Good news for "Research Parasites": NEJM takes it back, 8 years later

After years of debate, the National Institutes of Health finally rolled out a data sharing policy early this year, one that should greatly increase the amount of data that biomedical researchers share with the public. This week, three prominent scientists from Yale described, in an op-ed in the New England Journal of Medicine, how “the potential effects of this shift ... toward data sharing are profound.”

For some of us, it’s deliciously ironic that this op-ed appeared in NEJM, which just a few years ago coined the term “research parasites” to describe anyone who wants to make discoveries from someone else’s data. That earlier piece, written in 2016 by the NEJM’s chief editors, was simply dripping with disdain. It caused a huge outcry, including a response from me in these pages and a sharply worded response from the Retraction Watch team, published in Statnews. The editor backed down (slightly) in a follow-up letter just a few days later, but the damage was done.

One interesting consequence was that a group of scientists created a Research Parasite Award, now awarded each year (entirely seriously, despite the tongue-in-cheek name) at a major biomedical conference, for “rigorous secondary data analysis.”

The 2016 op-ed in NEJM was itself a response to a call for greater data sharing published in the New York Times by cardiologists Eric Topol and Harlan Krumholz–and Krumholz, we should note, is a co-author of the latest piece in NEJM. Meanwhile, the former editor of NEJM retired years ago, and it appears that the journal is now ready to join the 21st century, even if it’s a few decades late.

What is all this fuss about? Well, many people outside of the scientific research community probably don’t realize that vast amounts of data generated by publicly-funded research–work that is paid for by government grants–are not usually released to the public or to any other scientists.

On the contrary: in much of biomedical research, data sets collected with government funding are zealously kept private, often forever. The usual reasons for this are simple (although rarely admitted openly): the scientists who collected the data want to keep mining it for more discoveries, so why share it? Sometimes, too, researchers package up the data and sell it, which is completely legal, even though the government paid for the work.

(It’s not just medical research data, either: once I tried to get some data from a paleontologist, only to learn that he treated every fossil he ever collected as his personal property. But that’s a blog for another day.)

Many scientists have been fighting this culture of secrecy for a long time. Our argument is that all data should be set free, at least if it’s the subject of a scientific publication. It’s not just scientists making this argument: since the early 2000s, patient groups began to realize they couldn’t even read the studies about their own diseases unless they paid a for-profit journal to access the paper. Those groups lobbied–successfully, after a years-long fight–that any publicly-funded research had to be published on a free website, not locked behind the doors of private publishers. Their effort led to an NIH database called PubMedCentral, which contains the full text of thousands of articles.

The new NIH data sharing policy is one consequence of the Open Science movement (which I’m a part of), which argues that science moves much faster when it’s done in the open. This means sharing data, software, methods, and everything else. There’s now a U.S. government website dedicated to Open Science, open.science.gov, which includes more than a dozen federal agencies including NIH, NSF, and the CDC.

A bit more history: as far as I can tell, the earliest voices for data sharing emerged during the Human Genome Project, an international effort beginning in 1989 that produced the first draft of the human genome in 2001. When a private company (Celera Genomics) emerged in 1998, a dramatic race ensued, and as one strategy for competing, the public groups announced that, in contrast to the private group, they would release all their data openly on a weekly basis, long before publication. That wasn’t how things had worked before.

Very soon after that, scientists in genomics (my own field) realized that all genome data, whether from bacteria, viruses, animals, or plants, ought to be released freely. The publicly-funded sequencing centers received millions of dollars to generate the data, but they weren’t the only places who could analyze it. NIH and NSF agreed, and pretty soon they required all sequencing data to be released promptly.

This same spirit didn’t touch most medical research, though. Even though far more money–billions of dollars a year in NIH funds–is spent on disease-focused research, data from those studies remained locked up in the labs that got the funds. This is now changing.

As the Yale scientists (Joseph Ross, Joanne Waldstreicher, and Harlan Krumholz) point out in their NEJM editorial, open data sharing has already yielded tremendous benefits. For example, they point out that hundreds of papers have been published using public data from the NIH’s National Heart, Lung, and Blood Institute, including studies that revealed new findings about the efficacy of digoxin, a common drug used to treat heart failure.

