Hot Topics: Genetics

Blog Posts (124)

September 1, 2017

Questioning whether genes in human embryos were in fact successfully edited

Nature reports that the editing of a gene in human embryos–reported earlier in August and discussed recently on this blog–has been questioned by a different group of scientists. Read a fuller, general-public-level description here. The questioning scientists doubt a specific claim of the initial work; namely, that a faulty gene in human sperm was edited through a corresponding gene in the human egg fertilized by... // Read More »
August 29, 2017

Memo To White Nationalists From A Geneticist: Why White Purity Is A Terrible Idea

On August 14th, UCLA researchers Aaron Panofsky and Joan Donovan presented findings of their study,  “When Genetics Challenges a Racist’s Identity: Genetic Ancestry Testing among White Nationalists,” at a sociology conference in Montreal. They’d analyzed 3,070 comments organized into 70 threads publicly posted to the (sometimes difficult to access) “social movement online community”  Stormfront.

Former KKK Grand Wizard Don Black launched Stormfront on March 27, 1995. Posts exceed 12 million, ramping up since the 2016 election season. Panofsky and Donovan’s report has a lot of sociology speak, such as “scholars of whiteness” and “affiliative self-fashioning,” amid some quite alarming posts – yet also reveals a sophisticated understanding of genetics from some contributors.

A WHITE NATIONALIST ONLINE MEET-UP: STORMFRONT

“We are the voice of the new, embattled White minority!”proclaims the bold, blood-tinged-hued message on the opening page of Stormfront, the “community of racial realists and idealists.” It’s a site for white nationalists, who are a little less extreme than white supremacists, who want to dominate the world from their pinnacle of a perceived racial hierarchy. The Stormfronters seem more concerned with establishing their white purity – defined as “non-Jewish people of wholly European descent.”

Yet the lines between white nationalist and supremacist blur, as Stormfront states, “If Blacks or Mexicans become a majority, then they will not be able to maintain the White man’s social, cultural and economic systems because they do not have to (sic) minds needed to do so.”

The idea of white rights is rather new, catalyzed by the revolts of the truly marginalized, murdered, abused, ignored, and enslaved. In the past, whiteness was equated to lack of race, much as I thought as a child of vanilla as a lack of chocolate. Use of genetic ancestry testing to confirm one’s concept of pure whiteness is also somewhat new, a subversion of technology that is disturbing to this geneticist whose grandparents escaped the pogroms of eastern Europe.

Of the 153 folks on Stormfront brave enough to post their genetic ancestry test results, 53 were relieved. “Pretty much what I expected but it was good to get it confirmed,” proclaimed one. A participant named Sloth found out he has “pretty damn pure blood” from Scandinavia, the British Isles, and Iceland, prompting him to plan a getaway to Iceland and get a Thor’s hammer tattoo. Another relieved Stormfronter, worried that “Their (sic) might be American indian or jew in the mix because I tan really easily,” was happy to learn he’s “100% white! HURRAY!”

The other 100 genetic test-takers weren’t so thrilled with their results, seeking excuses. My favorite: “These companies are quite liberal about ensuring every white person gets a little sprinkling of non-white DNA (we know who owns and runs these companies).” ErikTheWhite helpfully added that the genetic testing company 23andMe is deploying Jewish DNA to create bioweapons to kill pure whites as if the DNA replication machinery checks in with the religion of the person.

But an impressive 1260 posts were about the science, several debating what DNA ancestry tests can and cannot do. I agree that the tests provide partial information that may, in fact, be trumped by a look in the mirror or a chat with great-grandma. Deep ancestry testing only provides partial glimpses of parts of the world where some ancestors may have come from. I have a map of my own roots – just what my grandmother told me.

GENETIC ANCESTRY TESTING IS NOT A FINAL ANSWER

DNA-based ancestry testing, from companies such as FamilyTreeDNA23andMe, and Ancestry.com compare parts of the genome that vary in DNA sequence among individuals from people living in different geographical areas, say Charlottesville and Kenya. In addition, mapping sequential changes in gene variant frequencies with places reveals ancient migration routes, which often jibe with historical knowledge.

