Category Archives: Human Genetics

As to diseases, make a habit of two things to help, or at least, to do no harm.

Hippocrates

The increasing ability of human beings to treat formerly lethal diseases has had a massive effect on the quality of our lives over the past century. However, many damaging genetic diseases such as Tay-Sachs and cystic fibrosis have remained outside of this pattern.

While certain drugs and treatments for these conditions do exist, they only can ameliorate the symptoms, not cure them.

Yet, the fact that the genomics industry is working to remedy this situation by developing gene-editing tools like CRISPR also provides new opportunities for investors. For instance, the ARK Genomic Revolution ETF (BATS: ARKG) provides investors with exposure to companies around the world that are involved in the genomics revolution, regardless of sector.

As of right now, most of its holdings are in U.S health care companies, most of which (71.93%) are in the biotech sector. Its other top sectors include advanced medical equipment and technology (12%), medical equipment, supplies and distribution (6.49%), health care facilities & services (4.21%) and pharmaceuticals (4.13%).

Its top holdings include Invitae Corp. (NYSE: NVTA), Illumina, Inc. (NASDAQ: ILMN), CRISPR Therapeutics AG (NASDAQ: CRSP), Intellia Therapeutics, Inc. (NASDAQ: NTLA), Compugen Ltd. (NASDAQ: CGEN), Editas Medicine, Inc. (NASDAQ: EDIT) and Teladoc Health, Inc. (NYSE: TDOC).

This funds performance has been solid in both the short run and the long run. As of February 10, 2020, ARKG is up 4.70% over the past month and up 19.95% over the past three months. It currently is up 6.59% year to date.

The fund currently has $514.19 million assets under management and an expense ratio of 0.75%, meaning that it is more expensive to hold in comparison to other ETFs.

Chart courtesy of http://www.StockCharts.com

While ARKG does provide an investor with a chance to profit from the world of genetics, the sector may not be appropriate for all portfolios. Interested investors always should conduct their due diligence and decide whether the fund is suitable for their investing goals.

As always, I am happy to answer any of your questions about ETFs, so do not hesitate to send me an email. You just may see your question answered in a future ETF Talk.

Continued here:
Accessing the World of Genetics - Stock Investor

RELIGION

Dhanyashtakam: Moksha Vidhyaananda Sarasvati, 4/14, MIG Flats, 4th Main Rd., Kotturgardens, 11 a.m.

Guru Mahimai: P. Swaminathan, Sri Kapaleeswarar Temple, Mylapore, 5.30 p.m.

CULTURE

Sahitya Akademi: Book discussion programme on Ku. Pa. Rajagopalanin Thernthedutha Sirukathaigal, Guna Complex, 2nd Floor, Anna Salai, Teynampet, 5 p.m.

Amar Seva Sangam: Inauguration of Early Intervention International Workshop, Minister V. Saroja participates, Hotel Hyatt Regency, 9 a.m.

Sri Ramachandra Institute of Higher Education and Research: Inauguration of 45th annual meeting of the Indian Society of Human Genetics, Porur, 9 a.m.

SRM Institute of Science and Technology: Awareness programme on Anti-Narcotics, Vadapalani, Noon

Smithsonian Institution and Water Matters: Talk on The Role of temple tanks ion South Indias Water Management, M.O.P. Vaishnav College for Women, Nungambakkam,. 10.30 a.m.

Fromage: Talk on Trutle Conservation, 47, Tamil Salai, Egmore, 5 p.m.

Hindustan Chamber of Commerce: Programme on Personal Data Privacy and Network Security, H.C. Kothari memorial hall, Greams Dugar, Thousand Lights, 6 p.m.

Skill Craft and NEC Technologies: Data Scientist Boot camp - launch of Artificial Intelligence Mastery a training programme, MMA Management Centre, Pathari Rd., 5.30 p.m.

ICWO; AHF-India and University of Madras and NSS: Inter College AIDS Gana contest, YMCA, Nandanam, 2.30 p.m.

D.R.B. Calavala Cunnan Chettys Hindu College: Programme on Industry - Institution Conclave, Pattabiram, 11 a.m.

MEASI Institute of Management: Programme on Research and Data Analysis using SPSS and AMOS, Peters Rd., Royapettah, 9.30 a.m.

G.S.S. Jain College For Women: Workshop on An overview of Budget 2020, Vepery High Rd., Vepery, 2 p.m.

Periyar Library Readers Circle: Meeting, Periyar Thidal, Vepery, 6.30 p.m.

Narcotics Anonymous: Meetings, Keep It Simple Group, St. Joseph High School,Vepery High Rd., Vepery, 7 p.m.

Al-Anon: Meetings, Caring and Sharing Group, Divine School, Perumal Koil St., S.V. Nagar, Padur; Santhome Boys HSS., Santhome; Tollgate Group, CSI Inbarasu Aalayam, Tollgate; Spiritual Service AFG, CSI Church, Nethaji Nagar, Tondiarpet; and Balwadi School, Kavarapalayam Main Rd., Avadi, 7 p.m.

Alcoholics Anonymous: Meetings, Church of Christ, Anna Nagar; Police Boys Club, Elango Nagar, Virugambakkam; Victory Child Development Centre, Muthalamman Koil St., Selaiyur; Church of Victorious Cross, Jawaharlal Nehru Salai, Ashok Nagar; St. Joseph Church, Cholapuram Rd., Ambattur; St. Sebastian Church, Madhavaram; C.S.I, Church, Tollgate; Good Shepherd Church, MMDA, Madhuravoyal; St. Joseph Church, Balayakarar St., Porur; Santhome HSS., Santhome High Rd., Mylapore; V.G.P. Pbhilominal School, Injambakkam; St. James Church Primary School, Ayanavaram, 7 p.m.

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Engagements in Chennai on February 13, 2020 - The Hindu

Feb 8th 2020

PERHAPS MORE than any other, cancer is seen as a disease of genes gone wrong. So, as genetic-sequencing technology has become cheaper and faster, cancer scientists are using it to check which changes to genes cause tumours to spread.

The latest insights from one group, the international Pan-Cancer Analysis of Whole Genomes (PCAWG), are revealed this week in Nature. In an analysis of the full genomes of 2,658 samples of 38 types of tumour taken from the bladder to the brain, the researchers give a blow-by-blow account of how a series of genetic mutations can turn normal cells into runaway clones. It provides the most comprehensive analysis yet of where to find this damaging disruption to DNA and, by unpicking the genetics of what makes cancer tick, just how hard it will be to tame.

For each of the cancer samples, the team produced a read-out of the tumour genomethe 3bn or so individual DNA lettersand compared it with the genome sequences of healthy cells taken from the same patients. In this way they could look for the genetic signatures of the cancer cells, where specific mutations had warped the genetic information.

