Research Translation Podcast

David Newman
  • 5.0 (4)
  • SCIENCE
  • UPDATED WEEKLY

Translating Medical and Health Research For All researchtranslation.substack.com

  1. How to Spot a Misleading Cancer Screening Study —Before It’s Even Published

    FEB 19

    How to Spot a Misleading Cancer Screening Study —Before It’s Even Published

    Get full access to Research Translation at researchtranslation.substack.com/subscribe

    18 min

  2. FEB 11

    The Case of the Missing Heart Attack

    When Arthur Conan Doyle wanted Sherlock Holmes to show off, he didn’t give him a bloody fingerprint or a dropped monocle. He gave him a dog that didn’t bark. In Silver Blaze, the silence was the clue. The horse didn’t vanish because of a stranger—the stable dog knew the intruder. The absence of noise told Holmes everything. That’s where we are with the newest trial of PCSK9s, a class of drug that dramatically lowers cholesterol levels. At first glance, the study looks like a triumph of modern pharmacology. It’s a massive, multinational, double-blinded trial done at hundreds of sites in a dozen countries, enrolling nearly three thousand people. The paper trumpets spectacular reductions in LDL (half or more!) and a power analysis north of 99%. Reviewers nodded. Editors smiled. Headlines followed. And yet: The dog never barked. This drug class exists for one reason: to reduce cardiovascular events—heart attacks, strokes, and deaths. Cholesterol is not the goal, it is the surrogate. Human outcomes are the prize. So where are they? Nowhere in the paper. Nowhere in the abstract. Nowhere in the results. Nowhere, even, in the discussion of limitations. Not a single Kaplan–Meier curve. No exploratory table. Not even the typical cowardly offering—“CV outcomes will be reported separately.” Just, silence. That is not an accident. Holmes would first note the power analysis (a window to the soul of a study): The authors insist the trial was designed to have more than 99% power to prove the drug can lower LDL. But that is absurd on its face. Sniff test: failed. No regulator requires 99% power to prove a biomarker outcome. Eighty percent is standard. Ninety if you’re nervous. But as I’ve pointed out before, increasing power, by upping the number of participants, can be a cover story for ulterior motives. And it’s pricey, to the tune of $50,000 or more per enrollment. Fiscally responsible companies don’t add study participants without a good reason. Which makes it notable that a standard power analysis for this trial suggests the researchers didn’t need to enroll three thousand people—they needed about twenty. Yup. Twenty. For the whole study. Both arms. The PCSK9 drugs drop cholesterol so powerfully that it takes very few participants to demonstrate it mathematically. Which means the company paid more than $140 million for seemingly extra, unnecessary enrollments. So, what’s really happening here? There is a clue that may at first seem small (Dr. Watson once said, "I am glad of all details, whether they seem to you relevant or not"): According to an online recruitment posting for this exact trial, the goal was not to lower cholesterol, but rather “to reduce major cardiovascular events, including cardiovascular death, heart attack and stroke, by lowering LDL-cholesterol.” Ahaa. There it is, in black and white. It takes thousands of subjects to find the tiny reductions in cardiac events that cholesterol lowering drugs can (under the best of conditions for the highest risk people) theoretically achieve. This explains the study’s size. Moreover, in a trial this expensive, CV events were not just possibly collected, they were inevitable. Logged. Coded. Reviewed. Sitting somewhere in a database. Which brings us back to the dog. Why not include the cardiovascular outcomes in the paper? Because they weren’t reduced. If CV outcomes had favored the drug, even weakly, they would have been mentioned or, more likely, headlined . But nary a mention. Not even, “Numerically fewer events, ” or “a favorable trend.” Journals allow that sort of nonsense. Regulators tolerate it. Marketing departments adore it. Instead, nothing. That is not sloppiness, it’s subterfuge. The brilliance of the design is that it allowed them to pivot. By claiming a primary endpoint of LDL reduction (a cakewalk for PCSK9s), and then massively inflating sample size, they could quietly chase their true goal, cardiovascular benefit—while still guaranteeing ‘success’. Heads they win. Tails they don’t lose. The drug succeeded at what was always easy: moving a lab value. But it failed at its secret raison d’être: helping humans. Sherlock Holmes would have closed the file already. The most telling result of this enormous, costly, meticulously planned trial is not what it reported—but what it very carefully did not. Get full access to Research Translation at researchtranslation.substack.com/subscribe

