NIH opens the floodgates to creating super-viruses

Some scientists really want to earn their "mad scientist" label. Ever since Mary Shelley's Frankenstein, novelists and screenwriters have shown us the dangers of letting mad scientists pursue their dreams without any controls. Of course, those stories are fiction.

In the microbial world, though, technology has caught up with fiction. Scientists today can create viruses from scratch, as they've already done with the polio virus, back in 2002. Using the tools of modern genomics, virologists and microbiologists can make pathogens much, much more deadly. But would anyone really want to do this? The answer, it turns out, is yes.

A few years ago, some virologists had the clever idea of modifying the bird flu virus to make it more deadly to humans. What would it take, they wondered, to turn the bird flu into a human flu? They decided to give it a try, and they announced their plans to the world. Then, just a few months later, they published results showing that they had succeeded, at least partially, using a bird flu called H7N9.

That wasn't even their first try. Only a year earlier, they did the same thing using a different flu virus (H5N1). Both of these bird flu strains have killed people, but the wild-type version of the virus rarely infects humans. The scientists running these experiments aimed to create a strain that could get into humans much more easily.

Many scientists were mortified. 18 leading microbiologists and infectious disease experts, including Nobel laureate Sir Richard Roberts, formed the Cambridge Working Group to oppose efforts to create super-viruses in the lab. Hundreds of other scientists, including 3 more Nobel laureates, joined the group as charter members.

In response to the concerns raised by scientists and other public health experts, NIH announced a moratorium on these so-called "gain of function" (GOF) experiments, at least in the U.S. (The scientists leading the charge for GOF experiments were based primarily in The Netherlands, although they did get some funding from NIH.) The NIH convened an expert panel, the NSABB, who commissioned a 1,000-page report and then issued their own report, which was released in May of 2016.

The NSABB panel avoids taking very strong positions, but they do raise some alarms. Here's their definition of "research of concern," for example:

"...research that could generate a pathogen that is: 1) highly transmissible and likely capable of wide and uncontrollable spread in human populations; and 2) highly virulent and likely to cause significant morbidity and/or mortality in humans." 

This does not sound like a good idea! So what does the NSABB recommend? Well, this:

"Research proposals involving GOF research of concern ... should receive an additional, multidisciplinary review, prior to determining whether they are acceptable for funding."

I can't argue that research like this doesn't need "additional" review–but the wording here suggests that at least some experiments like this might be worth funding. Mad scientists must be rubbing their hands together in glee.

And finally, just last week NIH announced it will end the moratorium on gain-of-function research. (They made this announcement just a week before Christmas, when many people are probably not paying attention. Coincidence? Perhaps.) In his statement announcing the end of the moratorium, NIH Director Francis Collins wrote:

"I am confident that the thoughtful review process ... will help to facilitate the safe, secure, and responsible conduct of this type of research in a manner that maximizes the benefits to public health."

I am not so confident. Harvard's Marc Lipsitch, one of the leaders of the Cambridge Working Group, commented that "we don't need to do these dangerous experiments. Indeed there are many ways that can (and have) been used to answer the public health question with greater generality, little to no safety risk, and much lower cost."

But just in case there is some question, let's weigh the pluses and minuses, shall we?
Pluses:

• Creating novel pathogens might lead to insights in the basic biology of viruses and bacteria.
• Creating hard-to-kill pathogens might help us develop better anti-virals and anti-bacterials, although more effective strategies already exist.

Minuses:

• The viruses could accidentally escape, and millions of people could die.
• The viruses could get into the wrong hands, and millions of people could die.

I don't know about you, Dr. Collins, but I'm leaning towards banning such research permanently.

No, Google didn't just create AI that could "build your genome"

Most scientists don't have their own PR machine to hype their work. After reading the announcement last week from Google's genomics group, I realized that's probably a good thing.

A Wired article last Friday reported that "Google is giving away AI that can build your genome sequence." Sounds impressive–two high-tech innovations (AI and genomes) in the same title! Unfortunately, the truth is somewhat different. It turns out that Google's new "AI" software is little more than an incremental improvement over existing software, and it might be even less than that.

I'm going to have to get into the (technical) weeds a bit to explain this, but it's the only way to set the record straight. The Wired piece opens with this intriguing challenge:

"Today, a teaspoon of spit and a hundred bucks is all you need to get a snapshot of your DNA. But getting the full picture—all 3 billion base pairs of your genome—requires a much more laborious process."

Interesting, I thought. The writer (Megan Molteni) seems to be talking about genome assembly–the process of taking billions of tiny pieces of DNA sequence and putting them together to reconstruct whole chromosomes. This is something I've been working on for nearly 20 years, and it's a fascinating but very complex problem. (See our recent paper on the wheat genome, as one of dozens of examples I could cite.)

So does Google have a new genome assembly program, and is it based on some gee-whiz AI algorithm?

No. Not even close. Let's look at some of the ways that the Google announcement and the Wired article are misleading, over-hyped, or both.

1. The Google program doesn't assemble genomes. That's right: even though the Wired piece opens with the promise of "getting the full picture" of your genome, the new Google program, DeepVariant, doesn't do anything of the sort. DeepVariant is a program for identifying small mutations, mostly changes of a single letter (called SNPs). (It can find slightly larger changes too.) This is known as variant calling, or SNP calling, and it's been around for more than a decade. Lots of programs can do this, and most of them do it very well, with accuracy exceeding 99.9%.

How could Wired get this so wrong? Well, the Wired piece is based on a Google news release from a few days earlier, called "DeepVariant: Highly Accurate Genomes With Deep Neural Networks," written by the authors of the software itself. Those authors, who obviously know what their own software does, make the misleading statement that DeepVariant is

"a deep learning technology to reconstruct the true genome sequence from HTS sequencer data with significantly greater accuracy than previous classical methods."

If you read on, though, you quickly learn that DeepVariant is just a variant caller (as the name implies). This software does not "reconstruct the true genome sequence." That's just wrong. To reconstruct the sequence, you would need to use a program called a genome assembler, a far more complex algorithm. (I should add that many genome assemblers have been developed, and it's an active and thriving area of research. But I digress.)

The Wired article also points out that

"the data produced by today’s [sequencing] machines still only produce incomplete, patchy, and glitch-riddled genomes."

Yes, that's true. Again, though, DeepVariant does nothing to fix this problem. It can't assemble a genome, and it can't improve the assembly of an "incomplete, patchy" genome.

2. Wild hyperbole: the caption on the lead image in the Wired piece says "Deep Variant is more accurate than all the existing methods out there."  The Google press release, presumably the source for that caption, claims that DeepVariant has "significantly greater accuracy than previous classical methods."

No, it does not. This is the kind of claim you'd never get away with in a scientific paper, not unless you rigorously demonstrated your method was truly better than everything else. The Google team hasn't done that.

How good is it? First, let me remind you that variant calling programs have been around a long time, and they work very well. An incremental improvements would be nice, but not "transformative" or a "breakthrough"–words that the Google team didn't hesitate to use in their press release. They also used the word "significant," which they'd never get away with in a scientific paper, not without statistics to back it up. Press releases can throw around dramatic claims like these without anyone to check them. That's not a good thing.

