Recent History of Socio-Political Anthropology Battles / Important

From Natural History Magazine:

Remembering Stephen Jay Gould

Human evolution was not a special case of anything.

By Ian Tattersall

For long-time readers of Natural History, Stephen Jay Gould needs no introduction. His column, “This View of Life,” was a mainstay of the magazine, starting in January 1974 with “Size and Shape” and concluding with the 300th installment, “I Have Landed,” in the December 2000/January 2001 issue. What made his columns so popular was not just Gould’s range of chosen topics, but also the way he regularly allowed himself to be carried away on any tangent that he found interesting.

Gould died on May 20, 2002. Last spring, on the tenth anniversary of his death, I was invited to join other scholars at a commemorative meeting in Venice organized by the Istituto Veneto di Scienze, Lettere ed Arti in collaboration with the Università Ca’ Foscari. It fell to me, as an anthropologist, to talk about Gould’s intellectual legacy to anthropology. Gould was, of course, anything but a primate specialist. But as it happens, in 1974, the year Gould started writing “This View of Life,” he and I were both invited to attend a specialized meeting on “Phylogeny of the Primates: An Interdisciplinary Approach.” Even at that early stage in his career, I learned, the reach of his writings had broadened well beyond his realms of invertebrate paleontology (he was a fossil-snail expert) and evolutionary theory. He came to address the roles of ontogeny (development of the individual) and neoteny (the evolutionary retention of juvenile traits in adults) in human evolution. What I personally found most interesting, however, was his preprint for the conference, which contained, among much else, a virtuoso canter through the history of human evolutionary studies. He effortlessly displayed mastery of a huge literature on a scale that many professional paleoanthropologists fail to achieve in entire academic lifetimes.

Despite a paucity of strictly technical contributions, there can be no doubt that Gould’s influence on anthropology, and on paleoanthropology in particular, was truly seminal. Foremost among such influences was his 1972 collaboration with Niles Eldredge in developing and publicizing the notion of “punctuated equilibria,” the view that species typically remain little changed during most of their geological history, except for rapid events when they may split to give rise to new, distinct species. This breakthrough enabled paleoanthropologists, like other paleontologists, to treat the famous “gaps” in the fossil record as information, a reflection of how evolution actually proceeded.

Similarly, it was Gould who, in collaboration with Yale paleontologist Elisabeth S. Vrba (then at the Transvaal Museum in Pretoria, South Africa), emphasized that an anatomical or behavioral trait that evolved to serve one function could prove a handy adaptation for an entirely unanticipated one—and that the term exaptation was a better name for this phenomenon than preadaptation, which implied some kind of inherent tendency for a species to follow a certain evolutionary path. Anthropologists were forced to recognize exaptation as an essential theme in the history of innovation in the human family tree.

Speaking of trees, I am convinced that Gould’s most significant contribution to paleoanthropology was his insistence, from very early on, that the genealogy of human evolution took the form of a bush with many branches, rather than a ladder, or simple sequence of ancestors and descendants. As he wrote in his April 1976 column, “Ladders, Bushes, and Human Evolution”:

“I want to argue that the ‘sudden’ appearance of species in the fossil record and our failure to note subsequent evolutionary change within them is the proper prediction of evolutionary theory as we understand it. Evolution usually proceeds by “speciation”—the splitting of one lineage from a parental stock—not by the slow and steady transformation of these large parental stocks. Repeated episodes of speciation produce a bush.”

Before World War II, paleoanthropologists had overwhelmingly been human anatomists by background, with little interest in patterns of diversity in the wider living world. And having been trained largely in a theoretical vacuum, the postwar generation of paleoanthropologists was already exapted to capitulate when, at exact midcentury, the biologist Ernst Mayr told them to throw away nearly all the many names they had been using for fossil hominids. Mayr replaced this plethora, and the diversity it had suggested, with the idea that all fossil hominids known could be placed in a single sequence, from Homo transvaalensis to Homo erectus and culminating in Homo sapiens.

There was admittedly a certain elegance in this new linear formulation; but the problem was that, even in 1950, it was not actually supported by the material evidence. And new discoveries soon made not only most paleoanthropologists but even Mayr himself—grudgingly, in a footnote—concede that at least one small side branch, the so-called “robust” australopithecines, had indeed existed over the course of human evolution. But right up into the 1970s and beyond, the minimalist mindset lingered. Gould’s was among the first—and certainly the most widely influential —voices raised to make paleoanthropologists aware that there was an alternative.

In his “Ladders, Bushes, and Human Evolution” column, Gould declared that he wanted “to argue that Australopithecus, as we know it, is not the ancestor of Homo; and that, in any case, ladders do not represent the path of evolution.” At the time, both statements flatly contradicted received wisdom in paleoanthropology. And while in making the first of them I suspect that Gould was rejecting Australopithecus as ancestral to Homo as a matter of principle, his immediate rationale was based on the recent discovery, in eastern Africa, of specimens attributed to Homo habilis that were just as old as the South African australopithecines.

Later discoveries showed that Gould had been hugely prescient. To provide some perspective here: In 1950, Mayr had recognized a mere three hominid species. By 1993, I was able to publish a hominid genealogy containing twelve. And the latest iteration of that tree embraces twenty-five species, in numerous coexisting lineages. This was exactly what Gould had predicted. In his 1976 article he had written: “We [now] know about three coexisting branches of the human bush. I will be surprised if twice as many more are not discovered before the end of the century.”

Indeed, his impact on the paleoanthropological mindset went beyond even this, largely via his ceaseless insistence that human beings have not been an exception to general evolutionary rules. Before Gould’s remonstrations began, one frequently heard the term “hominization” bandied about, as if becoming human had involved some kind of special process that was unique to our kind. Gould hammered home the message that human evolutionary history was just like that of other mammals, and that we should not be looking at human evolution as a special case of anything.

Of course, Gould had ideas on particular issues in human paleontology as well, and he never shrank from using his Natural History bully pulpit to voice his opinions. Over the years he issued a succession of shrewd and often influential judgments on subjects as diverse as the importance of bipedality as the founding hominid adaptation; the newly advanced African “mitochondrial Eve”; hominid diversity and the ethical dilemmas that might be posed by discovering an Australopithecus alive today; sociobiology and evolutionary psychology (he didn’t like them); the relations between brain size and intelligence; neoteny and the retention of juvenile growth rates into later development as an explanation of the unusual human cranial form; and why human infants are so unusually helpless.