    20 min
  3. Selling the Newest Flu Drug: A Masterclass in Distraction

    JAN 29

    Selling the Newest Flu Drug: A Masterclass in Distraction

    When readers sent me media articles touting baloxavir (‘Xofluza’), I started looking. In the interim, Sensible Medicine, a wonderful Substack by evidence-based doctors, published a podcast, and today a written piece, recommending the drug. I believe they have it deeply wrong. Fun! Check it out, tell me what you think. When I was seven years old I tried hard to see through a frosted glass window. My pediatrician, a silly and smiley man with a nasal voice, stood behind me. “You see that, across the street?” he quacked. Then, leaning forward, as if to sync his line of sight with mine, “See?” His hand was on my shoulder, squeezing gently. I squinted, and tried hard. “Wait… is that it?” “Ah, forget it” he said, smiling at my mother. “You missed it.” Which was true—I’d completely missed the shot in my shoulder. Research Translation is fully reader-supported. Like it? Consider becoming a paid subscriber to help me keep doing it. In addition to being a beloved and brilliant pediatrician, Dr. Gribbetz was a master of distraction. Unfortunately, that’s a skill drug company scientists have also mastered—for different ends—and they played it to perfection with a flu drug called baloxavir. In recent weeks The Atlantic and the Wall Street Journal, noting the rough flu season and weak effects of this year’s vaccine, ran articles extolling the virtues of baloxavir, a single-dose drug hoping to replace 5-day Tamiflu. Both media articles rely heavily on experts who have fallen hard for a 2018 trial published in the New England Journal of Medicine. To be fair, the study also convinced FDA reviewers who approved the drug. Though clearly, that ain’t tough, and the study is a crowded swamp of data. Reading it feels like trying to see through frosted glass. I’ll try to be efficient here, but for the geeks I’ll get into more detail on the podcast. The ‘study’ is actually two separate trials. One compared three doses of baloxavir to a placebo. The other compared baloxavir vs. Tamiflu vs. placebo. Which is remarkable because Tamiflu is a debunked drug, years ago revealed by many independent investigations as not just unhelpful but, to some critics, a premeditated fraud. As I’ve written and podcasted before, Tamiflu trades side effects for flu symptoms, adding as much misery as it subtracts, while failing to prevent serious illness. Meanwhile, symptoms—the only measure either drug even claims to affect—were identical with baloxavir. So the first and most obvious headline should be: BALOXAVIR WAS NO BETTER THAN TAMIFLU, A PROVEN FAILURE. That should end all discussion. But it won’t. The most interesting quirk about the baloxavir paper is that the first trial is an “FDA, Phase 2, dose-finding study”—a fancy way of saying it was done to find a dose, not prove efficacy. The trial had three drug groups of differing doses, plus a placebo group. And no group, when compared to placebo, had enough participants to say whether the drug works. That isn’t a flaw, it’s the point of Phase 2 studies. But it means efficacy claims drawn from them are, by definition, a mistake. Why? Because with three drug groups and one placebo, the drug is getting multiple shots on goal. Efficacy trials get one shot on goal—no more. Ever. And that’s why Phase 2 studies are, well, phase 2. Only Phase 3 studies can say whether a drug works. And in fact, it's weird to publish two studies of different design, from two separate FDA phases, together. It’s weird because the studies have different goals and are interpreted differently. Which is deeply distracting. So what were readers being distracted from? The paper’s much more pivotal Phase 3 study compared baloxavir to Tamiflu and placebo. And here’s where a red flag pops up, bright and tall: Why wasn’t the study a non-inferiority trial comparing the two drugs? ‘Non-inferiority’ is a special design statistically and methodologically focused on finding equivalence between drugs. That’s different from a classical superiority trial, designed to find a difference between drugs. For years non-inferiority has been the FDA’s favored design for testing when a new drug claims to be as effective as an older drug. Typically, in such cases the new drug offers some convenience upgrade, like being a pill instead of an injection. Or, perhaps, 1-day versus 5-day dosing. Like baloxavir. Baloxavir is a picture-perfect candidate for a non-inferiority study, but that’s not what the company did. Which means they probably expected more than equivalence with Tamiflu. They expected superiority. When that failed, they settled for (and pretended to celebrate) sameness. How can we know the trial aimed to show baloxavir was better, when the authors claim superiority based on dose-finding, placebos, and virologic results? The Methods section is the paper’s guilty conscience, confessing. The researchers used classical (non-parametric) superiority testing techniques to compare the drugs. Besides this, there is circumstantial evidence. For starters, early lab studies found baloxavir had better effects on viral load and biologic markers than Tamiflu. But that only matters when it translates into people feeling better or being safer, which didn’t happen. This probably surprised and dismayed company researchers, who—like the literati of medical evidence—surely know that Tamiflu is a failed drug. So when baloxavir failed, they changed the narrative: “It’s as good as Tamiflu—yay!” And sadly, most flu ‘experts’ are experts in virology, but not evidence. So when the red flag appeared—a failed superiority trial dressed up as success—they did what seven-year-olds do when asked to see through frosted glass. They squinted, nodded, and missed the shot. Tamiflu is a failed drug. Now we know baloxavir is too. Moreover, both represent a profound risk to public health, because both must be started within two days of first symptoms. If everyone with a sniffle runs immediately to their doctor, or ER, or clinic—resources already dangerously over-burdened—people in dire need of these resources will be harmed. So as I’ve written and podcasted about before, if you want one day’s relief from the flu, try silicon nasal sprays. They’re better, safer, and cheaper, and they’re over-the-counter. Get full access to Research Translation at researchtranslation.substack.com/subscribe

