evolution in four dimensions...,

evolution-institute |  One of the most mind-expanding books that you’ll ever read is Evolution in Four Dimensions by Eva Jablonka and Marion Lamb. They remind us that evolution is about variation, selection, and heredity, not genes. Genes provide one mechanism of heredity but there are others, including epigenetic mechanisms, forms of social learning found in many species, and forms of symbolic thought that are distinctively human. They provide a concise history of why evolutionary theory became so gene-centric during the 20^th Century and how it needs to be expanded to include the other three dimensions.

Eva Jablonka is a Professor at the Cohn Institute for the History of Philosophy of Science and Ideas at Tel Aviv University in Israel. I talked with her by Skype on November 6 2014. Our conversation provides a panoramic tour of evolutionary theory based on heredity, not just genes.

DSW: Welcome, Eva. I’m so pleased to be talking with you.

EJ: Hello, David.

DSW: I want to talk to you about the definition of evolution and the need for it to go beyond genetic evolution. This is the topic of your great book, Evolution in Four Dimensions, which I have adopted as the first text for almost all of my courses. That’s how much I think of it. Let’s begin by discussing your background. What is your training that enables you to write such a book?

EJ: I am a geneticist. I did a PhD in genetics and molecular biology; in fact, on DNA methylation and chromatin structure. Before that, I did a Masters thesis in microbiology. At the same time, I was deeply interested in philosophy of biology. While I was doing a PhD in genetics, I was also writing papers for philosophy of biology journals. I thought that I should combine the two because theoretical biology and evolutionary biology need a very strong conceptual basis. I ended up being in some kind of twilight zone between the two things. For me it was a productive combination.

DSW: Great! Everyone knows that Darwin knew nothing about genes. For him, evolution was about variation, selection and heredity, a resemblance between parents and offspring. Nevertheless, nowadays, whenever you say the word “evolution,” most people hear “genes.” That’s true for a professional evolutionist, as much as for the lay public. How is it that the study of evolution became gene-centric?

EJ: It is related to the strong focus on heredity that is apparent already in the second 19th century, when many  theories of heredity were developed. Once evolution became an accepted theory it was clear that one has to think very seriously about heredity. In order to have cumulative evolution, heredity is necessary.  Darwin himself had a theory of heredity, which was, in fact, one of the most Lamarckian theories of heredity around at the time!  The point is, however, that he needed a theory of heredity to consolidate his theory of evolution, and he  did develop one.

The other reason heredity became focal was because  of the Industrial Revolution. The population was growing and there was an urgent need to feed people so improvements in agriculture became pertinent. It was clear that breeding and selection were of great importance, and selection must be based on heritable variation. The study of heritable variation was  therefore  important from a practical point of view.

the gene is obsolete...,

psmag | In the aftermath of the Human Genome Project, biologists are struggling with the definition of a gene, but why should this matter to anyone else? It matters because the molecular concept of the gene that has dominated biomedical research for the last half-century is increasingly ill-suited for our efforts to understand the role of genetics in human biology. Giving a physical meaning to the concept of a gene was a triumph of 20th-century biology, but as it turns out, this scientific success hasn’t solved the problems we hoped it would.

The Human Genome Project was conceived as part of a research program to develop a set of clear molecular explanations for our biology. The idea was to inventory all of our genes and assign each of them a function; with this annotated inventory in hand, we would possess a molecular explanation of our genetic underpinnings and discover druggable target genes for specific diseases. While this gene-focused approach has been successful in many cases, it’s increasingly clear that we will never understand the role of genetics in our biology by merely making an annotated inventory of those DNA entities that we call genes.

Life isn’t so simple, and perhaps Wilhelm Johannsen’s more agnostic definition of a gene is a better match to the mixed bag of genetic elements in our genomes. The molecular concept of a gene was supposed to explain the influence of our DNA on our biology, our behaviors, and our ailments. That explanation is much more elusive than we hoped, and the role of DNA in our lives is more complex and subtle than we expected.

American Nations As Revealed In Identity By Descent (IBD) Networks

medium  |  Earlier this summer, I presented the American Nations: the eleven regional cultures that comprise the United States and North America. Their existence explains much about our history, our constitutional arrangements, and, indeed, our political fissures — past and present. If you have any ancestors who were living in North America prior to the Civil War, the existence of these rival nations is likely reflected in parts of your family tree and, according to a recent study published in Nature Communications, may very well have left a mark on your DNA.

I couldn’t miss this study, because shortly after it came out, readers of my 2011 book, American Nations: A History of the Eleven Rival Regional Cultures of North America, were stuffing my inbox and flooding my social media feeds with it. A glance at the thumbnail illustration that accompanied the study made it clear why: Unbeknownst to the scientists who’d written the paper, the map depicting the key results of their research on the patterns of genetic variation in North America over time and space mirrored the American Nations map to an uncanny degree.

Here they are for comparison:

Clustering of 770,000 genomes reveals post-colonial population structure of North america. Nature Communications 8 (2017)

This is remarkable because the American Nations paradigm is resolutely not about genetics or genealogy. Rather, it’s built on the late cultural geographer Wilbur ZeFrolinsky’s Doctrine of First Effective Settlement, which argues that when a “new” society is settled, the cultural characteristics of the initial settlement group will have a lasting and outsized effect on the future trajectory of that society — even if their numbers were very small and those of later immigrants of different origins were very large. These lasting characteristics, which inform the dominant culture of entire regions of North America, are passed down culturally, not genetically, which explains why the Dutch-settled area around New York City still has obvious and distinct characteristics inherited from Golden Age Amsterdam, even though the portion of people there reporting Dutch ancestry to census takers is a vanishingly small 0.2 percent. Culture is learned, not inherited.

And yet the Nature study — powered by the enormous cross-referenced genomics and genealogy databases of Ancestry.com — reveals that the regional cultures have left a significant genetic imprint as well. That’s because members of a regional culture tended to mate with one another, rather than with people from rival areas, even when those rivals lived nearby, in the very same colony or state.