Most mutations in the genome are harmless. But driver mutations, where genetic changes cause a cell to multiply more easily and faster than other cells, can trigger tumour growth. Many driver mutations have been found over the past decade and a handful have been translated into new medicines. In a fifth of breast cancers (pictured), for example, a driver mutation in the gene HER2 makes cells produce more of a protein on their surface that encourages them to grow and divide out of control. A series of drugs, including Herceptin, target this protein, and lead to significantly improved survival rates. The same HER2 mutation also appears in some lung cancers, raising hopes that similar therapies could work against that disease.

The problem is that most cancers have multiple driver mutations. Indeed, the PCAWG work found that on average each cancer genome carried four or five. And with some clever genetic archaeology they also found that some driver mutations can occur years before symptoms appear.

To discover this, researchers used a new concept called molecular time to reconstruct the cellular evolution of tumour cells. By comparing the DNA of cells within tumours, the researchers could place mutations in chronological order based on how many cells they appeared in. Earlier mutations occur more frequently. For example, driver mutations in a gene called TP53 were found to have originated at least 15 years before diagnosis in types of ovarian cancer, and at least five years before in types of colorectal and pancreatic cancer. Driver mutations in a gene called CDKN2A were found to have occurred in some lung cancers more than five years before diagnosis. In theory, that provides a window in which to find people at risk of developing these diseases, and perhaps prevent the cancer ever appearing.

The new study closes down talk that significant numbers of unknown driver mutations could lurk in the relatively unexplored regions of the human genome. One such driver mutation in non-coding DNA was found in 2013a mutation in the TERT gene across many different cancer types. To check for more like this, the consortium sequenced and analysed all the DNA letters of these non-coding regions (which account for 98% of human DNA) for the first time. They found that non-TERT driver mutations occurred at a rate of less than one per 100 tumours in these regions.

Peter Campbell of the Wellcome Sanger Institute in Cambridge, Britain, and a member of the PCAWG consortium, says an important contribution of the study is that by sequencing so many tumours it has raised the number of patients in whom a genetic contribution to their cancer can be identified from less than 70% to 95%. The goal, he says, is for genome sequencing of tumours to become routine. Efforts to introduce this are under way in some countries, including Britain, the Netherlands and South Korea, he adds.

Insights are all very well, but what about cold, hard clinical progress? Turning genome sequences into meaningful predictors of cancer will require comparisons between samples from tens of thousands of patients, say the researchers, along with data on their treatments and survival rates. Processing this would be beyond the reach of any single organisation. Instead, a follow-up project is planned that includes national funding agencies, charities and corporate partners from more than a dozen countries around the world. It aims to link full sequences of 200,000 cancer patients to their clinical data by 2025.

This article appeared in the Science and technology section of the print edition under the headline "Scientists reveal the most extensive genetic map of cancers ever made"

See more here:
Scientists reveal the most extensive genetic map of cancers ever made - The Economist

New research from the UK has revealed that the build-up of proteins in neuronal cellsthe hallmark of Alzheimers diseasemight be affecting the activity of genes implicated in the disease. This novel discovery may help shed more light on how and why these proteins build up, and how they lead to neuronal death and destruction.

Currently, no treatments are available that can change the course of Alzheimers disease. [This new information can be used to help scientists in their] understanding the interaction between genes and progression of the disease, said Prof. Jonathan Mill, of the University of Exeter Medical School, who led the project.[It] will help us identify new targets for treatment, which we hope will one day lead to drugs that can effectively treat this terrible disease.

Alzheimers disease is a disease of the elderly, commonly associated with loss of memory as it progressives, and eventual loss of all cognitive function. How it develops is not a well understood process, but it is suspected that genetics play a role. The tale-tell histological confirmation of Alzheimers disease is the presence of amyloid plaques and neurofibrillary tangles (made up of the protein tau)each the product of normal proteins which become over-expressed in diseased neuronal brain tissue to the point the neurons are poisoned and die. These proteins are found in lower amounts in normal brains, and the number of plaques and tangles found in patients tends to correspond to the severity of the disease phenotype.

Researchers at the University of Exeter, working in collaboration with Eli Lilly, and funded by Alzheimers Research UK and Alzheimers Society, have examined the brains of mice with mutations in the genes that code for amyloid and tau proteins, hoping to build an animal model to understand the disease better. The build-up of both proteins in specific regions of the brain is known to play a role in Alzheimers disease, so by recreating the genetic conditions, they hope to be able to determine what else must occur for disease development.

The results of this study were published inCell Reports, and the researchers found evidence that the levels of gene activity changed dramatically as tau and amyloid accumulated in the brain. The team also observed significant changes in the levels of gene expression involved with regulating inflammation through the immune system, which became more active as tau levels increased. The research also found new pathways potentially involved in the progression of Alzheimers disease, which adds weight to theories of brain inflammation being a key component in the build-up of tau.

First author Dr. Isabel Castanho, of the University of Exeter, said: Our results suggest that the genes which are disrupted through the build-up of tau and amyloid in the entorhinal cortex region of the brain influence the function of the immune response in the brain, which is known to be a key component of Alzheimers disease.

The team monitored the build-up of both proteins in the brain and the expression levels of their corresponding genes as the mutant mice aged, so they could track the same corresponding time associated in humans with disease worsening. The sequence of events is believed to be similar in the model organism.

Castanho and her team observed the expected build-up of both tau and amyloid, and noted that these changes corresponded to widespread changes in gene expression particularly in the case of tau.

This new information suggests that the accumulation of tau might have a more dramatic effect on gene regulation in the brain than amyloid. Furthermore, several genes observed to be upregulated in this experiment are also known risk factors for Alzheimers disease, and the overall changes observed in the mutant mice mirrored those seen in human Alzheimers disease brains, suggesting this is a sound model.

Dr. Sara Imarisio, head of Research at Alzheimers Research UK, added: Genetics plays an important role in the development diseases like Alzheimers and teasing apart the processes contributing to disease is crucial in the hunt for new breakthroughs, which will change lives. Future research capitalizing on genetic findings like this is a top priority for dementia researchers around the world. Its only thanks to the generosity of our supporters that Alzheimers Research UK is able to fund vital dementia research like this.

Original post:
Amyloid, Tau Buildup in AD Spur Gene Expression that Causes Brain Inflammation - Clinical OMICs News

In the past few years, something new has become possible in biology: cheaply printing DNA for insertion into a cell.