About a year ago, the Google team released a preprint on bioRxiv that shows that their method is more accurate (on a limited data set) than an earlier method called GATK, which was developed by the same author, Mark DePristo, in his former job at MIT, which he left to join Google. GATK is quite good, and is very widely used, but other, newer methods are much faster and (at least sometimes) more accurate. The Google team basically ignored all of the other variant calling programs, so we just don't know if DeepVariant is better or worse than all of them. If they want to get this preprint published in a peer-reviewed journal, they're going to have to make a much better case.

(As an aside: a much-less hyped method called 16GT, published earlier this year by a former member of my lab, Ruibang Luo, is far faster than DeepVariant, just as accurate, and runs on commodity hardware, unlike DeepVariant which requires special resources only available in the Google Cloud. And it does all this with math and statistics–no AI required. But I digress.)

(Another aside: if we really wanted to get into the weeds, I would explain here that the "AI" solution in DeepVariant is transformation of the variant calling problem into an image recognition problem. The program then uses a method called deep neural networks to solve it. I have serious reservations about this approach, but suffice it to say that there's no particular reason why treating the problem as an image recognition task would provide a large boost over existing methods.)

3. More wild hyperbole. The Google news release opens with a sentence containing this:

"in the field of genomics, major breakthroughs have often resulted from new technologies."

It then goes on to describe several true breakthroughs in DNA sequencing technology, such as Sanger sequencing and microarrays, none of which had any contribution from the Google team. Then–pause for a deep breath and a paragraph break–we learn that "today, we announce the open source release of DeepVariant." Ta-da!

I can only shake my head in wonder. Does the Google team truly believe that DeepVariant is a breakthrough on a par with Sanger sequencing, which won Fred Sanger the 1980 Nobel Prize in Chemistry? This is breathtakingly arrogant.

4. DeepVariant is computationally inefficient. Even if it is better than earlier programs (and I'm not convinced of that), DeepVariant is far slower. While other programs run on commodity hardware, it appears that Google's DeepVariant requires a large, dedicated grid of computers working in parallel. The Wired article explains that two companies (DNAnexus and DNAStack) had to invest in new GPU-based computer hardware in order to run DeepVariant. An independent evaluation found that DeepVariant was 10 to 15 times slower than the competition. Coincidentally, perhaps, Google's press release also announces the availability of the Google Cloud Platform for those who want to run DeepVariant.

No thanks. My lab will continue to use 16GT, or Samtools, or other variant callers that do the job much faster, and just as well, without the need for the Google Cloud. As a colleague remarked on Twitter, the "magic pixie dust of 'deep learning' and 'google'" doesn't necessarily make something better.

Genomics is indeed making great progress, and although I applaud Google for dedicating some of its own scientific efforts to genomics, it's not helpful to exaggerate what they've done so far, especially when they take it to this level. Both the Google news release and the Wired article contain the sort of over-statements that make the public distrust science reporting. We don't need to do that to get people excited about science.

Soon your Internet will look just like cable

The new FCC chairman, Ajit Pai, formerly worked as a lawyer for Verizon. His plan to eliminate net neutrality is a bigger gift to Verizon than anything he's ever done before.

In just a few weeks, the FCC will vote to eliminate net neutrality. The vote isn't in doubt: with Pai in charge, the anti-neutrality votes have a 3-2 edge. Without net neutrality, Internet service providers will be able to charge web companies for "fast lanes," which they can't do now. Smaller companies and individual's websites may be slowed down so much as to render them unusable. The biggest service providers (Netflix, Google, Amazon, and others) will have to cough up extra money, but the consumers won't see any of that–all the benefits will go to the ISPs. Consumers will see their rates go up.

Higher fees for lousier service. Does this sound familiar? That's how cable companies have operated for years.

Not surprisingly, virtually everyone hates this idea except the cable companies themselves. The telecommunications industry, though, is very excited about the prospect of all the money they're going to make. When previous FCC commissioner Tom Wheeler proposed to weaken net neutrality just a couple of years ago, the ensuing public outcry convinced him to reverse himself, resulting in a strong ruling in 2015 preserving neutrality. This week, Wheeler blasted Pai's new rules, saying that "this proposal raises hypocrisy to new heights."

But don't take my word for it. Check out this terrific and entertaining explainer from John Oliver, earlier this year:

If Ajit Pai and his telecom buddies get their way, here's what your Internet service might look like next year–I altered the first line, just to convey the idea; the rest is from a list of Comcast's current cable TV services:

That's right: your Internet service provider (ISP) will be allowed to bundle websites just like they bundle television channels. Of course, ISPs claim they will do no such thing, but why should we trust them?

If net neutrality goes away, no longer will anyone be able to set up a website and turn it into a thriving business by offering popular content. They'll first need to raise money to pay the ISPs, or else face being throttled back before their business even has a chance..

No one wants this change except a few large telecom companies. Interviewed by The Nation, former FCC Commissioner Michael Copps said

"There can be no truly open internet without net neutrality. To believe otherwise is to be captive to special interest power brokers or to an old and discredited ideology that thinks monopoly and not government oversight best serves the nation."

Ajit Pai, our new FCC chairman, clearly belongs to the former. Verizon is now in charge of the FCC.

Transgenic stem cells lead to a miraculous cure

Sometimes I read a science paper and I just say "Holy cow, this is amazing." I don't have that reaction very often, but I did last week.

Amidst all the hype, the hope, and the controversy about gene therapy and stem cell research, some very real progress is being made. Scientists can create working versions of human genes, package them into a virus, and then use the virus to deliver the genes to a real person. This approach creates "transgenic" cells that have bits of virus DNA within them, but the virus can be engineered to be harmless.

Last week, scientists reported in the journal Nature how they saved the life of a 7-year-old boy using transgenic stem cells. Twenty years ago, this would have been science fiction. Even today it is nothing short of astonishing.

Here's the story, summarized from the paper by Tobias Hirsch, Michele de Luca, and their colleagues. In June 2015, a 7-year-old boy was admitted to the Burn Unit of Children’s Hospital of Ruhr University, in Bochum, Germany, where Hirsch and his colleagues (Tobias Rothoeft, Norbert Teig, and others) work. The child wasn't suffering from burns: he had a devastating genetic disease, junctional epidermolysis bullosa (JEB), that had caused him to lose 80% of his skin.

Figure 1b from Hirsch et al. Schematic
representation of the clinical picture.
The denuded skin is indicated in red;
blistering areas are indicated in green.
Flesh-colored areas indicate currently
non- blistering skin. Transgenic grafts
were applied on both red and green areas.

Children with JEB suffer from constant blistering, wounds, and scarring. The disease is uncurable and children often die before reaching their teens. The 7-year-old boy was near death when he was admitted to the hospital–his weight had dropped to 17 kilograms (38 pounds) and he had severe skin infections from streptococcus and pseudomonas bacteria.

Dr. Hirsch and his team were struggling to keep the boy alive, and they had no treatments to offer. In desperation, they searched the scientific literature and found a possible treatment using gene therapy, developed by Michele De Luca, of the Center for Regenerative Medicine at the University of Modena and Reggio Emilia in Italy. Dr. De Luca had only tried this treatment twice before, and even then only on tiny patches of skin. He had never tried it on such a severe case.