“Who we are today — the genetics of Americans all over the place — is the result of all kinds of cycles of reproductive isolation and the release of that isolation,” says Catherine A. Ball, a geneticist and the chief scientific officer at Ancestry who oversees the company’s DNA work. “Who your mates would be was linked to geography, politics, religion, war, and all of that is showing today in people walking on the streets and who they are related to.”

Ball wasn’t familiar with American Nations before I spoke with her, but the results show that the boundaries of the regional cultures were very real when it came to human reproduction, creating reproductive clusters centuries ago that geneticists have been able to recreate through the examination of nearly a million living Americans’ DNA.

dna printing

NPR |  Here's something that might sound strange: There are companies now that print and sell DNA.

This trend — which uses the term "print" in the sense of making a bunch of copies speedily — is making particular stretches of DNA much cheaper and easier to obtain than ever before. That excites many scientists who are keen to use these tailored strings of genetic instructions to do all sorts of things, ranging from finding new medical treatments to genetically engineering better crops.

"So much good can be done," says Austen Heinz, CEO of Cambrian Genomics in San Francisco, one of the companies selling these stretches of DNA.

But some of the ways Heinz and others talk about the possible uses of the technology also worries some people who are keeping tabs on the trend.

"I have significant concerns," says Marcy Darnovsky, who directs the Center for Genetics and Society, a genetics watchdog group.

A number of companies have been taking advantage of several recent advances in technology to produce DNA quickly and cheaply. Heinz says his company has made the process even cheaper.

"Everyone else that makes DNA, makes DNA incorrectly and then tries to fix it," Heinz says. "We don't fix it. We just see what's good, what's bad and then we use the correct pieces."

Machine Learning and Data Driven Medical Diagnostics

labiotech |  Sophia Artificial Intelligence (AI) is already used worldwide to analyze next-generation sequencing (NGS) data of patients and make a diagnosis, independently of the indication. “We support over 350 hospitals in 53 countries,” CEO Jurgi Camblong told me.

With the new funds, Sophia Genetics is planning on increasing the number of centers using the technology. According to Camblong, this step is also key for the performance of the diagnostics algorythm, since the more data is available to the platform, the better results it can achieve.”By 2020, with the network, members and data we have, we will move into an era of real-time epidemiology,” assures Camblong.

Sophia’s growing network of hospitals is also the key to its ultimate goal: democratizing data-driven medicine. Until now, access to NGS equipment and analysis expertise was not affordable for all hospitals, especially those in underdeveloped regions of the world. Sophia Genetics is breaking this barrier by giving access to the network and its accumulated knowledge to small hospitals in Africa, Eastern Europe and Latin America without the resources to take on diagnostics themselves.

One of the areas Sophia AI can have a bigger impact is cancer, which currently makes up about a third of the 8,000 new patient cases registered in the platform each month. With the resources the cash injection will bring, the company wants to take on the project of implementing imaging data as well as genomic data to diagnose cancer and recommend the best treatment for each patient.  Fist tap Big Don.

nah, just what nicholas wade says about race...,

slate |  Wade’s argument has three parts: First, along with the divergence of physical traits such as skin color and types of earwax, racial groups have genetically evolved to differ in cognitive traits such as intelligence and creativity. Second, Wade argues that “minor differences, for the most part invisible in an individual, have major consequences at the level of a society.” Third, he writes that his views are uncomfortable truths that have been suppressed by a left-wing social-science establishment.

The word “inequality” does not appear in the book’s index, but what Wade is offering is essentially a theory of economic and social inequality, explaining systematic racial differences in prosperity based on a combination of innate traits (“the disinclination to save in tribal societies is linked to a strong propensity for immediate consumption”) and genetic adaptation to political and social institutions (arguing, for example, that generations of centralized rule have effected a selection pressure for Chinese to be accepting of authority).

Wade is clearly intelligent and thoughtful, and his book is informed by the latest research in genetics. His explanations seem to me simultaneously plausible and preposterous: plausible in that they snap into place to explain the world as it currently is, preposterous in that I think if he were writing in other time periods, he could come up with similarly plausible, but completely different, stories.

As a statistician and political scientist, I see naivete in Wade’s quickness to assume a genetic association for any change in social behavior. For example, he writes that declining interest rates in England from the years 1400 to 1850 “indicate that people were becoming less impulsive, more patient, and more willing to save” and attributes this to “the far-reaching genetic consequences” of rich people having more children, on average, than poor people, so that “the values of the upper middle class” were “infused into lower economic classes and throughout society.”

Similarly, he claims a genetic basis for the declining levels of everyday violence in Europe over the past 500 years and even for “a society-wide shift ... toward greater sensibility and more delicate manners.” All this is possible, but it seems to me that these sorts of stories explain too much. The trouble is that any change in attitudes or behavior can be imagined to be genetic—as long as the time scale is right. For example, the United States and other countries have seen a dramatic shift in attitudes toward gay rights in the past 20 years, a change that certainly can’t be attributed to genes. Given that we can see this sort of change in attitudes so quickly (and, indeed, see large changes in behavior during such time scales; consider for example the changes in the murder rate in New York City during the past 100 years), I am skeptical of Wade’s inclination to come up with a story of genetics and selection pressure whenever a trend happens to be measured over a period of hundreds of years.

Wade’s attitudes toward economics also seem a bit simplistic, for example when he writes, “Capital and information flow fairly freely, so what is it that prevents poor countries from taking out a loan, copying every Scandinavian institution, and becoming as rich and peaceful as Denmark?” The implication is that the answer is racial differences. But one might just as well ask why can’t Buffalo, New York, take out a loan and become as rich (per capita) as New York City. Or, for that matter, why can’t Portugal become as rich as Denmark? After all, Portuguese are Caucasians too! One could of course invoke a racial explanation for Portugal’s relative poverty, but Wade in his book generally refers to Europe or “the West” as a single unit. My point here is not that Haitians, Portuguese, and Danes are equivalent—obviously they differ in wealth, infrastructure, human capital, and so forth—but that it is not at all clear that genetic differences have much of anything to do with their different economic positions.

no easy answer - but them bowl haircuts though...,

nature |  Connecticut’s state medical examiner has requested a full genetic analysis of mass killer Adam Lanza, who shot 20 children, 6 school staff, his mother and himself in Newtown in December. At first glance, it is easy to understand why. Confronted with such senseless violence, it is human nature to seek solace in scientific explanations. After John Wayne Gacy was executed in 1994 for the murder of 33 young men and boys, his brain was preserved and examined for clues to what made him a monster. More than 80 years ago, scientists reportedly studied the brain of serial killer Peter Kürten, the ‘vampire of Dusseldorf’, who was executed in 1931.

