you like what you heard, be sure to get our latest content by following us on Facebook. Just click in the Facebook icon at

Caveat: This is the University of Utah, and nothing in Utah is not touched by Mormonism. Mormonism is highly magical in it’s foundational belief system, and there’s is simply no possibility that this underlying thinking is “magically turned off” within the Health Sciences division, even if individual employees have nonMormon personal histories and “science” loyalties. 

The overriding “goal” (as a radical branch of the Puritans who founded “America”) for Mormons today is business success = massive profits=expansion of the Mormon Empire, “funded by” the very modern pursuits of medicine and high-tech research and development. We need to recognize their commitment to these fields, but also to be wary of the “messages” being attached to their applications in “the real world” – which defend and promote the social status quo of control by elites over American thought and policy – these “elites” have always been dominated by religious groups.

Oh Look! It’s a USB sperm drive! 

Female Aspergers are often described as “Chameleon-like” in the propensity to take on the psychic and behavioral aspects of a social environment in order to (at least temporarily) hide in plain sight. This supposedly accounts for the common undiagnosed-state of female Aspies.

This is a gross misunderstanding of what Chameleons actually “do.”

Male Chameleons change to bright colors (red-yellow) to stand out against a natural green-brown environment. They are “showing off” in a mating display or other communication.

This obviously is not a correct analogy to the real or imaginary attempt by some female Aspergers to blend into the social scene.

Camouflage in it’s active form in Homo sapiens is a male specialty.


Modern humans have developed camouflage predominantly as a predatory strategy in military actions or in hunting. A vast (and extremely serious) subculture exists that promotes and supplies camo gear for use by civilians and professionals. Business is booming!

Camouflage has become a cult fashion bonanza: Pepto-Pink is mandatory for girls, which defeats the function of camouflage, unless one is trapped in the Pink Hell of American female fashion.  

So what are Asperger females doing to survive Neurotypical Social Hell?

(Do you really think that we would tell anyone?)




Chameleons, Camouflage and Selfies / Revised

Links to More Posts on American “Justice”

Criminal Justice System Flow Chart / Totally Bizarre

Is there any doubt as to why “justice” is a perverted concept in the U.S.? It’s a nightmare system in which “what is good for human beings” has been abandoned as a foundational idea that must direct social policy and governance.  

It does not matter what “psychiatrists” or “psychologists” claim about definitions of crime; what average people think about crime, what local communities want to do about crime, where resources are allotted in the perpetual Wars on Crime, what the “facts” reveal about crime, what “criminals” actually do, what “victims” experience, and what responses to crime are actually fair and effective.

It is, in fact, a highly subjective and predatory system, in which designated individuals within the Byzantine labyrinth are granted the power to dictate outcomes for criminals, victims and communities. for access to readable chart

Criminal Justice System Flowchart / The diagram below illustrates the sequence of events in the criminal justice system. To link to a text description of each section, click on any part of that section of the diagram or return to the Justice System page.




Psychiatry DSM 5 / Rape is a Crime not Mental Disorder

From Psychiatric Times

DSM-5 Confirms That Rape Is Crime, Not Mental Disorder

Blog | February 21, 2013 | On DSM-5, DSM-5, Forensic Psychiatry, Sexual Offenses

By Allen Frances, MD

DSM-5 has considered—and has roundly rejected—two proposed diagnoses that are frequently misused to justify involuntary psychiatric commitment under sexually violent predator (SVP) statutes. Not only were “Coercive Paraphilia” and “Hebephilia” denied status as official diagnoses, they were not even given a face saving place in the usually inviting DSM Appendix. This constitutes a total and unequivocal American Psychiatric Association (APA) rejection of these pseudo-diagnoses and compellingly confirms that they have no credibility in courtroom testimony.

Hopefully, the APA decisions will help clarify and correct a shameful travesty at the difficult interface between psychiatry and the law.

Sex offenders who have completed their prison sentences are now often detained (usually for life) in prison-like psychiatric facilities based on the completely mistaken assumption that their having committed sexual crimes somehow means they are also mentally ill. The action taken by DSM-5 has blown this argument completely out of the water. Diagnosing rape as mental disorder is an improper use of psychiatric diagnosis and promotes the abuse of psychiatric commitment to further what would otherwise be an unconstitutional form of preventive detention.

The proposal to create a mental disorder diagnosis for rapists has been raised and unequivocally rejected 5 times in the past 35 years—in 1976 for DSM-III; in 1986 for DSM-IIIR; in the early 1990’s for DSM-1V; in 1998 for an APA Task Force report; and now for DSM-5.

These repeated repudiations haven’t prevented poorly trained psychologists testifying as alleged experts in SVP cases from inventing the fake diagnosis—“Paraphilia Not Otherwise Specified, Nonconsent”—and using it as an excuse to justify what are in fact unjustifiable psychiatric commitments in SVP cases.