(Removed here; a narrative about the search for who had perpetrated the Piltdow Man hoax)

Gould’s devotion to the historically odd and curious, as well as his concern with the mainstream development of scientific ideas, is also well illustrated by his detailed account of the bizarre nineteenth-century story of Sarah “Saartjie” Baartman. Dubbed the “Hottentot Venus,” Baartman was a Khoisan woman from South Africa’s Western Cape region who was brought to Europe in 1810 and widely exhibited to the public before her death in 1815. Gould’s publicizing of the extraordinary events surrounding and following Baartman’s exhibition may or may not have contributed to the repatriation in 2002 of her remains from Paris to South Africa, where they now rest on a hilltop overlooking the valley in which she was born. But what is certain is that Gould’s interest in this sad case also reflected another of his long-term concerns, with what he called “scientific racism.”

Principally in the 1970s—when memories of the struggle for civil rights in the United States during the previous decade were still extremely raw—Gould devoted a long series of his columns to the subject of racism, as it presented itself in a whole host of different guises. In his very first year of writing for Natural History, he ruminated on the “race problem” both as a taxonomic issue, and in its more political expression in relation to intelligence. He even made the matter personal, with a lucid and deeply thoughtful demolition in Natural History of the purportedly scientific bases for discrimination against Jewish immigrants to America furnished by such savants as H. H. Goddard and Karl Pearson.

Gould also began his long-lasting and more specific campaign against genetic determinism, via a broadside against the conclusions of Arthur Jensen, the psychologist who had argued that education could not do much to level the allegedly different performances of various ethnic groups on IQ tests. And he began a vigorous and still somewhat controversial exploration of the historical roots of “scientific racism” in the work of nineteenth-century embryologists such as Ernst Haeckel and Louis Bolk.

But Gould’s most widely noticed contribution to the race issue began in 1978, with his attack in Science on the conclusions of the early-nineteenth century physician and craniologist Samuel George Morton, whom he characterized rather snarkily as a “self-styled objective empiricist.” In three voluminous works published in Philadelphia between 1839 and 1849—on Native American and ancient Egyptian skulls, and on his own collection of more than 600 skulls of all races—the widely admired Morton had presented the results of the most extensive study ever undertaken of human skulls. The main thrust of (Morton’s) study had been to investigate the then intensely debated question of whether the various races of humankind had a single origin or had been separately created. Morton opted for polygeny, or multiple origins, a conclusion hardly guaranteed to endear him to Gould. Along the way, Morton presented measurements that showed, in keeping with prevailing European and Euro-American beliefs on racial superiority, that Caucasians had larger brains than American “Indians,” who in turn had bigger brains than “Negroes” did. (Cranial-brain size DOES NOT correlate to intelligence)

After closely examining Morton’s data, Gould characterized the Philadelphia savant’s conclusions as “a patchwork of assumption and finagling, controlled, probably unconsciously, by his conventional a priori ranking (his folks on top, slaves on the bottom).” He excoriated Morton for a catalog of sins that included inconsistencies of criteria, omissions of both procedural and convenient kinds, slips and errors, and miscalculations. And although in the end he found “no indication of fraud or conscious manipulation,” he did see “Morton’s saga” as an “egregious example of a common problem in scientific work.” As scientists we are all, Gould asserted, unconscious victims of our preconceptions, and the “only palliations I know are vigilance and scrutiny.”

That blanket condemnation of past and current scientific practice was a theme Gould shortly returned to, with a vengeance, in his 1981 volume The Mismeasure of Man. Probably no book Gould ever wrote commanded wider attention than did this energetic critique of the statistical methods that had been used to substantiate one of his great bêtes noires, biological determinism. This was (is) the belief, as Gould put it, that “the social and economic differences between human groups—primarily races, classes, and sexes—arise from inherited, inborn distinctions and that society, in this sense, is an accurate reflection of biology.”

We are still plagued by this pseudo-scientific “justification” of poverty and inequality; of misogyny and abuse of “lesser humans” by the Human Behavior Industries. Remember, this is very recent history, and the forces of social “control and abuse” are very much still with us.  

It is alarming that the revolution in DNA / genetic research has shifted the “means” of this abuse of human beings into a radical effort to “prove” that socially-created and defined “human behavior pathologies” are due to genetic determinism. The race is on to “prove” that genetic defects, rather than hidden social engineering goals, underlie “defective behavior and thinking” as dictated by closet eugenicists. Racism and eugenics are being pursued in the guise of “caring, treating and fixing” socially “defective” peoples. Genetic engineering of embryos is already in progress

SEE POST August 11, 2017: First Human Embryos ‘Edited’ in U.S. / 7 billion humans not consulted

In Mismeasure, Gould restated his case against Morton at length, adding to the mix a robust rebuttal of methods of psychological testing that aimed at quantifying “intelligence” as a unitary attribute. One of his prime targets was inevitably Arthur Jensen, the psychologist he had already excoriated in the pages of Natural History for Jensen’s famous conclusion that the Head Start program, designed to improve low-income children’s school performance by providing them with pre-school educational, social, and nutritional enrichment, was doomed to fail because the hereditary component of their performance—notably that of African American children—was hugely dominant over the environmental one. A predictable furor followed the publication of Mismeasure, paving the way for continuing controversy during the 1980s and 1990s on the question of the roles of nature versus nurture in the determination of intelligence.

This issue of nature versus nurture, a choice between polar opposites, was of course designed for polemic, and attempts to find a more nuanced middle ground have usually been drowned out by the extremes. So it was in Gould’s case. An unrepentant political liberal, he was firmly on the side of nurture. As a result of his uncompromising characterizations of his opponents’ viewpoints, Gould found himself frequently accused by Jensen and others of misrepresenting their positions and of erecting straw men to attack.

