No, You Still Don’t Need Vitamin D Supplements!

The NY Times this week ran a story under the headline “Am I Getting Enough Vitamin D During the Winter?” I’ll give you one guess how they answered that one.

Yes, the days are at their shortest right now. (The shortest day of the year will be Wednesday, December 21.) And yes, your body synthesizes vitamin D when you’re out in the sun, so you make less of it this time of year.

You also get vitamin D from a variety of foods. The Times story quoted a skin cancer expert from NYU School of Medicine, Dr. Deborah Sarnoff from, who said “you don’t need to get it [vitamin D] from sunshine.”

So you don’t need to run out and take vitamin D supplements. as I pointed out emphatically in a column I wrote back in August, and in several earlier columns too. Scientists have conducted multiple major studies of vitamin D supplements, as I wrote before, and those studies–involving thousands of subjects and running for many years–showed that

• Vitamin D supplements do not improve bone density, and they do not reduce the risk of osteoporosis.
• Vitamin D supplements don’t prevent heart disease, weight gain, mood disorders, multiple sclerosis, or metabolic disorders.
• Vitamin D supplements (in the most recent study, involving 26,000 men and women followed for more than five years) don’t do anything to prevent bone fractures.

But the NY Times reporter (Rachel Peachman) really wanted to recommend supplements, it appears. She apparently wasn’t able to get a doctor to say that, so instead she quoted a dietitian nutritionist, who provided the quote, saying “Especially as we’re entering the winter months, most people would benefit from taking a supplement.”

Not surprisingly, the Times doesn’t quote an actual study that supports this recommendation, because that’s not what the science says. (To be fair, the dietitian also included some caveats, which are paraphrased in the article, including the point that “it’s difficult to suggest one blanket recommendation for everyone.”)

So no, NY Times, most people wouldn’t benefit from taking a supplement. As Drs. Steven Cummings and Clifford Rosen wrote last summer in the New England Journal of Medicine, “providers should stop screening for 25-hydroxyvitamin D levels or recommending vitamin D supplements, and people should stop taking vitamin D supplements to prevent major diseases or extend life.” And as five of my Hopkins colleagues wrote in a 2013 review in The Annals of Internal Medicine, “stop wasting money on vitamin and mineral supplements.” The science just doesn’t support it.

Cummings and Rosen also pointed out that more than 10 million blood tests for vitamin D levels are conducted in the US each year, with the vast, vast majority of these being unnecessary. These tests aren’t free, and our costly health care system doesn’t need the extra burden.

Finally, let me offer a caveat that I’ve written before: although routine supplementation is worthless and megadoses of vitamins can be harmful, if you think you have a vitamin deficiency, consult with your doctor. Serious vitamin deficiencies might be the result of other health problems that your doctor can help you address, and treatments for specific conditions or diseases may include vitamins.

We may get a universal flu vaccine, thanks to mRNA technology

The mRNA vaccines for Covid-19 are an amazing story: a new vaccine developed in a matter of weeks for a brand-new virus, SARS-CoV-2, at the beginning of the pandemic in early 2020. Clinical trials moved forward at record speed, and by December of that year we had an approved vaccine that was safe and over 90% effective against Covid-19.

Why not use this mRNA technology for other vaccines, especially for the flu? When I asked this question last year, I didn’t realize that a group of scientists at the University of Pennsylvania were already hard at work making this idea a reality. They’ve just published their first results, and the news is very encouraging.

But first, some background. Messenger RNA (mRNA) vaccine technology was the big breakthrough behind the Covid-19 vaccines. Invented by Katalin Karikó and Drew Weissman at the University of Pennsylvania, the idea is, at its core, very simple: take the genetic code for a protein from the virus (any protein can be used, and for Covid-19 this protein is called Spike), and inject it into someone’s arm. (The genetic code I’m referring to here is the mRNA that encodes the protein.) From there, the cells of the human host manufacture the protein–not too much, though, because mRNA quickly degrades once it’s in your body.