Displaying a surprising ignorance of (and careless indifference to) proper diagnostic practice, these psychologists routinely and rotely misdiagnose mental disorder in rapists who are in fact clearly no more than simple criminals. They repeatedly state as misguided (in) expert testimony that committing rape is by itself an indication of psychiatric illness.

These pseudoexperts are not dissuaded by the facts: that rape as mental disorder has been rejected by all the DSM’s and is almost universally opposed by the experts in forensics and in sexual disorders; that there is almost no scientific support for their pariah diagnosis of Paraphilia NOS, nonconsent; and that NOS diagnosis is inherently unreliable and can therefore never be taken seriously as expert forensic testimony.

I have reviewed “expert” reports and testimony in 39 SVP cases. In only 3 of these cases might the rapist’s behavior conceivably suggest some sort of unspecified form of paraphilia—and this could not be diagnosed even by me with the degree of reliability required in forensic testimony. All of the other offenders were straight out simple criminals—none of these represented a close judgment call. The hundreds of sloppy reports submitted by the misguided psychologists blithely misdiagnosed “Paraphilia Not Otherwise Specified, Nonconsent” without ever providing any evidence or rationale for their casual equating of criminal behavior with mental disorder.

Fortunately, the Department of Mental Health in California has taken active and effective steps to reform this bad diagnostic practice and to require more careful diagnosis and proper documentation of evidence and rationale. This has resulted in the dropping of weaker cases and a clearer to juries. Overall, more cases are now decided on merit rather than misinformation.

But a great deal more remains to be done to ensure that psychiatric diagnosis is not misused in SVP cases. Some evaluators still cling stubbornly to their idiosyncratic and discredited diagnostic practices. Let’s hope that they are weeded out and that other states follow California’s lead toward achieving much better quality control over errant evaluators.

I have absolutely no sympathy for rapists and believe they deserve longer sentences and less opportunity for quick parole than many have received—especially in the past. But I do have great concern when fake psychiatric diagnosis and unjustified involuntary commitment are misused to violate anyone’s civil rights—even a rapist’s.

The constitution says that when criminals do their time, they have the right to be released from prison. Making up a fake diagnosis to facilitate otherwise unconstitutional preventive detention is a clear violation of the individual’s civil rights and creates a very slippery and dangerous slope for our society. Unjustified psychiatric preventive detention was a convenient tool of political repression in the former Soviet Union and is reportedly also used today to quell economic complaints in China.
Protecting the constitutional rights of rapists who have served their sentences is not just a matter of fairness to them—it is necessary to protect the integrity of the judicial system and the rights of all the rest of us.

On another note, DSM-5 has also totally rejected “Hypersexuality” and “Sex Addiction” as diagnostic concepts. They are repudiated as official diagnoses and were given no place in the DSM-5 Appendix. These fake diagnoses also have no place in courtroom proceedings.

WELL! That’s strong language, and actually backs up my ongoing criticism of psychology as not scientifically valid, and that its pervasive influence in American culture is dangerous and destructive to human health, especially “behavioral / mental health” which the industry purports to “define and enforce” with religious-absolutist  authority.

This article also opens up critical questions too numerous and important to “dissect” without oodles more coffee and “unconscious percolation” with which this Asperger strives to connect myriad threads of experience and investigation around the dense topic: sexual behavior in social humans. 

AND – how rape and sex are presented by the entertainment industry…

Human Colonization / Living where we don’t belong Re-Post

There is nothing like a string of subzero days and nights to awaken the mind to hard core truth. (This morning it’s an overnight freeze and light snow) Humans are still tropical animals, molded by evolution for life within a consistent and moderate temperature range, under sunny nourishing skies, equipped for a life shaped by ease and plenty. A perpetual cheese and wine party punctuated by afternoon naps, walks along  sea shore, collecting “low tide stuff” for lunch, followed by craft time making dance costumes for all those oodles of festivals and rituals. Naked fun! Art! Music! Jewelry!

We draw smoothly curving lines of human dispersal ‘out of Africa,’ as if any wandering group of humans that strayed far enough north to encounter heavy snow, iced-over rivers and lakes, long periods of darkness, and instant death by freezing, looked upon the land and unanimously declared: “We like this! Let’s stick around.”

Every one of them would have promptly died of hypothermia and / or starvation. Homo erectus apparently ran up against a climate barrier and kept to a southern arc across Asia and into the SE Asian Archipelago and Southern Europe. Other than a few Neanderthals, no one moved permanently beyond southern Europe and the Middle East into subarctic areas, unless it was an act of seasonal nomadism or during interludes of warming climate.

An interesting geological proposition for migration of Homo erectus.

“the East African Rift and extreme Southeast Asia are endpoints on a grand east-west geotectonic pathway called the Tethys corridor (fig.1). During a rather brief period called the Olduvai subchron (1.98-1.79 mya), the Tethys corridor was extremely unstable. Homo erectus and companion mammals took advantage of open linear landscapes to migrate north from the Rift to the Caucasus, and then both ways across the Tethys corridor – west toward Gibraltar, east to the Himalayan fore slope, and then far east to current Java. By the end of the Olduvai subchron, Homo erectus had dispersed throughout the greater Tethys realm. See:

Neanderthal: general extent of occupation.