This quest to understand endures as technology advances. Now, instead of looking at cranial folds and frontal lobes for clues to the massacre, geneticists at the University of Connecticut in Farmington will scour Lanza’s genes. On its own, this hunt will be about as informative as studies of the brains of murderers: not very.

The Connecticut scientists will not talk about the job they have been handed. It is not clear what they will find, or even what they should look for. Suspend disbelief for a moment and pretend that a ‘mass-shooter gene’ exists — something that no serious geneticist believes — and scientists could still draw no conclusions from a single individual’s genome.

To be sure, many links and suggestions of links have been identified between genetics, mental illness and, to a lesser extent, violence. A study using Swedish registries (R. Kuja-Halkola et al. Dev. Psychopathol. 24, 739–753; 2012) found that children born to men older than 60 were more likely to be convicted of violent crimes than were those born to men aged 40–60 years, an observation that might be linked to increasing numbers of mutations in sperm as men age. Genetic risk factors have been identified for autism, depression and schizoid spectrum disorders, but they explain relatively little. People diagnosed with schizoid spectrum disorders are more likely to be convicted of violent crimes than are those with no such diagnosis, but the vast majority of people with mental illness do not commit crimes.

Such associations hold only for groups. Many healthy people carry mutations associated with disease; many people with mental illness carry no known risk factors. Mass shooters are often young white men, yet very few young white men become mass shooters. There is no one-to-one relationship between genetics and mental health or between mental health and violence. Something as simple as a DNA sequence cannot explain anything as complex as behaviour.

But there is a dangerous tendency to oversimplify, especially in the wake of tragedy.

are genes a "product of nature"?

BusinessInsider | The US Supreme Court heard the most high-profile genetics case in history on Monday, as justices considered whether private firms should be allowed to patent human genes linked to breast cancer.

The court's decision could have broad implications for research, patient health and the pharmaceutical industry, with nearly 20 percent of the approximately 24,000 human genes currently under patent, some linked to cancer and Alzheimer's disease.

At issue are the actions of Myriad Genetics, a Utah-based company which holds patents on genes known as BRCA1 and BRCA2, both associated with hereditary breast and ovarian cancer.

The firm says patents for the two genes, awarded in 1998, have helped it raise the money "necessary to decode the genes, design and deliver the tests, interpret the results, and help patients," to the benefit of a million people.

Critics accuse Myriad of barring research by other institutions on the BRCA genes and making the test too expensive for many patients, with a cost of $3,000 to $4,000.

"Competition is what leads to innovation and improvement," said Harry Ostrer, a medical geneticist and a plaintiff in the case.

"We don't want to tie up the uses of our genes," he told reporters, adding that if Myriad did not own the patents, "I would start offering testing to my poor patients in the Bronx."

Dozens of breast cancer survivors and women's health advocates assembled on the Supreme Court steps as the arguments were heard inside. Some hoisted signs, including one that read: "Corporate Greed is Killing My Friends."

What Does Responsibility Have To Do With Reproduction?

nursingclio |  Genetic counseling, as the previous two posts in this series suggested, has a lot to offer for navigating the tricky decisions things like prenatal testing and preimplantation genetic diagnosis raise. Well, in this post I’d like to make things a little more complicated. Enter the sheer messiness of history. I still believe genetic counseling is the best approach we have right now for helping prospective parents with hard choices, but it has a complicated — and not so distant — past that continues to shape counselors’ ways of interacting with clients and their decisions.

A LITTLE REVIEW

In the first post I shared a little bit of the history of genetic counseling in the United States and gave some examples of how, today, it can help prospective parents understand why they’re being tested and what those tests might mean. The second post discussed the history of blame and disability more broadly and introduced the fact that ideas about what disability means have changed over time — often significantly.

I’ve argued that genetic counseling has the potential to address feelings of blame, guilt, and confusion in the face of genetic testing results. Further, it can help answer questions like: What will life actually be like for parents and their children? What do genetic tests say and what don’t they say? What are the options after having a test?

My optimism about genetic counseling, evident in these two posts, is tempered by the fact that it has a complex and challenging past with origins in eugenics ideology that have influenced the way counseling is provided today. In a sense what I’m suggesting is that genetic counseling still has a lot of issues that need to be talked about and worked on, but that it’s way better than nothing.

Lets take a look at what I mean about how eugenic ideas shaped genetic counseling.

EUGENIC BEGINNINGS

Most of the first genetic counselors in the 1940s, 1950s, and 1960s were human geneticists, but the origins of human genetics lay in eugenics. Early genetic counselors identified self-proclaimed eugenicists like Charles Davenport, founder of the Eugenics Record Office at Cold Spring Harbor — one of the nation’s leading eugenics institutions between 1910 and the 1930s — as some of the first human geneticists in the United States. And four of the first five presidents of the American Society of Human Genetics, founded in 1948, were also board members of the American Eugenics Society.[1] Human geneticists tried to distance themselves from aspects of the traditional eugenics movement, particularly its racial prejudices and some of its scientific methods, but were still concerned about the eugenic effects of their work. They worried about what effect their counseling might have on the population as a whole.

The Genome Project - Write

NYTimes |  “By focusing on building the 3Gb of human DNA, HGP-write would push current conceptual and technical limits by orders of magnitude and deliver important scientific advances,” they write, referring to three gigabases, the three billion letters in the human genome.

Scientists already can change DNA in organisms or add foreign genes, as is done to make medicines like insulin or genetically modified crops. New “genome editing” tools, like one called Crispr, are making it far easier to re-engineer an organism’s DNA blueprint.

But George Church, a professor of genetics at Harvard Medical School and one of the organizers of the new project, said that if the changes desired are extensive, at some point it becomes easier to synthesize the needed DNA from scratch.