That means a scientist who needs a particular DNA sequence to, say, create new bacteria for research can now order that DNA sequence from a lab. That might seem like a niche technology how many biologists need to custom-print their own DNA? but DNA synthesis and assembly (as the printing process is called) are actually useful for an astonishing variety of research uses, and could have far-reaching implications for how we live. In labs around the world, tons of critically important, valuable biology research is advancing thanks to DNA synthesis, and things look likely to get even better as DNA synthesis gets even cheaper.

But as is often the case when a scientific field gets a lot better at what it does very quickly, progress in DNA synthesis has been so fast that coordination against bad actors has lagged. As a private individual, I can send a DNA sequence Id like synthesized to dozens of labs around the world that can print it out and send it to me.

But what if I asked them to print for me the genetic code of the influenza that caused the 1918 flu that killed millions of people? What if I sent them the instructions for a new disease that I have reason to believe is dangerous? What if I was doing legitimate research, but my lab didnt adhere to modern safety standards?

The answer is that a few DNA synthesis companies will send me what I asked for, with no screening to check whether theyre sending out a pathogen that ought to be carefully controlled. (Synthetic DNA is not a live virus, of course; Id have to be a talented biologist with specialized knowledge, lots of resources, and access to expensive tools to use it maliciously.)

Some companies including most industry-leading ones do follow US guidelines that require a background check and also check the DNA sequence against a list of known hazardous ones and would stop me from making this dangerous order but a recent report found no evidence of any laws requiring laboratories to follow those guidelines in any country in the world. Doing so adds some time and expense to the ordering process, so there is some incentive to cut corners.

Thats why many experts argue that we need to do better. Their proposals on how to fix the system vary, but they all agree on one thing: I shouldnt be allowed to order myself the 1918 influenza or a new coronavirus off the internet and have it delivered to my home.

And to establish screening for DNA orders on a global scale will take large-scale international coordination and so far, we have struggled to coordinate even for simpler countermeasures.

A few decades ago, researchers embarked on the Human Genome Project, which tried to determine the base pairs that make up all of human DNA. It was a 13-year project of enormous scope and complexity. The government had to invest billions of dollars to make it happen.

Since then, the world of genetics has changed. New technology has made us a lot better at scanning and manipulating DNA. It now costs about $1,000, instead of billions, to sequence a full human genome. Other critical aspects of genetics research are getting cheaper too.

Of particular importance? DNA synthesis.

When researchers wanted to produce copies of a DNA sequence theyre studying, they used to have no choice but to painstakingly clone an organism with the DNA they want, inserting or removing genes with splicing techniques. Now, that has changed. With todays techniques, we can artificially build DNA sequences, adding one base pair at a time, in a lab.

The process is fairly cheap and getting cheaper only about 8 cents per base pair added in this fashion though it does still add up with something as big as the human genome. But for many smaller projects, getting the DNA you need synthesized is a viable option. If I have on my computer a sequence of DNA which I want to work with in the lab, I can send those instructions to a DNA synthesis service and theyll send back the DNA, ready for lab work.

Lets consider a researcher who has modified the genome of a bacterium so that it will produce human insulin. Just a few years ago, it would have been expensive and an enormous hassle to get her DNA sequence printed all of the base pairs attached in order so that she could insert it into an organism and start her experiment. Just a few years before that, it would have been basically impossible.

But today, doing this is quite affordable. Thats amazing news for researchers, who can cheaply and quickly order DNA sequences online and get the DNA they asked for delivered straight to them at a reasonable price.

Lets be clear: This is great news. Advances in our ability to synthesize DNA open lots of avenues for promising new research. Researchers can test custom sequences and arrive at a better understanding of gene sequences and what they do. Progress on this front will make for better medicine, better crops, and better production of proteins we need for industrial processes.

But theres a critical security problem to be solved as DNA synthesis gets cheaper and easier.

Since DNA can be both beneficial and dangerous, experts agree that screening should happen. But most countries dont have laws or even guidelines on how to do it.

DNA is an inherently dual-use technology, James Diggans, who works on biosecurity at the industry-leading Twist Bioscience, told me. What that means is DNA synthesis makes fundamental biology research and lifesaving drug development go faster, but it can also be used to do research that can be potentially deadly for humanity. Thats the problem that biosecurity researchers in industry, in academia, and in the government are faced with today: trying to figure out how to make DNA synthesis faster and cheaper for its many beneficial uses while ensuring every printed sequence is screened and hazards are appropriately handled.

Where does policy stand on this? The US government has guidelines intended to prevent dangerous incidents, and If I went to a company like Twist, where Diggans works, and asked for a DNA sequence, they would conduct a background check to determine Is the customer on a watchlist, are there reasons to worry? Diggans told me. Theyd ensure I had a license and ship only to a legitimate lab.

The next step? Screen the sequence, said Diggans or check my request to compare it to known prohibited pathogens. If they noticed I was requesting a dangerous influenza virus, they would follow up with me to learn more about what Im researching.

But not every company follows those guidelines (though most synthetic DNA is produced by companies that do abide by them, and the International Gene Synthesis Consortium polices its members). And the guidelines dont cover short sequences, which are a growing share of biology research.

The technology has kind of outpaced where the government regulators are, Diggans told me.

So new screening and new regulations backing the international use of that screening is needed. The aim of a new screening regime should be to ensure that requests for DNA are checked to determine whether they contain prohibited, dangerous sequences, without adding too much to the expense of screening and without slowing down legitimate researchers, who should be able to access DNA for their projects cheaply and quickly.

We have this window of time to get screening right, Beth Cameron, who works on mechanisms for preventing illicit gene synthesis at the Nuclear Threat Initiative (NTI), told me. NTI is a nonprofit focused on global catastrophic risks and works to prevent attacks and accidents with nuclear, biological, and chemical agents. Last month in Davos, Switzerland, NTI and the World Economic Forum recommended a new international effort to establish a common mechanism for screening DNA orders. The report recommends creating a technical consortium to build and launch that mechanism for use by companies and labs around the world, with the goal of making screening a norm.

The Nuclear Threat Initiative also recommends establishing a new global entity focused on preventing biotechnology catastrophes a place whose mission is to oversee DNA synthesis screening. Since diseases can spread around the world, and DNA synthesis can be located anywhere, strong international cooperation is needed. Lots of international organizations are working together, but theres no good institution to coordinate it.

Another focus for biosecurity researchers should be on changing the incentives for how research is currently conducted.

Why do some companies choose not to screen? Well, screening is expensive. Comparing extremely long sequences of letters to a large database of prohibited sequences requires a lot of computer runtime. If a potential problem is identified, an expert biologist is needed to suss out whether theres a real issue. As DNA screening has gotten cheaper, Cameron told me, screening becomes a larger percentage of the cost.

That puts companies that are doing the right thing at a competitive disadvantage.