    43 min
  4. Autism, Tylenol, and the FDA

    JAN 23

    Autism, Tylenol, and the FDA

    Below marks my first critique of politics, and you’ll see why. For background: I have no political affiliation and do not care for party politics. Years ago I became deeply disenchanted with parties of all stripes. I do not seek a packaged bundle of beliefs or positions—I have my own. I care what works, one issue at a time, and I’m open. What I cannot stand, the attribute that repels me most, is the abuse and distortion of truth. On Tuesday the New England Journal of (oddly partisan) Medicine published two opinion pieces on autism—a favored topic of RT! The first addressed Trump and RFKjr’s September press conference on prenatal Tylenol, while the second discussed vague claims by FDA officials implying a chemotherapy drug can now treat autism. To jump into this cesspool of exaggerators and distortionists, we must first acknowledge an uncomfortable but obvious truth: When, on the campaign trail, you promise frenzied crowds that, once in office, you will quickly discover a cause and treatment for autism—a poorly defined neuro-developmental condition that has eluded researchers for decades—you have two options. Fail and concede, or fail and pretend. Guesses, anyone? After months of fishing through a swamp of poorly supported but rhetorically convenient pseudo-theories, RFKjr landed on the one entertained by stoner neuroscience grads munching funyuns at 3am. (Duuude. It’s totally the Tylenol.) I walked through the Tylenol-autism data in October, and last week a review published in a prominent journal confirmed: Put simply, Tylenol has—provably—zero connection to autism. This was self-evident to anyone who actually read the relevant studies. And yet, September 22nd, 2025 the Health Secretary, FDA head, NIH director, and President, acted out an SNL-ready skit, a tragicomedy of performance art. Speaking in the imperious tones of concern for their people, the four most powerful authorities in public health made a claim that wasn’t just weak—it was palpably b******t. The irony is thick. After years of furiously and publicly condemning Anthony Fauci and others for a crisis of public trust, they offered something far more corrosive than technocratic arrogance: A display of knowing dishonesty. This wasn’t confusion or misplaced confidence. It was the deliberate use of scientific authority to launder a claim that everyone involved knew was indefensible. That isn’t a mistake. It’s contempt—for evidence, for the public, and for the idea that science is anything more than a prop. Which is why recent FDA maneuvers around leucovorin, folate autoantibodies, and ‘folate deficiency associated with autism’ cannot be viewed in isolation. They sit in the same epistemic ecosystem. Once again a small, messy batch of weak studies became a nonsense narrative. To be fair, the folate-autism story is not proven nonsense—yet. It is, um, unfinished. Hypotheses deserve testing, not regulatory implication or political theater. The recent Lancet review, like mine months ago, showed what happens when you slow down and let the data breathe (scary headlines evaporate). And I have little doubt the brain-vitamin narrative will dissolve. But there’s work to be done. Bottom line? Autism doesn’t yield to deadlines. It yields to patience, rigor, and a tolerance for ambiguity—three necessary tools for science, ones in desperately short supply right now. When science is forced to perform certainty on command, what it produces isn’t truth—it’s theater. And this is the kind of theater that doesn’t merely fail to rebuild trust, it finishes it off. This administration didn’t set out to heal the public wound of scientific overreach. They inherited that wound and began poking at it deliberately. Trust wasn’t restored, because restoration was never the point. Control was. And a government that treats science as a stage prop shouldn’t be surprised when the audience stops believing anything it says. Get full access to Research Translation at researchtranslation.substack.com/subscribe

