Technological & Genetic Determinism: If It’s Feasible, Is It Inevitable?

Since MiT7 I’ve been musing about the confluence of two powerful streams of thought that I will call technological determinism and genetic determinism. While these ideas are not necessarily the same thing, they are mutually reinforcing. One is used to corroborate the other. Both express a futurist perception, a kind of faith, that if something can be done, sooner or later it will be done, and it’s futile to try to stop it.

I’ve been on the lookout for examples of the confluence in everyday discourse. Here are two.

Science writer Michael Specter published a New Yorker piece last month about Test-Tube Burgers. He reports on tissue engineering research in North America and the Netherlands that is developing experimental processes for growing meat cells in vitro. In an interview with NPR Fresh Air, Specter explains that the new technologies eventually could transform the world’s food supply. It’s simply a matter of scaling up:

I really think… the most important if really is the will of people to do this. But if you look at other technologies, if you look at the human genome project for instance, that was supposed to cost more than $3 billion and take 13 years to sequence the genome of one man starting in 1986, I believe. We can now do that in an evening for 1,000 bucks. It’s not that many years later.

You look at computer processing, things that cost literally a million dollars 50 years ago, are cheaper than I would put in a $10 watch right now. So that kind of thinking happened with this technology but it would need the support -that only happens when people want to buy the stuff and when they want to invest.

It’s sort of a weird snowball. You have to get someone to get excited and then when someone’s excited other people get excited. But until someone gets excited everyone’s sitting there saying eh, who wants to do this? How can we do this? But scientifically, technologically, there isn’t any reason why this couldn’t be really significant. “ [Transcript]

Commenting on Specter’s article, Razib Khan wrote this on his Gene Expression blog:

Raising raw tissue in cultures may seem ‘yucky,’ a point Specter covers in assessing the reaction of some environmentalists and animal-rights activists who don’t seem as excited by the shift from conventional livestock raising to growing tissue as one would expect if they ran the numbers, but it is probably inevitable if it is feasible.

Mapping Controversies in Citizen Bioscience

The academic buzzwords “bio-politics” and “citizen bioscience” at MiT7 led me into a discourse about science that was new to me. It came from a specialized cultural studies perspective that some call science studies, and Bruno Latour was an oft-cited source for its theoretical underpinnings. It isn’t the discourse of science journalism or the sociology or history of science, but a postmodern critical conflation of all those perspectives, and more.

“Narrative” – who owns it, who controls it, who disrupts it – was the holy grail of almost every argument at Media in Transition 7. After Marina Levina’s talk on Citizen Bioscience in the Age of New Media, I plunged passionately into a debate that seemed to be a reduction of individual vs. institutional narratives. I was alarmed by the notion that “citizen bioscientists” could conduct genetic research without the human protections oversight of the informed consent and institutional review board (IRB) process. To my surprise, I was defending Institutional Science, at least as far as it embraces the protection of human subjects in research. Even as I took on this role, I remembered something I wrote in the role of a disability rights activist in Not This Pig:

At the intersection of law, medicine, and science, institutions wield great power to shape both the information and the decisions we make in the informed consent process. According to Bruce Jennings, “We must not underestimate the power of science and technology to colonize and dominate the contemporary imagination” [13]. In other words, when we make decisions based on informed consent, especially in circumstances when our autonomy is most vulnerable, the marketplace of ideas may not be as free as it should be. Read more

Since MiT7 I’ve continued to wrestle with conflicting perspectives about human subjects research. I do not think that the reductionist schema of individual vs. institutional science is sufficient for understanding the potential risks of genetic screening and recombinant DNA technology. The schema needs to be expanded to include population perspectives, or what Karla F.C. Holloway calls cultural bioethics. And it needs to be grounded in a historical context that does not ignore the 20th-century legacy of eugenics, the Holocaust, and secret Cold War radiation experiments.

Maybe it’s cognitive dissonance. Maybe I’m working my way toward the process Bruno Latour calls mapping controversies.

Mapping Controversies (Wikipedia) | About MACOSPOL - Mapping Controversies on Science for Politics

Pondering Gene Therapy for Stargardt Disease (I)

Ethical questions about genetic disease and genetic research have been much on my mind since I heard a provocative talk on Citizen Bioscience in the Age of New Media, presented by Marina Levina, at MiT7. The protection of human subjects in research is one of my longstanding professional and scholarly interests. It also holds a deeper, personal significance for me. I have a genetic eye disorder called Stargardt disease.