“Editing doesn’t scale very well,” he said. “When you have to make changes to every gene in the genome it may be more efficient to do it in large chunks.”

Besides Dr. Church, the other organizers of the project are Jef Boeke, director of the Institute for Systems Genetics at NYU Langone Medical Center; Andrew Hessel, a futurist at the software company Autodesk; and Nancy J. Kelley, who works raising money for projects. The paper in Science lists a total of 25 authors, many of them involved in DNA engineering.

Autodesk, which has given $250,000 to the project, is interested in selling software to help biologists design DNA sequences to make organisms perform particular functions. Dr. Church is a founder of Gen9, a company that sells made-to-order strands of DNA.

Dr. Boeke of N.Y.U. is leading an international project to synthesize the complete genome of yeast, which has 12 million base pairs. It would be the largest genome synthesized to date, though still much smaller than the human genome.

The Omnigenic Model Of Complex Human Traits

quantamagazine |  The question most of genetics tries to answer is how genes connect to the traits we see. One person has red hair, another blonde hair; one dies at age 30 of Huntington’s disease, another lives to celebrate a 102nd birthday. Knowing what in the vast expanse of the genetic code is behind traits can fuel better treatments and information about future risks and illuminate how biology and evolution work. For some traits, the connection to certain genes is clear: Mutations of a single gene are behind sickle cell anemia, for instance, and mutations in another are behind cystic fibrosis.

But unfortunately for those who like things simple, these conditions are the exceptions. The roots of many traits, from how tall you are to your susceptibility to schizophrenia, are far more tangled. In fact, they may be so complex that almost the entire genome may be involved in some way, an idea formalized in a theory put forward last year.

Starting about 15 years ago, geneticists began to collect DNA from thousands of people who shared traits, to look for clues to each trait’s cause in commonalities between their genomes, a kind of analysis called a genome-wide association study (GWAS). What they found, first, was that you need an enormous number of people to get statistically significant results — one recent GWAS seeking correlations between genetics and insomnia, for instance, included more than a million people. 

Second, in study after study, even the most significant genetic connections turned out to have surprisingly small effects. The conclusion, sometimes called the polygenic hypothesis, was that multiple loci, or positions in the genome, were likely to be involved in every trait, with each contributing just a small part. (A single large gene can contain several loci, each representing a distinct part of the DNA where mutations make a detectable difference.)

How many loci that “multiple” description might mean was not defined precisely. One very early genetic mapping study in 1999 suggested that “a large number of loci (perhaps > than 15)” might contribute to autism risk, recalled Jonathan Pritchard, now a geneticist at Stanford University. “That’s a lot!” he remembered thinking when the paper came out.

Over the years, however, what scientists might consider “a lot” in this context has quietly inflated. Last June, Pritchard and his Stanford colleagues Evan Boyle and Yang Li (now at the University of Chicago) published a paper about this in Cell that immediately sparked controversy, although it also had many people nodding in cautious agreement. The authors described what they called the “omnigenic” model of complex traits. Drawing on GWAS analyses of three diseases, they concluded that in the cell types that are relevant to a disease, it appears that not 15, not 100, but essentially all genes contribute to the condition. The authors suggested that for some traits, “multiple” loci could mean more than 100,000.

views from the borders of mental illness...,

guardian | When the psychologist Peter Chadwick explained that he was trying to research psychosis he was given short shrift by one of his patients. "You're trying to climb rain, Peter, or sweep sun off the pavement." The desire to build a science of disabling mental states can sometimes seem like wishful thinking, especially to those who have experienced the turmoil of an unquiet mind.

It is therefore no accident that critics of psychiatry have always had a particular dislike for the use of diagnosis. There are those on the outer fringes who still argue that classifying anything as a "mental illness" is fundamentally flawed, but most of the debate centres on the possibility of distinguishing different forms of psychological disability. One of the key issues is whether different diagnoses such as schizophrenia, bipolar or depression represent distinct disorders that have specific causes or whether these are just convenient and perhaps improvised ways of dividing up human distress for the purposes of treatment.

This is a hot and newly contentious topic. The fifth edition of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM-5), the book that lists psychiatric diagnoses, is due out in May. The latest revision has emerged after a decade of unfriendly debates over what should be included and where the boundaries should lie.

The most medical approach sees each diagnosis as a separate disease with specific causes. For example, the National Institute of Mental Health, a US government research agency, describes schizophrenia as "a chronic, severe, and disabling brain disorder", something akin to a distinct condition linked to specific genetic risks and brain changes. But diagnoses are not usually derived from scientific discovery but are based on descriptions of experiences and behaviours, which are then tested for their coherence in scientific studies. For those who see mental illness as something best understood at the level of the brain and genetics, the discovery of specific biological differences associated with a particular diagnosis is considered to be good evidence for its validity.

An alternative approach is to see the definition of schizophrenia as a makeshift way of classifying mental distress that clinicians happen to agree on. From this point of view, rather than schizophrenia being a scientific discovery, it's a tradition – varying in its usefulness depending on your point of view. This difference of opinion turns out to be remarkably politicised: the medical model traditionally favours diagnosis, medication and biomedical science, while the social model is linked to the championing of individual experience, psychotherapy and social interventions.

But a growing body of evidence suggests that this divide is both unhelpful and misleading because some of the best evidence that diagnoses do not represent distinct disorders comes not from social criticism but from medical genetics. Observers may note that this is a deliciously uncomfortable situation for both parties. The hardline biological psychiatrists have had diagnoses undermined by exactly the techniques they use to support them and the social constructionists may have to accept that the best evidence for their "humane" conclusions are biological studies which they reject as supposedly "alienating".

meticulously planned parenthood WILL NOT be taken slowly because tards are scared of it...,

SA |  The official policy of the American Society of Reproductive Medicine is as follows: “Whereas preimplantation sex selection is appropriate to avoid the birth of children with genetic disorders, it is not acceptable when used solely for nonmedical reasons.” Yet in a 2006 survey of 186 U.S. fertility clinics, 58 allowed parents to choose sex as a matter of preference. And that was seven years ago. More recent statistics are scarce, but fertility experts confirm that sex selection is more prevalent now than ever.