Results seem overly simplistic. A “Genetic Ethnicity Summary” from Ancestry.com, for example, “reveals where your ancestors lived hundreds-perhaps even thousands of years ago”to be 57% Scandinavian, 32% British Aisles, 8% Eastern European, and 3% Uncertain. Many Stormfronters are disturbed by the uncertainty. The Jewish sprinkles?

The maps and diagrams the testing companies provide aren’t overtly racist, at least compared to the 1890 Census categories of mulatto (half black and half white), quadro (one-fourth black), or octaroon (one-eighth black).

The genomic points of comparison include autosomal swaths, but covering only parts of the non-sex-chromosomes – the autosomes – offers just signpoints, and are a far cry from comparing complete genome sequences. Mitochondrial and Y chromosome DNA sequences are considered too but must be interpreted in context, and with the proverbial grain of salt.

Mitochondrial DNA passes only from mothers, to all offspring, and is used to trace maternal lineage. Groups of linked genes (haplogroups) on the dinky Y are used to trace the paternal lineage. Mt and Y DNA can trace ancient migrations and the echoes of history, like stretches of Genghis Khan’s Y that today are in 1 in every 200 males (~16 million!) living between Afghanistan and northeast of China, reflecting waves of rapes by Genghis and his male descendants since the 13th century.

It’s easier to see that Y and mtDNA represent only a few of thousands of ancestors with a diagram. (DNAeXplained)

But there’s a hitch: mitochondrial and Y DNA comprise <1% of a genome and are only a tiny two of thousands of lineages contributing to the genome of a person living today.

Other problems lurk behind the pretty pie charts and percentages of ancestry test results:

• Tests don’t include all parts of the world.
• A new mutation could place a person in the wrong population group.
• Companies compare clients’ DNA to their own proprietary databases, and so white nationalists can shop around, seeking acceptable findings. It’s a little like my daughter’s elementary school approach to misspelled words on quizzes: “I just won’t ever use those words, mommy!”
• DNA ancestry testing projects current databases of population genetic variability back in time, assuming gene variant patterns were the same.
• Databases may not include people who’ve died young from a genetic disease.

SHARED AFRICAN ORIGINS AREN’T DETECTED BECAUSE THEY DON’T VARY!

That we all came from Africa is written into our genomes, represented by stretches of DNA so common, so much the same in all of us, that it would be nonsensical to include them in tests meant to detect varying DNA sequences. Even the most powerful KKK Imperial Wizard, if he understood genetics, couldn’t whitewash the reality of our African origins. Yet a Stormfront post comforted a man who was distraught that his Genetic Ethnic Summary included Senegal with “… you are simply related to some White fool who left some of his DNA with the locals in what is now Senegal.”

One post revealed a bizarrely accurate take on Mendelian inheritance. AngryGoy follows only mtDNA and Y chromosome information, despite their representation of <1% of the genome, because they are “pure.” His reasoning: Y chromosome DNA is transmitted entirely and unchanged from male to male and mtDNA is transmitted entirely and unchanged from female to all offspring. But autosomal DNA is halved at each generation as the two copies of each chromosome separate into different eggs or sperm.

He goes a step farther: a bi-racial female with a white mother or bi-racial male with a white father are “the lesser of two evils” because at least the mtDNA and Y DNA are untainted. This logic escaped me when I wrote the sections on mtDNA and Y DNA in my genetics books.

Stormfront considers the mtDNA and Y argument to be a version of the one-drop rule. Which leads me to the oft-evoked metaphor of blood for genetic ancestry, which isn’t even accurate because the red blood cells that impart the characteristic color do not even have any DNA!

BLOOD AS A SURROGATE FOR GENETICS

Claims Stormfront: “In a nutshell, the problem with humanity is not so much one of ideology – this or that religious, political, social, or economic doctrine – but rather one of blood. That is, that a great deal (possibly 90% or more) of a person’s intelligence and character is determined by their DNA, which determines the structure of their brain before they are born.”

The statement reeks of genetic determinism, the idea that our traits arise predominantly if not entirely from our genes. The 90% suggests a reference to heritability, which for intelligence ranges from 50% to 80%, depending upon the study consulted. But heritability isn’t the genetic contribution to a trait. Rather, it’s the genetic contribution to the VARIABILITY of a trait.

