Warm Beds Are Good fails to grapple with the most interesting question of all, however, which is how Arwen and Aragorn could possibly have developed the hots for each other in the first place. It turns out to be rather hard to come up with any theory of Elvish reproductive biology under which Arwen’s behavior makes any sense at all.
Aragorn’s end isn’t that much of a mystery. He’s an alpha male of a warrior culture, chock full o’ testosterone and other dominance hormones guaranteed to make him into a serious horn-dog. She’s a beautiful princess, broadcasting human-compatible health-and-fertility signals in all directions. If she doesn’t actively smell bad, tab A fits slot B just fine from the point of view of his mating instincts.
No, the fundamental problem is Arwen’s lifespan. She is supposedly something like two thousand, seven hundred years old when she meets Aragorn. That’s an awful lot of Saturday nights at the Last Homely Disco West of the Mountains; if she has a sex drive anything like a normal human female’s, she ought to have more mileage on her than a Liberian tramp steamer. On the other hand, if her sexual wiring is fundamentally different from a human female’s, what’n’the hell is she doing with Aragorn? He shouldn’t look or smell or behave right to trigger her releasers, any more than a talking chimpanzee would to most human women.
“B-b-but…” I hear you splutter “This is fantasy!”, to which I say foo! Tolkien was very careful about logical consistency in areas where he was equipped by temperament and training to appreciate it; he invented a cosmology, thousand of years of history, multiple languages; he drew maps. He lectured on the importance of a having convincing and consistent secondary world in fantasy. Furthermore, Tolkien never completely repudiated the intention that his fiction was a mythic description of the lost past of our Earth, and that therefore matter, energy and life should be consistent with the forms in which we know them.
Therefore, it is entirely appropriate to analyze Middle-Earth as though it were a science-fictional creation, to assume Elves and Men both got DNA, and to ask if the freakin’ biology makes any sense at all under this assumption.
And one of the facts we have to deal with is that humans and elves are not just interfertile, they produce fertile offspring. That means they have to be genetically very, very similar. If there are dramatic differences between elf and human reproductive behavior, the instinctive basis for them must be coded in a relatively small set of genes that somehow don’t interfere with that interfertility. In fact, technically, Elves and Men have to be subspecies of the same stock.
When this came up on my favorite mailing list just after the first movie came out, my hypothesis was that elves (a) have only rare periods of vulnerability to sexual impulses, and (b) imprint on each other for life when they mate, like swans. This pattern is actually within the envelope of human variation, though uncommon — which makes it a plausible candidate for being dominant in another hominid subspecies.
This ‘swan theory’ would be consistent with Appendix A, which (a) has Arwen meeting Aragorn when he was garbed like an elven prince and (as near as we can tell through Tolkien’s rather clotted chansons-de-geste style) falling for him hard right then and there, and (b) has Arwen’s family apparently operating under the assumption that once that had happened, the damage was done and she wouldn’t be mating with anyone else, noway, nohow.
One of the techies on the list shot the swan theory down by finding a canonical instance of an Elf remarrying (Finwe, father of Feanor; first wife Miriel, second Indis). In subsequent discussion, we concluded that it wasn’t possible to frame a consistent theory that fit Tolkien’s facts. The sticking-point turned out to be the half-elven; Tolkien tells us that they get to choose whether they will have the nature of Men or Elves, and it is implied that they do so at puberty.
Since that’s true, the difference between Men and Elves can’t properly be genetic at all. It must be in the cloudy realm of spirit, magic, and divine interventions. This is not an area in which Tolkien (a devout Catholic) gives us any rules or regularities at all. Elvish sexual behavior could be arbitrarily variant from human without any reasons other than that Eru keeps exerting his will to make it so, and He very well might be intervening to keep elf-maidens’ hormones from getting them jiggy Until It’s Time.