“A lot of U.S. clinics offer non-medical sex selection,” says Jeffrey Steinberg, director of The Fertility Institutes, which has branches in Los Angeles, New York and Guadalajara, Mexico. “We do it every single day. We did three this morning.”

In 2009 Steinberg announced that he would soon give parents the option to choose their child’s skin color, hair color and eye color in addition to sex. He based this claim on studies in which scientists at deCode Genetics in Iceland suggested they could identify the skin, hair and eye color of a Scandinavian by looking at his or her DNA. "It's time for everyone to pull their heads out of the sand,” Steinberg proclaimed to the BBC at the time. Many fertility specialists were outraged. Mark Hughes, a pioneer of pre-implantation genetic diagnosis, told the San Diego Union-Tribune that the whole idea was absurd and the Wall Street Journal quoted him as saying that “no legitimate lab would get into it and, if they did, they'd be ostracized." Likewise, Kari Stefansson, chief executive of deCode, did not mince words with the WSJ: “I vehemently oppose the use of these discoveries for tailor-making children,” he said. Fertility Institutes even received a call from the Vatican urging its staff to think more carefully. Seifert withdrew his proposal.

But that does not mean he and other likeminded clinicians and entrepreneurs have forgotten about the possibility of parents molding their children before birth. “I’m still very much in favor of using genetics for all it can offer us,” Steinberg says, “but I learned a lesson: you really have to take things very, very slowly, because science is scary to a lot of people.” Most recently, a minor furor erupted over a patent awarded to the personal genomics company 23andMe. The patent in question, issued on September 24th, describes a method of “gamete donor selection based on genetic calculations." 23andMe would first sequence the DNA of a man or woman who wants a baby as well as the DNA of several potential sperm or egg donors. Then, the company would calculate which pairing of hopeful parent and donor would most likely result in a child with various traits.

Illustrations in the patent depict drop down menus with choices like: “I prefer a child with Low Risk of Colorectal Cancer; “High Probability of Green Eyes;” "100% Likely Sprinter;" and “Longest Expected Life Span” or “Least Expected Life Cost of Health Care." All the choices are presented as probabilities because, in most cases, the technique 23andMe describes could not guarantee that a child will or will not have a certain trait. Their calculations would be based on an analysis of two adults’ genomes using DNA derived from blood or saliva, which does reflect the genes inside those adults’ sperm and eggs. Every adult cell in the human body has two copies of every gene in that person’s genome; in contrast, sperm and eggs have only one copy of each gene and which copy is assigned to which gamete is randomly determined. Consequently, every gamete ends up with a unique set of genes. Scientists have no way of sequencing the DNA inside an individual sperm or egg without destroying it.

“When we originally introduced the tool and filed the patent there was some thinking the feature could have applications for fertility clinics. But we’ve never pursued the idea, and have no plans to do so,” 23andMe spokeswoman Catherine Afarian said in a prepared statement. Nevertheless, doctors using PGD can already—or will soon be able to—accomplish at least some of what 23andMe proposes and give parents a few of the choices the Freemans made about their second son.

breaking away is the only viable option...,

churchandstate |  Many of us who have been paying attention to the state of the world over the last half century have now begun to realize with growing horror that the progressive deterioration we have been tracking shows no signs of resolution. In fact, to some of us it looks as though there is no way to resolve this deepening crisis. The end of the track is in sight. The planetary factory is in flames, and all the exit doors are barred.

Proposed technical solutions are utterly inadequate to the scale of the problem. Many ideas like geoengineering will simply make matters worse. There is no political constituency for degrowth – none at all. There is precious little political support for even putting a light foot on the brake. This road to Hell has been paved with the very best of intentions – giving our children a better life stands near the top of the list – but here we are nonetheless. The climate is signalling that our future may be a little warmer than we were expecting, once our seven-billion-passenger train passes those gates.

Now that the denouement is in sight, I’m setting aside the anger and outrage, the blame and shame, to focus my attention instead on why this outcome seems to have been utterly inevitable and unstoppable.

Why has this happened? I don’t buy the traditional “broken morality” or “flawed genetics” arguments. After all, our genetics seemed to be perfectly appropriate for a million years, and the elements of morality that some of us see as sub-optimal (the greed and shortsightedness) have been with us to varying degrees since before the days of Australopithecus. I don’t think it’s just a mistake on our part or a bug in the program – it appears to be a part of the program of life itself. It looks to me as though much deeper forces have been at work throughout human history, and have shaped this outcome.

The main difficulty I have with all the technical, political, economic and social reform proposals I’ve seen is that they run counter to some very deep-seated aspects of human behavior and decision-making. Mainly, they assume that human intelligence and analytical ability control our behavior, and from what I’ve seen, that’s simply not true. In fact it’s untrue to such an extent that I don’t even think it’s a “human” issue per se.

I have come to think that most of our collective choices and actions are shaped by physical forces so deep that they can’t even be called “genetic”. I haven’t written anything definitive about this yet, but the conclusion I have come to in the last six months is that a physical principle called the “Maximum Entropy Production Principle”, which is closely related to the Second Law of Thermodynamics, actually underlies the structure of life itself. Its operation has shaped the energy-seeking, replicative behavior of everything from bacteria to humans. All our intelligence does is makes its operation more effective.

breeding out disease?

cbsnews |  There are few fields of medicine that are having a bigger impact on how we treat disease than genetics. As we reported in October, the science of genetics has gotten so sophisticated so quickly that it can be used to not only treat serious diseases but prevent thousands of them well before pregnancy even begins. Diseases that have stalked families for generations -- like breast cancer -- are being literally stopped in their tracks. Scientists can do that by creating and testing embryos in a lab, then implanting into a mother's womb only the ones which appear healthy. While the whole field is loaded with controversy, those who are worried about passing on defective and potentially dangerous genes see the opportunity to breed out disease.

But with the promise of this technology also comes the fear that some parents would want to use it to select genetic traits in their children that have nothing to do with disease - a debate Lee Silver himself stoked when he wrote the patent for GenePeeks.