Writings from Nazi Germany mention “good blood” and “pure blood,” with a lone drop enough to confer non-purity. I’m reminded of the episode of All in the Family in which bigot Archie Bunker is horrified to learn he’s about to receive a transfusion from a black, female, West Indian physician who shares his rare blood type. “Not to worry,” she cautions him with a grin, “when you come out (of) the anesthetic, you might have a strange craving for watermelon.”

The Nazis quest for pure Aryan blood entailed both positive and negative eugenics. The Lebensborn program, begun in 1935, took the children from “unwed mothers” knocked up by the SS and placed them in good Aryan homes, and also placed appropriately blue-eyed, blond orphans in homes, while murdering millions who didn’t fit the Aryan definition of Nordic people from England, Germany, Denmark, Sweden, or Norway. Excluded whites were Roma, ethnic Poles, Slavics, and of course Jews, all deemed subhuman by the self-appointed master race.

The Nazi “Law for the Prevention of Hereditarily Diseased Offspring” provided a list. While hereditary blindness and deafness and “Hereditary chorea” are single-gene conditions, “Congenital Mental Deficiency, Schizophrenia, Manic-Depressive Insanity, Hereditary Epilepsy,” and “any severe hereditary deformity” are not. Yet Genetic Health Courts ruled on who should be sterilized to halt transmission of faulty genes.

REPRODUCTION: RESTRICTING GENE POOLS IS COUNTERINTUITIVE

Some people on Stormfront ask what to do after learning their genetic ancestry is not what they expected. Most answers are polite, but some are variations on “If you do care about the White race, don’t breed with any White women, therefore not polluting our gene pool.”

Intentionally restricting a gene pool (a term that describes a population, not a person or family) to promote a perceived superiority is a real headscratcher to anyone who knows any biology whatsoever.

Survival stems from genetic diversity – not sameness. That’s why sexual reproduction has been so successful: A plague can’t wipe out a population if some members are resistant to the pathogen thanks to gene variants. Conversely, a field of genetically identical anything is vulnerable to change. So Craig Cobb, the white nationalist who inspired Panofsky and Donovan’s project when he was mortified onstage when confronted with genetic ancestry test results indicating he’s 14% African, should instead be thankful that he’s not 100% white.

The idea is straightforward. Members of the same ancestral population having children together increases the chance that mutations inherited from recently shared ancestors will show up in a child. The close relationships amplify the distribution of mutations, and incidence of certain single-gene diseases increases.

The phrase “Jewish genetic diseases” isn’t prejudicial; it states a biological fact. The mass murders of Jews throughout history have strangled their genetic diversity, creating serial population bottlenecks that have concentrated certain disease-causing mutations that made it through the pogroms and Holocaust. And so we have Canavan disease, Tay-Sachs disease, familial dysautonomia, and some two dozen other illnesses that strike other families too, but us with higher frequency

The Amish and Mennonites too have much higher incidence of several single-gene diseases that they brought in from Europe. For example, maple syrup urine disease affects 1 in 400 newborns in these groups, but only 1 in 225,000 in the general population.

But wait! The Amish brought those bad genes in from Switzerland and the Mennonites from the Netherlands, and they’re certainly not Jewish. Pure white Europeans can have mutations???

Yup.

Consider cystic fibrosis. DNA in teeth discovered in a graveyard in Austria along the Danube left there between 544 and 255 BC yielded the most common CF mutation. (See Discovery of the Principal Cystic Fibrosis Mutation (F508del) in Ancient DNA from Iron Age Europeans).

Isn’t Austria more or less the epicenter of white purity?

Going from the population to the molecular level, new evidence has shown that if two people are carriers of certain CF mutations that affect opposite ends of the gene, the genes can complement, encoding correctly-folded proteins that function, so that their children don’t actually face the 25% risk of inheriting the disease. The best way to have parents carrying different mutations is for them to have come from different population groups.

Genetic diversity can protect; genetic sameness empowers mutations. I guess the Nazi list of Hereditarily Diseased Offspring missed the genetic diseases of European whites. It is selective pseudoscience.

And so scientifically, the white nationalists, white supremacists, and neo-Nazis have it all wrong. For DNA doesn’t discriminate – it just assorts itself in sync to our patterns of procreation.