Helluva way to run a universe, say I. Inelegant. A really craftsmanlike god would build his cosmos so it wouldn’t require constant divine intervention to function. It’s a serious weakness in Tolkien’s fiction, one that runs far deeper than anachronisms like domestic cats (which didn’t reach northern Europe until late Roman times) and tea (to Europe in 1610) in the Shire.
Eric S. Raymond, “Sex and Tolkien”, Armed and Dangerous, 2003-12-18.
October 3, 2016
May 26, 2016
Don’t get too smug, fellow Canuckistanis, as I suspect the numbers might be just as bad if Canadians were surveyed in this way:
You might have heard that Americans overwhelmingly favor mandatory labeling for foods containing genetically modified ingredients. That’s true, according to a new study: 84 percent of respondents said they support the labels.
But a nearly identical percentage — 80 percent—in the same survey said they’d also like to see labels on food containing DNA.
The study, published in the Federation of American Societies for Experimental Biology Journal last week, also found that 33 percent of respondents thought that non-GM tomatoes “did not contain genes” and 32 percent thought that “vegetables did not have DNA.” So there’s that.
University of Florida food economist Brandon R. McFadden and his co-author Jayson L. Lusk surveyed 1,000 American consumers and discovered [PDF] that “consumers think they know more than they actually do about GM food.” In fact, the authors say, “the findings question the usefulness of results from opinion polls as motivation for public policy surrounding GM food.”
My summary for laymen: When it comes to genetically modified food, people don’t know much, they don’t know what they don’t know, and they sure as heck aren’t letting that stop them from having strong opinions.
May 19, 2016
… it is not a bad time to remind ourselves how lucky we are to live on this damp little island.
I don’t mean this in a jingoistic way, and certainly when you look closely there is little to recommend Henry V’s brutal French raid. What there is to celebrate, of course, is Shakespeare’s poetic rendering of the campaign. It is our literary, scientific, technological, economic, political and philosophical achievements, rather than just our military milestones that we should occasionally pause to remember, amid our usual self-criticism.
All my life I have been told that Britain is in decline. But stand back and take a long, hard look. Even by relative standards, it just is not true. We have recently overtaken France (again) as the fifth largest economy in the world and are closing on Germany. We have the fourth largest defence budget in the world, devoted largely to peace-keeping. We disproportionately contribute to the world’s literature, art, music, technology and science.
We have won some 123 Nobel prizes, more than any other country bar America (and more per capita than America), and we continue to win them, with 18 in this century so far. In the field of genetics, which I know best, we discovered the structure of DNA, invented DNA fingerprinting, pioneered cloning and contributed 40 per cent of the first sequencing of the human genome.
On absolute measures, we are in even better shape. Income per capita has more than doubled since 1965 — in real terms. In those days, three million households lacked or shared an inside lavatory, most houses did not have central heating and twice as many people as today had no access to a car. When they did it was expensive, unreliable and leaked fumes.
In the 1960s even though there were fewer people in Britain, rivers were more polluted, the air was dirtier, and there were fewer trees, otters and buzzards. Budget airlines, mobile phones, search engines and social media were as unimaginable as unicorns. Sure, there was less obesity and fewer traffic jams, but there were more strikes, racism and nylon clothing. People spent twice as much of their income on food. There may be political angst about immigrants, but Britain is far more at ease with its multicultural self today than we might have dared to hope in the 1960s.
Matt Ridley, “Britain’s Best Years”, MattRidley.com, 2015-01-01.
October 8, 2015
In Wired, Sarah Zhang handicaps the horses in this year’s highly competitive Nobel Sweepstakes:
Nobel prize speculation, gossip, and betting pools kick off every fall around the time Thomson Reuters releases its predictions for science’s most prestigious prize. This year, one prediction was unusual: a genome-editing tool so hyped that it even got on the cover of WIRED.
(No, seriously, how often does molecular biology get to occupy the same space as Star Wars or Rashida Jones?)
