That’s a really good question. I can’t speak to the agenda of the National Cancer Institute, and why so little money, relatively speaking, is going into studying this process, which is what results in cancer’s lethality. With a few exceptions, cancer is only lethal when it spreads from the site of origin. And yet we don’t really have a clear sense of what it is that fosters the environment for spread. I wish I could offer you a better answer, but that’d require me to understand how the agencies think about these things, and I don’t have that insight.
Another line in the book says muscle cells aren’t susceptible to cancer. Now, this might be the stupidest question you’ll hear all book tour, but if we have more muscle, does that mean we’ll be less susceptible to cancer? Has anyone studied cancer rates in, say, hypertrophic individuals? What’s the practicality here?
It’s a good question—and you can get cancer in muscles, but it’s very rare—it’s called a sarcoma. They’re soft-tissue tumors in bones or in muscle, but they’re rare. Muscles aren’t a place where cancer develops the way we see it in the colon, liver or pancreas.
And I’m not aware of a study that asks the question you have asked, but it would have so many confounders in it that it’d be difficult to know if causality would be at play.
It’s almost the ultimate case of healthy user bias.
You’d have that on the positive side, and I suspect you’d have some things on the negative side: some of the most hypertrophic individuals might be full of growth hormone or anabolic steroids, and we don’t know what the long-term consequences of those would be.
You talk about the One True Church idea when speaking about different diets arguing online: there’s no nuance, and everyone disagrees. Why is nutritional data and experimental data so contradictory? Is it how it’s studied? Are there limits to applying it to real life?
It’s a couple of things. Nutrition’s a messy system to study. Start with what’s really easy to study: if I want to know if a particular pill lowers blood pressure, I’ll find people with high blood pressure, divide them into two groups, randomly, give one group a pill a day and another half a placebo, treat them identically, and in a few years there’s an answer. Did the pill lower blood pressure enough to reduce heart attacks and strokes? And even just with that, I won’t get perfect compliance: 20% won’t remember to take the pill.
Contrast that with nutrition: let’s say,10,000 people are in a study and I want to put them into two different diet groups. They now have to eat in line with the diet prescription day in, day out for five years. It’s been done—there’s an elegant example of this, like the PREDIMED study, but they basically sent people the food each week to nudge compliance. And that’s as good as it gets. What’s more commonly done is a “look back approach,” or asking how those 10,000 people have eaten for the past five years to predict what’s going to happen. I don’t know about you, but I can’t tell you what I ate five days ago—not with any fidelity. But this is the hallmark workhorse of nutrition research, which is this field of nutritional epidemiology. I’m not overstating it when I say it’s basically a farce. It offers no reliable knowledge beyond very broad strokes. And even there, it’s very difficult to extract causality because of many factors that are not present in other forms of epidemiology.
Sami Reiss
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