Neanderthal: general extent of occupation.





Humans who wanted to migrate into hostile country had to be prepared first; had to have control of fire and rudimentary technology.

Thousands of migrants in the 1800s died when trying to cross the western deserts and mountain ranges of the United States because they were totally unprepared and ignorant of the endurance the trip would demand. The colonization of Arizona, Nevada, and much of California,  dates to the recent invention of air-conditioning and massive water diversion – collection schemes. This “invasion” is proving to be a disaster – literally)

There had to have been much seasonal migration on the part of archaic humans to northern lands, with return trips, both temporary and permanent, to warm climates, before settlement outside the evolutionary comfort zone could take place. Let’s face it; without fire, food preservation, tools and warm clothing, humans could not have broken the climate barrier.

Modern humans face the same situation. Our bodies have only superficially adapted to life outside the tropics. Colonization of cold mountain climates (and desert, and arid plains) has only been possible by means of technology and animal domestication. Fire, clothing and primitive food preservation and storage may seem alien to us, but the refrigerator in my kitchen keeps food from freezing as well as rotting, and the heater that sits in my living room is little more than a campfire fueled by natural gas. Bundled into a cocoon of parka, hat, gloves and insulated boots, I’m like an astronaut leaving his or her spacecraft to enter utterly hostile conditions when I leave my house during our unlivable winters.

The steep (and untenable) rise in world population is the product of fossil fuels.

I began thinking about this yesterday when I looked out a kitchen window and saw a tiny woodpecker banging away at one of the trees. It looked so vulnerable and lost – as if it should have migrated south with most other birds that summer here. But then I realized, it’s ‘out there’ in sub zero weather and I’m essentially stuck in my artificial environment, in my life support system. And I thought of the deer, pronghorn, elk and moose, of the wild horses scraping the snow for dried grass, of the intense stinging cold that comes at night, which would freeze a human solid as a rock if he or she made a simple mistake and could not get back to ‘civilization’ – which in Wyoming isn’t much, but our human outposts provide what is necessary: warmth and food.

The bad news is that humans today exist in artificial, depleted, or hostile environments, and exist on the chain of energy and products, including medicine, food and “processed” water, heating and air conditioning, and transportation, all conveniences that are derived from fossil fuels.

While arguments about climate change go nowhere, we can see that the discussion has become irrelevant. Our fossil fuel technology has built a house of cards that a mere puff of chance will topple.

Chart of Neanderthal / Denisovan DNA in modern Humans

For article, go to:

“In some spots of our genome, we are more Neanderthal than human,” (what an unfortunate choice of words) said Joshua Akey, a geneticist at the University of Washington. “It seems pretty clear that at least some of the sequences we inherited from archaic hominins were adaptive, that they helped us survive and reproduce.”

“What allowed us to survive came from other species,” said Rasmus Nielsen, an evolutionary biologist at the University of California, Berkeley. “It’s not just noise, it’s a very important substantial part of who we are.”

Which raises the question, Were Neanderthal and Denisovan people actually members of “other species”? Had there been enough time, geographic isolation and adaptation to different geographic, geologic and climatological conditions, to actually result in these Archaic Homo being distinct species from African (warm climate) Homo (and vice versa) ? (The relationship may have been comparable to Polar Bear – Grizzly Bear as different versions of the same species, with distribution determined by climate.)

The Archaic Homo sapiens who left Africa, were not modern social humans, that is, as persistently claimed by modern biased researchers, exactly like us. Far from it!  

We would likely find them to be all but indistinguishable from their contemporary Neanderthal neighbors! 

It is possible that “Homo sapiens” was simply the Homo that stayed in Africa, developed there, and then a few, who migrated much later than the (eventual) Neanderthal – Denisovan groups, simply encountered these earlier migrants, who had adapted (at least partially – maybe not all that successfully) to colder and drier fluctuating conditions. Without the mutual reproductive compatibility that made possible the acquisition by African homo of N an D adaptive versions of genes, “we” simply could not have survived and spread to harsh cold / seasonal climates around the planet. 

The other necessary requirement for Homo sapiens to survive and prosper outside Africa, was  improved technologies and thus, an expanded range of skills, likely brought with them and then modified and improved to overcome the challenges presented by new environments – plus inventive additions developed along the journey. We see throughout advances in technology that the changing environments encountered by humans-in-migration, pushes innovation beyond “whatever works is okay” conservative repetition of tools and ideas in human culture. Modern humans, despite our technologies, remain “hoarders” of useless and even damaging cultural ideas and beliefs – innovation is the product of a few individuals, who meet growing needs.  

Clearly, it is technology that has been the “highlight” and foundation of Homo success. Artificial adaptation compensated for the slow pace of biological change and propelled “man” into a global species.  Modern social humans are a distinct “neotenic” type of Homo sapiens, an extremely recent version that has resulted from the agricultural – urban environment of the past few thousand years.