The tool, Crispr/Cas9, is essentially a pair of molecular scissors for editing DNA, so precise and easy to use that it has taken biology by storm. Hundreds if not thousands of labs now use Crispr/Cas9 to do everything from making super-muscled pigs to snipping HIV genes out of infected cells to creating transgenic monkeys for neuroscience research. But the Nobel prediction stands out for two reasons: First, the highly-cited paper describing Crispr/Cas9 came out a mere three years ago, a blip in the timescale of science. Second, the technique is currently at the heart of a bitter patent fight.
Thomson Reuters bases its predictions on how often key papers get cited by other scientists. Here, the paper in question has as its authors Jennifer Doudna, a molecular biologist at UC Berkeley, and Emmanuelle Charpentier, a microbiologist now at the Max Planck Institute for Infection Biology. Missing is Feng Zhang (no relation to this writer), a molecular biologist at the Broad Institute and MIT, who actually owns the patents for CRISPR/Cas9 and says that he came up with the idea independently. So let’s say Thomson Reuters gets it right. Could the patent for a discovery go to one scientist, and the Nobel prize for the discovery to someone else?
The two groups — or their patent lawyers, really — are in fact fighting over credit for CRISPR/Cas9. At stake are millions of dollars already poured into rival companies that have licensed patents from the two different groups.
But putting aside all the lawyers and all the money for a moment, obsessing over finding the one true origin of Crispr/Cas9 gets science all wrong. Casting the narrative as Doudna versus Zhang or Berkeley versus MIT is a misapprehension of history, creativity, and innovation. Discovery comes not from a singular stroke of genius, but an incremental body of research. “I’m not a great believer in the flash-of-genius theory. If you are a historian —” says Mario Biagioli, who is in fact a historian of science at UC Davis — “you quickly will realize exactly how many times there are independent discoveries of the same thing.” The dispute over credit for CRISPR/Cas9 is not the result of exceptional coincidence and disagreement. In fact, it illuminates how science always works.
July 28, 2015
In Nautilis, Adam Piore talks about the project to thoroughly map Icelanders’ DNA:
In the ninth century there was a Norwegian Viking named Kveldulf, so big and strong that no man could defeat him. He sailed the seas in a long-ship and raided and plundered towns and homesteads of distant lands for many years. He settled down to farm, a very wealthy man.
Kveldulf had two sons who grew up to become mighty warriors. One joined the service of King Harald Tangle Hair. But in time the King grew fearful of the son’s growing power and had him murdered. Kveldulf vowed revenge. With his surviving son and allies, Kveldulf caught up with the killers, and wielding a double-bladed ax, slew 50 men. He sent the paltriest survivors back to the king to recount his deed and fled toward the newly settled realm of Iceland. Kveldulf died on the journey. But his remaining son Skallagrim landed on Iceland’s west coast, prospered, and had children.
Skallagrim’s children had children. Those children had children. And the blood and genes of Kveldulf the Viking and Skallagrim his son were passed down the ages. Then, in 1949, in the capital of Reykjavik, a descendent named Kari Stefansson was born.
Like Kveldulf, Stefansson would grow to be a giant, 6’5”, with piercing eyes and a beard. As a young man, he set out for the distant lands of the universities of Chicago and Harvard in search of intellectual bounty. But at the dawn of modern genetics in the 1990s, Stefansson, a neurologist, was lured back to his homeland by an unlikely enticement — the very genes that he and his 300,000-plus countrymen had inherited from Kveldulf and the tiny band of settlers who gave birth to Iceland.
Stefansson had a bold vision. He would create a library of DNA from every single living descendent of his nation’s early inhabitants. This library, coupled with Iceland’s rich trove of genealogical data and meticulous medical records, would constitute an unparalleled resource that could reveal the causes — and point to cures — for human diseases.