    24 min
  5. Vitamins, Vaccines, Alcohol, and the Flu—HodgePodge 2026

    JAN 16

    Vitamins, Vaccines, Alcohol, and the Flu—HodgePodge 2026

    This week is an audio hodgepodge—lagniappe, if you will—a chance to discuss and explore recent headlines. Enjoy! Here are some of the relevant RT and news links. WSJ on vitamins -Vitamins piece on RT NYT on recent vaccine changes -Vaccines piece on RT (Covid for children, and related discussion) NY Times on Alcohol and Cancer, Alcohol and cardiovascular disease -Alcohol, alcohol, alcohol, and alcohol pieces on RT (relation to cancer) YLE on antivirals -Tamiflu, antivirals, and other flu treatments on RT (plus Tamiflu’s placebo effect!) RT is 100% reader supported. I’d love to keep doing it. If you agree, consider becoming a paid subscriber Get full access to Research Translation at researchtranslation.substack.com/subscribe

    39 min

  6. JAN 6

    Aspirin and Donald Trump: Schadenfreude Alert

    “Meet Virginia” is, I believe, one of the great rock singles of recent decades. It opens with a blue-sy, core-bending bassline and a thirsty guitar riff, as Pat Monahan etches a fantasy vamp. You will not forget Virginia. “Train” is the band’s eponymous first album, and with other tracks like “Free”, “I Am”, “Egglpant”, and “Rat”, it does not falter. Incredibly, it’s nearly matched by “Drops of Jupiter”, their second album. “She’s on Fire” and “It’s About You” are lyrically brilliant curtains of sound, and the title track is a magical tribute to Monahan’s deceased mother. And yet it’s the deep cut, “Mississippi”, that closes the circle: Train makes albums. Old school, full-package, musical journeys. Not singles. Albums. Which brings me to Donald Trump’s colorful hand, photographed and transmitted around the world this week: RT is 100% reader-supported. To keep it going, consider becoming a paid subscriber. While media outlets fluttered joyously over the president’s mysterious (possibly fatal!) affliction, my first thought was of “Bruises”, a song by Train. In it, Monahan and country singer Ashley Monroe re-connect after years, to find loss and pain have changed them. The chorus digs into a lesson learned by anyone who's been to their high school reunion: “We all got bruises.” Take heart, DJT, you’re not alone. Known in medical lingo as ‘ecchymosis’, bruises are bleeding under the skin. They happen with minor (or major) trauma, but sometimes they pop up spontaneously. As people age, the skin’s superficial vessels become increasingly fragile and bruising more common. Rarely, bruising is the flag for a disease—but rarely. When a man approaching 80 shows up with a hand bruise, it’s usually meaningless. But then we learned that Trump takes daily aspirin—DUN-DUN. And, at a higher dose than normal—DUN-DUN-DUN. There’s lots of data on the pros and cons of daily aspirin, which inhibits platelets and therefore makes blood clotting a bit less efficient. For a quick review (with help from Bill Murray in Meatballs) check out last year’s “It Just Doesn’t