Yet even after Mismeasure first appeared, the climax of the debate was yet to come. In 1994, Richard Herrnstein and Charles Murray published their notorious volume, The Bell Curve: Intelligence and Class Structure in American Life. At positively Gouldian length, Herrnstein and Murray gave a new boost to the argument that intelligence is largely inherited, proclaiming that innate intelligence was a better predictor of such things as income, job performance, chances of unwanted pregnancy, and involvement in crime than are factors such as education level or parental socioeconomic status. They also asserted that, in America, a highly intelligent, “cognitive elite” was becoming separated from the less intelligent underperforming classes, and in consequence they recommended policies such as the elimination of what they saw as welfare incentives for poor women to have children.

Eugenics has never died in American Science; it remains an underestimated force in the shaping of “what do about unacceptable humans”. It is neither a liberal nor conservative impulse: it is a drive within elites to control human destiny.

To Gould such claims were like the proverbial red rag to a bull. He rapidly published a long review essay in The New Yorker attacking the four assertions on which he claimed Herrnstein and Murray’s argument depended. In order to be true, Gould said, Herrnstein and Murray’s claims required that that what they were measuring as intelligence must be: (1) representable as a single number; (2) must allow linear rank ordering of people; (3) be primarily heritable; and (4) be essentially immutable. None of those assumptions, he declared, was tenable. And soon afterward he returned to the attack with a revised and expanded edition of Mismeasure that took direct aim at Herrnstein and Murray’s long book.

There can be little doubt that, as articulated in both editions of Mismeasure, Gould’s conclusions found wide acceptance not only among anthropologists but in the broader social arena as well. But doubts have lingered about Gould’s broad-brush approach to the issues involved, and particularly about a penchant he had to neglect any nuance there might have been in his opponents’ positions. Indeed, he was capable of committing in his own writings exactly the kinds of error of which he had accused Samuel Morton—ironically, even in the very case of Morton himself.

In June 2011, a group of physical anthropologists led by Jason Lewis published a critical analysis of Gould’s attacks on Morton’s craniology. By remeasuring the cranial capacities of about half of Morton’s extensive sample of human skulls, Lewis and colleagues discovered that the data reported by Morton had on the whole been pretty accurate. They could find no basis in the actual specimens themselves for Gould’s suggestion that Morton had (albeit unconsciously) overmeasured European crania, and under-measured African or Native American ones. What’s more, they could find no evidence that, as alleged by Gould, Morton had selectively skewed the results in various other ways.

The anthropologists did concede that Morton had attributed certain psychological characteristics to particular racial groups. But they pointed out that, while Morton was inevitably a creature of his own times, he (Morton) had done nothing to disguise his racial prejudices or his polygenist sympathies. And they concluded that, certainly by prevailing standards, Morton’s presentation of his basic data had been pretty unbiased. (WOW! What an indictment of current Anthropology) What is more, while they were able to substantiate Gould’s claim that Morton’s final summary table of his results contained a long list of errors, Lewis and colleagues also found that correcting those errors would actually have served to reinforce Morton’s own declared biases. And they even discovered that Gould had reported erroneous figures of his own.

These multiple “errors” DO NOT cancel each other out: this is a favorite social typical strategy and magical belief – Present the contradictions from “each side” and reach a “socially acceptable” deadlock. No discussion is possible past this point. The American intellectual-cultural-political environment is trapped in this devastating “black and white, either or, false concept of “problem-solving”. Nothing can be examined; facts are removed to the “supernatural, word-concept domain” and become “politicized” – weapons of distortion in a socio-cultural landscape of perpetual warfare. In the meantime, the population is pushed to either extreme. This is where we are TODAY and this “warfare” will destroy us from within, because the hard work of running a nation is not being done.

It is hard to refute the authors’ conclusion that Gould’s own unconscious preconceptions colored his judgment. Morton, naturally enough, carried all of the cultural baggage of his time, ethnicity, and class. But so, it seems, did Gould. And in a paradoxical way, Gould had proved his own point. Scientists are human beings, and when analyzing evidence they always have to be on guard against the effects of their own personal predilections.

And of the domination and control of their professions by the “elite and powerful” who promote a racist-eugenic social order and control how their work is “messaged” and used to achieve socioeconomic and biological engineering goals – worldwide.



TEDTALK / What is Beauty? I object to this “idea”

Anjan Chatterjee: How your brain decides what is beautiful

TEDTALK August, 12, 2017

It’s 1878. Sir Francis Galton gives a remarkable talk. He’s speaking to the anthropologic institute of Great Britain and Ireland. Known for his pioneering work in human intelligence, Galton is a brilliant polymath. He’s an explorer, an anthropologist, a sociologist, a psychologist and a statistician. He’s also a eugenist. In this talk, he presents a new technique by which he can combine photographs and produce composite portraits. This technique could be used to characterize different types of people. Galton thinks that if he combines photographs of violent criminals, he will discover the face of criminality. But to his surprise, the composite portrait that he produces is beautiful.

Galton’s surprising finding raises deep questions: What is beauty? Why do certain configurations of line and color and form excite us so? For most of human history, these questions have been approached using logic and speculation. But in the last few decades, scientists have addressed the question of beauty using ideas from evolutionary psychology and tools of neuroscience. We’re beginning to glimpse the why and the how of beauty, at least in terms of what it means for the human face and form. And in the process, we’re stumbling upon some surprises.

Galton’s finding that composite or average faces are typically more attractive than each individual face that contributes to the average has been replicated many times. This laboratory finding fits with many people’s intuitions. (preconceived assumptions) Average faces represent the central tendencies of a group. People with mixed features represent different populations, and presumably harbor greater genetic diversity and adaptability to the environment. Many people find mixed-race individuals attractive and inbred families less so.

The second factor that contributes to beauty is symmetry. People generally find symmetric faces more attractive than asymmetric ones. Developmental abnormalities are often associated with asymmetries. And in plants, animals and humans, asymmetries often arise from parasitic infections. Symmetry, it turns out, is also an indicator of health. (not really) In the 1930s, a man named Maksymilian Faktorowicz recognized the importance of symmetry for beauty when he designed the beauty micrometer. With this device, he could measure minor asymmetric flaws which he could then make up for with products he sold from his company, named brilliantly after himself, Max Factor, which, as you know, is one of the world’s most famous brands for “make up.”