What’s kind of amazing is that the human immune system will then recognize the Spike protein as an invader, and generate antibodies against it. From that point on, the person who received the vaccine will be prepared to fight off a real infection by Covid-19. In other words, they’ll be immunized.

The actual development of this technology was much more complicated than I’m describing here. First, you can’t just inject mRNA without causing a lot of inflammation, which can be dangerous. Weissman and Karikó solved that problem by using chemically modified mRNA. Second, you need to package the mRNA in something; the scientists discovered that they could use little packages of fat molecules called liposomes to make an effective container. Eventually, they got it to work, and the rest is (recent) history. Both the Moderna and Pfizer/BioNTech vaccines use mRNA technology.

Now about this new “universal” flu vaccine, and why it’s so much better than what we currently use. The annual flu shot contains pieces of one protein from 4 different influenza strains. Each year, as the flu itself evolves, the 4 strains used in the flu vaccine are fine-tuned in an effort to keep up. In some years, this effort fails and the vaccine just doesn’t work very well, for reasons I explained here.

One huge problem is that the current flu vaccine process grows the flu virus in chicken eggs, and sometimes the darned thing just won’t grow! So in those years, the vaccine manufacturers must switch to another flu strain, one not as well-matched to what’s circulating. The result is a vaccine that sort of sucks, although it’s usually better than nothing.

With mRNA, you don’t have to grow anything in chicken eggs, and you aren’t limited to just 4 strains. As the new research shows, you can put ALL 20 known influenza strains in the same vaccine, and it protects subjects against all of them. It even protects against other flu strains that weren’t in the vaccine. To create the vaccine, scientists simply synthesized the mRNA that encodes the surface protein of the flu, hemagglutinin, from 20 different flu strains. The synthesis process is already being done on an industrial scale for the Covid-19 vaccines, and the same process will work for any mRNA, from any virus.

In the new research, scientists at UPenn led by Scott Hensley and Drew Weissman (the co-inventor of the mRNA vaccine) inserted all 20 flu strains in a single vaccine. They found “that the vaccine dramatically reduced signs of illness and protected from death, even when the animals were exposed to flu strains different from those used in making the vaccine.”

Did I mention that the subjects in the new study were mice and ferrets, not people? Well, this experiment is just the beginning: we’ll need further trials to test the safety and efficacy of this vaccine in people. Those are much, much more costly, though, and it’s not clear when or even if those trials will happen.

If we had a universal flu vaccine, we might no longer need the annual flu shots that we beg everyone to get each year. So when can we expect to see this new 20-strain vaccine?

Well, there’s the rub. Even if this new flu vaccine works perfectly in human testing, we might never get it. At the moment, we are completely dependent on private companies to develop vaccines. At the beginning of the Covid-19 pandemic, the U.S. created incentives for vaccine manufacturers by promising to buy millions of doses, and–fortunately–that worked. We’ve never tried anything like that with the flu vaccine.

We need to re-think our dependence on private, for-profit companies for this critically important public health technology. Perhaps it’s time for the government to step in and make sure we get this vaccine, whether through incentives like the ones used to create the Covid-19 vaccine, or through a direct effort by the government itself (as other countries have done) to create a universal flu vaccine. A universal flu vaccine will save tens of thousands of lives every year. Let’s hope we get there.

College football continues to corrupt our universities. At least we could pay the players

More than ten years ago, I wrote that it was time to get football out of our universities because the sport was corrupting the universities’ mission. Not surprisingly, I got a lot of pushback about that, but I’ve continued to make this point, both here at Forbes and in The New York Times.

This weekend, I watched a college football game for the first time in years. I was struck by how much worse things are–and by worse, I mean driven by money.

Don’t get me wrong. Football is entertaining for its millions of fans, and college football is extremely popular, especially for those who live in cities without a professional team. I’m not so naive as to think people will give this up.

The problem is that major college football is a professional sport where everyone makes money except the main participants: the players. Worse, the players are being told by their coaches, assistant coaches, athletic directors, and university presidents that they’re getting a great deal. We give you free education! And you get to play football for our great team, and everyone will cheer for you!