The new NIH policy covers all of NIH, not just one institute, and we can hope it will unlock new discoveries by allowing many more scientists to look at the valuable data currently kept behind closed firewalls.

But simply requiring scientists to have a “data management and sharing policy,” as the NIH is now doing, might not be enough. Many thousands of scientific papers already say they share data and materials–but as it turns out, the authors don’t always want to share.

A study published last year illustrated how toothless some current policies are. That study identified nearly 1800 recent papers in which the authors said they would share their data “upon request.” They wrote to all of them, only to find that 93% of the authors either didn’t respond at all, or else declined to share their data. That’s right: only 7% of authors shared their data, despite publishing a statement that they would.

The NEJM editorial proposes a different solution, one that could be far more effective: putting scientific data into a government repository. This is something the government itself can enforce (because they control the funding), and once the data is in a public repository, the authors won’t be able to sit on it as (some of them) now do.

It’s good to see NEJM joining the open science movement. Science that is shared openly will inevitably move faster, and everyone–except, perhaps a few data hoarders–will benefit.

A simple trick to make better coffee: cut the static!

 

You’d think that coffee afficionados had tried everything by now, and that few if any tricks remained undiscovered. Well, you could be right–but there’s one trick that most ordinary coffee drinkers probably don’t know, and it’s remarkably easy to do.

I’ll jump right to the punchline, and then I’ll explain the (new) science that explains it. To make richer coffee in the morning, simply spritz a little water on your beans before grinding them. That’s it!

So what happens when you do this, and why does it make better coffee? Well, as explained in this new paper in the journal Matter, by Christopher Hendon and colleagues at the University of Oregon, it’s all about reducing the static electricity that the grinding process creates.

Grinding coffee causes triboelectrification. If you’ve never heard of that, not to worry–neither had I, until I read the paper. Basically, when the beans rub together, they create static, and that makes the ground coffee clump together (and sometimes fly into the air).

Then when you make the coffee, the clumping means that the water flows through the grounds unevenly, absorbing less of the coffee particles than it might. Ideally, all the coffee grounds should be evenly and densely packed, and static electricity prevents that.

Water reduces triboelectrification quite a bit, it turns out.

So what happens? Well, after extensive experimentation–and I do mean extensive–the scientists found that the amount of coffee solids in a cup of espresso increased from 8.2% to 8.9% when adding a bit of water to the beans before grinding. That’s a relative increase of 8.5%. Richer coffee!

Reading the paper, I realized these scientists had a lot of fun doing these experiments. They measured the water content in 31 types of coffees, and tried a wide range of settings for their grinders, for the water temperature, and more.

They also roasted their own beans to varying degrees of darkness. They tried dozens of combinations of beans and roasting strategies, measuring the water content after roasting and the amount of static electricity generated upon grinding. They observed that darker roast coffees usually generate finer ground particles, and finer particles in turn generate more static electricity.

They drank a lot of coffee to get this right! But hey, sometimes science requires sacrifices, right?

I should mention that the trick of adding a little water to the beans is already known to some experts, although the precise science behind it was unknown until now. It even has a name (as the paper points out): the “Ross Droplet Technique.”

As the paper concludes, “a few simple squirts of water [may] have solved the problems of clumping, channeling, and poor extractions while aiding in the pursuit of attaining the tastiest espresso.” You only need a few drops of water–give it a try.

One important caveat is that if you use the French press method to make coffee, where the grounds are immersed in water, then this trick won’t make any difference.

What’s next? Well, I should point out that this study focused entirely on espresso. Does it work for regular coffee as well? Probably so, but more research is needed.

Vaccines Show Surprising Link To Reduced Risk Of Alzheimer’s

Well, the anti-vaccine community is not going to like this one.

A growing body of evidence, buttressed by a new report out last month, shows that people who are vaccinated have a significantly lower risk of Alzheimer’s disease.