This talk by Anjan Chatterjee popped up in the inbox this morning: I confess that something about TED talks feels creepy. I had an argument once with a friend who kept sending me links to “talks” – I signed up for notifications in order to be “open-minded” and tried watching when the topic was of interest. But there’s something about TED that creeps me out.

Coincidentally, I spent some time yesterday looking at “faces” from a collection of Native American period photographs posted on this website:

These are faces created by the life the person lived; not faces made by “shaming” the face one was born to have, and which is a treasure map of the experiences of a single unique human being.

And yet, modern social humans subscribe to a social injustice: your face is not good enough. It must be disguised to be acceptable. It must not reveal your life; your experiences, trials or triumphs. And now, “science” is going to tell you that this “lie that is your made-up face” magically “fools” other humans into believing that you are “genetic perfection” in the flesh; an object of prime real estate for reproducing the species. That you are fertile, healthy, and a preferred choice for having children.

It’s all nonsense. It’s cultural distortion. It’s “psychosocial” Eugenics. It’s a perversion of life processes that have produced millions of “beautiful species” and the individuals of those species and not by the warped dictates of one person or group of modern social humans, but by  incremental changes over unimaginable time; by natural “crisis” engineering when the environment changes radically and quickly. By “optimization” of systems, not by slavish “copying” of ideal forms – especially as “presented by” the cultural imposition of ideas that simply do not pass the scrutiny of “what actually exists” in front of our “noses”.

Case in point: My face. There is no “pride” in stating that my face appears to fulfill the “requirements” that ostensibly advertise “health and good genes” and therefore a slam dunk for “positive” reproduction. I am not: By evolutionary standards, I’m a failure. Non-conforming to “female” design as the “baby-growing” half of the species; the product of a dysfunctional “Asperger, bipolar, schizophrenic” – producing family line – ostensibly caused by “bad genes” And I’m certainly not the only exception to this “eugenic” rule of beauty = healthy genes and reproductive success. I have no children. There are millions of “beautiful criminals” and “ugly saints”. No one can predict which individual humans will contribute the genetic diversity which must be available to a species in order to adapt to changeit is in the genetic “fringes” of a population where adaptation occurs, and not within the typical or average bulk of the species.

Beauty is: the universe is beautiful, but mostly in ways that we don’t understand. The face of an individual is beautiful – not unlike a weathered and broken outcrop of rock, a cobble shaped in a turbulent river, a fossil trace of a fragile bit of life that existed  millions of years ago.

From the soft unformed face of a baby to the “being” who is sculpted by the forces of nature and culture and by the inborn will to grow and to become – that is always a surprise.

I would say that I have outgrown my face and my “genetic destiny”. That process is beautiful.



First Human Embryos ‘Edited’ in U.S. / 7 billion humans not consulted

The work, which removed a gene mutation linked to a heart condition, is fueling debate over the controversial tool known as CRISPR. Two days after being injected with a gene-editing enzyme, these developing human embryos were free of a disease-causing mutation.

Two Words: “Unintended Consequences”

By Erin Blakemore

PUBLISHED by National Geographic, August 2, 2017

What if you could remove a potentially fatal gene mutation from your child’s DNA before the baby is even born? In an advance that’s as likely to raise eyebrows as it is to save lives, scientists just took a big step toward making that possible.

For the first time, researchers in the United States have used gene editing in human embryos. As they describe today in the journal Nature, the team used “genetic scissors” called CRISPR-Cas9 to target and remove a mutation associated with hypertrophic cardiomyopathy, a common inherited heart disease, in 42 embryos.

DNA Hacking Tool Enables Shortcut to Evolution

Scientists who want to explore the technique hail it as a biomedical advance that could one day give people the option not to pass down heritable diseases. The tool could also reduce the number of embryos that are discarded during fertility treatments because of worrisome genetic mutations.

“The scientists are out of control,” says George Annas, director of the Center for Health Law, Ethics & Human Rights at the Boston University School of Public Health, who thinks that scientists should not edit the genomes of human embryos for any reason. “They want to control nature, but they can’t control themselves.”

Healing Hearts

According to the Centers for Disease Control and Prevention, hypertrophic cardiomyopathy occurs in about one in 500 people. The condition causes the heart muscle to thicken and can lead to sudden cardiac arrest. It takes only one gene mutation to cause the condition, and you can get the disease even if only one of your parents has the mutated gene. If you inherit it, there’s a 50 percent chance you will pass it on to your children.

For their work, Shoukhrat Mitalipov, principal investigator at the Oregon Health and Science University’s Center for Embryonic Cell and Gene Therapy, and his colleagues targeted the genetic mutations that cause the majority of hypertrophic cardiomyopathy cases.

First, they created 58 human embryos from the sperm of a male donor with the mutation and the egg of a female without the mutation. Then, they used CRISPR to cut the mutation out of the gene. When things go right, the DNA repairs itself and the mutation disappears.

The technique isn’t always successful. In previous studies, some CRISPR-edited embryos developed mosaicism, a condition in which some cells have the unwanted mutations and others don’t. All in all, the team was able to repair the gene mutation in about 70 percent of the embryos, and the study showed no unwanted changes at other sites in the edited DNA.

The team allowed the fertilized cells to develop into blastocysts—the stage at which embryos are usually implanted into the mother during fertility treatments. They showed normal development, the team reports. Then, the embryos were destroyed.

Science in Motion

“Of course further research and ethical discussions are necessary before proceeding to clinical trials,” study coauthor Paula Amato, adjunct associate professor of obstetrics and gynecology at OHSU, said during a press briefing on August 1.

Earlier this year, the National Academy of Sciences and National Academy of Medicine asked an international committee of scientists and ethicists to weigh in on the benefits and risks of genome editing in humans. (Find out why scientists think gene editing is both terrifying and terrific.)