So heres another idea: Make grants for biologists who do research with DNA synthesis contingent on using labs that follow screening guidelines. Most of the grants for DNA research actually comes from the US government. By mandating that scientists only buy their DNA from organizations that are employing state-of-the-art, agreed-upon screening procedures otherwise they dont get the grant we can turn DNA screening from a competitive disadvantage into a competitive advantage, and hopefully drive more labs to get on board.

Those research dollars should go to companies that screen responsibly, Diggans told me. With research dollars only going to compliant companies, companies that currently do not screen as encouraged by the US guidelines would likely start complying with them.

Some researchers think the system could be improved along other dimensions as well.

Kevin Esvelt, at MIT, is one of them. Esvelt led early research on CRISPR gene drives, and hes been thinking about misuse of biotechnologies for just as long.

He points at a key limitation of even the best proposed screening programs. In order for companies to know what pathogens to screen for, they need to have a database with the DNA sequences of all the dangerous biological agents we know of so they can cross-check between that database and requests from customers.

But maintaining that database creates some problems. If a new pathogen is added to it, then any bad actor can see that it was added and knows it might be an interesting threat. If a bad actor wants to get dangerous DNA past the screening process, they can review the database and learn whether their sequence will be flagged. Thats why lots of secure systems do not make the details of what test you have to pass publicly available.

There are a few ways to solve this problem. One is to aim to design a comprehensive screening system that is safe even if people have full access to the database of potential hazards.

Esvelts proposed solution goes in the other direction, by arranging for the database to be secure and inaccessible. His proposal is the product of work by cryptographers as well as biologists. The line of research has a few elements.

Current DNA screening sometimes requires an expert to review a potential match and determine whether its a real match. This is expensive, takes up a lot of time, and requires a database of hazards.

Esvelt and the researchers he works with want to make some major changes. The key idea is that they want to develop a comparison system that counts only exact matches, instead of the near-matches counted under current systems. Thatd reduce false positives and make it possible to automate screening. Itd also mean we dont need to compare each new customer request with the full genome of every dangerous biological agent out there. Instead, we can pick some essential segments of dangerous biological agents segments that those agents couldnt function without. (We could also find alternate versions of those segments that are predicted to have the same functionality.)

That would ideally mean theres less to screen for making screening faster without missing any dangerous pathogens the old method would have caught. And there wouldnt be the need for a database of full sequences that could lead to disaster if it fell into the wrong hands. Instead, the database would be distributed and encrypted so no one could access it but everyone could compare sequences to it.

Not every expert I spoke to was convinced that all the measures above were necessary or even feasible to get international agreement on. Experts are divided about whether hash matching Esvelts approach would be an improvement on the current gold standard for screening, IARPAs Fun GCAT. But all of them agreed that to make progress on DNA research security, screening needs to get faster, cheaper, and better coordinated.

Technological solutions will almost certainly be a significant part of the picture as we make DNA screening safe and cheap enough that it can be universal. (One complication to look out for: The technology is now arriving for biology labs to have their own bench-top DNA synthesis. These machines can be equipped from the outset to conduct screening. But if theyre released without any of the capabilities that would make screening possible, itll be very hard perhaps impossible to retrofit that in later.)

But legal and regulatory changes, and international cooperation, will have to be a significant part of the picture too. Its been about coalition building between companies like Twist, nonprofits, and governments internationally, Diggans told me of Twists work on screening.

Over the last two years, we have seen a tremendous sense of urgency from companies and technical experts in developing a global process, Cameron said about the NTI Biosecurity Innovation and Risk Reduction Initiative. But theres a lot of work to make biosecurity a mainstream part of technology research and development.

Any technical solution will only make the world safer to the extent that governments and research funders around the world can adopt it and help make it happen.

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Why DNA synthesis is so important and why it needs to be better regulated - Vox.com

Adapted from the cover of Human Diversity(Twelve)Human Diversity: The Biology of Gender, Race, and Class, by Charles Murray (Twelve, 528 pp., $35)

The dumb kids at Middlebury College had no idea what they were setting in motion when they stopped Charles Murray from speaking. At an instantly infamous 2017 lecture, students shouted down his speech, waited through a livestreamed discussion between him and a faculty member given from a private location, and swarmed him after the event, injuring the faculty member.

Murray, you see, had been thinking about swimming back toward the fraught waters he and the late Richard Herrnstein had explored in 1994s The Bell Curve notions that traits such as intelligence are hugely important in determining who gets ahead in modern societies, and that gaps on those traits among social groups, including racial groups, could be partly genetic in origin. His wife had been telling him not to.

Confound it! he recalls her saying after the Middlebury affair (. . . or two syllables to that effect). If theyre going to do this kind of thing anyway, go ahead and write it. And now, three years later, we have Human Diversity: The Biology of Gender, Race, and Class.

This isnt an intemperate screed meant to trigger oversensitive 19-year-olds, however. Instead, its a patient and generally cautious explanation of where the science stands in the three highly contentious areas mentioned in the subtitle: the biological underpinnings of sex differences, social-class differences, and racial differences.

Those whove been following developments in these areas will find little thats surprising. But those new to the topics will learn a lot, so long as they understand basic statistical concepts well enough to follow Murrays often-a-bit-technical prose. Murray provides some of his own entry-level instruction, but its a little scattershot in terms of what concepts get an explanation in the text, which definitions are relegated to an appendix, and what terms the reader is simply expected to know.

Murray begins with sex differences because theyre the most obvious and hard to deny, so Ill do the same. Men and women have measurably different abilities, preferences, and behaviors; many of those differences do not seem to be shrinking in societies that strive for gender egalitarianism; and new research is establishing some connections between the sexes behaviors and their brains.

Theres a long list of sex differences that researchers have found repeatedly, and they go well beyond physical size. Men are more likely to have autism, women depression. Women are more concerned with the well-being of others; men are more assertive. Men have stronger visuospatial skills, women better verbal ability. Men tend to have higher variation in ability; for example, the sexes have the same average IQ, but men are overrepresented among people with very high or very low IQs. Men and women also have markedly different interests, especially in that men are more likely to prefer working with things, women with people.

These gaps are no doubt at least partly due to socialization and culture, but at least some almost certainly have a biological component. One way of seeing this is to look at what happens when societies adopt stronger norms in favor of gender equity: Do the gaps shrink, as would be expected if socially enforced gender norms caused the gaps to begin with?