In 1996, Stefansson founded a company called Decode, and thrust his tiny island nation into the center of the burgeoning field of gene hunting. “Our genetic heritage is a natural resource,” Stefansson declared after returning to Iceland. “Like fish and hot pools.”
May 15, 2015
On the face of it it sounds like the nice narrative we are fed every time something like this happens. I haven’t been following the international scene, and frankly it wouldn’t even surprise me if Europe headed for nativism and blood-related nationality. It is what is at the basis of their nation states (even if it’s often a lie. For instance I’d hazard that a lot of people in Portugal — yes, d*mn it, I’ll do the DNA testing. Let the house sell and let me have some money first — are as mixed as Americans. My kids call Portugal the reservoir tip at the end of Europe, which is unkind but somewhat accurate since that portion of land was part of the Celtic commonwealth, before being invaded by Carthaginians, Greeks, Romans, Germanic tribes, Moors (though their contribution in the North is minimal as the North was usually administered by overseers with little or no actual colonization) French crusaders, Viking raiders. Then there were British and Irish merchants due to ties going back before the Carthaginians who would set up trading posts, send their younger sons over, sometimes engage in a bit of raiding, etc. There are unkind proverbs about blue eyed Portuguese, but there are also a lot of them. (Two of my grandparents. A third was green eyed.) And in the end sometimes I think all of us are the result of some girl who tripped (on purpose or not) while evading a foreigner. All this to say that when my dad talks of the “The Portuguese Race” (and boy, does he) he’s mostly talking of a mythical entity. But it’s one they all believe in as hard as they can.)
Sarah A. Hoyt, “Multiculturalism IS Racism”, According to Hoyt, 2015-04-04.
March 20, 2015
Epigenetic researchers – “We can double the size of these bugs!” Everyone else – “No, thanks. We’re good.”
Science can be a great source of fascinating experiments. Doubling the size of insects is perhaps not the best way to advertise your particular speciality, however:
Researchers have changed the size of a handful of Florida ants by chemically modifying their DNA, rather than by changing its encoded information. The work is the latest advance from a field known as epigenetics and may help explain how the insects — despite their high degree of genetic similarity — grow into the different varieties of workers needed in a colony.
This discovery “takes the field leaps and bounds forward,” says entomologist Andrew Suarez of the University of Illinois, Urbana-Champaign, who wasn’t connected to the study. “It’s providing a better understanding of how genes interact with the environment to generate diversity.”
Ant nests have division of labor down pat. The queen spends her time pumping out eggs, and the workers, which are genetically similar sisters, perform all the other jobs necessary to keep the colony thriving, such as tending the young, gathering food, and excavating tunnels. Workers in many ant species specialize even further, forming so-called subcastes that look different and have different roles. In Florida carpenter ants (Camponotus floridanus), for example, workers tend to fall into two groups. Minor workers, which can be less than 6 mm long, rear the young and forage for food. Major workers, which can be almost twice as long, use their large jaws to protect the colony from predators.
A team from McGill University in Montreal, Canada, suspected that the mechanism involves DNA methylation: the addition of a chemical to DNA. Genome sequencing and other methods suggest that these physical differences don’t usually stem from genetic differences between individual ants. Instead, environmental factors help push workers to become majors or minors — specifically, the amount of food and coddling that young ants receive. But just how do these factors change the size of ants?
February 20, 2015
In Nature, Claire Ainsworth explains why it’s becoming more difficult to discuss sex as a binary:
Sex can be much more complicated than it at first seems. According to the simple scenario, the presence or absence of a Y chromosome is what counts: with it, you are male, and without it, you are female. But doctors have long known that some people straddle the boundary — their sex chromosomes say one thing, but their gonads (ovaries or testes) or sexual anatomy say another. Parents of children with these kinds of conditions — known as intersex conditions, or differences or disorders of sex development (DSDs) — often face difficult decisions about whether to bring up their child as a boy or a girl. Some researchers now say that as many as 1 person in 100 has some form of DSD.