The boy and his parents had no other options to save his life. They agreed to let Dr. De Luca try.

In September of 2015, De Luca took a small patch of undamaged skin (4 square centimeters) back to his lab in Italy. There, he used a retrovirus containing a functioning copy of the LAMB3 gene–the gene that was mutated in the boy–to infect the skin cells. The retrovirus integrated itself into the genome of many of the skin cells, giving them the ability to function normally. Then De Luca grew the repaired cells into new skin grafts, enough to cover 80% of the child's body.

In a series of surgeries starting in October 2015, Hirsch and his colleagues applied the skin grafts to the young boy. The results were amazing.

As reported in the paper itself:

"Virtually complete epidermal regeneration was observed after 1 month.... Over the following weeks, the regenerated epidermis surrounding the open lesions and the epidermal islands spread and covered most of the denuded areas."

In other words, it worked. The new skin completely replaced the missing or damaged skin on 80% of the boy's body. What's even more remarkable is that two years later, his skin remains normal. The new skin is functioning perfectly and the young boy has returned to school.

The science behind this treatment represents the culmination of decades of research into gene therapy, stem cells, retroviruses, and genomics. To make it all work, we had to know: the identity of the gene that caused the disease (LAMB3); the DNA sequence of a normal LAMB3 gene; how to insert the human gene into a retrovirus; how to create a modified retrovirus that wouldn't harm humans; and much more.

The success of the therapy also revealed new insights into stem cells in human skin: the small patch of undamaged skin from the boy contained many cells, a few of which were stem cells (holoclones) that could replenish the skin indefinitely. It was these stem cells that allowed the skin grafts to take hold and continue to function, hopefully for the rest of the boy's life.

Sometimes science and medicine converge, and miracles happen.

(Note: the paper is "Regeneration of the entire human epidermis using transgenic stem cells" by T. Hirsch et al.)

The new Star Trek series gets biology terribly, terribly wrong.

The new Star Trek: Discovery series is based on a massive scientific error. Can it survive?

It didn't have to be this way. Those of us who have followed Star Trek through its many TV series and movies, including the excellent trio of recent moves (2016's Star Trek Beyond is the latest) were eager to jump on board the newest show, Star Trek: Discovery.

Despite some rather uneven acting in the pilot, I was willing to give it a chance. So were millions of other Star Trek fans.

But alas, the writers have stumbled into a scientific error so egregious, and so entangled in the entire plot line, that I fear the new Star Trek cannot recover. (Note: a few mild spoilers ahead.)

Episodes 4 and 5, released on October 8 and 15, revealed that the USS Discovery, the ship that the series revolves around, has an advanced form of transport that allows it to travel anywhere in the universe instantaneously. Unlike all previous Star Trek transport tech, this one uses a biological mechanism, based on mushrooms.

Yes, you read that right. The DASH (Displacement Activated Spore Hub) drive uses mushroom spores as its power source. They've discovered a special fungus whose root system extends "throughout subspace" all over the galaxy. Using spores from this fungus, the ship can jump into subspace (or something like that) and jump out somewhere else in real space, light years away, in a matter of seconds. As bizarre and this sounds, the worst is yet to come.

To power its DASH drive, the Discovery maintains a large greenhouse full of spore-producing mushrooms. (Mycologists might love this, but how big a fan base can they be?) The problem for the Discovery, in the first few episodes, is that the experimental drive will only let them jump short distances.

Then they discover the tardigrade. Tardigrades are a real thing: they are microscopic animals, only 0.5 millimeters long, that live all over the planet. Here's a picture of one:

Electron microscope image of Milnesium tardigradum,
from E. Schokraie et al., PLoS ONE 7(9): e45682.

They are also surprisingly cute for a microscopic animal, and they are colloquially known as water bears, moss piglets, or space bears. "Space bears" comes from their ability to survive in extreme environments, possibly including interplanetary space.

Star Trek Discovery's tardigrade is, shall we say, rather different. It looks a bit like the picture shown here, but it's the size of a large grizzly bear, incredibly strong, and extremely fierce. On the show they call it a "giant space tardigrade."

But that's not all. Thanks to a unique biological property that the show's writers apparently misunderstood, the space tardigrade can access the mushroom network to travel throughout the universe, wherever and whenever it chooses.

Here's how the space tardigrade accomplishes this remarkable feat of interstellar travel, as explained by Michael Burnham, the show's central character (in Episode 5, "Choose your pain"):

"Like its microscopic cousins on Earth, the tardigrade is able to incorporate foreign DNA into its own genome via horizontal gene transfer. When Ripper [the space tardigrade] borrows DNA from the mycelium [the mushroom], he's granted an all-access travel pass."

And just like that, not only the tardigrade but the entire spaceship jump across the galaxy. Is this sounding a bit crazy? It should.

Horizontal gene transfer (HGT) is a real thing. It's a process through which bacteria sometimes take up DNA from the environment and integrate it into their own genomes. Animals can't do HGT, but rather infamously, a paper was published in December 2015 that made the bold claim that tardigrades had a unique ability to absorb all kinds of DNA. That paper was instantly controversial in the scientific community, and not surprisingly its findings were being disputed in the Twittersphere within days of its appearance. Surprisingly, the same journal (PNAS) that published the bogus HGT claim published a second paper just a few months later showing that tardigrades do not absorb foreign DNA into their genome. That plus a third paper showed that the original paper had mistakenly identified contaminating DNA as part of the tardigrade's own genome. This rapid correction of the record was a win for science; I've used this example to demonstrate to my undergraduate class how sloppy science (the first paper) can lead one astray.

So: a minor scientific controversy, quickly debunked.

Until, that is, one of the Star Trek writers got their hands on it. Apparently one of them heard the tardigrade story, perhaps someone who'd had a bit of biology in college (I'm guessing here), and got so excited that they turned it into a wildly implausible premise for an intergalactic space drive.

The idea of using horizontally transferred DNA for space travel is so nutty, so bad, that it's not even wrong. Even if tardigrades could absorb foreign DNA (they can't), how the heck is this supposed to give them the ability to tap into the (wildly implausible) intergalactic spore network? DNA that's been taken up through HGT isn't connected to the source any longer. This is no more plausible than asserting that people could connect to the mushroom network by eating a plate of mushrooms. And how would the space-traveling tardigrade take the entire ship with it? Are we supposed to assume it's creating some kind of mushroom-DNA field?

Star Trek has had faster-than-light warp drives for 50 years. Although physically implausible, warp drive isn't laughably ridiculous. The DASH drive is.

And now the entire series seems to be based on a combination of magic (an intergalactic mushroom network in subspace) and scientific errors (horizontal gene transfer by tardigrades).

I can't watch this nonsense. I'm willing to suspend disbelief for the sake of a good story (warp drive!), but I can't accept obviously bogus claims. I don't know how the Star Trek writers can get themselves out of this one, but if they don't, then Star Trek Discovery is finished. If they're reading this, here's my plea: ditch the DASH drive and find something to replace it–and for god's sake, hire a competent science consultant.