Sometimes, sometimes not. Murray goes through a long list of different trends. Male overrepresentation among high scorers on the math portion of the SAT, for example, has shrunk steadily for decades. Womens movement into jobs that involve working with things rather than people, though, happened speedily in the 1970s and 1980s and stopped thereafter, with women still underrepresented in things jobs. (This Murray shows through a fascinating original analysis of federal job classifications and survey data.) Meanwhile, the most gender-egalitarian countries actually have bigger gaps in certain outcomes, such as the share of women who score highly in STEM (science, tech, engineering, and math) tests but choose not to go into those fields. Some theorize that living in an advanced country allows talented women to do what they want rather than what pays most. Another important fact is that women who score highly in STEM tend to have better language skills, and thus more non-STEM job options, than do men who score highly in STEM.

Theres also a growing body of research that looks directly at the effects of male and female hormones and differences in the brains of men and women. Changes in hormone levels tend to exaggerate or reduce sex differences in exactly the direction youd expect people injected with testosterone become more impulsive; prenatal exposure to testosterone predicts a childs future visuospatial ability, autism risk, empathy, and interest in children. As for brains, women have stronger functional connectivity in regions involved in emotion processing and social cognition, and there are sex differences in the sizes of numerous brain regions as well.

Murrays discussion of class differences, meanwhile, relies heavily on a much older body of evidence: the research of behavioral genetics, especially twin studies. Over a period of decades this work has shown that genes are incredibly powerful, though hardly all-powerful, in shaping how a person turns out within a given society whether its his personality, health, intelligence, or education while the shared environment, which is to say the effect of being raised in the same home (with the same income, neighborhood, parenting philosophy, etc.), is generally weak. Newer methods, involving the DNA sequencing of thousands of subjects, actually pinpoint some of the specific genes that affect important traits, and these methods can even be used to generate a polygenic score that predicts from DNA (very imprecisely, but far better than chance) how strongly a person will exhibit a trait.

The clear role of genes in life outcomes, coupled with a weak role for the home environment, implies that social class is not just a matter of privilege and oppression and public policy, and not just a matter of personal responsibility and effort, but also heavily a function of natural abilities. This is not exactly a shocking conclusion, though it does challenge some of the more extreme narratives put forth by both Left and Right.

One criticism Ill make of Murray here, though, is that in noting the limits of public policy he could have dealt more thoroughly with various strains of research showing that environments do matter, sometimes a lot, including Raj Chettys work on how neighborhoods affect social mobility and Susan Dynarskis recent study showing that something as simple as promising financial aid up front, rather than later in the process, can make poor kids much more likely to go to a top-tier college. Educational attainment, by the way, is an important trait that is affected by the shared environment quite a bit: 25 percent in a table presented here, though its also 50 percent genetic.

Lastly, theres race the topic that attracted nearly all of the controversy associated with The Bell Curve despite taking up only a minority of its pages. Interestingly, Murray is more circumspect now than he was in that tome a quarter century ago, when he and Herrnstein wrote that it was highly likely that part of the gap between blacks and whites IQ scores was genetic. Here he is more interested in debunking the notion that race is nothing more than a social construct that has nothing to do with genes at all.

Even on that front hes pretty timid. Indeed, he begins by agreeing to dispense with the word race when talking about genetics, because the word carries so much baggage and the professional geneticists have mostly abandoned it. Instead he goes with population, while noting that the ancestral populations that geneticists distinguish from one another overlap heavily with commonly used racial categories.

Yes, these groups can be identified using nothing but DNA, and yes, there are some important genetic differences among populations: Some less controversial ones affect skin color, malaria resistance, and adaptations for living at high altitudes. In other words, humans have continued to evolve in lots of ways since they spread out across the globe, and different changes have taken hold in different environments. But what about hot-button psychological characteristics such as intelligence?

Youd think wed be getting close to answering that question by now. Recall that weve actually identified a lot of genes that affect these traits, and even developed scoring systems that roughly predict from someones DNA how hell turn out. One imagines you could just apply these techniques to the average DNA profile of each racial group excuse me, population and get a simple answer, albeit a tentative one that would become more precise as methods improved and additional influential genes were discovered.

But its not that easy. For a variety of technical reasons, you cant apply a single scoring system across multiple populations, at least with current methods. Murray notes that the genetic variants weve singled out as playing a role in assorted traits often show up more frequently in some populations than others a point he makes more painstakingly than he probably needs to, with a series of scatterplots and tabulations but he admits these gaps are only grist for future, more sophisticated research. His bottom line is not much different from the point made by the prominent Harvard geneticist David Reich in a 2018 New York Times piece: Human populations differ at the genetic level, and we have to prepare for the possibility that these genetic differences substantively affect traits wed rather they didnt, but we dont know the specifics yet.

In 1994, Herrnstein and Murray lit the world on fire with a book that made highly controversial claims about IQ, class, and race. Human Diversitys publicists no doubt hope for a repeat performance; I had to sign a nondisclosure agreement to see the text before the release date. But the result is actually, as Murray himself promises early on, pretty boring for those already familiar with the topics it covers. What it is, is an excellent primer for the uninitiated at least for a few years, by which point new science will likely have superseded much of the research discussed here.

Hopefully the Middlebury kids and their ilk will bother to read it before denouncing it.

This article appears as The Power of Genes in the February 24, 2020, print edition of National Review.

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'Human Diversity: The Biology of Gender, Race, and Class' Book Review - National Review

While the Wuhan coronavirus dominates health news headlines, less exotic viral foes are still around: influenza, the rhinovirus, adenovirus, and respiratory syncytial virus behind the common cold, norovirus outbreaks aboard cruise ships, and always hepatitis and HIV.

What these viruses share is RNA as their genetic material, a nucleic acid less familiar than DNA. Among the RNA viruses are also West Nile, chikungunya, and those behind Ebola and Marburg hemorrhagic fevers, dengue, rabies, and yellow fever.

When science writer David Quammen made the media rounds recently to discuss the Wuhan coronavirus, he glommed right over the RNA part dont worry about that right now. But his excellent book Spillover: Animal Infections and the Next Human Pandemic, which charts the predictions of the current situation starting nearly a decade ago, details the significance of RNA viruses.

RNA is a nucleic acid like its cousin DNA, but has uracil in place of thymine as one of the four nitrogen-containing bases that carry each molecules encrypted information. RNAs sugar ribose has an oxygen atom in a place that DNAs deoxyribose doesnt. DNA is the same in every cell of an individual, whereas shorter and shorter-lived RNA molecules carry out the specific DNA instructions that sculpt different cell types and functions.

The inability of RNA to repair itself, as DNA can, allows mutations to accrue in RNA viruses, enabling them to replicate wantonly and spread explosively. And our bodies help them. New viral particles spew from coughs and sneezes, are propelled in vomit, and ooze from blood and diarrhea, often before our immune systems begin to respond.

All viruses are just nucleic acids in protein coats theyre not cells, not even considered to be alive. I recently recounted their discovery here.