If this is really so great, then why don’t the coaches work for free? College football coaches are paid multimillion-dollar salaries, usually far higher than anyone else at the same university, even the university president. The average salary of NCAA Division I coaches this year is $1.75 million, and some coaches make over $10 million. In most states, a football coach at a public university is the highest-paid state employee.

But the players get zero. This situation, to put it bluntly, is unethical. Universities with large football programs are profiting handsomely off the unpaid labor of their own students.

Universities have been told this before. In 2011, civil rights historian Taylor Branch wrote a ground-breaking cover story in The Atlantic titled “The Shame of College Sports,” As Branch wrote then:

“Big-time college sports are fully commercialized. Billions of dollars flow through them each year. The NCAA makes money, and enables universities and corporations to make money, from the unpaid labor of young athletes.”

That was 11 years ago. The situation has only gotten worse.

What’s striking about watching a college football game on television, as I did this past weekend, is the degree of commercialization of the sport. The game is interrupted constantly with advertisements from sponsors, and the stadiums are decorated with ads as well. ESPN has a large, professional team of announcers covering every aspect of the game. The television work is highly coordinated and professional, with many cameras covering every angle of every play.

There is a LOT of money in college football.

I listened to interviews with some of the (winning) players after the game. They were excited, and they praised their coaches and fellow teammates as they were supposed to. They seemed to believe that the game they’d just won was supremely important, and that their performance (an upset victory) was meaningful and even “historic” (as one player said).

But it wasn’t. Football is just entertainment.

What’s especially sad, to me, is that nearly all of these players are getting short-changed on their education. They spend most of their time on football for a good portion of their year, despite the laughable pretense by the NCAA that these are “student athletes.” They’re athletes, certainly, but they don’t have time to be students, not during football season. The universities (and especially the football coaches) just don’t seem to care, despite their continual protestations to the contrary.

Only 1.6% of college football players make it into the NFL. Or to put it another way: at the end of their college years, 98.4% of college football players will be spit out into the real world, with poor job prospects because they didn’t focus on their education.

And it’s actually even worse than this. We’ve learned in recent years that football carries serious risk of permanent neurological damage, due to repeated blows to the head that happen to many players. It’s a violent contact sport, and the ever-greater size of today’s players has made it much more dangerous than in its early years in the mid-20th century. (I wrote about this too, back in 2019.)

Universities could start to fix this unethical situation by paying the players what they’re worth. Here’s one idea: if universities are seriously concerned about the education of these young men, they should separate their football programs from their education programs. Teams could pay to license the university’s name, hire and pay players, and pay fees to use the football stadiums. (Football fans claim that the sport makes a profit, and if this is true, the teams should do just fine in this scenario.) The athletes could be offered full 4-year scholarships that they could use after their playing years were over, or perhaps in the off seasons, so that they would be able to truly focus on their education.

But meanwhile, as The Atlantic‘s editors put it over 10 years ago,

“the real scandal is the very structure of college sports, wherein student-athletes generate billions of dollars for universities and private companies while earning nothing for themselves.”

Pay the players. That’s the only way to fix this.

New report says COVID was probably a lab leak: should we believe it?

 

A week ago, Vanity Fair and ProPublica published a long exposé on the origins of Covid-19, in which they revealed new evidence of a lab leak in the Wuhan Institute of Virology (WIV) in November 2019.

The big reveal: the report makes it appear much more likely than before that Covid-19 originated through an accident at WIV, where presumably one of the scientists was exposed to the virus. The new evidence in the ProPublica report largely centers on the work of a translator, Toy Reid, who claims to have a unique gift for interpreting the “secret language of Chinese officialdom.” Even native Chinese speakers can’t really follow it, he claims in the article.

Reid scrutinized a collection of internal and external communications from WIV, and says that he found messages in the fall of 2019 that indicated “inhumane working conditions and hidden safety dangers.” And most significantly, a message on November 12 refers to some kind of biosecurity breach, which might have referred to an accidental exposure of someone in the lab to a virus.

The date of this incident appears to coincide with an incident described in a 2021 article in the Wall St. Journal, which reported that 3 WIV employees sought hospital care in November of 2019. This incident has never been confirmed to involve Covid-19 infections.