Should we all be on statins? (reprise)

Should you be on statins? New guidelines and an online calculator may allow you to answer this question yourself.

Back in 2011, I asked whether we should all be on statins. At the time, it was clear that statins offered benefits for people who had already suffered heart attacks or other serious cardiovascular problems. But for the rest of us, it wasn't clear at all. A number of studies had been published suggesting that millions more people (in the U.S. alone) might benefit from statin therapy, but most of those studies were published by drug companies that made statins. As I wrote at the time, "we need more data from completely unbiased studies."

So has anything changed? Actually, it has. Last year, the U.S. Preventative Services Task Force (USPSTF) reviewed all of the evidence and updated its former (from 2008) recommendations. The evidence now suggests that some people–even those who have never suffered a heart attack–would benefit from statins.

Here's what the current USPSTF recommendations suggest. If you've never had a heart attack and have no history of heart disease, you still might benefit from statins if:

• you're 40-75 years old,
• you have one or more "risk factors" for cardiovascular disease (more about this below), AND
• you have a 10-year risk of cardiovascular disease (CVD) of 7.5%-10%, using a "risk calculator" that I'll link to below.

Now let's look at those risk factors for CVD. There are four of these, and any one of them puts you in the category of people who might benefit from statins: diabetes, high blood pressure (hypertension), smoking, or dyslipidemia.

Most people already know their status for the first 3, but "dyslipidemia" needs a bit more explanation. This is simply an unhealthy level of blood cholesterol, defined by USPSTF as either "an LDL-C level greater than 130 mg/dL or a high-density lipoprotein cholesterol (HDL-C) level less than 40 mg/dL." You can ask your doctor about these numbers, or just look at your cholesterol tests yourself, where they should be clearly marked.

For that last item, how do you calculate you 10-year risk of CVD? Most people should ask their doctor, but if you want to see how it's done, the calculator is at the American College of Cardiology site here. It's quite simple and you can fill it in yourself to see your risk.

A big caveat here, as the USPSTF explains, is that the "risk calculator has been the source of some controversy, as several investigators not involved with its development have found that it overestimates risk when applied to more contemporary US cohorts."

Another problem that I noticed with the risk calculator is that using it for the statin recommendation involves some serious double counting. That's because the risk calculator relies in part on your cholesterol levels and blood pressure, but those same measurements are considered to be separate risk factors for CVD. This puts a lot of weight on cholesterol levels–but on the other hand, statins' biggest effect is to reduce those levels.

The USPSTF is a much more honest broker of statin recommendations than industry-funded drug studies, so we can probably trust these new guidelines. Note that if the risk calculator puts you in the 7.5%-10% range, you will only get a very small benefit from statins–as the USPSTF puts it, "Fewer persons in this population will benefit from the intervention."

Don't rush to go on statins without giving it some serious thought. As Dr. Malcolm Kendrik put it last year (quoted by Dr. Luisa Dillner in The Guardian),

“If I was taking a tablet every day for the rest of my life, I would want to know how long I would have extra to live. If you take statins for five years and you are at higher risk, then you reduce the risk of a heart attack by 36%. But if you rephrase the data, this means on average you will have an extra 4.1 days of life.” 

So no, we shouldn't all be on statins. But until something better comes along (and I hope it will), they are worth considering for anyone who is in a higher-risk group for cardiovascular disease.

Clever food hacks from Cornell Food Lab might all be fake

Have you heard that serving your food on smaller plates will make you eat less? I know I have. I even bought smaller plates for our kitchen when I first heard about that study, which was published in 2011.

And did you know that men eat more when other people are watching? Women, though, behave exactly the opposite: they eat about 1/3 less when spectators are present. Perhaps guys should eat alone if they're trying to lose weight.

Or how about this nifty idea: kids will eat more fruits and vegetables at school if the cafeteria labels them with cool-sounding names, like "x-ray vision carrots." Sounds like a great way to get kids to eat healthier foods.

Or this: you'll eat less if you serve food on plates that are different colors from the food. If the plate is the same color, the food blends in and it looks like you've got less on your plate.

And be sure to keep a bowl of fruit on your counter, because people who do that have lower BMIs.

Hang on a minute. All of the tips I just described might be wrong. The studies that support these clever-sounding food hacks all come from Cornell scientist Brian Wansink, whose research has come under withering criticism over the past year.

Wansink is a professor at Cornell University's College of Business, where he runs the Food and Brand Lab. Wansink has become famous for his "kitchen hacks" and healthy-eating tips, which have been featured on numerous media outlets, including the Rachel Ray show, Buzzfeed, USA Today, Mother Jones, and more.

Last week, Stephanie Lee at Buzzfeed wrote a lengthy exposé of Wansink's work, based on published critiques as well as internal emails that Buzzfeed obtained through a FOIA request. She called his work "bogus food science" and pointed out that

"a $22 million federally funded program that pushes healthy-eating strategies in almost 30,000 schools, is partly based on studies that contained flawed — or even missing — data."

Let's look at some of the clever food hacks I described at the top of this article. That study about labeling food with attractive names like "x-ray vision carrots"? Just last week, it was retracted and replaced by JAMA Pediatrics because of multiple serious problems with the data reporting and the statistical analysis.

The replacement supposedly fixes the problems. But wait a second: just a few days after that appeared, scientist Nick Brown went through it and found even more problems, including data that doesn't match what the (revised) methods describe and duplicated data.

How about the studies that showed people eat more food when others are watching? One of them, which found that men ate more pizza when women were watching, came under scrutiny after Wansink himself wrote a blog post describing his methods. Basically, when the data didn't support his initial hypothesis, he told his student to go back and try another idea, and then another, and another–until something comes up positive.

This is a classic example of p-hacking, or HARKing (hypothesizing after results are known), and it's a big no-no. Statistician Andrew Gelman took notice of this, and after looking at four of Wansink's papers, concluded:

"Brian Wansink refuses to let failure be an option. If he has cool data, he keeps going at it until he finds something, then he publishes, publishes, publishes."

Ouch. That is not a compliment.

Soon after Gelman's piece, scientists Jordan Anaya, Tim van der Zee, and Nick Brown examined four of the Wansink's papers and found 150 inconsistencies, which they published in July, in a paper titled "Statistical Heartburn: An attempt to digest four pizza publications from the Cornell Food and Brand Lab." Anaya subsequently found errors in 6 more of Wansink's papers.

It doesn't stop there. In a new preprint called "Statistical infarction," Anaya, van der Zee and Brown say they've now found problems with 45 papers from Wansink's lab. Their preprint gives all the details.

New York Magazine's Jesse Singal, who called Wansink's work "really shoddy research," concluded that

"Until Wansink can explain exactly what happened, no one should trust anything that comes out of his lab."

In response to these and other stories, Cornell University issued a statement in April about Wansink's work, saying they had investigated and concluded this was "not scientific misconduct," but that Cornell had "established a process in which Professor Wansink would engage external statistical experts" to review many of the papers that appeared to have flaws.

And there's more. Retraction Watch lists 14 papers of Wansink's that were either retracted or had other notices of concern. Most scientists spend their entire careers without a single retraction. One retraction can be explained, and maybe two or even three, but 14? That's a huge credibility problem: I wouldn't trust any paper coming out of a lab with a record like that.