When genetics is taken into consideration, the boundary between the sexes becomes even blurrier. Scientists have identified many of the genes involved in the main forms of DSD, and have uncovered variations in these genes that have subtle effects on a person’s anatomical or physiological sex. What’s more, new technologies in DNA sequencing and cell biology are revealing that almost everyone is, to varying degrees, a patchwork of genetically distinct cells, some with a sex that might not match that of the rest of their body. Some studies even suggest that the sex of each cell drives its behaviour, through a complicated network of molecular interactions. “I think there’s much greater diversity within male or female, and there is certainly an area of overlap where some people can’t easily define themselves within the binary structure,” says John Achermann, who studies sex development and endocrinology at University College London’s Institute of Child Health.
These discoveries do not sit well in a world in which sex is still defined in binary terms. Few legal systems allow for any ambiguity in biological sex, and a person’s legal rights and social status can be heavily influenced by whether their birth certificate says male or female.
“The main problem with a strong dichotomy is that there are intermediate cases that push the limits and ask us to figure out exactly where the dividing line is between males and females,” says Arthur Arnold at the University of California, Los Angeles, who studies biological sex differences. “And that’s often a very difficult problem, because sex can be defined a number of ways.”
February 19, 2015
Published on 18 Feb 2015
Almost every cell in your body has the same DNA sequence. So how come a heart cell is different from a brain cell? Cells use their DNA code in different ways, depending on their jobs. Just like orchestras can perform one piece of music in many different ways. A cell’s combined set of changes in gene expression is called its epigenome. This week Nature publishes a slew of new data on the epigenomic landscape in lots of different cells. Learn how epigenomics works in this video.
February 9, 2015
Last month, in his Times column, Matt Ridley explained why — until we discover a treatment for aging itself — rising cancer rates are a weird form of good news:
If we could prevent or cure all cancer, what would we die of? The new year has begun with a war of words over whether cancer is mostly bad luck, as suggested by a new study from Johns Hopkins School of Medicine, and over whether it’s a good way to die, compared with the alternatives, as suggested by Dr Richard Smith, a former editor of the BMJ.
It is certainly bad luck to be British and get cancer, relatively speaking. As The Sunday Times reported yesterday, survival rates after cancer diagnosis are lower here than in most developed and some developing countries, reflecting the National Health Service’s chronic problems with rationing treatment by delay. In Japan, survival rates for lung and liver cancer are three times higher than here.
Cancer is now the leading cause of death in Britain even though it is ever more survivable, with roughly half of people who contract it living long enough to die of something else. But what else? Often another cancer.
In the western world we’ve conquered most of the causes of premature death that used to kill our ancestors. War, smallpox, homicide, measles, scurvy, pneumonia, gangrene, tuberculosis, stroke, typhoid, heart disease and cholera are all much rarer, strike much later in life or are more survivable than they were fifty or a hundred years ago.
The mortality rate in men from coronary heart disease, for instance, has fallen by an amazing 80 per cent since 1968 — for all age groups. Mortality rates from stroke in both sexes have halved in 20 years. Cancer’s growing dominance of the mortality tables is not because it’s getting worse but because we are avoiding other causes of death and living longer.
It is worth remembering that some scientists and anti-pesticide campaigners in the 1960s were convinced that by now lifespans would be much shorter because of cancer caused by pesticides and other chemicals in the environment.
In the 1950s Wilhelm Hueper — a director of the US National Cancer Institute and mentor to Rachel Carson, the environmentalist author of Silent Spring — was so concerned that pesticides were causing cancer that he thought the theory that lung cancer was caused by smoking was a plot by the chemical industry to divert attention from its own culpability: “Cigarette smoking is not a major factor in the causation of lung cancer,” he insisted.