To add some context: Reid’s findings were released by a Republican U.S. Senator, Richard Burr, in a report that was not endorsed by the full Senate committee investigating COVID-19’s origins. Burr’s report concluded that Covid-19 was “more likely than not, the result of a research-related incident.”

Not surprisingly, this new report has been getting a lot of attention.

The report initially might seem convincing, until you realize that it doesn’t include any actual biological evidence: no reports of actual infections, and no specifics about any viruses that might have escaped from WIV at the time. It seems to be based entirely on the translation super-powers of Toy Reid.

It didn’t take long for other experts to weigh in. There are plenty of Chinese-language speakers out there, including native speakers who are likely much more fluent than Toy Reid. One translator wrote on Twitter that Reid “screwed up.” Another said that a critical passage identified by Reid “doesn’t suggest a biosafety problem had occurred at all.”

Hmm. Here I have to admit that I have no idea who is right here, since I don’t speak or read Chinese. However, it does appear that ProPublica and Vanity Fair may have put too much faith in a single translator who might have had a political bias.

And there’s more. A number of virologists weighed in to point out that the Vanity Fair piece had ignored work that pointed to the Huanan Wholesale Seafood Market (in Wuhan) as the source of the virus. I wrote at length about that research in March, when 3 new scientific papers had just appeared (as preprints), all pointing fingers at the seafood market as the source of the pandemic.

Unfortunately, all of the evidence in those papers was circumstantial. None of them found an infected animal that was the true source of Covid-19. Instead, they found that many early cases in people were centered on the seafood market. Even supposing that is correct (and it might not be, because China never allowed outside scientists to go to Wuhan and test people all over the city), it is still just circumstantial. Perhaps a scientist from WIV got infected and stopped by the seafood market that day–we may never know.

But let’s return to this week’s controversy, shall we? A virologists who led one of the papers I discussed back in March, Michael Worobey, was also quoted in the Vanity Fair article. He had major objections to what they wrote, and he posted them in a lengthy Twitter thread here, which is well worth reading.

Vanity Fair described Worobey’s work as providing evidence that a natural zoonotic origin (in other words, an origin in an animal at the Wuhan seafood market) for Covid-19 was “plausible.” Worobey objected, pointing out that his comments were much more definitive, and that his position is that:

"OUR TWO RECENT PAPERS establish that a natural zoonotic origin is THE ONLY plausible scenario for the origin of the pandemic." (all-caps in original)

After Worobey’s Twitter thread appeared, Vanity Fair and ProPublica updated their stories to include exactly that quote, without the all-caps.

Worobey makes a compelling case that Vanity Fair and ProPublica misquoted him (or at least omitted important details), and it seems they have fixed that error. However, neither the Twitter thread nor Worobey’s scientific paper make a definitive case that, as he puts it, a natural origin is the “only plausible scenario” for Covid-19.

Not at all. The paper by Worobey and colleagues concluded that “the earliest known COVID-19 cases from December 2019 were geographically centered on this market.” Let’s grant that this statement is accurate: even so, their data does not prove that the market was the “origin” of the pandemic, especially because they failed to find any animals infected with Covid-19 from that market. They only found human cases. This leaves open the question of where the very first human case occurred: it’s entirely possible that the first human was infected elsewhere–perhaps at the Wuhan Institute of Virology–and that human visited the seafood market while actively spreading the virus.

And their data relies on samples collected in Wuhan, which is of course controlled by the Chinese government. Note the wording of that conclusion from the paper, which refers to “the earliest known cases.” China does not want the world to think that the Wuhan Institute of Virology might have caused the pandemic, so how can we ever know if there were early cases originating from WIV?

On the other hand, as I wrote back in March, China has known for decades that their live animal markets are a source for novel human viruses, including the 2003 SARS outbreak and multiple cases of avian influenza jumping from birds into people. And yet they have done nothing to shut down those markets.