RNA viruses are everywhere, from subway railings, to deep sea habitats, to jungles, taking up residence in all types of organisms. Here are three that are far less familiar than the flu and coronaviruses, but that for a brief time made the news because they, too, make people sick.

The supposedly first outbreak of hantavirus pulmonary syndrome struck in May 1993, in The Four Corners where Arizona, New Mexico, Colorado, and Utah meet.

Patient zero was a young, previously healthy and fit man of Navajo ancestry who developed shortness of breath and died soon after arriving at a hospital in New Mexico. His fiance had died a few days earlier, also with a sudden respiratory illness. Two healthy young people suddenly sick within a week alerted medical sleuths, who soon discovered five other cases.

After ruling out the usual suspects, like a poison or the flu, local officials notified the CDC. Their Special Pathogens Branch, with state health departments, the Indian Health Service, the Navajo Nation, and university researchers, pursued the cause of the illness.

At the CDC, matching patient tissue samples to known viral genes led to Hantaan virus, the cause of Korean hemorrhagic fever, transmitted by mice. Hantaan affects the kidneys, not the lungs. But could its RNA sequence lead epidemiologists to the source of the new outbreak?

The investigators in the Four Corners trapped and shipped nearly 1,700 rodents to the CDC in Atlanta over the summer for dissection and testing for Hantaan, which would turn out to be a close relative of what would soon be named hantavirus the viral variants are distinguished by human body part affected and geographical distribution.

The deer mouse Peromyscus maniculatus quickly emerged as the reservoir species for hantavirus. Pathogens collect in reservoir species, in which they may or may not cause illness, and are transmitted through vector species to vulnerable hosts. (Heres a great glossary of epidemiology terms.)

Nearly a third of the deer mice tested at the CDC carried hantavirus. The mice are in homes, barns, and live just about anywhere people do in the rural southwestern setting. But what had made some people sick, and not others?

Contact with mice. The homes of the infected people had many more rodents, and the victims did housecleaning, gardened, or worked in nearby fields.

Did the infected folks need to touch the pathogen, or just breathe in a poop-tainted breeze? It probably hadnt mattered, because a confluence of environmental factors prolonged drought, followed by snow and rain that rapidly replenished rodent populations led to a ten-fold explosion in the numbers of mice. Human-to-human spread, which doesnt happen with hantaviruses, wasnt necessary.

By November 1993, the CDC special pathogens team had isolated the new virus, dubbing it the Sin Nombre virus (SNV), causing hantavirus pulmonary syndrome (HPS). Ultimately, 10 people would die in the outbreak. But HPS wasnt new.

When researchers re-examined stored lung tissue from people whod died of unexplained acute respiratory distress, other cases came to light. The first recognized case had been a 38-year-old man whod gotten sick in Utah in 1959!

Although the Navajo people had been aware of the infectious disease, and the link to deer mice, for many years, it was news to the CDC. Once epidemiologists knew what to look for, other variations on the hantavirus theme were reported in the following months:

Hantavirus infections have also popped up in Argentina, Brazil, Chile, Paraguay, Uruguay, and Canada.

Fruit bats, aka flying foxes, are the reservoir species for the related Hendra and Nipah viruses. They belong to genus Pteropus.

These viruses adhere to a peculiar rule of six. If a mutation adds or removes DNA bases so that the size of the viral genome isnt a multiple of six, its kaput.

Like hantavirus, the genetic material of Hendra and Nipah is a single strand of RNA. Each genome has only 6 genes, but RNA editing cuts and pastes gene segments, expanding the protein repertoire of each virus. The 2011 film Contagion was purportedly based on Hendra and the 2019 film Virusbased on Nipah.

Christopher Basler, director of the center for microbial pathogenesis at Georgia State University and colleagues reported on how the viruses make us sick in Nature Communications. A viral protein, called simply W, interferes at pores in the membrane that defines the nucleus, wherein lies our DNA. This action blocks the gene activity that jumpstarts the innate immune response, enabling the viruses to replicate unchecked.

Hendravirus came to public attention in September 1994, in Hendra, a suburb of Brisbane, Australia. The index case was Drama Series, a mare who snorted virus-laden froth onto her dozen stable mates and two trainers, one of whom died. Hendra virus fills the lungs with bloody fluid and can also shut down the kidneys.

If a person survives the pneumonia, inflammation of the membranes around the brain (meningitis), may occur months later. One such delayed case alerted authorities to the fact that a second Hendra virus outbreak happened in August 1994, a month before what was thought to have been the first.

Several other outbreaks have all been in Australia, in forested or coastal areas. Only a handful of people have been infected, but all were near sick horses. The fatality rate is 60% among humans and 75% among horses, and a vaccine for horses became available in 2012.

Nipahvirus infection causes encephalitis and pneumonia, through pigs. An outbreak in 1998 from pig farms on the Malaysian peninsula killed 105 of 265 infected people. Pigs sent from Malaysia to an abattoir in Singapore infected 11 people there, killing one, in early 1999.

The virus was isolated and described soon after, but may have been percolating around the Malaysian peninsula for two years. Since then limited outbreaks have occurred in India and Bangladesh.

Bats bring us coronaviruses; hemorrhagic fevers like Lassa, Marburg, and Ebola; and rabies. The bats seem healthy despite their bodies teeming with virus, and pass the pathogen to us through intermediate hosts, like horses and pigs.

So why bats? Let me count the ways.

We will likely never be able to stay ahead of the ever-mutating viruses. A study published in Virus Evolutionin 2017 implicated bats on a scale larger than limited outbreaks. Investigators from Columbia Universitys Mailman School of Public Health and the University of California, Davis One Health Institute in the School of Veterinary Medicine led the project.

Researchers from 20 nations, over 5 years, identified viruses in 19,192 bats, rodents, and primates, including us. They collected samples from places where viruses could easily jump species, such as ecotourism sites, areas of deforestation, and animal sanctuaries. People encroaching on the habitats of mammals that can fly anywhere is a recipe for disease disaster.

They found 100 species of coronaviruses, and that more than 98 percent of the animals harboring them were bats 282 species in all. Extrapolating for all known bat species suggests that the coronaviruses we know about may be the tip of an iceberg.

Perhaps researchers can zero in on RNA sequences common to all coronaviruses to develop a multipotent vaccine that could be stockpiled and easily provided at the first signs of an outbreak if those signs can be reported.

Ricki Lewis is the GLPs senior contributing writer focusing on gene therapy and gene editing. She has a PhD in genetics and is a genetic counselor, science writer and author of The Forever Fix: Gene Therapy and the Boy Who Saved It, the only popular book about gene therapy. BIO. Follow her at her website or Twitter @rickilewis

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Will scientists ever get ahead of fast-mutating deadly health viruses? Exploring the coronavirus and the genetics of other viral outbreaks - Genetic...