But how about those clever-seeming food ideas I listed at the top of this article? They all sound plausible–and they might all be true. The problem is that the science supporting them is deeply flawed, so we just don't know.

Finally, an important note: Brian Wansink is a Professor of Marketing (not science) in Cornell's College of Business. He is not associated with Cornell's outstanding Food Science Department, and I don't think his sloppy methods should reflect upon their work. I can only imagine what the faculty in that department think about all this.

How much brain damage is too much? NFL players head for the exits.

The smartest player in the NFL just quit.

Not because he was unable to play, and certainly not because of his age–he's only 26. No, Baltimore Ravens' player John Urschel decided to quit because the risk of permanent, irreversible brain damage is just not worth it.

Urschel is a very smart guy. He's currently pursuing a Ph.D. in mathematics at MIT, one of the best and most demanding science universities in the world. Until this summer, he was (impressively) balancing his studies with being a full-time NFL player.

But when Dr. Ann McKee and colleagues published a new study showing that 110 out of 111 former NFL players had suffered serious brain damage, Urschel could no longer pretend he wasn't putting his future at grave risk. McKee's study, the largest study yet of chronic traumatic encephalopathy (CTE), showed alarmingly high rates of CTE in college and high school players as well (91% of former college players).

Let's get one point out of the way: everyone involved with the study, including Dr. McKee, knows that it was biased. The scientists examined brains of deceased players that had been donated to the study because family members–or the players themselves, before they died–suspected something was wrong. So perhaps the true risk of brain damage is lower than 99%. Maybe it's only 50%, or 20%. Do young men playing football want to take that risk?

John Urschel isn't the first player to quit because of the growing realization that football may cause irreversible brain damage. In 2015, San Francisco 49ers player Chris Borland retired at the age of 24, and in 2016 Kansas City Chiefs player Hussain Abdullah retired at 30, both over concerns about concussions and brain damage.

The NFL has been denying or downplaying the risk for years. A few years ago, after the suicide of former player Junior Seau, they announced a $30 million partnership with the NIH to study the risks of football on the brain. As results started coming in, showing that the risk was far more serious than most people knew, the NFL backed out of the deal with $16 million still unspent.

Meanwhile, the chorus of warnings has been growing steadily louder from the medical community. Last year, a former team doctor and a former football player and coach wrote in JAMA that

"unless there is a way to reduce the number of TBIs [traumatic brain injuries] caused by the sport, football will remain a threat to the brains and health futures of the players, including impaired cognitive function and reasoning, memory loss, emotional depression, and other sequelae that profoundly erode quality of life."

Earlier this year, a study out of the CDC reported that "3 high school or college football players die each year from traumatic brain and spinal cord injuries that occur on the field," most them as a result of being tackled during games.

Over the years, football players have grown ever larger (the average NFL lineman today weighs over 300 pounds) and the intensity of the violence on the field has grown with them. It's not just in the NFL, either: last year, three high school teams in the state of Washington forfeited their games against a local team out of a legitimate fear that players would be badly injured by the opposing team's 300-plus pound linemen. Their fears were justified: the human head simply wasn't built to withstand the repeated blows that players endure.

All players might do themselves a favor by listening to John Urschel. He explained his decision–and his abiding love for the game of football–in a lengthy interview on the Freakonomics podcast a couple of weeks ago. That interview should be required listening for young players, and even more so for parents who might be dreaming that their sons have a future career in football.

Houston, we have a problem. It's called global warming, whether you admit it or not.

Hurricane Harvey poured more rain on Texas and Louisiana last week than this country has ever seen from a single storm. The city of Houston is now suffering from historic flooding, with many calling this a "1000-year flood." Congress is likely to pass a huge bailout bill in the coming days, starting with a $14.5 billion "down payment," suggesting much more is to come.

The storm's eventual costs could rise even higher than the costs of 2005's Hurricane Katrina, which cost $160 billion according to NOAA.

Let's not dance around the issue: Hurricane Harvey was a direct consequence of global warming, which in turn is a direct consequence of human activities.

It's ironic that Texas (and Houston in particular) has an economy that is dominated by on oil and fossil fuels. Burning these fuels is what got us in this mess.

It's also ironic that Texas Senator Ted Cruz, who is now at the front of the line asking for a federal government rescue package, is a scientifically illiterate climate change denier. As I wrote shortly after he announced his candidacy for President in 2015, Cruz not only denied that global warming was happening, but he then went on to compare himself to Galileo, as if he were taking a brave and bold scientific position. Right.

A few facts: the Gulf of Mexico is 4 degrees warmer than normal this year, and it has been getting worse. Back in March of this year, the Washington Post's Jason Samenow reported that the Gulf was "freakishly warm, which could mean explosive springtime storms." Warm water feeds hurricanes, and Harvey feasted on it, sucking up energy and using it to dump ridiculous amounts of water onto south Texas.

Noted climate scientist Michael Mann, writing in The Guardian, took the slightly more nuanced position that "climate change made Hurricane Harvey more deadly." True enough: if you want to be strictly accurate, we can't prove that warming temperatures are the sole cause of Harvey. Maybe with cooler temperatures, we'd have had a hurricane anyway–but it would have been a far smaller one, and the damage would have been far less severe.

Mann also pointed out that global warming has already caused sea levels to rise over half a foot, which made the flooding in Houston significantly worse than it would have been otherwise.

Now it's time to rebuild, which raises a dilemma. The U.S. can't just abandon Houston, one of our country's largest cities, even if most of its residents deny the reality of global warming (and perhaps they don't). But given that global warming is well under way, with rising sea levels and warming oceans, more catastrophic flooding events like Harvey are highly likely. Should we pay to rebuild the city exactly as it was, basically ignoring the problems of floodwater management as Houston has done until now? Or should we use the government bailout funds to reduce the risk from future flooding?

Actually, it might do even more good to impose a simple requirement, before Texas gets any of our bailout funds. Let's require U.S. senators Ted Cruz and John Cornyn, and Texas governor Greg Abbot, to state publicly that global warming is real, that humans are making it worse, and that they will work in the future to mitigate the risks posed by continued climate change. Wouldn't that be something? A simple statement, nothing more, to unlock billions of dollars in aid.

If we just rebuild everything like before, then Houston will continue to have a problem.

(*Note about the title of this article. The original quote was "Houston, we've had a problem," famously utterly by Apollo 13 astronaut Jim Lovell. In the movie Apollo 13, actor Tom Hanks (playing Lovell) instead said, "Houston, we have a problem.")

NIH institute purges climate change references, but not very well

Last week, one of NIH's institutes, the National Institute for Environmental and Health Sciences (NIEHS), did something rather mysterious. The institute purged references to climate change on its website by replacing the phrase "climate change" with "climate."