So it’s complicated. In any case, as Matthew Iglesias pointed out in The Guardian, even if the entire Vanity Fair article is wrong, the lab leak hypothesis is still plausible–very much so. The fact remains that one of China’s major virology research institutes, which was known to be conducting research on SARS-like viruses, and which was known to be collecting viruses from bats, is located just a few miles from the live animal seafood market. That’s one heck of a coincidence.

Finally, let’s take a step back: why all this attention to whether the virus originated from a virology institute or from a live animal market? Either way, the implication is that humans caused this pandemic. As I wrote back in March, we should take away at least two lessons from this experience: first, that live-animal food markets should be shut down, especially those that sell wild animals rather than farm-raised ones; and second, that gain-of-function research on deadly viruses should be shut down as well.

So let’s stop arguing about the precise origin of the pandemic, and start taking steps to prevent the next one.

Gain-of-function experiments at Boston University have created a deadly new COVID virus. Who authorized this?

Schematic of the Covid-19
 virus, SARS-CoV-2

After all the controversy over the past few years about gain-of-function research on viruses, especially the Covid-19 virus, I thought this kind of work was on hold, at least in the U.S. Indeed, the controversy grew so hot that NIH issued a statement in May of 2021 declaring that it wouldn’t support such work.

Nonetheless, some scientists continue to pursue gain-of-function work. In a new study, just released on the preprint server bioRxiv, a group of virologists at Boston University did the following. They took the Spike protein from the Omicron BA.1 strain of SARS-CoV-2 (that’s the strain that spread throughout the world last winter, often slipping past the protection offered by vaccines) and combined it with an early 2020 strain of the Covid-19 virus.

This experiment gave them a brand-new, never-before-seen strain of Covid-19. Was it more deadly? You bet!

In their experiments, the BU scientists infected laboratory mice with the original Omicron virus, which caused “mild, non-fatal infection.” But when they infected mice with their new, recombinant virus, which they called Omi-S, 80% of the mice died. To quote from their article:

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“the Omicron S-carrying virus inflicts severe disease with a mortality rate of 80%.”

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Well, that’s just great. Making matters worse, the researchers found that the new recombinant virus also replicated much faster in mice: “Omi-S-infected mice produced 30-fold more infectious virus particles compared with Omicron-infected mice.” Yes, you read that right: Omi-S might grow 30 times faster than the garden-variety Omicron strain.

This, dear readers, is what we mean by “gain of function” research. The scientists took sequences from two different strains of the Covid-19 virus, one of which was relatively mild, and created a new strain that is far more infectious and far more deadly. As many scientists (and others) have pointed out, research like this carries great risks, foremost among them the chance that an accidental lab leak could create a new pandemic, killing millions of people.

And the benefits? There must be some pretty major benefits to offset this risk, right? Well, not exactly. The researchers say that these experiments show that the pathogenicity of the Covid virus is determined primarily by something other than the Spike protein. That’s a pretty narrow finding, and the authors don’t seem to consider that they might have learned this without creating an entirely new, more-lethal virus.

Does this work violate NIH policies? The NIH director has stated that

“neither NIH nor NIAID have ever approved any grant that would have supported ‘gain-of-function’ research on coronaviruses that would have increased their transmissibility or lethality for humans.”

First, let me point out that this is a very narrow statement: the NIH doesn’t deny that it funds gain-of-function work on viruses, because it does. They even put a “pause” on such work for 3 years, but they lifted it (regrettably) in 2017. I wrote about that at the time (“NIH Re-opens the Door to Creation of Super-Viruses,” December 2017).

Second, the NIH policy carefully says they don’t support work that would make viruses more deadly for humans. The BU study only looked at mice, so one might argue that it wasn’t making the viruses more deadly in humans–but there’s simply no way we can tell that, not unless we intentionally infect someone. Having read the paper, this work seems to me to be a clear violation of NIH rules.

Boston University and the researchers who led the study disagree. In a statement issued last week, BU officials wrote:

“First, this research is not gain-of-function research, meaning it did not amplify the Washington state SARS-CoV-2 virus strain or make it more dangerous.”