By: Editorial | Updated: February 10, 2020 9:10:58 am Global science would also benefit from a mapping project in one of the worlds most diverse gene pools, which would provide data useful for the mapping of the spread and migration of a range of life forms in the Old World, from plants to humans.

The Genome India Project, a collaboration of 20 institutions including the Indian Institute of Science and some IITs, will enable new efficiencies in medicine, agriculture and the life sciences. The first obvious use would be in personalised medicine, anticipating diseases and modulating treatment according to the genome of patients. Several diseases develop through metabolic polymorphisms the interplay of the environment with multiple genes, which differ across populations. For instance, one group may develop cancers and another may not, depending on the genetically-determined pathways by which they metabolise carcinogens. Cardiovascular disease generally leads to heart attacks in South Asians, but to strokes in most parts of Africa. If such propensities to disease can be mapped to variations across genomes, it is believed public health interventions can be targeted better, and diseases anticipated before they develop. Similar benefits would come to agriculture if there is a better understanding of the genetic basis of susceptibility to blights, rusts and pests. It may become possible to deter them genetically, and reduce dependence on chemicals.

Global science would also benefit from a mapping project in one of the worlds most diverse gene pools, which would provide data useful for the mapping of the spread and migration of a range of life forms in the Old World, from plants to humans. Traversing from the worlds tallest mountain range to warm seas through multiple bio-zones demarcated by climate and terrain, India could provide much information on the interplay of species and genetic groups within them. Eventually, a deeper understanding of ecology could emerge from the material thrown up.

However, some caution must be exercised in the field of human genetics, because the life sciences sometimes stray into unscientific terrain and heighten political bias. The mapping of brain regions to mental functions spun off the utterly unscientific and racist field of phrenology. The work on cranial volume measurements of the physician Samuel Morton regarded in America as the father of scientific racism justified slavery before the US Civil War. In India, a nation riven by identity politics and obsessed with the myths of pristine origins and authenticity, scientific work in mapping genetic groups may become grist to the political mill of the unscientific notion of race. Projects in genetics generally extend over long periods of time, which should be used by makers of scientific policy to ensure that the data which emerges is not interpreted for political ends.

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Mapping life - The Indian Express

Paleoanthropology studies the origin and evolution of man and tries to reconstruct the history of biological and cultural changes experienced by our ancestors since the lines that have led to humans and chimpanzees split some six million years ago. One of the main bodies of evidence on which the study of human evolution draws is fossils of extinct hominid species.

Mara Martinn-Torres is director of the National Research Center on Human Evolution in Spain.

This frequently leads to the erroneous idea that paleoanthropology is an area of study cloistered in the past. In fact, research into human evolution over the last decade has invalidated that paradigm in both the methodological and conceptual sense with research on the very horizon of knowledge that has contributed previously unknown knowledge about our own species. The past is now uncovered using technology of the future. The need to make the dead talk and to maximize the information that can be extracted from cherished and rare fossils and archeological finds has led paleontologists and archeologists to perfect and fully exploit current methodssometimes to define new lines of investigation.

Over the last decade, the analysis of ancient DNA has emerged as cutting-edge research that uses methods (genetics) and concepts (hybridization) not previously common in the field of anthropology. Today, we are the only human species on the planet, but we now know that we had offspring with others that no longer exist and have inherited some of their genes. Both genetic and fossil evidence gathered over the last decade offer a more diverse and dynamic image of our origins. Many of the keys to Homo sapiens success at adapting may possibly lie in this miscegenation that not only does not harm our identity, but probably constitutes a part of our species hallmark and idiosyncrasies.

Privileged with a variety of advanced physical and intellectual capacities, modern humans would have spread to all of the continents no more than 50,000 years ago. That is the essence of the Out of Africa theory, which suggests that in its expansion across the planet Homo sapiens would have replaced all archaic human groups without any crossbreeding at all. Molecular analyses have now dismantled that paradigm, revealing that modern humans not only interbred and produced fertile offspring with now-extinct human species such as Neanderthals, but also that the genetic makeup of todays non-African human population contains between two and four percent of their genes.

Both genetic studies and fossil evidence from the last 10 years offer a more diverse, rich, and dynamic view of our own species. Many of the keys to our successful adaptation as we conquered ever-wider territories and changing environments may well be the result of precisely the cosmopolitan miscegenation that has characterized us for at least the last 200,000 years. This mixture not only does not weaken our identity as a species; it is probably part and parcel of our idiosyncrasy. Human evolution rests precisely on biological diversity, an advantageous and versatile body of resources on which nature can draw when circumstances require adaptive flexibility. Endogamic and homogeneous species are more given to damaging mutations, and it is even possible that the Neanderthals prolonged isolation in Europe over the course of the Ice Age may have made them more vulnerable in the genetic sense.

Part of the flexibility that characterizes humans today came from other humans who no longer exist.

Part of the flexibility that characterizes us today came from other humans who no longer exist. We are the present and the future, but we are also the legacy of those who are no longer among us. Despite being from species who probably recognized each other as different, humans and others now extinct crossbred, producing offspring and caring for them. This inevitably leads us to reflect on current society and its fondness for establishing borders and marking limits among individuals of the same species that are far more insurmountable than those dictated by biology itself.

What is our level of tolerance toward biological and cultural diversity? We continue to evolve. Natural selection continues to function, but we have altered selective pressures. Social pressure now has greater weight than environmental pressure. With the rise of genetic editing techniques, humans now enjoy a superpower that we have yet to really control. Society must therefore engage in a mature and consensual debate about where we want to go, but that debate must also consider our own evolutionary history, including our species peculiarities and the keys to our success.

By any measure, what made us strong was not uniformity, but diversity. Today, more than ever, humanity holds the key to its own destiny. We boast about our intelligence as a species, but what we do from now on will determine how much insight we really possess. In 10, 20, or 100 years, our past will speak for us, and it will be that past that issues the true verdict on our intelligence.

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Anthropology: What we have learned over the last decade - MIT Technology Review

A heated battle over the future of animal gene-editing in the US has intensified following the publication of dueling articles from the Food and Drug Administration (FDA) and the editorial board of the journal Nature Biotechnology.

In an analysis of genome-edited cattle and an accompanying letter to the editor, the FDA defended its proposal to regulate gene-edited animals as veterinary drugs, arguing the regulation would help prevent unintended consequences that could arise from the use of new breeding techniques such as CRISPR-Cas9. Nature responded in a sharply wordededitorial claiming the agencys proposal is at odds with the evidence, and saying it appears primarily designed to avoid legal battles with litigious anti-GMO groups.