For example, a page formerly titled "Health Impacts of Climate Change" is now titled "Health Impacts of Climate," a title that obscures the main point of the page's content, which is all about climate change. Another page formerly called "Climate Change and Human Health" is now called "Climate and Human Health." Ironically, the web addresses of both these pages still contains the term 'climatechange':

•   https://www.niehs.nih.gov/research/programs/geh/climatechange/health_impacts/
•   https://www.niehs.nih.gov/research/programs/geh/climatechange/

which is something of a smoking gun showing the after-the-fact alterations. The attempted purge was first revealed by the nonprofit group EDGI, a group dedicated to addressing "potential threats to federal environmental and energy policy." The Washington Post revealed that these changes were made by Christine Flowers, the NIEHS Director of Communications. As quoted in the Post, Flowers explained that:

"It’s a minor change to a title page, but the information we provide remains the same. In fact, it’s been expanded."

True, the contents of these pages seem to be unchanged. But in that case, why change the titles and headings? Clearly something more is afoot. Is NIEHS trying to pretend that climate change isn't real, or that it has no effect on human health? If so, this would undermine the very mission of the institute. Are the NIEHS staff fearful that one of Trump's minions will attack them for describing objective scientific facts? If so, perhaps they should get another job.

NIEHS's attempt to re-write its own history has been woefully ineffective. It's easy to find other NIEHS webpages devoted to climate change, such as:
https://www.niehs.nih.gov/health/topics/agents/climate-change
which has the title "Climate Change" right at the top, and which links to a major report called "The Impacts of Climate Change on Human Health in the United States: A Scientific Assessment." There's also the NIEHS Climate Change and Environmental Exposures Challenge, a competition sponsored by NIEHS to create graphical visualizations showing the effect of climate change on health.

The WashPost story did not mention whether the NIEHS director, Dr. Linda Birnbaum or her boss, NIH Director Dr. Francis Collins, had plans to restore the original language to the website. I've written to them both to ask, and I'll post an update here if they do.

Reject this incompetent Trump appointee

Sam Clovis standing next to Trump during the campaign.

Trump has nominated a non-scientist to be chief scientist at the U.S. Department of Agriculture. This is an outrageous slap in the face to science. It's also a slap in the face to Congress.

As I predicted back in May, Trump has nominated Sam Clovis, a former right-wing radio talk show host and failed Senate candidate from Iowa, to be the chief scientist of the USDA. ProPublica was the first to break this story, and they also pointed out that Clovis was a vocal climate change denialist. Clovis has an undergraduate degree in politics and graduate training in business, but he has no formal training in science at all.

Clovis does have one qualification, though. As ProPublica pointed out, he has been a "fiery pro-Trump advocate on television." Sounds like a good candidate for a chief scientist job to me.

Fortunately (perhaps), the Senate has to approve this appointment. The Senate itself stipulated, in a bill that Congress passed in 2008, that the USDA's chief scientist (the Under Secretary for Research, Education, and Economics) must be appointed from

"distinguished scientists with specialized or significant experience in agricultural research, education, and economics."

The law also says, just to make it crystal clear, that the Under Secretary "shall hold the title of Chief Scientist of the Department."

Why is this appointment so wrong? I'll repeat what I wrote back in May:

Overseeing the USDA's research programs requires strong expertise in biological science. A non-scientist has no basis for deciding which research is going well, or what questions need further study, or which questions present the most promising avenues for research. A non-scientist is simply incompetent to choose among them–and I mean this in the literal sense of the word; i.e., not having the knowledge or training to do the job. This does not mean that I think Sam Clovis is incompetent at other things; I don't know him and he might be very capable in other areas. Among other problems, a non-scientist leader of a scientific agency will be incapable of using scientific expertise to set priorities, and instead can make up his own priorities.

If the Senate has any backbone at all–if Republicans are willing to show that they are capable of doing something other than rubber-stamping every action, no matter how damaging, of our self-absorbed, ignorant President–then they will turn down this nomination. Sam Clovis is so obviously unqualified that this should be easy to do.

Actually, if Mr. Clovis cared about the USDA's mission, he would recognize that he's the wrong man for the job and refuse the nomination. Even Dan Glickman, the former Secretary of Agriculture, said "I wouldn't be qualified for that job" (about himself–he's a lawyer) in a recent interview about Clovis' appointment. The current and previous Chief Scientists at the USDA have Ph.D.s and extensive scientific publication records. Mr. Clovis does not. (Note that when I wrote to Mr. Clovis in May to ask about his pending appointment, he declined to respond on the record.)

The Senate's Republicans have confirmed all of Trump's nominees so far, and I fear they will rubber-stamp this one as well. Let's hope that a few of them (and only 3 have to object, assuming all 48 Democrats vote no) realize that appointing a non-scientist to be Chief Scientist of the USDA is a slap in the face not only to science, but to Congress itself, because the appointment scoffs at Congress's own law, passed during the George W. Bush administration.

Trump can find another political appointment for Sam Clovis, as he has for other Trump loyalists. But appointing a former talk radio host, a non-scientist who has never published a single scientific paper, as the Chief Scientist of the USDA is a gross insult to the thousands of hard-working real scientists at the USDA, and to millions more who depend on, and benefit from, the USDA's research programs. Senators: do the right thing and tell Trump to appoint a real scientist to this job.

Will this be the end of college football? The risk of brain damage is startlingly high.

Parents send their kids off to college with high hopes and great expectations. Universities, in turn, have a responsibility to provide an education in an environment that supports and also challenges the students.

Universities are not supposed to encourage activities that may result in permanent brain damage.

And yet, they do. As revealed in a new report by Jesse Mez and colleagues from Boston University, just published in the Journal of the American Medical Association, a shockingly high number of former football players, from both college and professional teams, suffered chronic traumatic encephalopathy (CTE) later in life, likely as a result of their years playing football.

The study authors looked at 202 deceased former football players whose brains had been donated for research, and found that 87% of them had some degree of CTE. The highest rates of CTE were among former NFL players, which affected 110 out of 111 players. CTE was nearly as bad in college football players, though, with 91% of them (48 out of 53) suffering from CTE.

Over half of the high school players (27) had "severe pathology." The authors noted that in deceased players with severe CTE, the most common cause of death was neurodegenerative disease. As they also explain:

"There is substantial evidence that CTE is a progressive, neurodegenerative disease."

In other words, CTE is a death sentence.

The authors of the study stated their conclusions carefully, noting that the study was not randomized, and that players and their families may have been motivated to participate because they were concerned about a possible link between football and CTE. Nonetheless, even if the risk of CTE is much lower than found in this study, universities should be taking a very hard look at the risks that they are exposing their students to.

Or to put it another way, is it okay to ask young men to play football if the risk of permanent brain damage is only 50%? What if it's just 10 or 20%? Is that okay? Is football that important?

Readers of this column know my answer: no. College is not about football, and if it disappears completely, universities will be just fine. The University of Chicago eliminated its football program in 1939, and brought it back in decades later as much-reduced program, now in NCAA Division III. The university itself has remained a powerhouse, routinely ranked in the top universities in the country academically.

As I've written before, football is corrupting our universities, blinding them to their true mission (education and research) in the pursuit of a profitable entertainment business. University presidents seem helpless to stop or even slow down the enormous machine that is big-time college football. For example, in 2015 the University of Maryland (where I used to be a professor) paid millions of dollars to buy out the football coach, so that he could quit a year early and the university could pay millions more to a new coach. Ironically, Maryland had done exactly the same thing in 2011 to buy out the previous coach, at a time when the entire state had hiring and salary freezes in place. None of these actions benefitted the university or its students.