Let’s take a look at this denial, shall we? First, let me reiterate that the new experiments combined 2 strains of the Covid-19 virus: the Omicron strain, which has been the main strain infecting humans since last winter, and an earlier strain that was collected from a patient in Washington state in 2020. The Omicron strain causes only mild infections in mice, but the new Omi-S strain–the one that Boston University scientists created in their lab–kills 80% of them. The Washington state strain, which is no longer circulating in people and thus isn’t a current threat, kills 100% of mice.

So that is the BU argument: because Omi-S is less deadly than one of its parental strains, the research doesn’t meet the definition of gain-of-function.

Sorry, but this argument is just nonsense. You don’t get to redefine gain-of-function in the same sentence where you’re denying you’ve done it. These experiments created a brand-new, recombinant strain of Covid-19, and that strain was much more infectious and much more deadly than Omicron, which is one of the strains it was created from. This is precisely what most scientists mean when they describe gain-of-function research and the risks that it carries.

Furthermore, we have no idea how this virus will behave in humans. It might be far more deadly than Omicron in people. Let’s hope we never find out.

And what about that 80% mortality rate? According to Prof. Ronald Corley, Director of BU’s National Emerging Infectious Diseases Laboratories (NEIDL), “This was a statement taken out of context for the purposes of sensationalism, and it totally misrepresents not only the findings, but [also] the purpose of the study.”

Out of context? Well, here’s what the scientists themselves wrote in the very first paragraph (the abstract) of their paper: “We generated chimeric recombinant SARS-CoV-2 encoding the S gene of Omicron in the backbone of an ancestral SARS-CoV-2 isolate and compared this virus with the naturally circulating Omicron variant.... In K18-hACE2 mice, while Omicron causes mild, non-fatal infection, the Omicron S-carrying virus inflicts severe disease with a mortality rate of 80%.”

That’s the scientists’ own statement, and it’s not out of context. The authors themselves were emphasizing this dramatic mortality rate.

The experiments also present another problem for BU. Despite being funded by multiple NIH grants, neither the scientists themselves nor Boston University appears to have informed NIH about this work, which is a requirement for gain-of-function research.

BU officials addressed this problem by stating, first, that the NIH funds only supported some of the underlying “tools and platforms,” and that NIH funds did not directly support the research. Really, BU? How stupid do you think we are? Money, as we all know, is fungible.

Second, according to BU, “there was no gain of function with this research. If at any point there was evidence that the research was gaining function, under both NIAID and our own protocols we would immediately stop and report.” (Read the full BU statement here.)

Well, I would say that when those mice started dying, you had some pretty good evidence that “the research was gaining function.”

I’ve been in touch with multiple virologists who take a similar view. Simon Wain-Hobson, an Emeritus Professor at the Pasteur Institute, wrote to tell me that the BU research “is a GOF outcome in that the recovered virus is more pathogenic than the parental (backbone) virus, albeit in a transgenic mouse setting.” Prof. Wain-Hobson also pointed out that this work “provides a road map to [creating] a virus that might be dangerous to man. By posting this, these authors are making life easier for the next person or copycat.”

Another virologist, Dr. Valentin Bruttel of the University of Würzburg, pointed out the same problems and more, writing that:

• [the experiments] could have produced a virus that is “way more lethal” than the original SARS-CoV-2 strain
• “the study is useless for the general population, because the chance that exactly this Omi-Spike [would] recombine with an extinct variant [the Washington state strain] are zero,”
• “the chimeric virus could cause more severe disease in humans than estimated from mouse data.”

Like Prof. Wain-Hobson, Dr. Bruttel also pointed out that “any terrorist group could copy the BU group’s protocols.”

What does NIH think? They don’t appear convinced by the BU denials. According to an article in The Hill, “NIH is examining the matter to determine whether the research” fits the definition of gain-of-function. And as reported by Helen Branswell in Stat last week, an NIAID official said that NIH should have been informed, at a minimum so that they could determine whether or not the research was permitted under NIH’s gain-of-function rules.

I contacted the lead author of the study to get his response, but he did not reply.