A WHITER SHADE OF PALE

To a geneticist, the idea of supremacy, intellectual or otherwise, based on minimal distribution of a pigment molecule in skin is meaningless, if not outright idiotic. Yet it has dictated so much of our history, fueled so much senseless hatred. So I’ll end with an explanation of human skin color, from my human genetics textbook:

“The definition of race based largely on skin color is more a social construct than a biological concept, because skin color is only one of thousands of traits whose frequencies vary in different populations. We may classify people by skin color because it is an obvious visible way to distinguish individuals, but this trait is not a reliable indicator of ancestry. The concept of race based on skin color falls apart when considering many genes. That is, two people with very dark skin may be less alike than either is to another person with very light skin. Overall, 93% of varying inherited traits are no more common in people of one skin color than any other.”

Skin color arises as melanin molecules are produced and packaged into sacs called melanosomes in cells called melanocytes. The pigment-packed melanocytes snake between the tile-like epidermal cells, releasing melanin granules that are broken into bits and pushed upward as the skin cells divide below. The bits of color darken the skin, protecting it from ultraviolet radiation.

Several genes control melanin production and dispersal, and we vary in skin color. Having more melanin is an adaptation, not a liability! So where did white people come from? The prevailing hypothesis has been that white skin captures more sunshine, making it possible to produce vitamin D and keeping bones strong. A study from David Reich’s lab at Harvard identified 3 genes that brought white skin to Europe.

People who left Africa for Europe about 40,000 years ago had dark skin. Then about 8500 years ago, hunter-gatherers from Spain, Luxembourg, and Hungary brought in variants of the genes SLC24A5 and SLC45A2, which impair the ability to make and distribute melanin. Farther north, where the lower light would have made white skin even more advantageous, evidence from southern Sweden shows contribution from the third gene, HERC2/OCA2, which conferred not only pale skin but blue eyes and blond hair too. Finally, farmers from the Near East also brought in gene variants for white skin. Amid all this mixing, natural selection and perhaps human behavior favored whiteness. Completely wiping out these genes causes albinism, so if anyone could be called mutant, it’s white people, not the brown and black.

Could one type of pigment molecule, controlled by just 3 of our 20,633 genes, fuel so much bigotry?

A FINAL THOUGHT

I applaud Panofsky and Donovan’s revelation of the twisting of genetic ancestry testing to validate white nationalism and its slippery slope to white supremacy. The technology has been helpful in many ways: solving crimes, reuniting families dispersed by slavery, and finding relatives after disasters. Let’s hope that the taking of genetic testing to the dark side of white supremacy backfires, bringing a greater appreciation of our essential biological diversity.

The Alden March Bioethics Institute offers a Master of Science in Bioethics, a Doctorate of Professional Studies in Bioethics, and a Graduate Certificate in Clinical Ethics. For more information on AMBI's online graduate programs, please visit our website.  

 

 

 

August 17, 2017

Search and destroy—or at least, select

This week’s issue of Nature carries a feature article on the explosion of preimplantation genetic diagnosis (PGD) in China.  Because women are having children later in life, partly because of relaxation of the old one-child policy; because Chinese culture sees it as a duty to seek to bear healthy children; because some Chinese want to try to enable their kids to exploit some features of... // Read More »
August 15, 2017

CRISPR and Identity

Dr. Joel Reynolds, a postdoctoral fellow at The Hastings Center recently wrote a very poignant essay in Time magazine arguing that our increasing ability to edit our own genetic code risks eventually eliminating the very genetic code that results in people like his younger brother Jason, who was born with muscle-eye-brain disease, resulting in muscular dystrophy, hydrocephalus, cerebral palsy, severe nearsightedness and intellectual disability. In... // Read More »
August 8, 2017

Charlie Gard Post-Mortem: Could He Have Been Saved?

Charlie Gard would have turned one year old tomorrow.

Two days before the British infant died of a mitochondrial disease on July 28, a short article in MIT Technology Review teased that Shoukhrat Mtalipov and his team at Oregon Health & Science University and colleagues had used CRISPR-Cas9 to replace a mutation in human embryos, a titillating heads-up that didn’t actually name the gene or disease.

Yesterday Nature published the details of what the researchers call gene correction, not editing, because it uses natural DNA repair. I covered the news conference, with a bit of perspective, for Genetic Literacy Project.

Might gene editing enable Charlie’s parents, who might themselves develop mild symptoms as they age, to have another child free of the family’s disease? Could anything have saved the baby?