All the while, universities pretend that they are educating the players. Here's a quote from Bleacher Report's interview with star UCLA quarterback Josh Rosen:

"Look, football and school don't go together. They just don't.... No one in their right mind should have a football player's schedule, and go to school."

This from one of the top college football players in the country. (On this topic, Taylor Branch's 2011 exposé in The Atlantic is particularly worth reading. Or this article by a disillusioned former Michigan fan.)

Universities now face an ethical dilemma far more serious than merely taking advantage of athletes' skills to entertain football fans and pay inflated salaries to coaches. The JAMA study reveals that by running a football program, universities are not just robbing young men of four years that might be better spent getting an education and preparing for life: they might be robbing their students of life itself.

ClinicalTrials.gov, a great resource for patients, is being abused to market bad medicine

This wasn't supposed to happen.

Since 1997, the National Institutes of Health has maintained a database of clinical trials, ClinicalTrials.gov, that lists trials under way in the U.S. and throughout the world. It's an invaluable resource, providing a single source for patients trying to find where to get the newest experimental treatments, and for doctors and scientists looking to enroll patients in their trials.

In recent years, companies offering questionable stem cell therapies got the bright idea that they could describe their treatments as clinical trials, register them on ClinicalTrials.gov, and thereby get some free advertising. Most stem cell treatments are not FDA-approved, and many have little or no data supporting their effectiveness, but clinics can still register their "trials" on the NIH site, making it appear that they are supported and endorsed by the government. A new study by Leigh Turner, published this week in Regenerative Medicine, reveals the growing extent of this problem.

What's especially worrisome is that some stem-cell treatment clinics charge patients very high fees to participate in their "trials." Some patients (perhaps most) don't know that legitimate clinical trials virtually never charge fees.

Consider this example, reported last July by Emily Bazar at Kaiser Health News: California resident Linda Smith has knee osteoarthritis, and was looking for treatments that could restore her knees to health without surgery. She found a stem cell trial at ClinicalTrials.gov that was run by StemGenex, a clinic in La Jolla. The clinic promised it could inject stem cells into her knees to replace lost cartilage. When she inquired about signing onto the trial, Smith was shocked to learn that StemGenex wanted a $14,000 fee for her to participate.

StemGenex claimed that “The actual treatment is not part of the study protocol”: you pay for the treatment, they explained, and the study is merely a followup to see how you did afterwards.

What nonsense. I checked the StemGenex site today (a year after the quotes above), and they proudly boast that they are registered on ClinicalTrials.gov, and that

"Stem cell therapy for Osteoarthritis is being studied for efficacy in improving the complications in patients through the use of their own stem cells."

Hmm. This sure sounds like the study is about the treatment. StemGenex's site strongly suggests that their therapy works wonders:

"The goal of each stem cell treatment is to inject the stem cells into the joint to create cartilage (chondryte cells)."

Sounds good, right? If only it were true.

I've got bad knees myself, so I've been following the research on stem cell treatments for cartilage replacement for years. I would love to be able to get a simple injection that could repair my damaged cartilage. Alas, though, no one has yet developed an effective stem cell treatment for bad knees, although it is plausible, and legitimate trials are under way right now (here's one).

Unfortunately, the lack of evidence hasn't stopped clinics from offering stem cell injections right now, accompanied by all sorts of promises that are not backed by science. It's not just knee injections, either: this past March, Sharon Begley at STAT reported on three women who were blinded by stem cell therapy injected into their eyes.

Most patients think, mistakenly, that if a clinic offers stem cell therapy, it must have been approved by the FDA. That's not true–clinics offering these therapies don't have FDA approval, and they argue that they don't need it (which might be correct, but that's a topic for another day).

Patients also assume that trials listed on ClincialTrials.gov must have been approved by some government agency, but that's not true either. The site is a clearinghouse that uses the honor system, nothing more, to ensure that trials listed there are legitimate. If you read their Disclaimer (but who does?), you find that studies listed on the site are not necessarily funded by NIH or approved by the FDA.

Turner's study found 7 trials that openly state they charge patients to participate. At least they're honest about it. Turner found many more (including several run by StemGenex) that appear to charge patients despite not explaining their policy on ClinicalTrials.gov. For example, a stem cell trial by Cell Surgical Network plans to enroll 3000 patients and will charge each of them $6000 or more to participate. As Turner writes

"Cell Surgical Network uses its registered ClinicalTrials.gov study as a powerful marketing device. Press releases and the websites of the clinics that are part of this network emphasize that the study is registered on ClinicalTrials.gov."

NIH needs to start policing this site before the situation gets worse. Coincidentally, I know just where they can find the resources to do it. NIH just announced that it's about to start regulating all sorts of basic science studies as clinical trials, a move that will cause a "massive amount of dysfunction and paperwork," according to one MIT scientist. Rather than over-regulating basic science, NIH should devote those same resources to cleaning up and then continuously monitoring the ClinicalTrials.gov database.

What these stem cell clinics are doing is not a clinical trial, and advertising their services through ClinicalTrials.gov is reprehensible. For now, if a doctor or clinic tries to charge you to participate in a clinical trial, your best course may be to find another trial–and another doctor.

CRISPR gene editing controversy - does it cause unexpected mutations?

Just over a month ago, a short paper appeared in Nature Methods saying that the gene editing technique known as CRISPR-Cas9 has a big problem: it creates unexpected mutations all over the genome. This was startling news for a technique that has been hailed worldwide as a dramatic breakthrough, not only because it is the easiest gene-editing method yet invented, but also because it is (supposedly) very precise.

This new paper, by Kellie Schaefer and colleagues, found hundreds of mutations (in experimental mice) that weren't supposed to be there. The results contradicted earlier studies that showed CRISPR caused very few of these "off-target" mutations. One of the authors, Stephen Tsang, commented that

"We feel it's critical that the scientific community consider the potential hazards of all off-target mutations caused by CRISPR."

Not surprising, the resulting news headlines were gloomy. The stock in three companies trying to commercialize gene editing–Editas Medicine, Intellia Therapeutics, and CRISPR Therapeutics–all fell sharply.  (Interestingly, the stocks started falling on May 24, and bottomed out on May 31. The paper appeared online on May 30.) Scientists involved with these companies quickly responded, arguing that the study was flawed, but of course those scientists have a lot of money at stake.

Who was right? Well, a new paper by Caleb Lareau and colleagues, just released in the bioRxiv preprint repository, re-examines the same data and concludes that CRISPR is just fine. I've read both papers so you don't have to. Here's what seems to be going on.

The study by Schaefer et al. used CRISPR-Cas9 to create mutations in two mice (called F03 and F05), and then sequenced their genomes. They also sequenced the genome of a third mouse, called FVB. All three mice were supposed to be genetically identical.

Then they compared all three genomes to a "reference" mouse to find mutations. (Aside: this is something my own lab does all the time, so I know the techniques well.) They found over 1,500 mutations in each mouse (which wasn't surprising, because the reference mouse differs from their 3 lab animals), but they found hundreds more mutations in the two CRISPR-edited mice. That was the main surprise from Schaefer's paper, and it's the basis for their claim that CRISPR causes numerous off-target mutations.