Matter.” In it I write (and talk) about how recent trials re-confirmed what I found in 2015 after reviewing the data: For people without known heart disease, daily aspirin is, on balance, more harmful than helpful. But as the NY Times highlights in their finger-wagging explainer about Trump’s aspirin addiction, until 2022 the USPSTF (United States Preventive Services Task Force) was recommending daily aspirin. Why? The USPSTF and I saw the same data, but they’re bad at translating it. Which is sad, since their reviews set standards for insurance (insurance is legally forced to pay for many tests and treatments that are provably worthless because of the USPSTF). But I’ve discussed the task force’s failures, and while I believe there are good, well-intended people there, it was 100% predictable that aspirin would fail in the recent primary prevention trials—because it already had. But I digress. The bigger point here is that aspirin is a wonderful example of a preference-sensitive medicine. That is, people should know the pros and cons—and choose their poison. So here’s the (summarized) deal on daily aspirin for primary prevention: * It does NOT reduce mortality (i.e. it doesn’t prevent death). * It DOES prevent nonfatal heart attacks and strokes, for about 1 in every 250. * It CAUSES bleeding in the brain for 1 in 1,000. * It CAUSES other life-threatening bleeding (mostly gastrointestinal) for 1 in 200. We can turn this into an easy comparison: For every 1,000 who take daily aspirin for primary prevention, 4 avoid a heart attack or stroke, 1 bleeds in their brain, and 5 have a different life-threatening bleeding problem. A few factoids: First, any heart attack or stroke aspirin prevented was likely to be followed by full recovery. Meanwhile, bleeding in the brain is real real bad and typically leads to serious long term disability. Finally, the other bleeding problems mean hospitalization and treatment, but they too are rarely fatal and lead to full recovery. So what does it all mean for our fearless leader, the new President of Venezuela? There’s a better chance Trump will be harmed than helped, and he won’t live longer. BUT HE GETS TO CHOOSE. Perhaps he’s most afraid of a nonfatal heart attack or stroke, and doesn’t mind hand bruises and a 1 in 200 chance of serious bleeding. Though he IS taking a bigger dose of aspirin than in most trials, so his chance of bleeding is even a bit higher. But the worst part for him, it seems to me, is that the press will be waiting for him to bleed, then lapping it up like a parched vampire. They will hover like vultures to bathe in the world’s most public case of bloody schadenfreude. But in reality, as the tiny numbers for aspirin make clear, whether he bleeds or doesn’t, has a stroke or doesn’t, and dies or doesn’t, is far more likely to be determined by his genes, lifestyle, and luck. Which calls to mind another Train song, “Calling All Angels.” Trump should check it out. Get full access to Research Translation at researchtranslation.substack.com/subscribe