The panel recommended that in the case of the human germline—genes passed down from generation to generation—scientists refrain from editing genes for any purpose other than treating or preventing a disease or disability. (No more neurodiverse people will be allowed to be born? Where does this “elimination” of genetic diversity end?) The report also insisted on a more robust public debate before such experiments begin. (Oh sure, as if anyone in power will listen to the “peasants” at the bottom of the pyramid)

In the United States, there’s currently a ban on using taxpayer funds for any research that destroys human embryos. In this case they used institutional and private funds. If the team can’t move ahead as quickly as desired in the U.S., (blackmail?) they’ll consider pursuing their research in other countries.

Of course, poor and developing countries need the money and will sacrifice their embryos, and the “outcomes” for the population, good or bad, gladly…)

Debating the Future

It’s already possible to screen for genetic defects within embryos during in vitro fertilization using a process called preimplantation genetic diagnosis. The team thinks their CRISPR technique could eventually be applied to gene mutations associated with other diseases, like cystic fibrosis.

In their paper, the team writes that their method may one day “rescue mutant embryos, increase the number of embryos available for transfer and ultimately improve pregnancy rates (for the Elites who can $$$$ pay for it)

“That’s just absurd,” says Annas. “They admit right up front that if you want to avoid having a baby with [the mutation], you can just not implant the embryos that are affected.”

Mitalipov disagrees: “Discarding half the embryos is morally wrong,” he tells National Geographic. “We need to be more proactive.”

The embryos in this experiment were destroyed!

This is unbelievable: taking over the future evolution of our species, is “morally” right? Nature provides genetic variation which is necessary for organisms to adapt to a changing environment – we are not smart enough to interfere with this process.

Has anyone asked 7 billion  humans if they think it’s a slam dunk “moral good” for a handful of scientists, who obviously are not the least concerned about morality or ethics, to just “go ahead” and terminate 3.5 billion years of evolution?

Either way, Annas says, it’s time to revisit the conversation about how to regulate CRISPR in the United States. “My guess is that the regulators will be horrified.” (Until $$$$ decides the issue)

But for Mitalipov, the debate is a chance to inform the world about the technique’s potential. And for a scientist who has also cloned monkey embryos and even cloned human embryos to make stem cells, he knows plenty about how to ignite public debate.

“We’ll push the boundaries,” he says.

Of course, “the rest of” Homo sapiens just don’t count; we have no choice but to submit to a future dictated by individuals who regard themselves as “GODS” The track record of “ethical nightmares” in human recent history (Eugenics, genocide, the Holocaust, chemical and biological warfare, and other mass murder of “defectives” – who are simply people of another race, religion, or ethnicity) has proven over and over that the power-insane “Male Psychopaths” at the top of the social pyramid are destroyers of Nature.








Female “Autistic” Mice / Funding Bonanza for “Crap Science”

Madness: The government and the “Autism” industry have truly gone bonkers: Political agendas dictate funding for research, not scientific value or the needs of real children and adults who are “Autistic” 


Can Female Mice Improve Autism Research?

Researchers angling for government funds must now include both sexes in their animal studies—or explain why they don’t

In a lab in Sacramento, California, a wall of plastic boxes lined with corncob bedding holds around 800 mice. Even in this clean and bright room, the smell of so many mice concentrated in one place is overpowering — pungent, and familiar to anyone who has spent time with a pet hamster or gerbil. Most of the boxes hold four adult mice, which flit about, noses twitching as they stare out at the humans staring in. But in one of the boxes, a sleek white mouse is tucked in a corner suckling her litter of half a dozen or so squirmy, dark-furred pups.

In most research labs, the fate of these (MICE) pups would be determined by their sex. The males (MICE) would spend their lives as test subjects. The females (MICE) would either be kept for breeding or simply euthanized because they’re not ideal for experiments: They’re supposedly more difficult to work with and generate less consistent data than males do (translation: researchers make sure that the data “support” their preconceived “results”) and it costs too much to maintain both males and females, which must be housed separately. Or so the rationale has gone.

But these little female (MICE) pups are different. The lab where they live is run by Jill Silverman and Mu Yang, researchers at the University of California, Davis (UC Davis) MIND Institute. The two scientists study the behavior of about 15 autism mouse models, and they have always included both males and females in their work.

When the pups get older, they will learn to paddle through water mazes or bury black marbles in their bedding, giving researchers insight into how their memory and behavior compare with that of typical mice. Finding the best animal behavioral models of autism is essential because (MOUSE) behavior is at the heart of the disorder. In people, autism is diagnosed based on behavioral criteria: abnormal social interactions, difficulties with communication and repetitive actions.

Therefore, MICE, which have been genetically engineered to produce behaviors that supposedly duplicate or “mimic” autistic behavior, are mis-represented as scientifically valid “equivalent animals” to human children and adults who are “diagnosed” as “autistic” – a vast, poorly-differentiated spectrum of both problematical and unwanted  (socially annoying) behaviors. THIS IS GARBAGE – the cross species “leap” to identifying a specific genetic “cause” for autism, is not valid: this ‘magical idea” in no way explains, or even acknowledges, the complex learning that characterizes the human brain, the vital contribution of language, problems during pregnancy, and the highly variable interaction of REAL human children with diverse (and often damaging) environments. Children are not “genetically-defective” MICE: These are ARTIFICIAL LIFE FORMS whose behavior is created and controlled by the “requirements” dictated by “researchers” and their funding and  publishing goals. This “reductionist and rigged” research is the barely disguised agenda of  Eugenics.

Ideally, these mice should be as much like their human counterparts as possible. Of course, there are limits to how much a tiny, nocturnal rodent can be like a brainy bipedal primate. But if a mouse isn’t the same as a man, a male mouse is even less like a woman, particularly when it comes to the things that define autism. (“Things” that are not empirically nor logically determined, but are “chosen” subjectively by those who are motivated by profit and social status: by those who have created the “Autism Industry) Boys are typically diagnosed four times more often than girls, and autism manifests differently depending on sex; in girls, the disorder is often subtler and more difficult to detect.

“Girls have autism. Maybe it’s not as prominent as boys in the statistics, but girls do have autism and there is significant research that shows that girls with autism have a very different type than boys do,” says Silverman. “So I think females are equally as important to study.”