I had a big problem with this claim even before reading Lareau's paper. Just TWO mice? That's a ridiculously tiny sample. But I digress.

Lareau et al. pointed out, correctly, that Schaefer's conclusion depends on the mice being genetically identical. But what if the two CRISPR mice (F03 and F05) were closer to each other than to the third mouse, FVB? (It's analogous to comparing two siblings with a first cousin, although these mice are much more inbred than any humans.) In that case, the result falls apart.

Fortunately, Schaefer et al. made all their data available (props to them for doing that), so Lareau could answer this question quite precisely.

It turns out that F03 and F05 are much closer to each other than either one is to FVB.  Lareau discovered that the two CRISPR mice share thousands of mutations that FVB doesn't have.

What does this mean? Lareau and colleagues conclude that the "unexpected" mutations in the CRISPR-edited mice were already there before the experiment began, and were not caused by gene editing. As they put it,

"the CRISPR-treated embryos most likely already harbored these private SNPs and indels prior to nuclease treatment whereas the control mouse did not."

In other words, it seems highly unlikely that CRISPR gene editing caused hundreds of unexpected mutations in these mice.

Even though CRISPR is being over-hyped right now, it is nonetheless genuinely exciting technology. Nature Methods was probably too eager to publish a controversial result, an all-too-common problem with big-name journals, and they seem to have done a poor job managing peer review. (Aside: I'd love to see what the reviewers said. Did they miss the obvious problems, or did the journal editors ignore the reviewers? I doubt we'll ever know.)

A final note: this kerfuffle illustrates the tremendous value of rapid publication through pre-print archives. Lareau et al.'s paper appeared a few days ago (July 5) on bioRxiv, along with all the data they used to support their arguments. We'll probably see a journal version too, but that will take months. Getting this paper out faster was a win for science.

(Postscript: two of the authors on the bioRxiv paper have financial interests in CRISPR technology companies, which they disclosed in the paper. I have no financial interests in any of these companies.)

Gwyneth! How did you learn so much about health?

Gwyneth Paltrow has invented stickers that promote healing. Yes, stickers. Little circular stick-on thingies that you might give to your 1st-grader as a reward for doing her homework.

Gwyneth, though, has discovered something much deeper about stickers. If you make them with just the right materials, and then stick them on your body in the right places, they "rebalance the energy frequency in our bodies."

(A quick warning: if you follow the links in this article, put down your coffee first. You might laugh so hard that you'll spill it all over yourself.)

Until a day or two ago, Gwyneth Paltrow's Goop website–a "lifestyle" business that sells all things Gwyneth–advertised these stickers as using "NASA space suit material," which presumably was the source of their magic healing properties. Then Gizmodo called someone at NASA to check out this claim, and got a very clear answer.

Nope. Goop's stickers are not made of space suit material. (Not that space suit material has healing properties in the first place–it doesn't.) Gizmodo's quote from a former NASA scientist, Mark Shelhamer, sums it up nicely:

“Wow,” Shelhamer told Gizmodo. “What a load of BS this is.”   

Goop quickly updated their site, and now they don't claim anything about NASA space suits in their stickers. But they didn't dial back any of their magical healing claims. Here's what Goop says now, in an article called "Wearable Stickers that Promote Healing (Really!)":

"Human bodies operate at an ideal energetic frequency, but everyday stresses and anxiety can throw off our internal balance, depleting our energy reserves and weakening our immune systems. Body Vibes stickers come pre-programmed to an ideal frequency, allowing them to target imbalances."

Wow. What gobbledygook. I see what that NASA scientist meant. But wait, there's more! Goop tells us:

"Studies have shown that when your frequency slips, your immune system is compromised, which opens the door to getting sick."

Studies? No such studies exist. People don't have a "frequency," and there's nothing to "slip." I think it's fair to say that the Goop claims about these stickers are so ridiculous that they're not even wrong.

These stickers are powerful, though, so you must be careful. Goop warns that

"We recommend starting with 1 or 2 for sensitive people. Wearing more than 4 may cause some dilution of the individual frequencies."

Oh boy.

Paltrow sells these magic stickers (and all of her products) using pictures of beautiful models doing healthy activities while wearing stickers. This is part of Goop's appeal: Paltrow is suggesting, in essence, "I'm beautiful and healthy and I'm in my forties, so I know the medical secrets that will keep you beautiful too."

Of course, the special Goop stickers aren't cheap: they cost $60 for a 10-pack.

Not surprisingly, Goop sells lots of overpriced dietary supplements too, such as a bottle of multivitamins with fish oil for $90, which comes with claims about keeping the immune system strong. Almost no one needs these supplements, and they don't do anything for your immune system, as I've explained before.

It took me just a few seconds to find that you can get a sheet with about 50 "dreams come true" stickers at stickersgalore.com for less than $2. These don't come with any wild health claims, but they do make kids happy. I recommend trying these before you get the Goop stickers.

Goop's (and Gwyneth's) claims about their stickers are so ridiculous, so laughably nutty, that I can't really feel sorry for the people who fall for them. Anyone who can afford to waste $60 for a pack of stickers probably has too much money and not enough sense. It's just too bad that they're giving their money to a wealthy actress rather than donating it to some worthy cause.

Finally, I should note that I've always liked Paltrow as an actress, in movies such as Emma and Shakespeare in Love from the 1990s through the recent Iron Man franchise. But why would her acting skills make her an expert on human health? They don't.

Apple's next iPhone iOS will save lives

There's no way that we can convince people to stop texting while driving. It's incredibly dangerous, selfish, and reckless. According to the National Highway Traffic Safety Administration, distracted driving killed at least 3,477 people in 2015 alone. Many states have outlawed texting while driving, including my own state of Maryland, but every day I pass people on busy roads who are looking at their phones.

The only solution is technological. The phone itself needs to stop distracting you while you're driving. People aren't going to put their phones down voluntarily.

Apple's iOS 11, coming this fall, finally offers a solution. It may not solve the problem entirely, but it will likely save lives.

Apple's IOS 11, coming in the fall of 2017,

will offer Do Not Disturb while driving

The solution is very simple, technically speaking. Your phone already knows when it's on a roadway, and it knows that it's moving. So the phone's software–iOS, if it's an Apple phone–can simply disable any apps that might cause distractions.

Apple's preview of iOS11 says it will do more than that. It will not only silence all incoming calls, text messages, and other notifications, but it will text people back automatically and tell them that you're driving.

You'll still be able to use maps and GPS for directions, which is an extremely useful feature that many people just can't do without (and that doesn't cause traffic accidents).

This is a great idea that is long overdue. Apparently, Apple couldn't resist allowing passengers in the car to override the do-not-disturb mode, which I think is a pretty terrible idea. I doubt that the phone will recognize when a passenger just hands it to the driver, but I'll have to wait and see how Apple implemented this override feature. I hope it's really hard to do.

iOS 11 is coming in the fall. Google hasn't yet said anything about whether Android phones will have a similar feature, but I hope they will. This is desperately needed, and it will save lives.

Google, the ball is in your court.