In fact it turns out that pollution causes very little cancer and cigarettes cause a lot. But aside from smoking, most cancers are indeed bad luck. The Johns Hopkins researchers found that tissues that replicate their stem cells most run the highest risk of cancer: basal skin cells do ten trillion cell divisions in a lifetime and have a million times more cancer risk than pelvic bone cells which do about a million cell divisions. Random DNA copying mistakes during cell division are “the major contributors to cancer overall, often more important than either hereditary or external environmental factors”, say the US researchers.
To sum it up, until or unless medical research finds a way to stop the bodily effects of aging, cancer becomes the most likely way for all of us to die. Cancer is a generic rather than a specific term — it’s what we use to describe the inevitable breakdown of the cellular division process that happens millions or even trillions of times over our lifetime. As Ridley puts it, “even if everybody lived in the healthiest possible way, we would still get a lot of cancer.” I’m not a scientist and I don’t even play one on TV, but I suspect that the solution to cancers of all kinds are to boost our immune systems to more quickly identify aberrant cells in our bodies before they start reproducing beyond the capability of the immune system to handle. The short- to medium-term solution to cancer may be to make us all a little bit cyborg…
December 5, 2014
Michael White says we need to follow up our success in reading our own genetic code by decoding a different one:
There are thousands of mutations that occur in the breast cancer-linked genes BRCA1 and BRCA2. Some of these cause breast or ovarian cancer, while others are harmless. When we design a genetic test for predisposition to breast cancer, we have to know which ones to test for. The same is true of almost any gene that plays a role in disease — you’ll find many mutations in that gene in the general population, only some of which cause health problems. So how do we know which mutations to worry about?
We start by using the genetic code. The genetic code, cracked by scientists in the 1960s, makes it surprisingly easy to “read” our DNA and understand how a particular mutation affects a gene. As genetic testing takes on a bigger role in predicting, diagnosing, and treating disease, we rely on this code to help us make sense of the data. Unfortunately, the genetic code applies to less than two percent of our DNA. In an effort to read the rest, researchers are trying to crack a new genetic code — and this next one is turning out to be much more difficult to solve than the first. In fact, scientists may have to give up the idea that we can use a “code” to “read” the rest of our DNA.
When scientists were working out the original genetic code in the 1950s and ’60s, all sorts of complicated schemes were proposed to explain how information is stored in our genes. The problem they were trying to solve was how a gene, made of DNA, codes the information to make a particular protein — an enzyme, a pump, a piece of cellular scaffolding, or some other critical component of the cell’s working machinery. They were looking for a code that would translate the four-letter DNA alphabet of genes into the 20-letter amino acid alphabet of proteins.
Thanks to its simplicity, the genetic code is a powerful tool in our hunt for mutations that cause disease. Unfortunately, it has also led to the genetic equivalent of a drunk looking for his lost keys under the lamppost. Researchers have put much of their effort into looking for disease mutations in those parts of our genomes that we can read with the genetic code — that is, parts that consist of canonical genes that code for proteins. But these genes make up less than two percent of our DNA; much more of our genetic function is outside of genes in the relatively uncharted “non-coding” portions. We have no idea how many disease-causing mutations are in that non-coding portion — for some types of mutations, it could be as high as 90 percent.
May 7, 2014
In Forbes, Matthew Herper looks at how Novartis is transforming itself in an attempt to conquer cancer:
“I’ve been an oncologist for 20 years,” says Grupp, “and I have never, ever seen anything like this.” Emily has become the poster child for a radical new treatment that Novartis, the third-biggest drug company on the Forbes Global 2000, is making one of the top priorities in its $9.9 billion research and development budget.
“I’ve told the team that resources are not an issue. Speed is the issue,” says Novartis Chief Executive Joseph Jimenez, 54. “I want to hear what it takes to run this phase III trial and to get this to market. You’re talking about patients who are about to die. The pain of having to turn patients away is such that we are going as fast as we can and not letting resources get in the way.”
