Subscribe
Share
Share
Embed
Truth Seekers: Where Data Meets Reality
Tired of sensational headlines and conflicting health advice? Join Alex Barrett and Bill Morrison as they cut through the noise to uncover what scientific research actually says about the claims flooding your social media feed.
Each week, Alex and Bill tackle a different health, nutrition, or wellness claim that everyone's talking about. From "blue light ruins your sleep" to "seed oils are toxic," they dig into the actual studies, examine the methodologies, and translate the data into plain English.
No agenda. No sponsors to please. No credentials to fake. Just two people committed to finding out what's really true by going straight to the source—the research itself.
Perfect for anyone who's skeptical of influencer health advice but doesn't have time to read every scientific study themselves. New episodes drop regularly, delivering clarity in a world full of clickbait.
Question everything. Verify with data. Find the truth.
Disclaimer: Truth Seekers provides educational content based on published research. Nothing in this podcast should be considered medical, financial, or professional advice. Always consult qualified professionals for decisions affecting your health and wellbeing.
Now I'll rewrite the script with all these natural conversation elements:
---
**Exercise Shrinks Tumors by 60%—Or Does It?**
Alex: So there was this Yale study last month—exercise shrinks tumors by sixty percent.
Bill: I saw that one.
Alex: Sixty percent, Bill. That's the kind of number that makes people think we've cracked the code on cancer prevention.
Bill: And the mechanism they proposed actually makes sense. Exercise starves cancer cells of energy by redirecting glucose to your muscles instead. It's biologically plausible, which is probably why—
Alex: Which is exactly why it spread everywhere. It's not some bizarre claim—it sounds like solid science. But here's what I'm wondering... if this is such a breakthrough, why aren't oncologists prescribing treadmills instead of chemo?
Bill: Right. Because when you actually look at what they tested, it's not what the headlines make it sound like.
Alex: Go on.
Bill: Okay, so the study comes out of Yale, published in PNAS—that's a legitimate journal. The researchers used isotope-labeled glucose to trace where energy goes in the body during exercise. Genuinely clever methodology for this kind of work.
Alex: Mmm.
Bill: And what they found was that during exercise, glucose gets redirected away from tumors and toward muscles. Which makes sense physiologically. Your muscles need fuel, they're working, they pull glucose from the bloodstream.
Alex: Right.
Bill: But the subjects weren't humans. They were mice. Specifically, obese mice that had been fed a sixty percent high-fat diet, then injected with human cancer cells.
Alex: Wait, hang on. So they gave mice cancer artificially, then put them on running wheels?
Bill: Exactly. For four weeks. And yeah, compared to obese mice that stayed sedentary, the ones that exercised had about sixty percent smaller tumors.
Alex: That's quite different from what the headlines implied, though. When people read "exercise shrinks tumors," they're picturing their own bodies, their own cancer risk. Not obese lab mice with injected tumors.
Bill: And here's the thing—the sixty percent reduction is specific to that exact scenario. Obese mice, artificial tumors, four weeks of voluntary wheel running. The study didn't even report whether the effect size was the same in lean mice.
Alex: Okay, so we don't know if it's the exercise itself, or just the fact that obese mice lost weight and reversed some metabolic dysfunction?
Bill: We don't. That's a huge confound. When you take an obese mouse and give it a running wheel, you're changing multiple variables at once—fitness, weight, metabolic health. The study doesn't cleanly separate which one is doing the work.
Alex: This reminds me of when I was covering health stories—you know, before I left the paper. You'd get a press release with one compelling finding, and by the time it became a headline, all the caveats were just... gone.
Bill: Yeah.
Alex: Every single one of them. The editor would say "people don't want to read about limitations," and I'd say "but that's the actual story."
Bill: How'd that go over?
Alex: Not well. Anyway, what did the researchers actually say about limitations in this study?
Bill: Oh, they were appropriately cautious. One of the lead authors, Brooks Leitner, wrote on his own Substack that there are limitations—rodent exercise dose varies, they didn't have human tumor data to compare. And in the paper itself, they explicitly say scientists still need to see if these same processes work in humans.
Alex: So they said "we're keen to investigate this in humans," and the headlines heard "we've proven this works in humans."
Bill: Exactly. The scientists are doing their job—proposing a mechanism, testing it in a model system, calling for human studies. The media just skipped the part where none of this has been validated in actual people.
Alex: But hang on, because I've definitely seen solid evidence that exercise reduces cancer risk. That's real, isn't it?
Bill: It is. Meta-analyses of human studies—actual people followed over years—show exercise is associated with fifteen to thirty-seven percent lower cancer risk. There was a 2016 study in JAMA that pooled data from 1.44 million participants and found lower risk for thirteen different cancer types.
Alex: So exercise and cancer protection—that connection exists. It's just not coming from this mouse study.
Bill: Right. The mouse study might eventually help us understand *why* exercise protects against cancer in humans, but we're nowhere near there yet. This is early mechanistic research, not proof of how human cancer works.
Alex: What else is dodgy about translating this to humans?
Bill: Okay, so the mice had human cancer cell lines injected under their skin. That's called a syngeneic tumor model.
Alex: Okay.
Bill: It's useful for controlled experiments, but it's not how cancer naturally develops in people. Real human cancers evolve over years, even decades. Your immune system is constantly fighting back, selecting for cancer cells that can evade detection. The tumor develops in the context of your specific metabolism, your gut bacteria, all of it.
Alex: Right.
Bill: But in these mice, researchers injected the cancer cells all at once, then started the exercise. It's like the difference between a wildfire that spreads naturally and one you set in a lab. The immune interaction, the gradual evolution—all of that is missing from the model.