Silverman and Yang’s research not only includes mice of both sexes, but analyzes their behavior separately. For a long time, this approach wasn’t required, but now others must catch up with them. A year ago, the National Institutes of Health (NIH) rolled out the first phase of a new mandate that requires researchers funded via NIH grants to either include plans for how they will use animals of both sexes or explain why they will work with only one. (This is not a scientific decision; it’s political – and dangerous – this “government mandate” will now define “female autism” by whatever “new” conclusions are made, regardless of the idiocy or prejudice behind them. Autism in female humans will be “defined” using illegitimate research results. Whatever is “discovered, created, invented” will become diagnostic DOGMA. Generations of girls may suffer the wrong diagnosis and “treatment” due to this reckless political move.) The hope is that by studying both males and females, (MICE) scientists will gain better insights into sex differences (IN MICE) ranging from behavior to brain anatomy to drug metabolism.

The new rules raise intriguing questions for the field as a whole: Because autism is more common in boys, should researchers use a proportionate amount of resources for studying male mice? Should researchers focus on females in studies that are relevant to Rett syndrome, which primarily affects girls? If scientists begin to include both sexes in each experiment, who’s going to pay for the extra mice?


 If you don’t believe that this “research” is bullshit, here’s the link to a previous post about the $1.1 BILLION Lab Rat scam industry.


In order to accommodate this new reality, scientists will need to think more deeply about when sex matters and when it doesn’t. (Yes, and by past results, we can predict that this will be highly biased or simply nonsensical neurotypical thinking) In the year the NIH mandate has been in effect, it has so far changed only how researchers write their grants and plan their studies. “I would say within a few years, it should be possible to start seeing differences in publications,” (PC agenda differences) says Annaliese Beery, a neuroscientist at Smith College in Northampton, Massachusetts, who has been calling for researchers to address sex differences since 2009, and whose work was part of a larger movement that led to the NIH mandate.

The results of those studies may nudge autism research forward in unexpected ways. If autism mostly affects males, understanding the differences between the sexes could explain why, which in turn may reveal something about the fundamental causes of the disorder. (No, the ongoing political-social take-over of science will promote the fixation and obsession with genetic reductionism-determinism basic to Eugenics – dehumanization of “unwanted” groups of humans.

Excuses, excuses: Historically, women were often excluded from clinical studies because sex wasn’t considered a major factor in health or illness. Even when sex was suspected to be a factor, researchers thought women were too variable to study because of their monthly hormone cycle. They also worried that experimental treatments might harm pregnant women or their babies, especially after the 1960s, when the morning sickness drug thalidomide was found to cause birth defects. “Women of childbearing potential should be excluded from the earliest dose-ranging studies,” asserted a 1977 report from the U.S. Food and Drug Administration (FDA).

That guidance had a chilling effect across all stages of clinical research, notes a 2012 report from the Institute of Medicine: Biomedical researchers were afraid to include women in their studies. What little research women participated in focused on reproduction. For much of the rest, researchers generalized data collected from men to women despite the fundamental differences in physiology, hormones and neurology.

“The underlying assumption is that if you study males, that’s enough and you can extrapolate to everyone else from there,” says Beery. “We’ve seen many examples where that assumption clearly doesn’t hold, where there are really important biological sex differences.”

For example, women have anxiety and depression more often than men do, and they are also more prone to strokes and thyroid disease. Women metabolize drugs differently, too, and are more likely to experience side effects.

Among the most infamous examples of this is the insomnia drug zolpidem, marketed as Ambien, which was approved by the FDA in 1992. Many women metabolize the drug so slowly that it is still in the bloodstream the morning after a dose, leaving them too impaired to drive or to do other tasks that require mental acuity. It took more than a decade after zolpidem launched for the FDA to formally address the issue; in 2013, it halved the recommended dose for women.

The women’s health movement — a political force emerging in the 1960s that initially focused on reproductive rights — pushed against the assumption that the results of male-only studies applied equally to women. Activists demanded improved healthcare for all women and an end to sexism in the health system. The NIH officially responded in 1986 with a report acknowledging that women’s health matters beyond reproduction and recommended that both sexes be included in research. In 1993, new rules required that NIH-funded researchers include more women in clinical trials. (What an astoundingly minimal “solution” to vast cultural, social and religious stupidity (misogyny) that is rampant in the U.S.)  

Today, more than half of NIH-funded clinical trial participants are women. But in preclinical research — work with animals and cells — the preference for males has remained steadfast. In a 2011 meta-analysis, Beery and Irving Zucker, professor of psychology at the University of California, Berkeley, dug into 10 areas of biological research, such as biology and pharmacology, to see just how bad the sex bias was in animal studies.

What they found is that it was pretty bad: 8 of the 10 disciplines showed a strong bias in favor of males. Their study wasn’t granular enough to analyze autism research, but the most prominent discrepancy it found was in neuroscience, in which studies using only males outnumbered those with only females by more than a factor of five. “And that didn’t even count the studies where they didn’t declare sex in the methods, which probably were often just males,” Beery says.

That lopsided approach may mean that some studies misconstrue the way animals actually behave. Like men and women, male and female rodents have unique sex-based characteristics. In mice, depending on the strain, the sexes may exhibit different levels of anxiety, detected by how willing the animals are to explore new objects or spaces. Females have maternal instincts, whereas males can be aggressive and territorial. (That is, laboratory “mice” and other laboratory “animal torture victims” are so thoroughly screwed up by artificial breeding and genetic manipulation and inhumane treatment, that they are useless as “a foundation species” for biological study of human health and behavior. 

There are also differences in the brain, says Jason Lerch, professor of medical biophysics at the University of Toronto. For example, the bed nucleus of the stria terminalis and parts of the amygdala — brain structures that play a role in social behaviors — are typically larger in male mice than in females. Males and females also have different levels of sex hormones, which affect brain development and function.

The reasons for excluding female animals are familiar: that females’ regular hormonal fluxes during the estrus cycle make their behavior and physiology less predictable, and that this natural variability can make data from relevant tests unreliable.

Those things may be true, but can be accounted for, says Lerch. “We’ve looked explicitly to see how the estrus cycle affects the brain across different stages of the cycle,” he says. “And it does, particularly in the hippocampus, but it’s very subtle.”