Yes, that’s right: in addition to the obvious benefit of protecting you from infections, multiple different vaccines have now been shown, in two large studies, to be associated with fewer cases of Alzheimer’s.

How big is the effect? Well, the earlier study, published about a year ago, looked at the flu vaccine. Scientists from the University of Texas Health Science Center, led by neurologist Paul Schulz, collected data on more than 1.8 million older patients from around the U.S., of whom half had received the flu vaccine and half had not. Their average age was 74 years, and the scientists examined health records for four subsequent years to see how many developed signs of Alzheimer’s in that time.

In the vaccinated group, nearly 48,000 patients (out of 936,000) developed Alzheimer’s during the four-year follow-up period, about 5.1% of all patients. That might sound like a lot, but in the unvaccinated patients, nearly 80,000 developed Alzheimer’s. To put it another way, patients who got the flu vaccine had a 40% lower risk of Alzheimer’s, 5.1% versus 8.5%.

It appears this benefit isn’t specific to the flu vaccine, though. In the newer study published this September, the same group from the University of Texas looked at three more vaccines: the Tdap vaccine (tetanus, diphtheria, and pertussis), the shingles vaccine and the pneumococcus vaccine. They were able to collect records on 1.65 million people, among whom more than 500,000 had received one or more of the vaccines. All of the patients were over 65 years old.

Remarkably, all three of the vaccines showed similar and quite significant benefits against Alzheimer’s disease. In an eight-year follow-up period, the risk of Alzheimer’s was 30% lower (7.2% versus 10.2%) in patients who had the Tdap vaccine versus those who hadn’t. For the shingles vaccine, the reduction in risk was 25%, 8.1% versus 10.7%. And for the pneumococcal vaccine, the risk was 27% lower, 7.9% versus 10.9%.

(Note that this study looked at the older shingles vaccine. The newer one, Shingrix, has only been widely available since 2017. The scientists hypothesize that the newer vaccine, because it’s more effective against shingles, may provide even greater protection against Alzheimer’s.)

So how might this work? Is Alzheimer’s caused by an infection, and the vaccines prevent Alzheimer’s by preventing the infection? Well, the short answer is no, probably not. Although we don’t know the cause of Alzheimer’s, we don’t have any strong evidence that it’s the direct result of an infection.

Furthermore, with data showing that at least four different vaccines offer similar levels of protection against Alzheimer’s, the evidence indicates that the effect cannot be specific to the flu vaccine, or the Tdap vaccine, or with any of the other vaccines or their ingredients.

The University of Texas group that published the study speculated that vaccines might work to protect against Alzheimer’s by “long-term reprogramming of innate immune cells,” also called “trained immunity.” This hypothesis is far too complex to try to explain here–and it involves immunology, which I don’t really understand myself and which is “absurdly intricate” as science writer Ed Yong put it. So let’s just say that this is an intriguing idea that needs more research.

And for anyone who thinks that getting an infection and recovering (instead of getting vaccinated) might offer the same benefit, that doesn’t seem to work: another study looked at precisely this question and found no connection between the number of influenza infections and the risk of Alzheimer’s. So the vaccine seems to confer a benefit that the disease itself does not. (I mention this because a popular–but wrong–claim of anti-vaccine activists is that you get better immunity from infection by catching the disease and then recovering. Not a good idea.)

Also, I have to add that these studies report correlation, not causation. So even though the effects are large and significant, we don’t know for certain that vaccines do something to directly prevent Alzheimer’s. Maybe people who get vaccinated also have other behaviors that help them avoid Alzheimer’s–although the study design tried to minimize this possibility.

Vaccines have enormous, extensively documented benefits: they prevent suffering and disease, and they’ve saved countless millions of lives. And now it appears that they offer something else: a lower risk of Alzheimer’s. So if you haven’t received your boosters, now you have one more reason to get them.

Most of our common cold medicines don’t work

We still don’t have a cure for the common cold. In your local pharmacy, though, you can find many shelves filled with products that claim to treat the symptoms.