A successful trial would prove a milestone in the fight against the demon that has plagued living things since dinosaurs roamed the Earth. Coupled with the exploding capabilities of DNA-sequencing machines that can unlock the genetic code, recent drugs have delivered stunning results in lung cancer, melanoma and other deadly tumors, sometimes making them disappear entirely – albeit temporarily. Just last year the Food & Drug Administration approved nine targeted cancer drugs. It’s big business, too. According to data provider IMS Health, spending on oncology drugs was $91 billion last year, triple what it was in 2003.
But the developments at Penn point, tantalizingly, to something more, something that would rank among the great milestones in the history of mankind: a true cure. Of 25 children and 5 adults with Emily’s disease, ALL, 27 had a complete remission, in which cancer becomes undetectable. “It’s a stunning breakthrough,” says Sally Church, of drug development advisor Icarus Consultants. Says Crystal Mackall, who is developing similar treatments at the National Cancer Institute: “It really is a revolution. This is going to open the door for all sorts of cell-based and gene therapy for all kinds of disease because it’s going to demonstrate that it’s economically viable.”
H/T to Megan McArdle for the link.
December 17, 2013
At Ace of Spades HQ, Ace explains why a court decision from the 1970s set a very bad precedent for today’s legal and technological world:
Fifty years ago the police had a very limited ability to utilize your fingerprints record to harm you. If you became a suspect in a case — and only in that case — they could painstakingly compare your fingerprints to those found at a crime scene using slow, precious human labor resources.
There were serious practical limits on what could be done with citizen data held in government files. Yes, the government could use that data to put people in jail, but analysis and comparison was a labor intensive process that at least served as a naturally-existing limiting principle on government intrusion: Sure, the government could search your personally-identifying data to connect you with a crime, but, as a practical matter, it was so time-consuming to do so that they generally would not do so, not unless they had a strong suspicion you were actually a culprit.
They wouldn’t just compare every fingerprint on file with every fingerprint found at unsolved crime scenes, after all.
Well, today, they can — and do — actually do that. So there is no longer any practical limitation on the government’s ability to use your DNA to connect you with unknown DNA found at a crime. They can run everyone’s DNA through the database with virtually no effort.
I exaggerate; there is some lab work needed to process the DNA and reduce it to a 13 allele “genetic fingerprint.” Nevertheless, this can all be done fairly inexpensively, and running it through the database once reduced to a short code is very nearly cost-free.
But within the next ten years all of this will become entirely cost-free.
This is why I disagreed with the Supreme Court’s reliance on an old precedent in claiming that the police can take a DNA sample from every single person arrested. Merely arrested, not convicted. They relied on a precedent established at the dawn of investigatory police science, that every arrestee’s fingerprints may be collected and catalogued.
But way ‘back then, there were natural limitations on the State’s power to make use of such data which simply no longer exist. What would have been considered a silly hypothetical sci-fi objection back then — “But what stops the state from merely searching these fingerprints against every fingerprint ever lifted at a crime scene?” — is actual reality now.
The same arguments apply to all police/FBI/NSA mass data collection: cell-phone usage, internet activity, license plate scanning, facial recognition software, and so on. It resets the baseline assumptions of civil society, where the authorities only look for suspects in actual criminal cases, rather than tracking everyone all the time and deducing “criminal” actions without needing to detect the crime. If your first reaction is to think “if you’ve done nothing wrong, you’ve got nothing to fear”, remember that you cannot possibly know all the laws of your country and that statistically speaking, you probably violate one or more laws every day without realizing it (one author suggests it’s actually three felonies per day).
Update: Ayn Rand explained this phenomenon fictionally in Atlas Shrugged.