The bottom line here is that some virologists (by no means a majority) believe that conducting gain-of-function research on the Covid-19 virus is just fine. Many other scientists disagree, and strongly. Some have pointed out that this work is qualitatively no different from biowarfare research. I’ve been warning about the risks for years, and I’m certainly not the only one.

Merely requiring scientists to inform the government, which is the current NIH policy, is not enough. We need to shut this research down and take a long, hard look at it before any such experiments can go forward again.

Why the new COVID vaccine boosters are safe and likely very effective

In case you haven’t heard, there’s now a new set of vaccine booster shots that protect against the latest variant of Covid-19, BA.5. This new variant is highly infectious, and the original vaccine doesn’t protect people against it as well as it protected against earlier variants.

Now, before someone takes that last sentence out of context, let me emphasize that the original Covid-19 vaccines are still highly effective at preventing severe disease and hospitalization. Anyone who isn’t vaccinated would be well-advised to get one of those, if that’s their only option.

But the new vaccines protect against two different strains of Covid-19: the original strand and the latest Omicron variant, BA.5. BA.5 just emerged in August, and it’s spreading extremely fast–it now accounts for 88% of the cases in the U.S. The FDA authorized these “bivalent” boosters on August 31.

My main point today is to explain how this happened so quickly, and why it didn’t involve many months of clinical trials the way that the original vaccines did. Some people have expressed suspicion about the speed with which these boosters appeared, but those suspicions are entirely unfounded.

First of all, we do have data showing that the new vaccine boosters are safe: a study showing these data for the Moderna booster just appeared in the New England Journal of Medicine. That study also showed that people generated robust antibodies against the BA.1, BA.4, and BA.5 Omicron variants after getting the new booster.

Second, to explain why that’s all the data we need, let me explain something about the flu vaccine. Many people are well aware that we have a new influenza vaccine every year–but what they might not know is that each year’s vaccine contains a different strain of the flu virus from the previous year. (Actually, it has up to four different strains, and any or all of them could be new.)

And yet we don’t run large, months-long clinical trials of the flu vaccine each year to measure it’s efficacy. Why not? Well, the basic designs of the flu vaccines (there’s more than one) have been tested in large clinical trials, and we know they’re safe. Replacing the vaccine strain with a new one doesn’t affect the safety of the vaccine, as decades of experience with the flu vaccine have now demonstrated. And because flu mutates quickly, we need to change the vaccine strain every year if we want the vaccine to work.

So that’s what we do: we change the flu vaccine strain to match whatever seems to be circulating, but everything else about the vaccine design remains the same.

This is exactly what scientists have done with the new Covid-19 booster shots from Pfizer/BioNTech and Moderna: they simply added a new strain, in this case to match the latest Omicron variant.

Both of the new boosters are mRNA vaccines, which means the vaccine contains a tiny bit of genetic code (mRNA) with instructions on how to make the “spike” protein from SARS-CoV-2, the Covid-19 virus. When you get the vaccine, your own cells follow those instructions to make a limited number of copies of the spike protein–but nothing else. The virus itself can’t be created without many other genes, and the spike protein alone can’t form a virus.

But your immune system recognizes that an invader is present–that spike protein–and it generates antibodies against it. After that, your immune system is primed to recognize and defeat Covid-19, if it ever infects you.

So the new boosters contain mRNA from the BA.5 spike protein as well as the original spike protein, and now you get protection from both old and new strains. Other than that, it’s the same vaccine as before.

The vaccine makers have produced safety data showing that the booster is just as safe as the original vaccine (see that NEJM article I mentioned above). But the FDA didn’t require them to prove that the booster really works better against BA.5, because that would require months of trials, and by that time the virus could mutate again. So while it’s possible that the boosters won’t help against BA.5, it’s very, very likely that they will.

One of the big advantages of mRNA vaccines is precisely this: we can swap out the mRNA easily, allowing us to respond quickly to mutations in circulating viruses. That’s a good thing, and it might be our only path to controlling Covid-19.

The bottom line is that the new boosters should be very safe, and they will likely provide much better protection against the current strains of the Covid virus. I’ve already gotten my booster, and I hope everyone else will too.