I’ve written about my own complex ethical debate in deciding whether or not to join a research study in the 1990s that sought to identify a Stargardt gene (see the essay Not This Pig). I ultimately decided not to join that study because the informed consent process was not made accessible to me. That was a serious limitation in a study involving people who were legally blind. Intellectual curiosity led me to the study initially, but I had reservations about it that took a long time to understand.  I wrote in 2003:

Hoping for an experimental cure for my eye disease… is not even a blip on my sonar screen. A geneticist who has heard my stories asked me once about this difference in attitudes. The simplest answer is this: unlike heart disease in both its acute and chronic dimensions, I do not experience vision loss as a disease. It is a different way of perceiving the world, and it is rich with its own sensory skills and sweet satisfactions. I think of myself as socially blind; the deficits associated with my blindness result more from society’s limitations than from a disease process active in my body. Read more

Now, after four decades of living with Stargardt disease, there is the possibility of an experimental treatment. Phase I/IIa clinical trials, which are designed to test safety rather than efficacy, are scheduled to begin sometime this summer. They involve gene therapy using a viral vector. I won’t be rushing to join those studies, but I plan to follow their progress.

I should note here that the scientist whom I called Dr. X in Not This Pig is NOT the investigator featured in this news release from Columbia University Medical Center:

The path from basic research to clinical trials is long and arduous?and most new treatment ideas never make it out of the laboratory. This is especially true with gene therapy, which is still in its early stages. One of the few gene therapy treatments to make it to clinical trials is for Stargardt disease, an inherited form of early-onset macular dystrophy that affects approximately 1 in 10,000.The gene for Stargardt was discovered in 1997 by Columbia geneticist Rando Allikmets, and Phase I/IIa clinical trials are scheduled to begin in summer 2011. The hope is that if and when the treatment comes to market, a single dose will restore at least some vision long term, or even permanently.

Allikmets took a circuitous scientific path to the genetics of Stargardt and other eye disorders. Born in Estonia, he spent his childhood studying birds and thought he wanted to become an ornithologist. In college, he decided that molecular biology had more career possibilities. His PhD research at the Institute of Bioorganic Chemistry in Moscow involved building human genome libraries of various organisms and cloning various genes.

In 1991 Allikmets moved to the National Cancer Institute, in Maryland, where he cloned genes of ABC transporters, which are proteins that help transport various molecules across cell membranes. While cloning the ABC transporters, he discovered more than 30 new ones, including one called ABCR. In 1997, he found that ABCR?now called ABCA4?was responsible for Stargardt disease.

Allikmets admits that the road to pinpointing ABCA4 as the cause of Stargardt was simpler than usual. “We were lucky,” he said. “When we mapped the gene, we realized that it was in a region on human chromosome 1 that Baylor College of Medicine researchers had already defined as harboring the Stargardt gene.  At that time, scientists could study a region for years without finding the disease-causing gene.”

The discovery spurred Allikmets to concentrate on eye genetics. In 1999, he moved to Columbia, where today he heads the Laboratory of Molecular Genetics in CUMC’s Department of Ophthalmology and is director of research at the Edward S. Harkness Eye Institute.

When Foundation Fighting Blindness (FFB) invited Allikmets to search for a gene therapy treatment for Stargardt, he resisted, citing his lack of experience in gene therapy. But the foundation was persuasive. Allikmets asked Columbia ophthalmology colleagues Peter Gouras and Janet Sparrow to join him, in particular because of their experience with mouse models and with cell biology. The researchers then asked the biopharmaceutical company Oxford BioMedica to work with them. The Columbia team had been using an HIV-based lentiviral gene-delivery system, while Oxford BioMedica was able to provide them with an equine infectious anemia virus (EIAV)-based one, which was more efficient and less of a safety concern. (Lentiviruses are a subset of retroviruses.)

Allikmets and his team also had to go up against the common knowledge that lentiviruses would be inefficient at targeting the eye’s photoreceptors. Although this was the case with mice, they worked superbly with monkeys?which makes sense, as the monkey eye, like the human eye and unlike the mouse eye, has a macula in the center of the retina.

In 2008, Allikmets, Gouras, Sparrow, and other Columbia colleagues, together with Oxford BioMedica, coauthored a Gene Therapy paper on the successful treatment of Stargardt disease in a mouse model, using an EIAV-based vector to add a normal ABCA4 gene to the eye. The paper offered the “proof of principle,” showing that the treatment idea was workable.