    18 min

  7. 12/24/2025

    Flu Vaccine and Dog Park Etiquette

    I wrote and posted this last year, but with the respiratory season now gripping local and national stats—and me spending time with my family, including two boys with the flu—I thought I’d repost this for anyone interested. Turns out no new flu research has changed anything below. And for a list of prior dives into flu-related studies (including a treatment that works!) see the links at the bottom of the page. Happy Holidays, everyone! My boys found our dog, Jazz, earlier this year. She was eating out of a trash can behind an office building. Collarless and homeless, she was also mangy and thin—but somehow pathologically optimistic. On the car ride home her attitude felt contagious, which led me to record her first ever entry into our house. We went inside, Jazz locked eyes with me and, sporting a winsome grin, shat on the couch. The video plays like a teaser for the horror movie Smile. Jazz’s assimilation into local canine culture has also been rocky. There is, I learned, an unspoken code of behaviors in the dog park. Thankfully she’s not a humper or a poop-eater, traits that can lead to doggy censure. And she’s not a fighter. But she plays rough and, worst of all, looks like a pit bull. Which may be partly because she’s a pit bull. Mostly this hasn’t been a problem. Dogs don’t mind her style of play, but many owners do and recently we had a hiccup. A bougie Pomeranian pranced into the park wearing a harness. I’m not sure why an owner chooses the asylum-style, thoracic harness with a rubber handle on top, but Jazz knew what to do with it. Unfortunately, as Jazz shook her new toy the owner screamed. Like, blood-curdling. I practiced emergency medicine for 25 years in the streets, the ER, and combat support hospitals in Iraq, and I swear to you the following: I’ve never heard anyone make that sound. People ran, men flexed, the dogs were separated. The woman took her pom-pom and left, and there seemed to be broad consensus we should too. Perhaps it was my soft jog as the crisis unfolded. Or the eye roll. In any case, we shame-walked to the gates as breathless owners held their loved ones close. Jazz never wavered, doing her best Marilyn Monroe. Naturally, I’ve been hesitant to go back, despite the fact that Jazz mostly loved her time there, and was loved. It’s probably irrational, but even rare bad moments can have that effect. Which brings me to the seasonal influenza vaccine. Does it work? Should everyone have it? What are the downsides? The flu vax is, to me, a fascinating case study with lots of defensible arguments on all sides. Here are some facts: * The Northern hemisphere vaccine changes each year, built on guesses using flu strains found in the Southern hemisphere where flu season starts earlier * The guesses are pretty good but every five years or so the vaccine uses the wrong strains, like in 2021 * Flu vaccine was intended to reduce deaths and serious illness in the elderly, but randomized trials and lots of good observational data suggest it didn’t work; some argue there aren’t enough trials to know for sure * In the late 20th century vaccine uptake rose precipitously—along with flu deaths * In trials, the vaccine consistently reduces getting the flu or a flu-like illness—for kids, healthy adults, elderly people, and even immuno-suppressed adults * The flu vaccine may have reduced serious illness for heart patients at the highest risk (i.e. people with heart failure or known heart disease) Okay so let’s accept some easy and some hard realities. First, the good news: getting vaccinated makes a flu-type illness less likely. That’s a good thing. True, the numbers are small: only about 1 in 30 vaccinated people avoids a flu episode because of the vaccine. But why would anyone not want to reduce their chances of getting the flu? The answer, of course, is because of the downsides. These include effort, and cost, and inconvenience. Most vaccines also involve a needle (for healthy adults there’s now a nasal spray). Also, about 1 in every 125 people experiences a fever because of the vaccine. Finally, there are rare serious reactions. Unfortunately, adverse effects aren’t closely tracked partly because the formula changes yearly, and there aren’t new randomized trials every year. So it’s tough to know how much harm the vaccine might be causing. Studies in past years found the vaccine increased non-flu sicknesses, or (rarely—like 1 in 50,000) may have caused narcolepsy. It was also linked to miscarriages in one study, though the CDC says newer data refute that finding. So… what’s it all mean? For me, there are a few bottom lines. First, the flu vaccine probably isn’t saving anyone’s life. That’s a claim the CDC makes based on zero rigorous data. Therefore the vaccine probably isn’t accomplishing it’s original goal, and that has led some trustworthy experts to suggest marketing and money are behind the yearly push. On the other hand I love the idea it might keep me from getting sick—but only if it’s not going to do anything bad. Is the rare fever, or a super-rare chance of narcolepsy or some other bizarre problem, going to keep me from taking advantage? Not sure yet. But Jazz sure does love playing in the dog park. The RT influenza library: -The new mRNA flu vaccine study—and the one STILL unpublished (both) -A fancy new flu drug, that’s actually not new at all (and doesn’t work) (both) -A not-at-all fancy, or new, flu drug that works (written) -A not-at-all fancy, or new, flu drug (podcast/audio) -Tamiflu (written); Tamiflu (audio) -Sore throats, and mindless medicine (both) -Tamiflu and the double-dog placebo (audio only) - Get full access to Research Translation at researchtranslation.substack.com/subscribe

    21 min
  8. Does Reducing Blood Sugar Prevent Heart Disease?