Norah O'Donnell: We read your patent and it says your technology could be used to assess whether a child could have other traits, like eye color, hair color, social intelligence, even whether a child will have a widow's peak? If your company is so focused on preventing disease, why would you include those traits?

Lee Silver: The purpose of the list of traits is simply to demonstrate that our technology can be used to study anything that's genetically influenced. That doesn't mean we're going to actually do that.

Norah O'Donnell: OK. But you're running a company? That could be big business?

Lee Silver: We are the ones who invented this technology and we're going to use it to study pediatric disease. At the moment, we will make sure the technology is used only for that purpose.

And at the moment, you'll have to take his word for it because there are no real rules in this country limiting what this kind of technology can be used to screen for, leaving those decisions up to scientists like Lee Silver and Mark Hughes.

Norah O'Donnell: So we should trust you to set the boundaries?

Dr. Mark Hughes: If I'm setting a boundary saying, "I'm not willing to do that," that's no different from any other field of medicine. So sure.

Norah O'Donnell: But do you wrestle with this at all? I mean, who is the gatekeeper?

Dr. Mark Hughes: That's the question. Should it be some group sitting around a mahogany table or should it be all left up to the patient? If it would get to the point where it was like cosmetic surgery, that would be downright awful. But I'd think those are all straw men arguments. And people asked me these very questions that you're asking me right now, 25 years ago. And it hasn't happened.

on human self-domestication, psychiatry, and eugenics

peh-med | Abstract: The hypothesis that anatomically modern homo sapiens could have undergone changes akin to those observed in domesticated animals has been contemplated in the biological sciences for at least 150 years. The idea had already plagued philosophers such as Rousseau, who considered the civilisation of man as going against human nature, and eventually "sparked over" to the medical sciences in the late 19th and early 20th century. At that time, human "self-domestication" appealed to psychiatry, because it served as a causal explanation for the alleged degeneration of the "erbgut" (genetic material) of entire populations and the presumed increase of mental disorders.

Consequently, Social Darwinists emphasised preventing procreation by people of "lower genetic value" and positively selecting favourable traits in others. Both tendencies culminated in euthanasia and breeding programs ("Lebensborn") during the Nazi regime in Germany. Whether or not domestication actually plays a role in some anatomical changes since the late Pleistocene period is, from a biological standpoint, contentious, and the currently resurrected debate depends, in part, on the definitional criteria applied.

However, the example of human self-domestication may illustrate that scientific ideas, especially when dealing with human biology, are prone to misuse, particularly if "is" is confused with "ought", i.e., if moral principles are deduced from biological facts. Although such naturalistic fallacies appear to be banned, modern genetics may, at least in theory, pose similar ethical problems to medicine, including psychiatry. In times during which studies into the genetics of psychiatric disorders are scientifically more valued than studies into environmental causation of disorders (which is currently the case), the prospects of genetic therapy may be tempting to alter the human genome in patients, probably at costs that no-one can foresee.

In the case of "self-domestication", it is proposed that human characteristics resembling domesticated traits in animals should be labelled "domestication-like", or better, objectively described as genuine adaptations to sedentism.

studying the extended phenotype...,

NYTimes | The investigation of the genetics of behavior is a huge scientific enterprise, with great progress being made in a variety of species — roundworms, fruit flies, lab mice, sticklebacks. Dr. Hoekstra’s work is unusual in that it deals with a naturally occurring, complicated behavior in mammals that is important for survival. And it is significant that she has been able to separate that behavior into two modules controlled by separate and independent DNA regions — burrow length, and escape tunnels.

Dr. Bargmann said she was impressed at Dr. Hoekstra’s success in unpacking the behavior into modules, a result that adds to the likelihood of one day finding simple genetic controls underlying the mystifying diversity of natural behavior patterns. The extraordinary variety of animal body shapes, after all, has been found to grow out of a relatively few master control genes.

“I really believe that there are rules for behavior that go all the way back,” Dr. Bargmann said.

One component of Dr. Hoekstra’s success has been oddly low-tech: the kind of fast-hardening foam that can be purchased in a hardware store for home repair. It quickly produces an easily measured mold — behavior solidified.

Another important factor is as high-tech as tech gets. Decades ago the evolutionary biologist Richard Dawkins suggested that one could study the evolution and genetics of behavior just the way one studies the evolution of body shape: concentrate on what animals build — birds’s nests, beaver dams, termite mounds — and treat them like beak length or coat color. Writing before the development of enormously powerful technology for analyzing DNA, he regretted that his proposals were hypothetical.

They are hypothetical no longer.
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You always have to watch the NYTimes like a hawk. Its reporting of topics in "evolutionary biology" always dangerously skirts Big Don-ism. Any time you mix molecular biology with a nonsensical theory in a disturbing mess of facts and factoids, you run the risk of creating a narrative that will be opportunistically co-opted for knuckledragging political ends. If you're going to talk about molecular biology as evolutionary biology, it is important first and foremost, to establish the clear understanding that molecular biologists will be studying differences in burrowing behavior which are nutrient-dependent and pheromone-controlled via epigenetic effects on genetic predispositions - as these consistently express across species - from microbes to man.

THOSE - are genetic mechanisms of behavior.

Stupid, ignorant, political opportunists will instead leap to unfounded conclusions about IQ, aggression, and a host of other non-molecular, non-falsifiable narrative correlations suited to their own political agenda. 

Bad molecular biologists will lose track of the complex machinery under consideration and fall prey to darwinian nostrums relating the study of beak length and coat color "random mutation" as the cause of adaptive evolution. 

The smart money, symbiogenetically enlightened molecular biologists, will stay focused on the more compelling understanding that adaptive evolution is nutrient-dependent and pheromone-controlled through epigenetic feedback mechanisms within symbiotic cohorts, and that optimized and protracted symbiosis gives rise to speciation, not "red in tooth and claw" random mutation.

the double-helix takes the witness stand

cell |  Advances in understanding genetic predispositions to behavioral and neuropsychiatric syndromes are squarely in the sights of the legal profession. With data suggesting substantial genetic contributions to the risk for criminal behavior (Tuvblad et al., 2011), attorneys have begun to explore the potential uses of genetic evidence in their clients’ defense (Denno, 2011). In addition, the first signs that genetic data may be of interest to the civil justice system have begun to appear. As is true whenever scientific data are introduced in court, these developments hold potential for assisting judges and juries with some of the difficult judgments that they face—but they also bring a substantial risk of misinterpretation and misuse.