Well, it turns out that one of the most widely used ingredients, long believed to be effective at treating congestion, doesn’t work at all. The ingredient, phenylephrine, has been in use for decades, and it’s in many common cold medicines that are taken by millions of people each year, including Nyquil Severe, Sudafed PE, Robitussin CF, Tylenol Cold & Flu and others.

It turns out that phenylephrine was never properly studied for effectiveness. How can this be? It’s FDA approved, which usually means it has to be safe and effective, right? Not exactly, as I explain below.

As for phenylephrine: well, the studies have finally been done, and last month an FDA panel unanimously concluded, after reviewing the results, that phenylephrine is “useless and no better than a placebo.” It probably won’t cause you any harm, but it won’t have any effect on your stuffy nose.

To understand how this happened—and why it might be true of many other FDA-approved remedies that you can buy at the pharmacy—you have to know about how the FDA approval process has changed over the years. Pharmacists Randy Hatton and Leslie Hendeles, who worked for years trying to get phenylephrine properly reviewed, explained in a recent New York Times editorial that when the FDA was originally created, way back in 1938, it was only required to ensure that drugs were safe.

At the time, that was tremendous progress. Prior to 1938, drug manufacturers could claim pretty much whatever they wanted to.

But it wasn’t under 24 years later, in 1962, that Congress required the FDA to show that drugs were also effective. Therefore the thousands of drugs approved prior to 1962 were mostly safe, but they might not actually treat the disease they were intended to treat. After 1962, the FDA created a process to check those previously approved drugs, but they’ve never had enough staff or funding to check most of them. So phenylephrine was never properly reviewed, until now.

What’s next for phenylephrine? The FDA might ban it from the market, but that will take time, and it might not happen, because the FDA doesn’t have to follow the advice of its panels, although it usually does. Meanwhile, you can still buy cold remedies with phenylephrine, and they still claim to treat congestion.

And don’t even get me started on other treatments that are not only ineffective but that aren’t even subject to review by the FDA, such as homeopathic remedies. These include Zicam, which claims in large print on the front of its packaging that it “shortens colds.” It doesn’t, and Zicam’s manufacturer doesn’t even have to prove it, because it’s homeopathic. If you zoom way in one of the labels on the Zicam website, you’ll find the disclaimer that “Claims [are] based on traditional homeopathic practice, not medical evidence. Not FDA evaluated.” On some of the packages, I couldn’t even find the small print.

(Aside: Congress protected homeopathic preparations from FDA scrutiny way back in 1938, thanks to a homeopath who was also a U.S. Senator, and who helped write the original FDA legislation.)

I wrote about Zicam and other ineffective cold remedies in 2014 (”The Top Five Cold Remedies that Do Not Work”), and that advice still holds. Now we can add another one to the list.

We simply don’t have any drugs that work particularly well for the common cold, despite the many claims you can find online and on the labels of so-called cold remedies. The best thing you can do is just drink warm liquids such as tea or lemon-infused water, stay home and get plenty of rest.

West Virginia Says It’s Too Poor To Support Its Only Major University

As students and faculty prepared for the start of the new academic year this month, the president of West Virginia University, Gordon Gee, made a startling announcement: he’s eliminating 169 faculty jobs, about 16% of the full-time professors, and dropping 32 undergraduate and graduate degree programs, including all of its foreign language programs.

No foreign language classes? No French, Spanish, Chinese, Russian, anything other than English? Apparently not–and in response to questions, the university suggested that students might be offered an online app instead. It’s not just humanities, either: WVU is also getting rid of its graduate program in mathematics.

These cuts came as a shock to the students and faculty of WVU, who are understandably dismayed. The university administration says it’s just about money, as they face a $45 million deficit that they must do something about.

I’m not buying it. What really seems to be going on (and this is not unique to West Virginia), is that the state has steadily cut its support for WVU over the years, creating ever-larger deficits. The problem now is that the current president, Gordon Gee, seems to be saying that’s all fine with him. He didn’t even ask the state if it could help before he imposed these drastic cuts: as quoted in the Washington Post, Gee said “If I had gone down and asked for $45 million from the state legislature, they would have thrown me out.” Perhaps, but did you even try?