A TRAGIC CASE

The court hearing testimony on the case between Great Ormond Street Hospital (GOSH) and the family, published April 11, chronicles the sad story. The hospital had requested discontinuing life support based on the lack of tested treatment.

Charlie was born August 4, 2016, at full term and of a good weight, but by a few weeks of age, his parents noticed that he could no longer lift his head nor support any part of his body. By the October 2 pediatrician visit, Charlie hadn’t gained any weight, despite frequent breastfeeding. After an MRI and EEG, Charlie had a nasogastric tube inserted to introduce high-caloric nutrition.

By October 11, the baby was lethargic, his breathing shallow. So his parents, Connie Yates and Chris Gard, took him to GOSH. There, physicians noted Charlie’s “persistently elevated lactate.” It was an ominous sign.

Remember Bio 101? When cellular respiration in the mitochondria fails, an alternate pathway releases lactic acid – this is what causes muscle cramps in a sprinter right after a race. It’s what was happening to the thousands of mitochondria in Charlie’s muscle cells; they weren’t extracting enough ATP energy from digested nutrients, and so the baby was limp, unable to reach or react much. His brain was running out of energy too.

Lactic acid buildup in muscles when oxygen is depleted causes cramping. Charlie had persistently elevated lactic acid.

On October 25, a muscle biopsy indicated only 6% of the normal amount of mitochondrial DNA, well below the 35% that indicates a mitochondrial DNA depletion syndrome (MDDS). But which one did Charlie have? Which gene was mutant? That’s important. With a judge discussing “strains” of the syndrome, as if it is a bacterial infection and not a monogenic disease, confusion loomed.

In mid November, sequencing of Charlie’s genome found two mutations in the gene RRM2B, causing “infantile onset encephalomyopathic MDDS.” It affected the brain and muscles – that was obvious – but he was also deaf and had heart and kidney abnormalities. With these findings, the Ethics Committee at GOSH advised against a ventilator.

Charlie’s disease is a “block to the machinery in charge of supplying nucleotide building blocks for mitochondrial DNA synthesis,” Fernando Scaglia, professor of medical and human genetics at Baylor College of Medicine, told me when I picked his brain on whether gene editing might help Charlie’s parents.

(A quasi-technical aside: RRM2B encodes an enzyme [ribonucleotide reductase] that, with three other subunits, removes an oxygen from the sugar part of nucleic acid building blocks, leaving deoxyribose as the sugar rather than ribose, with two phosphates attached. This happens just outside the mitochondria. Once these precursors get into the mitochondria, a third phosphate is added, forming the DNA nucleotide building blocks of the 37 mitochondrial genes. Charlie inherited a RRM2B mutation from each parent – the gene is in the nucleus, but it is essential to supply the mitochondria with nucleotides. RRM2B’s enzyme works only in cells that aren’t dividing – hence the extreme effects on Charlie’s muscles and brain.)

Charlie’s seizures started on December 15 and never let up. Experts began weighing in, including by the end of the month Michio Hirano from Columbia University, who had experience using nucleoside bypass therapy on 18 patients with MDDS due to mutations in a different gene, TK2. A ray of hope?

(Dr. Nakeya Dewaswala, Medicowesome)

Nucleoside bypass therapy provides precursors to the DNA building blocks that have only one of the three phosphates, to circumvent the disabled enzyme, and because the full forms are too highly charged to easily enter cells. But the paper analyzing the strategy, from 2012, clearly showed that it didn’t work in an experimental system for Charlie’s disease – “myotubes,” bits of non-dividing muscle in a dish:

“First we suggest that not only myotubes (post-mitotic cells), but also myoblasts and possibly other dividing cells can show mtDNA depletion in RRM2B deficiency. Second, supplementation with dNMPs, as expected, had no beneficial effect in RRM2B deficiency. Based on the function of this protein supplementation with dNDPs could be tried as an alternative strategy in RRM2B deficiency.” (This isn’t a sentence, albeit the crucial one for the case; it means trying two phosphates instead of one.)

I’m guessing that these three sentences are what catalyzed the parents’ GoFundMe effort and desire to take their baby to the US. But “there’s never been a proper clinical trial for nucleoside therapy,” said Dr. Scaglia, although 18 patients in Spain and Italy with mutations in a different gene, TK2, have so far tolerated it. But that form only affects muscle. The treatment might not have crossed the blood-brain barrier to reach Charlie’s more extensive disease.