In considering current and future uses of behavioral and neuropsychiatric genetic evidence, the unhappy history of genetics in the courtroom cannot be ignored. Even before the structure of DNA was identified and the transmission of genetic information elucidated, courts recognized that behavioral traits could be handed down in families. However, judges’ understanding of genetics typically reflected the science of the day, and the consequences of their reliance on contemporary knowledge were not always salutary. For example, in the U.S. Supreme Court’s decision in Buck v. Bell (274 U.S. 200, 1927), which upheld Virginia’s involuntary sterilization statute, Justice Oliver Wendell Holmes, appealing to the popular view that intellectual disability was passed from parent to child and was associated with promiscuity and crime, notoriously declared, “It is better for all the world, if instead of waiting to execute degenerate offspring for crime, or to let them starve for their imbecility, society can prevent those who are manifestly unfit from continuing their kind.”

Presumptions about the relationship between crime and hereditary intellectual deficiencies appear to have influenced the lower courts as well, with defendants who were viewed as “defective delinquents” often sent to state institutions where they could be confined indefinitely, rather than being sentenced to a fixed term in a correctional facility (Willrich, 1998). But the first use of genetic tests in the courts for their presumed relationship to criminal behavior did not arrive until the late 1960s and was based on data purporting to show that the XYY karyotype was linked to violent crime (Denno, 1996). Derived from a number of studies demonstrating overrepresentation of XYY men in correctional populations, the data were recruited by enterprising defense attorneys to argue that their clients’ violence was driven by genetic factors beyond their control, and thus that they could not be held criminally responsible for their behavior. Courts, however, were skeptical about the validity of data suggesting a causal link between the XYY karyotype and violent behavior and generally declined to admit karyotyping of defendants into evidence. As it turned out, the courts’ skepticism was fully justified—the purported link between XYY and violence has never been generally accepted (Stochholm et al., 2012).

Related To Montagnier's Concern About mRNA? Extrachromosomal DNA Drives Tumor Malignancy

thescientist |   Despite being treated with drugs designed to target this gene, the patients were not getting better, and when we interrogated the genomes of their cancers after the tumors were surgically removed following treatment, we saw that they had changed. The tumors had dramatically reduced the number of copies of the targeted epidermal growth factor receptor (EGFR) gene, presumably giving them an advantage to escape the drugs, and they had evolved these genetic differences at a rate that seemed to make no sense—within just one to two weeks. 

Normally, we think of cancers evolving over many cell divisions, as the cells carrying genetic changes that provide a fitness advantage—such as an ability to resist a particular treatment—will be more likely to survive and divide. Here, we were noticing a change in the copy number of the gene within just a few generations. There was no way that we could explain how the tumors were altering their DNA so quickly. 

Even stranger, we could take any cell from the tumor, and whether it had high or undetectable protein levels of EGFR, it would give rise to a new tumor when cultured in the lab or implanted into a mouse. Each of these new tumors would then display the full spectrum of cells found in the original tumor, varied in their EGFR copy number. This makes no sense according to what we know about classical genetics. We would have expected that tumors arising from a cell with low levels of EGFR would give rise to a tumor with low EGFR levels, whereas a tumor arising from a cell with high levels of EGFR would give rise to a tumor with high EGFR levels. 

When we removed the treatment with the EGFR inhibitor from cultured tumor cells, EGFR copy number quickly rebounded, but again, not on chromosomes. When we saw this, we realized that ecDNA might explain why some cancers can become resistant to treatment so quickly, allowing tumors to evolve at a rate that far exceeds anything that could be accounted for by classical genetics. We published our results in Science in 2014, but they were not immediately accepted by the community. Although we had only studied one tumor type, glioblastoma, we began to wonder whether this might be the tip of the iceberg. 

Without realizing it, this study led us, and now others, to a series of discoveries that have changed the way that researchers view cancer in general, revealing frightening ways that tumors can evolve. We have learned that ecDNA is central to the behavior of some of the most aggressive forms of cancer, enabling remarkably elevated levels of oncogene transcription, creating new gene regulatory interactions, and providing a powerful mechanism for rapid change that can drive very high oncogene copy numbers or allow cancer cells to resist treatment. Fist tap Woodensplinter

a search on "entheogens" yields zip, zilch, nada...,

ISHE | Like rivers histories of scientific disciplines have many tributaries. The human ethology tributary I know best begins in a paper given by Eibl-Eibesfeldt at a 1965 conference in Minnesota. Eibl was invited by the originators of the conference - Eckhard Hess, a one-time-student of Lorenz, and several child psychologists interested in strengthening interdisciplinary connections. In his paper Eibl (1967) argued that the concepts of fixed action pattern, IRM, releasing stimuli, spontaneity, and play that ethologists found useful were also of great importance for every student of human behavior (p. 141). As far as I can determine, this melding of ethology with human research interests was a first in the area of child behavior and development. A year earlier, Detlev Ploog (1964) made an analogous move aimed at establishing connections between psychiatry and ethology. In a very scholarly paper, written in German and hence virtually unknown to English-speaking readers, Ploog laid the foundations for a comparative/behavioral approach to psychiatric phenomena: his suggestions covered topics ranging from 'brain mechanisms and instinctual behavioral stereotypies to social behavior and structures.

As Eibl started moving his program forward, Dan Freedman, working in Chicago, was establishing novel links between evolutionary theory and human infant behavior, as well as pioneering an evolutionary approach to research on the life cycle. At the same time, others such as Ambrose, Bowlby, Blurton Jones, van Cranach, Crook, Esser, Ekman, Hutt & Hutt were also in the process of establishing connections between ethology and psychology. In short, by the end of the sixties, a variety of tributaries were feeding into the slowly widening river channel of human ethology.

