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Why Do We Develop Pre-Diabetes? · So That's Why

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Jen: Welcome to the So That's Why podcast, where we unpack the
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science behind everyday questions.
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I'm Jen.
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Jamie: I'm Chris.
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And I'm Jamie.
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Jen: Okay.
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Right.
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Here's a question with a strange twist built into it.
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Why do we develop pre-diabetes?
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So the twist being, it might be the only common diagnosis where experts can't
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reliably agree on who has it, and where a good chunk of people have, you know,
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they get told that they've got it, but they quietly get better on their own.
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Jamie: That is strange.
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Most diagnoses are at least confident about being bad news.
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Yeah.
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This one turns up, has a look around, and goes, "Well, maybe."
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Chris: Yeah.
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It really does sit in a, an odd spot, doesn't it?
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Because the short version here is that pre-diabetes is a stage, not a disease.
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Um, so it's where the system that keeps your blood sugar steady starts slipping,
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and the surprising part is how early.
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So for a lot of people, it's about 10 years or more before
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anyone measures a thing.
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Jen: Which is the bit for us to think about.
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So you feel completely fine, you get on with your life, but the groundwork's
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been quietly laid for about a decade.
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Jamie: So by the time the letter lands- Mm … you're not still at
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the start of the story, you've been handed a book already at chapter nine.
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Chris: Yeah, that's a really good way to put it.
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And the hopeful flip side, which we'll come back to, is that chapter nine still
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leaves a lot of chapters you can change.
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Jen: So by the end of this episode, you'll hopefully know why fat in the
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wrong place is at the heart of this, and why the cells that make insulin
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can go quiet without dying off, and why even experts argue about whether
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pre-diabetes is a helpful word at all.
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Jamie: And that's a lot for us to unpack.
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Jen: It is.
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But before we get into the biology, let's chat about the
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scale of it, which we always like to do, because this is not niche.
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So worldwide, something like 541
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million adults have one of the main forms of diabetes, and in the UK, the
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NHS has found around 3.6 million people.
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So it had, sorry, around 3.6 million people on its books by 2023.
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Jamie: 3.6 million people, and that's only the ones tested and counted.
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Jen: Mm.
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Jamie: The number of people actually walking around is probably much bigger.
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Jen: Yeah.
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Chris: Yeah, not only that, it's rising fast too.
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So that UK figure jumped by almost a fifth in a single year, and the
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part that got me was the under 40s, which is up about a quarter.
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Jamie: Mm. So the thing people think is a problem for later
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is quietly moving towards them.
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Jen: Yeah, and I think being in my 40s now too, that puts, it puts it on my radar.
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So if you've been waving it off as a someday problem, you're in good company.
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Chris: Yep, and being in my 30s, um, or yeah, 40s, like Jen, yeah, this is
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definitely the window to think about it.
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Jen: Um, but it's worth understanding, isn't it, rather than panicking though.
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So let's, let's see what's happening and what's going on in the inside.
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Chris: Yeah, so the simplest way to look at it is, um, as two things going
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on, well, going slightly wrong at once, and they make each other worse.
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Mm. And the first is what's known as insulin resistance.
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Jamie: And insulin is the hormone that tells sugar where to go, right?
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Chris: That's right.
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So when you eat, your blood sugar rises and insulin tells the cells to take
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the sugar in and to use it, and that insulin resistance is when the cells
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stop listening as well as they used to.
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So the sugar's knocking, but the door is slow to open.
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Jamie: So it ends up hanging around in the bloodstream
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because nobody is letting it in.
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Jen: Yeah, and that's where it stays.
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And so the cells that go deaf first are the ones that nobody
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suspects, which are your muscles.
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So they're the biggest customer for blood sugar.
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They take up about three-quarters of it after a meal.
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So when they stop listening, a lot of the sugar has nowhere to go,
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so it builds up for 10, even 20 years before there's any diagnosis.
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Jamie: 20 years, so it's not a breakdown, it's a drift.
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Mm. Two quiet decades, then a letter.
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Jen: Yeah.
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Chris: It really is, isn't it?
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Um, and the second thing is in the pancreas.
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So there's a cell in the pancreas, which is the beta cell, and the beta cell's
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one job is making insulin, and over those same years, it gradually stops keeping up.
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Jen: And this is, this is a part that I find genuinely hopeful, because
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the, the old assumption was that those cells were simply dying off,
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and once gone, like, they're gone
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Jamie: And they're not?
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Chris: So increasingly, it looks like they're not, no,
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at least not early anyway.
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So some great, uh, research work has found that under that pressure,
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beta cells largely don't die.