Alex: So the timeline is compressed too.
Bill: Yeah, exactly. Four weeks in a mouse's life, given their metabolic rate, doesn't translate to years of human cancer development. A mechanism that works in a four-week window might not persist long-term.
Alex: Because the tumor could adapt.
Bill: Exactly. Tumors are incredibly adaptive. Even if glucose competition works initially, cancer cells might switch to using fatty acids, amino acids, other fuel sources. The study only looked at glucose.
Alex: What's the actual translation rate from mouse studies to human cancer treatment? Because I'm guessing it's not great.
Bill: It's terrible. About ninety percent of drugs that work in mice fail when you test them in human clinical trials.
Alex: Ninety percent?
Bill: Ninety percent.
Alex: Christ. Hang on, didn't we talk about this before? That thing about curing cancer in mice?
Bill: Oh, the NAD+ episode. Yeah—we can cure cancer in mice every week, we can't cure most cancers in people.
Alex: Right, that was it. So this is just... this is the same problem all over again.
Bill: Well, yes and no. I mean, it's the same translation gap, but—
Alex: But what? If ninety percent of this stuff fails, why are we even doing mouse studies? That's abysmal.
Bill: Because we need them to understand mechanisms. You can't just test drugs in humans without knowing what they do biologically first.
Alex: But clearly what they do in mice doesn't predict what they'll do in humans.
Bill: Not perfectly, no. But it gives us a starting point. Like, syngeneic models—the kind they used here—have even worse translation rates because they lack the immune complexity of naturally occurring human tumors. But that doesn't make them useless. It makes them a specific tool for answering specific questions.
Alex: Such as?
Bill: Such as "does glucose repartitioning happen during exercise" or "do cancer cells in this controlled environment respond to energy availability." Those are real questions. They're just not the same as "will exercise shrink my tumor by sixty percent."
Alex: Okay. That's fair. But the headlines don't make that distinction.
Bill: No, they don't. When I was working in tech and we saw a ninety percent failure rate on anything, we knew that model wasn't predictive. But we'd still use it for early-stage exploration, you know? Just not as proof of what would happen in production.
Alex: So even though the science within the mouse study is solid, the leap to humans is just... not supported.
Bill: The science is actually quite good for what it is. Using isotope tracers to show glucose repartitioning, looking at gene expression changes, testing multiple tumor types—it's rigorous preclinical work. The problem isn't the researchers. It's the headlines that marketed this as "we now know how exercise shrinks human tumors."
Alex: When what they actually showed is "in obese mice with injected tumors, exercise might reduce tumor size, possibly through glucose competition, and we should probably test this in humans someday."
Bill: That's the accurate version. Way less catchy.
Alex: But it matters, doesn't it? Because if someone with cancer reads that headline and thinks, "I can shrink my tumor sixty percent by exercising," and then that doesn't happen...
Bill: That's the harm. False hope in a cancer context is not trivial. People might delay effective treatment, or feel like they've failed when exercise doesn't shrink their tumor by sixty percent—which it won't, because that figure comes from obese mice in artificial conditions.
Alex: And it's not like exercise is bad for cancer patients. There's real evidence it helps with outcomes, quality of life, all of that. But the mechanism and the magnitude—those are still open questions.
Bill: Right. The epidemiological evidence is solid. Exercise is associated with lower cancer risk in humans. But that's from decades of observational studies, not from this mouse research. This study is a hypothesis about why that association might exist, not proof that it does.
Alex: What would actually prove this mechanism in humans?
Bill: You'd need a few things. Ideally, a randomized controlled trial where you assign people to exercise or not, then measure actual cancer incidence over time. Or mechanistic studies in human tumor biopsies showing the glucose repartitioning effect. Or clinical trials in cancer patients showing that exercise dose-dependently slows tumor growth.
Alex: And none of those exist yet.
Bill: None. That's what "keen to continue investigation" means. It's scientist-speak for "we have an interesting lead, but we haven't tested it where it matters."
Alex: There's something almost perverse about how this played out, though. The researchers did good work, were appropriately cautious, called for more research—did everything right. And then the media turned it into definitive proof.
Bill: It's a pattern. Preclinical research is about exploring mechanisms, generating hypotheses. It's not meant to be clinical advice. But somewhere between the journal and the public, that distinction gets obliterated.
Alex: Because "exercise might work through glucose competition in mice" doesn't get clicks.
Bill: Right.
Alex: "Exercise shrinks tumors sixty percent" does.
Bill: And the correction—if it even happens—never reaches the same audience as the original headline.
Alex: Huh. So what should people actually take away from this?
Bill: If you exercise because it's associated with lower cancer risk, keep going. That evidence is real, from human studies. But don't expect sixty percent tumor shrinkage, and don't think we've proven exactly how exercise protects against cancer. This mouse study is early-stage mechanistic research. It's a piece of the puzzle, not the whole picture.
Alex: And if you see a health headline with a dramatic percentage, check whether it's from human studies or animal models. That's not a trivial distinction.
Bill: Especially in cancer research. The translation failure rate is just too high to assume what works in mice will work in us.
Alex: Which doesn't mean animal research is useless—
Bill: Right.
Alex: —it's essential for exploring mechanisms. It just means we need to be honest about what it can and can't tell us.
Bill: And the media needs to stop stripping out the caveats that scientists include for a reason. Those limitations aren't boring details. They're the difference between "we found something interesting" and "we solved cancer."
Alex: The Yale researchers knew that.
Bill: Yeah.
Alex: Shame the headlines didn't.