In the same article, State Senator Eric Tarr (R) also said he “wholeheartedly” believes that WVU president Gee is doing the right thing. And yet in the same interview, Sen. Eric said “We have never not supported WVU.”

Hmm, really? Over the past decade, the state has cut its support for WVU by 36%, or nearly $100 million. So it’s pretty clear that the legislature is not supporting WVU, at least not like they did in the past.

With support like that, who needs detractors?

According to one analysis, if West Virginia’s legislature had simply kept WVU’s funding flat for the past decade, WVU’s deficit right now would be far smaller, just $7.6 million rather than $45 million.

President Gee, did you ask the legislators about that?

I can’t help noting that WVU just renewed Gee’s contract for another year, at $800K per year. So they do seem to be able to come up with money for administrators. Gee’s only the 4th highest-paid WVU employee, with the football and basketball coaches each making over $4 million. I wasn’t able to find out how much WVU paid the consulting company rpk Group, whom Gee hired to come up with these severe cuts, but I’ll bet they weren’t cheap.

The state of West Virginia has only one R1-class research university, West Virginia University, with some 25,000 students on its main campus in Morgantown. If this trend continues, the state might no longer have even one major research university. That’s too bad.

And despite what WVU’s Gee and the consultants he hired might claim, this is not just about money; it’s about priorities. Currently, only five states don’t have an R1 level university: Alaska, Idaho, South Dakota, Vermont, and Wyoming. Does West Virginia want to join that club?

It’s true that West Virginia is one of the poorest states in the U.S., with a poverty rate of 16.8%. But can it really not afford even one major university? For West Virginia residents, WVU is the only R1 university that most of them can afford, because in-state tuition is far cheaper than out-of-state tuition at any other state university.

The way to fix this problem isn’t to eliminate the core elements of a college education, which include foreign languages. The fix is simple: the legislature should step up and say they truly support WVU, and cover its deficit without eliminating any programs. Then they should find a university president who is willing to ask for the funds that a major university needs. I’m sure they can find someone willing to do the job, maybe for even less than $800K per year.

Let’s Consider The Benefits Of Raw Milk

As reported this past week in the New York Times and elsewhere, more than half the states in the U.S. now allow the sale of raw milk. In some states, you can only buy raw milk at a farm, but in 14 states you can buy it in stores.

So why are some people excited about raw milk? Well, the implication is that if’ it’s less processed, it must be better, right? After all, we learned recently that ultra-processed foods are pretty bad for you. (There’s pretty good evidence for that.) And milk is one of those products that people associate with health. For the first few months of life, we humans live entirely on milk–but that’s milk from a woman’s breast.

Cow milk is a different matter. It’s not nearly so, shall we say, clean.

It only took a minute for me to find claims that raw milk has all kinds of benefits: supposedly it helps you digest food better, it has more vitamins and minerals, it boosts your immune system, and it’s better for people with lactose intolerance. (I won’t link to any of those claims because they’re all bogus, and I don’t want to give scammers any more web traffic.)

Before listing some of the special properties of raw milk, let’s consider how it’s processed. The main thing we do to milk is pasteurization: a very simple process where the milk is heated just enough to kill any bacteria in it. It’s not boiled, and the mild heating doesn’t destroy any of milk’s nutrients.

Pasteurization is named after the French scientist Louis Pasteur, who invented the process in the 1860s. Originally it was used to preserve wine, but people eventually discovered it worked just as well for milk and other foods. Back in the 1860s, people didn’t even know that bacteria caused disease, and Pasteur was one of the pioneers who figured that out.

So what does raw milk have in it? Well, it can carry a long list of delightful bacteria, including the ones that cause tuberculosis, brucellosis, scarlet fever, salmonella. And of course there is E. coli, including strains that can cause terrible diarrhea.