In January 2020, Genetic Literacy Project released its Global gene-editing regulation tracker and index, evaluating nations based on how their laws encourage or hinder innovation. These tools illustrate that the US is a pioneer in agricultural gene-editing research, ranking seventh in the world by maintaining sensible rules that protect public health while developing novel food crops that are addressing important nutritional and environmental challenges.

The one exception in US policy is animal biotechnology. Brazil, Argentina, Japan, Canada and Australia have thus far taken a much more progressive stance on this issue. There are currently no gene-edited animals approved for human consumption in the US.

Under the FDAs oversight, only one genetically engineered animal, the transgenic (GMO) fast-growing AquAdvantage salmon developed by AquaBounty has received regulatory approval, which took roughly 20 years. Because of political wrangling, the salmon is not yet sold in the US, but salmon eggs imported from Canada are being raised at an AquAdvantage fish farm in Indiana. In May 2016, the Canadian Food Inspection Agency approved the sale of the GM fish, and AquaAdvantage salmon fillets became available to customers in Canada.

The FDA is now poised to classify gene-edited animals as veterinary drugs, which would put them in the same regulatory bucket as GMO animals, such as AquaBountys salmon, which is engineered in part using genes from another fish species.

Critics contend this proposed policy would trigger extensive, costly premarket regulatory review that would severely limit the ability of scientists to breed gene-edited animals, though the FDA says it will balance its guidelines to protect public health without hampering innovation. The agencys proposal has been panned by animal biotech scientists, some of whom have moved their breeding programs to countries with less restrictive regulations.

FDA stands its ground

Writing in Nature Biotechnology on February 7, FDA Center for Veterinary Medicine (CVM) Director Steven Solomon explained the rationale guiding the agencys proposal. Citing the examples of a gene-edited bull whose genome was unintentionally altered to contain bacterial DNA and a conventionally bred animal from the 1950s, Solomon argued that:

The intended genome edit sought to introduce the Celtic POLLED allele into Holstein cattle. This allele exists in some other cattle breeds and results in the animals lacking horns (or being polled) . [H]owever, the editing also produced unintended modifications . Unintended alterations can have unexpected and deleterious consequences no matter the size of the alteration or how it was produced . There is a particularly compelling example of the risks of occult genomic alterations in cattle produced by traditional breeding techniques: a high incidence of bovine leukocyte adhesion deficiency (BLAD) syndrome, a lethal autosomal recessive disease, in Holstein calves.

The selection of a particular Holstein bull for superior milk production genetics resulted in wide dissemination of carrier bulls semen for breeding beginning in the 1950s and 1960s. It turned out that the selected bull was a carrier of a naturally occurring single point mutation that causes BLAD when two copies are present. The extensive use of carrier bulls semen led to an eventual 23% BLAD carrier frequency in Holstein calves in the United States. It took a decade to effectively breed the genetic mutation that causes BLAD out of dairy cattle genetics.

. We recognize that there is tremendous excitement over quickly embracing and bringing to market the fruits of genome editing technology, as well as the critical importance of adequately identifying potential risks, efficiently evaluating whether the risks do in fact exist, and determining whether the risks pose an actual safety hazard in a timely manner.

It is the FDAs role to balance these competing imperatives. We want to support the timely development of beneficial products, but not at the expense of abdicating our critical role in protecting consumer and animal health. We have a public health obligation to protect consumer and animal health that we must balance with the potential of this innovative technology to enhance human and animal health and food production.

Experts unconvinced

Nature Biotechnologys editorial board found Solomons case unpersuasive. If anything, they wrote, his examples undermine the justification for strict FDA oversight of gene-edited animals:

BLAD is not a justification for mandatory regulation of all gene-edited animals . [I]t illustrates that conventional breeding might warrant tighter FDA oversight, especially when rapid breeding expansion programs thrust particular genetic profiles to the fore . [I]f the BLAD case history tells us anything, it is that the origin of a DNA arrangement (conventional breeding, recombinant DNA or gene editing) makes little difference to an animal.

While the editorial authors conceded that the presence of extraneous donor plasmid in the gene-edited POLLED Holstein DNA was unexpected and initially missed, they said the unintended edit should be properly contextualized. The genomes of domesticated cattle contain north of 86 million mutationsinsertions, deletions and single nucleotide variantsand none of these changes is linked to negative health outcomes in humans who consume milk or meat from cows. Amidst this background of innocuous variation, how can the presence of one identifiable variant justify the costs and delays of mandatory FDA oversight? the authors asked.

The answer, they continued, has more to do with politics than science. Anti-GMO groups have utilized every tool at their disposal to restrict the progress of agricultural biotechnology. One of their most potent weapons has been a constant stream of litigation aimed at the USDA, FDA and EPA, the three federal agencies tasked with oversight of biotechnology. Activist litigation was a primary factor in the delayed approval of AquaBountys salmon, for example. The groups behind the mass of lawsuits have also successfully stoked consumer concern about the alleged risks of genetically engineered crops and animals. Meanwhile, the relatively small animal biotechnology industry doesnt have anywhere near the same the public relations and legal resources. As the editorial explained:

[T]here are very few companies in this sector to argue the case for genetically engineered (including gene-edited) animals . On the other hand, there is a powerful and litigious anti-GMO/pro-organic lobby that repeatedly challenges the legitimacy of regulatory rulings and attempts to block market access following approval.

Life-saving biotech drugs gain wide support in Washington. But there is little political capital invested in backing gene-edited animals. Food remains plentiful and, if anything, the public mood is shifting to vegetarianism and animal-substitute products. Scientists and breeders want to use new technology in agriculture, but public sentiment nostalgically harks back to Victorian farming practices in a way that it doesnt for Victorian medical practices.

A cautious, process-based regulatory route keeps the FDA out of trouble and lowers litigation risks for CVMs lawyers.

The authors ended with a proposal of their own, urging the FDA to regulate gene-edited animals based on the risks they may pose to human health, not the process that was used to breed them:

Mandatory oversight could be phased out to a system whereby the agency exercises discretion over which gene-edited animals are regulated according to the hazard represented by the introduced trait. This would be consistent with USDA policy and longstanding US regulatory policy. It would give the animal biotech sector a chance to bloom. And it would counter the narrative of fearmongers who would taint all gene-edited animals as hazardous to public health and injurious to animal welfare.

Cameron J. English is the GLPs senior agricultural genetics and special projects editor. He is a science writer and podcast host. BIO. Follow him on Twitter @camjenglish

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FDA defends CRISPR-edited animal rules likely to block most uses: Is the agency trying to avoid litigation from anti-GMO groups? - Genetic Literacy...