Justice Francis knew the limitations of what some in the media called the “pioneering treatment,” if not the difference between a microbe and a gene. “In fact, this type of treatment has not even reached the experimental stage on mice let alone been tried on humans with this particular strain of MDDS,” he wrote.

Charlie’s disease blocks the supply of DNA building blocks to the mitochondria, but his mutant gene is in the nucleus. 
(NHGRI)

From January 9th until the 27th, Charlie had an unrelenting storm of seizures, his EEG erratic even when he wasn’t obviously seizing. This setback caused postponement of an ethics committee meeting and all but Dr. Hirano to give up. Perhaps he thought it a “theoretical possibility” because of that one sentence in the 2012 paper that suggested giving DNA precursors with 2 phosphates instead of one.

For a time, Columbia University considered treating Charlie, with what I don’t know. Meanwhile, nurses noted and then testified that the baby was gaining weight but making no obvious progress, countering the parents’ observations that Charlie felt pain, distress, pleasure, and subtly communicated with them.

Then an EEG from March 30 convinced even Dr. Hirano that an attempt at any treatment would be futile – a term that so dominated the court hearing that Justice Francis defined it: “for the avoidance of any doubt, the word “futile” in this context means pointless or of no effective benefit.” Goals began to focus on preventing suffering.

Yet the Pope and the President weighed in circa July 4, offering to welcome the baby for unspecified treatment to the Vatican or US. What did they know that the English doctors didn’t? And I had to wonder, where are these notables when similar things happen to many other babies born with rare genetic diseases? (See No Ice Buckets or Pink Ribbons for Very Rare Genetic Diseases)

For a time, discussion at the hearing devolved into a UK vs US scenario of the Brits taking a more reasoned approach in denying a futile therapy whereas US docs would try anything if parents could just raise enough money.

As the Pope and President were making their kind offers, pretty much all the experts were reaching agreement that Charlie should be taken off life support. Still, and understandably, the parents grabbed at any hope. “We truly believe that these medicines will work,” the father told the court, although nucleoside bypass was more an untested hypothesis than a medicine. Belief can’t alter biochemistry.

And so Charlie passed away on July 28.

COULD ANYTHING HAVED SAVED CHARLIE?

It was too soon for nucleoside bypass therapy, nor were approaches for other mitochondrial diseases such as cofactor supplementation (which I wrote about here), liver transplant, or stem cell transplant applicable. Nor can a recently-described peptide-like molecule that silences mitochondrial genes help, because Charlie’s mutant genes are in the nucleus. (A mitochondrion only houses 37 genes.)

Gene therapy or gene editing couldn’t have saved Charlie, because the intervention would have to have infiltrated his many muscle and brain cells, damaged beyond repair. But could either approach enable his parents to avoid having another child with two doses of the RRM2B mutation? (Gene therapy introduces a functioning copy of a gene; gene editing can replace it.)

Couples who are carriers of the same recessive condition already have options to avoid passing on the disease: prenatal genetic testing to identify an affected fetus and ending the pregnancy, or preimplantation genetic diagnosis (PGD) following IVF and selecting healthy embryos to continue development in the uterus.

Unfortunately, yesterday’s Nature paper about gene correction of a heart condition doesn’t apply to Charlie’s family. The researchers used CRISPR-Cas9 to snip a dominant mutation from sperm at the brink of fertilizing an egg, jumpstarting a natural DNA repair mechanism that copies a normal version of the gene from the egg to reconstitute two functioning copies — a little like me giving my husband a Women’s March tee-shirt to match mine and replace his Jets tee-shirt. The approach wouldn’t work for a sperm and an egg each bearing a recessive mutation in the same gene, the scenario for Charlie and 1 in 4 of his potential siblings, because there wouldn’t be a healthy gene to copy.

PGD tests one cell of an 8-celled embryo. If all is ok, the remainder is transferred to a woman’s uterus to continue development.

“It’s easier to do PGD and select those embryos that would not have a mutation in the particular gene, as is done for many other conditions,” Dr. Scaglia said. However, editing-out mutations can potentially help older women undergoing PGD by upping the percentage of okay embryos — both the number of eggs and their quality decline precipitously with age. A more pressing problem, Dr. Scaglia added, is controlling the cost of PGD and getting insurance to cover it, rather than pursuing gene editing.