Bacteria just love milk, it turns out. Raw milk is teeming with them, and many of them are really not good for humans. Fortunately for most of us, pasteurization kills bacteria very effectively.

And there’s one more special thing you get in raw milk that you won’t get in pasteurized milk: cow poop. Funny thing, though: on the advertisements I found for the benefits of raw milk, none of them mentioned this.

So sure, get your raw milk and live like it’s 1850 again! Never mind that pasteurization has saved countless millions of lives. Seriously, folks: there’s no reason whatsoever to drink raw milk. And states that allow the sale of raw milk are endangering the health of their own people.

Does Taurine Really Extend Life? Maybe.

 Readers of this column will know that I’m highly skeptical of dietary supplements. So you might imagine my reaction when I saw headlines a few days ago about “Taurine, the elixir of life?” (at CNN) and “Supplement slows aging in mice and monkeys” (NY Times).

Unlikely, I thought. But I read the scientific article behind these reports, and now I’m intrigued.

What is taurine? And could it really slow down aging? Well, it seems like it could, just maybe. A new study published last week in Science (one of the top journals in all of science) seems to show, for the first time, that taking large doses of taurine, an essential amino acid, might provide a host of benefits that include slowing down the aging process.

First question first: what is taurine? It’s an amino acid, but it’s not one of the 20 amino acids that comprise all the proteins in your body. It’s a slightly different one, and our bodies naturally produce it in small amounts. We need more than our bodies produce when we’re very young, but we get it from breast milk, and it’s added as a supplement to infant formula.

We also get extra taurine from our diet: the best foods for taurine are meats, especially shrimp and other shellfish, but also beef and the dark meat in chicken and turkey.

What did the new Science paper show? Well, first the authors (from Columbia University, India’s National Institute of Immunology, and the Sanger Institute in the UK) describe how taurine levels clearly decline with age in humans and other mammals. Now, just because taurine declines doesn’t mean that replacing it will reverse the aging process, but at least it establishes plausibility.

They then describe a series of experiments, mostly in mice but also in monkeys, where they fed the animals relatively large amounts of taurine each day, and the results were pretty darned impressive:

1. Life span in the mice increased by 10-12%.
2. In mice that started taurine supplements in middle age, life span increased by 18-25%.
3. Bone density increased in female mice and osteoporosis seemed to be cured.
4. Muscle strength increased in both males and females compared to mice who didn’t get taurine.
5. The number of senescent cells–cells that don’t do much except emit damaging inflammatory signals–seemed to be reduced.

Of course, there’s always a big caveat with results in mice: they’re mice, not humans! And many, many times we’ve seen results in mice that just don’t carry over into humans. So the scientists also did a study (a smaller one) in monkeys, which are much closer to humans genetically. This also had some very good results:

1. Bone density increased in the spine and legs.
2. Body fat was lower than it was in monkeys that didn’t get taurine.
3. Several measures of inflammation decreased.

Monkeys live a lot longer than mice, so the scientists don’t yet know if taurine increases the monkeys’ life span, but all the signs are promising. I was skeptical going into this article, but I couldn’t find any obvious flaws.

In an accompanying article in Science, U. Penn’s Joseph McGaunn and Joseph Baur point out that we don’t know for sure what the risks of long-term supplementation with taurine would be, but it is already widely taken as a supplement in baby formula and in energy drinks, with no known ill effects.

However, the amounts used in the Columbia study were very high, much higher than you’d get from energy drinks or even from standard taurine supplements. I looked up a few, and typical formulations offer 1000 or 2000 mg (which is 1-2 grams) per day. The doses given to monkeys in the study, if converted to a 150-pound person, is equivalent to about 5500 mg (5.5 grams) per day. That’s not very much by weight, and it would be easy enough to take this much taurine, but no one knows the effects in humans of such high doses.

The bottom line: this study is really intriguing. More studies are needed, especially to measure the effects of taurine on humans, but all the signs are positive. I’ll be watching closely to see if the effects in mice and monkeys carry over, and if they do, we may all be taking taurine supplements one day. And I just ordered some taurine powder for myself–why not?