“Did you really think that we want those laws to be observed?” said Dr. Ferris. “We want them broken. You’d better get it straight that it’s not a bunch of boy scouts you’re up against — then you’ll know that this is not the age of beautiful gestures. We’re after power and we mean it. You fellows were pikers, but we know the real trick, and you’d better get wise to it. There’s no way to rule innocent men. The only power any government has is the power to crack down on criminals. Well, when there aren’t enough criminals, one ‘makes’ them. One declares so many things to be a crime that it becomes impossible for men to live without breaking laws. Who wants a nation of law-abiding citizens? What’s there in that for anyone? But just pass the kind of laws that can neither be observed nor enforced nor objectively interpreted — and you create a nation of law-breakers and then you cash in on the guilt. Now that’s the system, Mr. Rearden, that’s the game, and once you understand it, you’ll be much easier to deal with.”
December 2, 2013
Kyle Smith on the FDA’s sudden interest in shutting down private DNA testing company 23andMe:
… the FDA has the power to regulate medical devices, which is the pretext it is using to stop 23andMe. Ordering it to stop selling its personal genome service, the FDA declared that the tube “is a device within the meaning of section 201(h) of the FD&C Act, 21 U.S.C. 321(h), because it is intended for use in the diagnosis of disease or other conditions or in the cure, mitigation, treatment or prevention of disease, or is intended to affect the structure or function of the body.’
It would seem that 23andMe could simply put the words, “not intended for us in the diagnosis, cure, mitigation, treatment or prevention of disease” on its website and satisfy the FDA, but we all know that the motto of today’s federales is “We make it up as we go along.” The FDA seems determined to conduct a lengthy war with 23andMe.
Using the same reasoning, the FDA might as well shut down WebMd.com because people might type their symptoms into the site, and the response might affect whether or not they choose to go to a doctor. Any computer or iPhone thereby becomes a “medical device” that people can use for the “diagnosis, cure, mitigation, treatment or prevention of disease.”
Come to think of it, that thermometer you use to check your temperature is pretty dangerous too — it might give you either a false positive or a false negative — but why stop there? You exercise to mitigate or prevent disease, don’t you? Maybe the FDA should take your running shoes and your yoga pants away.
November 29, 2013
Nick Gillespie on the mindnumbingly awful exercise of FDA regulatory power in shutting down personal DNA testing company 23andMe:
Personal genetic tests are safe, innovative, and the future of medicine. So why is the most transparent administration ever shutting down a cheap and popular service? Because it can.
In its infinite wisdom, the Food and Drug Administration (FDA) has forbidden the personal genetic testing service 23andMe from soliciting new customers, claiming the company hasn’t proven the validity of its product.
The real reason? Because when it comes to learning about your own goddamn genes, the FDA doesn’t think you can handle the truth. That means the FDA is now officially worse than Oedipus’s parents, Dr. Zaius, and the god of Genesis combined, telling us that there are things that us mere mortals just shouldn’t be allowed to know.
23andMe allows you to get rudimentary information about your genetic makeup, including where your ancestors came from and DNA markers for over 240 different hereditary diseases and conditions (not all of them bad, by the way). Think of it as the H&M version of the haute couture genetic mark-up that Angelina Jolie had done prior to having the proactive mastectomy that she revealed this year.
Peter Huber of the Manhattan Institute, a conservative think tank, has an important new book out called The Cure in the Code: How 20th Century Law is Undermining 21st Century Medicine. Huber writes that whatever sense current drug-approval procedures once might have had, their day is done. Not only does the incredible amount of time and money — 12 years and $350 million at a minimum — slow down innovation, it’s based on the clearly wrong idea that all humans are the same and will respond the same way to the same drugs.
Given what we already know about small but hugely important variations in individual body chemistry, the FDA’s whole mental map needs to be redrawn. “The search for one-dimensional, very simple correlations — one drug, one clinical effect in all patients — is horrendously obsolete,” Huber told me in a recent interview. And the FDA’s latest action needs to be understood in that context — it’s just one more way in which a government which now not only says we must buy insurance but plans whose contours are dictated by bureaucrats who arbitrarily decide what is best for all of us.