August 4, 2017

The Age of Designed Babies Arrives

by Craig Klugman, Ph.D.

In the film Gattaca, a couple desiring to have a child visits their neighborhood geneticist:

Geneticist: You have specified hazel eyes, dark hair and fair skin.

July 28, 2017

Human genetic editing (engineering) is here

A “hat tip” again to Wesley Smith, who at the National Review Online blog, provided a link to this week’s report in the MIT Technology Review that the first editing of genes in human embryos in the US is underway—and apparently not yet formally published—at an academic center in Portland, Oregon.  Similar efforts have been undertaken in China, but US scientists have been a little... // Read More »
May 11, 2017

All we like SHEEFs, Part 2

Carrying on with last week’s musings… In thinking further, I think my attempt was confused by conflating the moral status of a SHEEF—a synthetic human entity with embryo-like features, something more than a clump of cells of human origin, but less than a human being—with reasons why I might want to hold that nobody should ever make certain sorts of SHEEFs. Again, SHEEFs are human,... // Read More »
May 5, 2017

All we like SHEEFs (?)

So, how should we address the moral status of synthetic human entities with embryo-like features (“SHEEFs”)? First, we should consider that these are human, as opposed to non-human, if they arise entirely from cells of human origin.  Human/non-human hybrid creatures are just that, and partially human, biologically.  But are any of these human beings, as in, in California the crime of murder is described as... // Read More »
May 5, 2017

All we like SHEEFs (?)

So, how should we address the moral status of synthetic human entities with embryo-like features (“SHEEFs”)? First, we should consider that these are human, as opposed to non-human, if they arise entirely from cells of human origin.  Human/non-human hybrid creatures are just that, and partially human, biologically.  But are any of these human beings, as in, in California the crime of murder is described as... // Read More »

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Published Articles (61)

American Journal of Bioethics: Volume 17 Issue 7 - Jul 2017

Modernizing Research Regulations Is Not Enough: It's Time to Think Outside the Regulatory Box Suzanne M. Rivera, Kyle B. Brothers, R. Jean Cadigan, Heather L. Harrell, Mark A. Rothstein, Richard R. Sharp & Aaron J. Goldenberg

AJOB Primary Research: Volume 8 Issue 2 - Apr 2017

When bins blur: Patient perspectives on categories of results from clinical whole genome sequencing Leila Jamal, Jill O. Robinson, Kurt D. Christensen, Jennifer Blumenthal-Barby, Melody J. Slashinski, Denise Lautenbach Perry, Jason L. Vassy, Julia Wycliff, Robert C. Green & Amy L. McGuire

American Journal of Bioethics: Volume 17 Issue 5 - May 2017

Genetic Fingerprints and National Security Beau P. Sperry, Megan Allyse & Richard R. Sharp

American Journal of Bioethics: Volume 17 Issue 4 - Apr 2017

Psychiatric Genomics and Mental Health Treatment: Setting the Ethical Agenda Camillia Kong, Michael Dunn & Michael Parker

American Journal of Bioethics: Volume 17 Issue 4 - Apr 2017

Psychiatric Genetics in a Risk Society Nicole Martinez-Martin

American Journal of Bioethics: Volume 17 Issue 1 - Jan 2017

A Framework for Unrestricted Prenatal Whole-Genome Sequencing: Respecting and Enhancing the Autonomy of Prospective Parents Stephanie C. Chen & David T. Wasserman

American Journal of Bioethics: Volume 17 Issue 1 - Jan 2017

Modern Pregnancies and (Im)Perfect Babies Stephanie A. Kraft

American Journal of Bioethics: Volume 16 Issue 12 - Dec 2016

Does Lack of “Genetic-Relative Family Health History” Represent a Potentially Avoidable Health Disparity for Adoptees? Thomas May, Kimberly A. Strong, Kaija L. Zusevics, Jessica Jeruzal, Michael H. Farrell, Alison LaPean Kirschner, Arthur R. Derse, James P. Evans & Harold D. Grotevant

AJOB Primary Research: Volume 7 Issue 3 - Jul 2016

Concerns about genetic testing for schizophrenia among young adults at clinical high risk for psychosis Ryan E. Lawrence, Phoebe Friesen, Gary Brucato, Ragy R. Girgis & Lisa Dixon

AJOB Primary Research: Volume 7 Issue 3 - Jul 2016

Clarifying ethical responsibilities in pediatric biobanking Merle Spriggs & Craig L. Fry

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News (895)

September 5, 2017 9:00 am

F.D.A. Approves First Gene-Altering Leukemia Treatment, Costing $475,000 (The New York Times)

The Food and Drug Administration on Wednesday approved the first-ever treatment that genetically alters a patient’s own cells to fight cancer, a milestone that is expected to transform treatment in the coming years.