    12/19/2025

    Does Reducing Blood Sugar Prevent Heart Disease?

    More than a decade ago, large data reviews found that using drugs to tightly control blood sugar in people with type 2 diabetes does more harm than good. In careful studies, it didn’t save lives, reduce heart problems, or prevent kidney failure. And while on rare occasions it helped to avoid or delay limb amputations (1 in 250 people), forty times more often it caused life-threatening episodes of low blood sugar (1 in 6 people). These findings, and the fact that newer drugs prevent heart problems and deaths independent of glucose lowering, have led to a merciful shift away from obsessing over sugar levels. As a former ER doc, I saw countless hypoglycemic episodes—some of them tragic—during the era of “tight glycemic control.” [To read about one strange case, check out this post from last year.] So when I saw the New York Times headline, “Controlling Blood Sugar Cut Heart Disease Risk in Half, Study Says,” I was concerned. Predictably, however, the Times has virtually everything about the study wrong. Less predictably, so do the study’s authors. The Times writer claims the new study, published this week in a Lancet journal, highlights the effects of treatment to lower glucose. It doesn’t. In actuality, the study compared long-term (20-year) outcomes among people with borderline diabetes in two trials that started in the ’90s. Both compared lifestyle changes and pills with no treatment, but found mostly small differences in progression to diabetes. The new paper, however, did a post hoc secondary analysis comparing participants whose sugars normalized in the first year with those whose didn’t, and tracked heart problems. In other words, the researchers compared people whose abnormal sugars quickly resolved—regardless of treatment, including in the placebo group—with people whose sugars stayed too high. And what did they find? Extra! Extra! Read all about it!! We got a doozy, folks: People who were healthier twenty years ago were sometimes healthier today, too. Science!!! Which brings us to the Times headline: “Controlling Blood Sugar Cut Heart Disease Risk in Half.” For starters, the new study didn’t look at ‘controlling’ sugar. That would be treatment, and the study didn’t compare outcomes based on treatment; it compared outcomes based on changes in sugar irrespective of treatment. Then the writer uses a relative number—“cut in half”—rather than an absolute number, to glaze the result. BTW, for a one-minute primer on absolute vs. relative risk, see our new video, posted last week. So what was the absolute number that was cut in half? It was 7%. Which is pretty amazing. Only 7% of people with persistent prediabetes or diabetes went on to have a heart problem over twenty years. For those whose sugar resolved immediately, it was about 3%. That is a 4% difference. That is the difference the researchers tout, the journalist trumpets, and readers are supposed to be impressed by: 4%. Yay? I mean, dude. The New York Times has GOT TO LEARN HOW TO READ A STUDY. So do the (Stanford and Johns Hopkins) doctors who offered breathless quotes like “an incredible finding!” I realize it’s exciting to be asked to comment for the Times, but you need to read the study—and think, please—before you talk to a reporter. To be fair to the journalist, the worst part is that the researchers who did the new study spun their results, and the editors and peer reviewers at Lancet allowed it. All parties ignored the paper’s methods (a secondary analysis of sugar levels, not treatment) and seem not to know the proven history of harms from treating numbers, rather than people. This illiteracy across the scientific and lay-press ecosystem is what allowed and amplified the study’s wrongheaded conclusion. The researchers’ conclusion statement was: “Targeting remission might represent a new approach to cardiovascular prevention.” New?!? Targeting low glucose levels is not new. It’s a failed and harmful approach. And it’s not what their study tested. The study tested what happens to people whose prediabetes quickly disappeared—spontaneously, treatment-related, or otherwise. The answer was 4% fewer heart problems, twenty years later. So thank you, NYT, for always offering deranged, uneducated, misleading research translation. And thank you, Lancet, for the same. Couldn’t do it without you. For a little more depth, check out the podcast. Research Translation is fully reader-supported. To support my work and keep it going, please consider becoming a paid subscriber. Get full access to Research Translation at researchtranslation.substack.com/subscribe

    23 min
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