A 2014 study from the University of Chicago and the University of California, Berkeley proved the point further. The researchers analyzed 293 scientific articles that looked at a range of traits in both male and female mice at varying stages of the latter’s estrus cycle. They found not only that females are no more variable than males, but that males are actually more variable in certain conditions. The title of the report proclaimed: “Female mice liberated for inclusion in neuroscience and biomedical research.”

Model behavior
So far, there are only a few autism studies in which the sex of animals seems to make a difference, but that may be because scientists have only just begun to look.

Some of the most commonly used mouse models of autism are knockout mice, which are engineered so that certain genes are either missing or turned off. These genetic modification techniques debuted in the 1980s, but the first autism knockout mice took a while longer to develop, emerging only in the early 2000s.

To date, researchers have created 676 mouse models that supposedly capture some features of the disorder. No one model is a complete representation of autism, notes Yang. “An analogy would be: None of the instruments in the philharmonic sounds like the symphony.”

Any scientist would also be quick to point out that even the best model mouse does not actually have autism, which is a uniquely human condition. But because mice are naturally social and communicative, and their normal activities — such as how often they groom or play — are well known, those that diverge from the norm are fairly easy to study. Even models that are approximations can be enormously valuable ($$$$$$$$$$$$$$$$$$$) making it possible to identify biological mechanisms underlying a disorder, or drugs that could help treat it. (In case you haven’t caught on yet THIS IS THE PROFITMAKING GOAL of MEDICAL RESEARCH)

In labs such as the one at UC Davis, researchers test the mutant mice for behaviors that might be analogous to symptoms of autism.

One example is the milkshake memory test. At her desk just a couple of floors up from the mouse lab, Silverman pulls up a video on her computer screen. It’s a black-and-white aerial view of a gray mouse sitting in a triangular enclosure, like a surveillance tape from a miniature convenience store security camera. In front of the mouse are two touchscreens flashing simple images — an airplane to the left and a spider to the right. The mouse nudges the spider with its nose, and then scurries to the rear of the enclosure where a trap door opens to reveal a sip of strawberry milkshake.

After the mouse learns which image yields the reward, Silverman says, the researchers can switch the rules, perhaps making the airplane yield the sweet treat. Normal mice can relearn the order of the images, but autism models (See above: “Any scientist would also be quick to point out that even the best model mouse does not actually have autism, which is a uniquely human condition”) are usually more hesitant to veer from the original path — reminiscent of the perseverative behavior seen in people with autism. THIS IS NOT SCIENCE; it’s not even pseudoscience!) Other behavioral tests examine sociability, giving the mice the choice to spend time either with other mice or with inanimate objects; risk-taking, in which the mice either venture out on to a high open ledge or hide in a dark enclosed space; and repetitive behavior, where the focus is on excessive grooming or jumping. (Pathologies induced by captivity, abuse, and genetic design)

How old is this type of moronic “reward punishment” experimentation? How archaic, how repetitive and stupid? And yet so-called “researchers” have so little scientific awareness and mental capacity for “original” ideas that this standard, Western Culture mechanical concept of “understanding” human behavior gets funded over and over and over again!

Silverman calls up a set of raw data from her team’s recent experiments: bar charts comparing sex differences in six different strains of mice across various tests intended to detect behaviors relevant to autism. In this limited dataset, there are no significant differences between the sexes. But that doesn’t mean that sex differences don’t exist, Silverman says. (We’re “manufacturing data as fast as we can. – We need more funding, of course!)

“There are tests that are more sensitive, more sophisticated, that might be able to pick it up,” adds Yang, who is peeking over Silverman’s shoulder. The differences may show up, for example, in more complicated behavioral assays and drug tests, which Silverman and Yang are exploring.

In other labs, some intriguing differences between male and female mice test subjects have already begun to emerge. One example comes from the lab of Sheryl Moy, professor of psychiatry and director of the mouse behavioral phenotyping core at the University of North Carolina’s Carolina Institute for Developmental Disabilities. Moy’s work focuses on the hormone oxytocin, which can be given as a drug to autism model mice and may encourage them to be more social. Her group showed in 2013 that males and females from a strain called C58/J, which has repetitive behaviors and low sociability, do not react the same way to oxytocin. In females, pro-social effects happened sooner and lasted longer. “These results suggest that oxytocin might be particularly effective in females — something we would not have observed just looking at the male mice,” says Moy, who is now comparing oxytocin responses across sexes in other autism models.

Brain imaging research — in which scientists scan tiny mouse brains to understand neuroanatomical differences in autism models — has also revealed sex-based patterns. In 2014, Lerch’s group used magnetic resonance imaging to compare the brains of 26 different autism mouse models to see whether they have common abnormalities. The researchers found that the areas of the brain that are most strikingly different between male and female mice, such as the bed nucleus of the stria terminalis and amygdala, are also areas that are abnormal across many of the 26 mouse models. It’s a strong suggestion that sex differences might be important, says Lerch, although the exact role sex plays is unclear. “These are the things that we don’t know yet,” he says. “But I think we are going to need to understand them to understand autism.”

The issue of sex is particularly acute in preclinical studies of Rett syndrome, a disorder caused by mutations in a gene located on the X chromosome. Boys who have the mutated gene die young, and girls survive, albeit with developmental problems that include features of autism and motor problems that usually get progressively worse as they age. Likewise, male mice with a Rett mutation have much more severe symptoms than the females do, says Zhong-wei Zhang, associate professor at the Jackson Laboratory in Bar Harbor, Maine. Because these severe symptoms develop quickly and are easy to detect, many researchers prefer to work only with the male mice.

This bias may mean that the researchers are missing valuable information about the syndrome, says Huda Zoghbi, professor of neurobiology and genetics at Baylor College of Medicine in Houston, Texas. Because the mutation takes longer to affect female mice, researchers have an opportunity to study how it changes behavior and brain function over the entire lifespan. “There is really a lot of value to studying the females because they have this slow progression of the onset of symptoms,” Zoghbi says, “which is what we see in the human patient.”

Soft money
The little white mouse mother and her neighbors at the Sacramento lab enjoy unusually nice digs. They breathe air that recirculates 15 times every hour and drink only purified water. Researchers and lab technicians speak in whispers when the animals are running through tests, so as not to disturb them.