August 22, 2017 9:00 am

China’s embrace of embryo selection raises thorny questions (Nature)

Early experiments are beginning to show how genome-editing technologies such as CRISPR might one day fix disease-causing mutations before embryos are implanted. But refining the techniques and getting regulatory approval will take years. PGD has already helped thousands of couples. And whereas the expansion of PGD around the world has generally been slow, in China, it is starting to explode.

August 16, 2017 9:00 am

Commit to talks on patient data and public health (Nature)

Of course it was going to happen — and now it has. Last week, an international team reported the use of CRISPR–Cas9 gene-editing techniques to correct a heart-wrenching mutation in human embryos. These attempts worked several times more efficiently than previous ones had, and avoided introducing new genetic errors. Although the embryos were never destined to be used for pregnancies (and have now been destroyed), the work — carried out mainly in the United States — makes it easy to foresee practical applications to genetically alter human embryos.

August 15, 2017 9:00 am

Horse Clones Start Heading to the Races (Bloomberg News)

So far, the big winner in the great clone race has been Alan Meeker, chief executive officer of Crestview Genetics. Since 2010 the 52-year-old Texas oil heir has created close to 100 horse clones valued at $500,000 to $800,000 each, depending on how long the company’s raised them.

August 14, 2017 9:00 am

Americans are becoming more open to human genome editing, survey finds, but concerns remain (Science)

CRISPR, the powerful genome-editing tool, does a molecular tango to cut and modify DNA that is highly nuanced. The same subtlety applies to the public’s views on how best to use genome editing in humans, a new survey of adults in the United States shows.

August 11, 2017 9:00 am

CRISPR fixes disease gene in viable human embryos (Nature)

An international team of researchers has used CRISPR–Cas9 gene editing — a technique that allows scientists to make precise changes to genomes with relative ease — to correct a disease-causing mutation in dozens of viable human embryos. The study represents a significant improvement in efficiency and accuracy over previous efforts.

August 8, 2017 9:00 am

CRISPR patent battle in Europe takes a ‘wild’ twist with surprising player (Science)

MilliporeSigma, a subsidiary of pharmaceutical giant Merck KGaA of Darmstadt, Germany, has become a new major player in the complicated European patent battles over CRISPR, the revolutionary genome-editing tool.

July 25, 2017 9:00 am

US defense agencies grapple with gene drives (Nature)

The JASONs, a group of elite scientists that advises the US government on national security, has weighed in on issues ranging from cyber security to renewing America’s nuclear arsenal. But at a meeting in June, the secretive group took stock of a new threat: gene drives, a genetic-engineering technology that can swiftly spread modifications through entire populations and could help vanquish malaria-spreading mosquitoes.

July 24, 2017 9:00 am

Scientists record videos in strands of DNA using CRISPR (Science)

With the help of the gene editor CRISPR, scientists can now save videos in DNA, Nature writes. The researchers encoded five grayscale images into 104 DNA fragments per image, each made up of 33 DNA letters. One image per day was then introduced to the Escherichia coli bacterium. Because CRISPR adds DNA snippets to its host genome in sequential order, researchers were able to recover the recorded images after sequencing and put them together to see the movie.

July 10, 2017 9:00 am

How Canadian researchers reconstituted an extinct poxvirus for $100,000 using mail-order DNA (Science)

A group led by virologist David Evans of the University of Alberta in Edmonton, Canada, says it has synthesized the horsepox virus, a relative of smallpox, from genetic pieces ordered in the mail. Horsepox is not known to harm humans—and like smallpox, researchers believe it no longer exists in nature; nor is it seen as a major agricultural threat. But the technique Evans used could be used to recreate smallpox, a horrific disease that was declared eradicated in 1980.

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