By 1972, as a result of informal contacts among Chicago, Eibl's group in Seewiesen and Minnesota, a small group of somewhat innocent, self-labeled human ethologists held the first international meeting at the University of Minnesota. Attendance consisted mostly of German. Canadian, and American studcnts. It was a modest beginning to say the least, but it did lead later to two much larger, more sophisticated meetings. The first was held in Percha/Starnberg (Eibl's first research station); the second immediately followed in London under the sponsorship of Nick Blurton Jones. Both meetings were very well-attended and, despite much healthy disagreement on about nearly everything, it became apparent that substantive scientific enterprise was a in the making.

But more than meetings were taking place in 1972. That year Blurton Jones' Ethological Studies of Child Behavior appeared in print. This collection of very promising papers launched a serious commitment to do two things most human ethologists liked to do back then - develop objective methods for observing, categorizing, and organizing behavior, and talking about their subject matter in terms of evolutionary theory. In the foreword top the volume, Tinbergen gave the newly emerging discipline a boost by stressing the need for psychology ("not yet really a science") to build its foundations on "the observation and description of .... natural phenomena" (p. vii), undertaking, in the process, the work of building ethograms, a labor-intensive program of research so productively engaged in by him and Lorenz.

During this same year, Bill McGrew's (1972) volume, An Ethological Study of Children, also appeared; it was a methodological tour de force demonstrating ways to meet the challenge posed by the task of observing and categorizing preschoolers' behavior. Also, at the time, John Bowlby's work on attachment was awakening child psychologists and psychiatrists to the value of taking evolutionary theory seriously. In summary, things were on the move but much of the activity critics claimed, was at the level of "ethologizing". Human ethologists reputedly were over-speculating on the evolutionary origins and functions of human behavior, and wildly extrapolating from animals to humans when they should have begun building human ethograms and discovering novel phenomena.

As a personal note, when I met Eibl, I had grown tired of testing children for Piagetian cognitive structures. I had come to Piaget via general developmental psychology. About a decade earlier, I had been introduced to comparative/experimental psychology by Bob (W.R.) Thompson and ended up working in his rat laboratory at Wesleyan University (Connecticut). Other professors, at that time, did not share Bob's biological leanings, so using the term "instinct" in some classes was a misdemeanor quickly to be corrected by appropriate extinction methods. I realize the weaknesses (operational and conceptual) of the term, but they did not seem to me any more pronounced than the weaknesses of the term "learning". In addition to comparative animal research, Thompson was also well into behavior genetics with John Fuller even though genetics was unpopular in psychology at the time.

As an occasional champion of unpopular causes, I was motivated to extend the biological approach to the study of children when I went to Cornell. When I arrived, I quickly discovered that environmentalism was in strong command. Interestingly, though, animal work was always recognized as a possible source of hypotheses about human behavior, especially if it had anything to do with critical periods for learning. Harlow's work on the effects of social deprivation on rhesus monkeys quickly captured everyone's attention (and devout allegiance) in child development. I found this curious because other animal analogues usually got short shrift if they suggested that instincts were lurking somewhere within them. What was also curious was that Lorenz was condemned by a sizable segment of the faculty as a reactionary nativist. The same faculty, though, enthusiastically acknowledged his imprinting studies, which, it was obvious (to me at least), were classical examples of a gene/environment interaction rather than unmitigated genetic determinism.

Also at the time, it became apparent to me that caging and depriving monkeys was not scientifically superior to studying them in their natural habitats. After two years of experimenting with pregnant rats at Wesleyan, it was refreshing later to hear Eibl describe his warm and humorous relationship with his polecat. It struck me that a significant difference between ethologists and comparative psychologists at the time was that the former viewed their research subjects as friends to understand while the latter viewed them as research objects to manipulate. Recognizing individuals for what they are (as well as what their peculiar environments require of them) seems to me a much more interesting and humane way to study and deal with humans (and animals) than conceptualizing them solely as objects to be used to test hypotheses.

Of course, psychologists have been studying individual differences since the 19th century, but their data have been mostly test scores (reaction time, intelligence. personality, etc.) and hardly ever observational data connecting such differences with differences in success and failure in everyday adaptation. Studying individuals adapting to their environments is very different from testing them; it is also a lot more difficult.

As I got to understand ethology better, a number of its features struck me as very interesting. The major one was that, for a human ethologist perhaps more than for any other behavioral scientist, daily experience and scientific scholarship can never be totally separate. The former feeds the latter with a steady stream of fresh ideas and potential data; the latter controls the former and keeps it from becoming a subjective, unproductive morass. But what really makes this happy symbiosis distinctively ethological is evolutionary theory: it is always lurking in the background suggesting that what happens today on a daily basis may be a very old story with a predictable, long term outcome, or, maybe, a new story with a significant but unknown end. How can one lose?

Another feature of ethology I find attractive was best expressed by the mother of Barbara Pym (modern British author) when she presumably was giving Barbara tips on studying people as potential characters in her books: Mother said, "See what you can find out without asking." Those of us who work with infants or young children understand such advice so well. Asking children questions can be frustrating and perplexing, as well as hilarious (especially when asking gifted children). Asking adults questions, especially questions having to do with resources and inclusive fitness matters, can frequently be an unproductive enterprise.

Establishing human ethology as a branch of ethology, as we all know, has not been free of impediments. Accepting a biological (and especially an evolutionary) approach to studying human behavior has frequently released a whole range of accusations - genetic predeterminism, reductionism, over-simplificationism, sexism, racism, the especially pernicious aim of telling too many adaptationist stories, etc. Much of this criticism is understandable when it comes from those unfamiliar with how science operates and the difficulties ethologists face when doing research on subject matter that is both complex and virtually always out of control. It is less understandable when it comes from other ethologists. Robert Hinde (l979), for example, has noted that "carving up science along phyletic lines smacks of a regression to nineteenth century science" (p. 645) and that "human ethology comes near to being a contradiction in terms" (p. 646). Hinde's main worry seemed to be that human ethologists would not only lose the comparative approach that proved so useful to ethology in general, but also be very tempted to attribute more causal status to evolution in accounting for human behavior than warranted.