The luxury comes at a price. Daily upkeep for one cage, which holds four mice, costs about $1.10. According to Yang and Silverman, a typical behavioral test aims for 20 mice per group in order to achieve sufficient statistical power. Most tests require three groups: controls, genetically altered mice with one copy of the gene of interest, and genetically altered mice with two copies of that gene. That adds up to 60 mice per test. Such tests require more animals than in other areas of research, in part because there are already so many variables that can cause statistical noise in a behavioral experiment — anything from the temperature of the room to whether the handlers are wearing a new cologne.

With the new NIH mandate, that minimum may double in order to get the same amount of data for each sex, because both datasets will often be reported separately (unless there are no discernible differences, in which case the researchers may pool the datasets to boost statistical power). Caging expenses would double, not only because there would be twice as many animals but also because the males and females must be separated so they don’t mate. Given that behavioral tests can take up to two months and mice usually live four to five months in the lab, the mandate’s costs add up quickly.

It’s not clear where researchers will find the money for this extra tab — the NIH hasn’t promised an increase in grant dollars for people trying to fulfill the requirement. “I think it’s great that we’re doing this now, but how does that impact funding?” asks Stacey Rizzo, who teaches a course in characterizing mouse behavior at the Jackson Laboratory. “My colleagues who are applying for grants haven’t seen an increase in the award amounts to compensate for [the new mandate].”

In response to such concerns, Jackson Laboratory scientist Gary Churchill ran hypothetical design scenarios through statistical models to figure out how many more mice an average researcher might need. The calculations included information about the type of test, how much of an effect could be expected, and how variable the responses might be.

Depending on the type of study, some researchers might need twice as many animals, he found. Others might need to add just a few more to their experiments. “The answer depends on the fundamental unknown, which is: In what way do the sexes differ?” he says.

Janine Clayton, director of the NIH Office of Research on Women’s Health, agrees that populations of research mice won’t necessarily have to double. The NIH will evaluate grants not only on whether they include both sexes, she says, but how they consider the ways in which sex affects their research questions and design. “In the long run, money can be saved when scientists study both sexes early in basic and translational science,” she says.

Rat race
About 20 miles west of Sacramento, Silverman steps into a lab that nearly mirrors her group’s mouse lab, with two notable differences: Everything is bigger, and instead of mice, the lab houses rats.

Historically, mice have been the rodents of choice for autism research, partly because there are so many models representing a broad range of autism-relevant genetic mutations, and partly because they’re small and relatively cheap. But Silverman and principal investigator Leonard Abbeduto began building this lab in 2012 because they say the rat may be a more promising model.

Mice and rats diverged between 12 and 24 million years ago, and the latter evolved to be bigger and more socially complex. Their social behavior could make features of autism — as well as sex differences — easier to recognize in tests.

“See these guys? They’re wrestling and playing,” says Silverman, pointing into a cage where a few white adolescent rats tumble across the floor, taking turns pouncing on one another’s backs. “Mice would never do that. Rats are just way more social.”

Rats are also smarter. Consider the milkshake test: When mice take it, they nudge one touchscreen image or the other with their nose. According to Silverman, rats quickly learn to bypass the rules by hitting both screens simultaneously with their nose and a paw to get their treat. A rat must be given a more advanced version, which includes a small ledge that measures the pressure from its paws, forcing it to use its nose to select one image at a time.

The downside is that rats are more expensive. Originally, Silverman and Baumann planned to use only male rats in their pilot studies because the cost of including both sexes would be substantial; housing and feeding a single adult rat runs to more than a dollar a day.

Ultimately, given the NIH mandate, the researchers decided it made more sense to start the new project with both females and males from the very beginning. Silverman says that is ultimately a good thing for understanding sex differences in autism models. “There wasn’t enough varied behavior [in the mice] to see that difference,” she says. “Now it is closer to being a realistic possibility, because we’ll have a bigger signal.”

She pulls out another plastic cage, occupied by a large white rat with red eyes that is nursing a dozen 21-day-old pups. They’ll soon be weaned and separated by sex into new cages and eventually run in behavior and memory tests just like their smaller counterparts in Sacramento.

How this work plays out at UC Davis and at other autism labs across the country will only reveal itself in time as researchers sort out how to include both sexes and the data start rolling in. But at the very least, it’s time for the sleek white mouse and the big red-eyed rat — and their female pups — to have the chance to show what they’ve got.

By showing how sex differences in autism happen at the most basic level, these animals may change our fundamental understanding of autism. Silverman recognizes that the new policy is going to cost more money — but she says it’ll be worth it. “We should embrace the NIH mandate,” she says. “It’s really important that every one of these models be looked at with males and females separately.”

Artificial Evolution Videos / Seeing is better than believing!

Published on Nov 25, 2013

We present a control method for simulated bipeds, in which natural gaits are discovered through optimization. No motion capture or key frame animation was used in any of the results. For more information, see…


Published on Jun 30, 2016

Accompanying video for: F. Corucci, N. Cheney, H. Lipson, C. Laschi and J. Bongard, “Evolving swimming soft-bodied creatures”
The Fifteenth International Conference on the Synthesis and Simulation of Living Systems (ALIFE XV) – Late Breaking Abstract

See also our growing soft robots exploiting morphological computation:

More on:…


Published on Jun 29, 2014

The research field of evolutionary robotics abstracts some of the major themes in biological evolution (heritable traits, genetic variation, and competition for scarce resources) as tools to allow computers to generate new and interesting virtual creatures. One of the recent themes in this field is towards more embodied robots (those that produce interesting behavior through the design of their bodies, as well as their brains). Here, we build on previous work evolving soft robots to demonstrate the low level embodiment of electrical signals passing information through muscle tissue. Through this work we attempt bridge the divide between embodied cognition and abstracted artificial neural networks. We hope you find the video interesting and entertaining!

This video accompanies the following paper:
Cheney, N., Clune, J., Lipson, H. (2014) “Evolved Electrophysiological Soft Robots”. Proceedings of Artifical Life 14: The Fourteenth International Conference on the Simulation and Synthesis of Living Systems (ALife14). MIT Press.