Oxford BioMedica completed the required biodistribution studies, which track the distribution of the virus to tissues other than the treatment target, as well as safety studies for the treatment, called StarGen. In March 2011, the company received FDA approval to proceed to Phase I/IIa clinical trials. These trials will study three dose levels for safety, tolerability, and biological activity. If they are successful, the next step will be Phase IIb trials, to test effectiveness of the treatment. Larger, multicenter Phase III trials will further determine efficacy. Fourteen years after Allikmets discovered the gene for Stargardt disease, Stephen Rose, Ph.D., chief research officer for FFB, commended his perseverance in working to advance his early-stage research from lab to clinic.

I couldn’t find a citation yet for the proposed studies on, which currently lists seven clinical studies for Stargardt disease.

According to the Wikipedia entry on gene therapy:

On 1 May 2023 Moorfields Eye Hospital and University College London‘s Institute of Ophthalmology announced the world’s first gene therapy trial for inherited retinal disease. The first operation was carried out on a 23 year-old British male, Robert Johnson, in early 2007.[26] Leber’s congenital amaurosis is an inherited blinding disease caused by mutations in the RPE65 gene. The results of the Moorfields/UCL trial were published in New England Journal of Medicine in April 2008. They researched the safety of the subretinal delivery of recombinant adeno associated virus (AAV) carrying RPE65 gene, and found it yielded positive results, with patients having modest increase in vision, and, perhaps more importantly, no apparent side-effects.[27]

Hamster Cages, Participatory Surveillance, and the Quantified Self

I’m still catching up on news and media I missed last week while I was pondering media theory at MiT7.The conference’s fundamental issue crystallized for me during the Saturday night forum (Power and Empowerment) when Richard Rogers invoked the phrase “participatory surveillance to” suggest the dark side of platforms monetizing user-generated content (a.k.a. “hamster cages”). Unbeknownst to me at the time was last week’s edition of On the Media, devoted to data, with a story on The Personal Data Revolution. It makes me wonder, whose revolution is it, anyway, and whose wallet should I watch?

One of the sources for OTM’s story was Gary Wolf, who publishes a blog called The Quantified Self. He told OTM:

BROOKE GLADSTONE: So all those individual unique data points have the potential to reveal our society’s workings. Good stuff. But amassing all that revelatory data demands that we all engage in staggering amounts of self-tracking. What does all that navel-gazing do to us?

Gary Wolf, contributing editor of Wired and cofounder of The Quantified Self, a blog about, quote, “self-knowledge through numbers,” started this whole thing, so I pummeled him with my fears.

GARY WOLF: We hear a lot at The Quantified Self the worry that this is just the ultimate stage in a kind of narcissistic apocalypse, so that we will soon not notice anything that goes on more than a few inches from our own nose.


GARY WOLF: I think that that is a fear without a foundation. And one of the things that happens when people begin to pay attention to themselves in new ways is that they see in a different light what they have in common with other people.

BROOKE GLADSTONE: What keeps us optimistic is a sort of fantasy of who we are and what we might become, and don’t we run the risk of losing hope when confronted with the harsh numerical reality of what we really are?

GARY WOLF: I think that’s a very good question. There is a whole industry devoted to selling the possibility of change to people, for instance, health clubs, which see that huge uptick in membership after January 1st [LAUGHS]. And many, many things that we see in our consumer culture are based on hopes that never come true.

And one of the things that happens in The Quantified Self is people begin to see how related all of their behaviors are and how difficult it is to change one thing in isolation, and then, at the same time, how difficult it is to change many things at once.

On the one hand, this is discouraging, whether it’s weight loss or extreme improvements in happiness or great leaps of productivity. The promise of radical change is one of the things that we live on in our society. At the same time, I think trading fantasies of radical change for possibilities of small important changes is a tradeoff worth making.

BROOKE GLADSTONE: Do you think it makes us smarter than our consumer culture?

GARY WOLF: I hope it does.

BROOKE GLADSTONE: If you track yourself over a long period of time, you will inevitably quantify your own physical and cognitive decline, right?


BROOKE GLADSTONE: That’s depressing.

GARY WOLF: We probably do need to tune up our capacity to handle that truth, especially as our demographic shift, at least in this country, towards an older population creates incentive to sell people [LAUGHS] fantasies that their cognitive decline is ultimately preventable, rather than merely manageable.

When you fail to see those clear realistic limits, you’re vulnerable to being exploited and you’re vulnerable to terrible crashes. [LAUGHS] So I think the overall effect of this is very healthy, but not easy. [transcript]