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They do something which is more like, um, changing job, maybe slipping back
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from being a specialist insulin maker into more of a basic generic state.
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Jamie: So they haven't quit.
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They've downed tools.
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They're still in the building- … they're just not doing the skilled bit.
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Chris: That's it.
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And, and it matters because if they've gone quiet rather than gone for good,
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there's a route back, isn't there?
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And, um, a study of people at this stage backs that up, whereby the
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number of beta cells is about the same, it's their performance that drops.
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Jen: Which is what reframes it, so less damage, more dormancy, so muscles not
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listening, insulin makers downing tools.
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But what is actually causing this?
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Chris: Yeah, so this is the idea that pulls it together, and it's very domestic.
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So if you, um, if you picture your body's fat as something that you would store in a
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cupboard, sounds a bit gross, doesn't it?
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Um, most of that fat is meant to live there under the skin safely, but
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every cupboard has a size, doesn't it- Mm … like a person capacity,
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and it's different for everyone.
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Jamie: So it's not about how much fat you've got, it's about it
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spilling into the wrong places.
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Jen: Yeah, and that explains something that confuses people, doesn't it?
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So you can be fairly slim and still develop this because your personal fat
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storage cupboard, it might be a small one.
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Um, it's why people of like South Asian heritage, they can develop these problems
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at lower body weights and why screening thresholds are set lower for some groups.
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Jamie: So the bathroom scales are never really telling the interesting story.
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Same weight, completely different amount of fat in the places that matter.
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So we basically can't judge purely on a number.
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Chris: No, that's absolutely true.
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And of course, the modern angle here is that our bodies haven't changed,
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it's the world around them that has.
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So we now have food at all hours- Mm … far less movement built into the day.
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So that fat storage cupboard might be the same size.
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We're just filling it faster and emptying it less than we would've
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done a few generations ago.
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Jamie: Okay.
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Fat in the wrong place is useful to know, but what everyone r- is really
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asking is, does this apply to them?
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And the answer, the honest answer is, it depends on who you are.
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Jen: Yeah, it does.
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So take age.
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In the US, more than half the over 65s fit the criteria, yet the
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fastest growth is in younger people.
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It's expanding at both ends at once.
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Chris: It is, and something to point out here i- is it's not even.
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So, um, UK data put it- At around twice the rate in Black and Asian groups
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compared to white groups, with South Asian heritage, as Jen mentioned, carrying a
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particularly high risk, and younger- Mm
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which is worrying.
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Jamie: And here it gets awkward, because my understanding is one
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of the main tests we lean on isn't even-handed across everyone.
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Chris: That's right, and, um, the most common test here is
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what's known as the HbA1c test.
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Rolls off the tongue, of course.
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Mm. And this partly depends on your red blood cells, but on average, it reads a
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touch higher in Black patients for the very same blood sugar as white patients.
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So it might be small on paper, but it's big enough to tip some people
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over the line that they're not actually necessarily really over.
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Jen: Which is, it's at the heart of why a pre-diabetic diagnosis gets argued over.
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The tests don't even agree.
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So there are three ways to diagnose it, and depending on which you use, the
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share of people who count swings wildly.
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So one analysis found it ranged from about 4% of a group to over 40.
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Same people, different test.
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Jamie: Wow.
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A tenfold swing depending on which test you happen to get.
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If three referees watched the same match and one said nil-nil, and another
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4-3, dunno about the third, you'd, you'd stop trusting the referees.
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Jen: I never- You would, absolutely
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never trust referees
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Chris: anyway.
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Jen: But that, it feeds the, the biggest myth, that pre-diabetes
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means diabetes is definitely coming, and nothing can be done.
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So the pre, it makes it sound like a countdown.
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It isn't.
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Over a few years, very roughly about a quarter progress, half stay put, and
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the other quarter drift back to normal.
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Jamie: So a quarter effectively get the all clear.
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Jen: Mm.
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Jamie: Sometimes doing nothing dramatic, which is why some health
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bodies aren't keen on the word, and would rather just describe the blood
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sugar and skip the ominous prefix.
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Jen: Mm.
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Chris: And there's a fair case there, isn't there?
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So nobody disputes that some people are genuinely on the road to type 2
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diabetes, but the question is, how wide should the prediabetes category be?
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So the, the highest risk group is usually the one identified by a glucose
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tolerance test, whereas the broader definition's pulling millions more
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people, many of whom, as you said, may never develop diabetes at all.
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Jen: Mm.
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Chris: And that's why this remains an active scientific debate
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rather than a settled fact.
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Jen: But debated or argued over isn't ignore it.
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Um, even the critics agree it's a useful nudge for a lot of people.
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The honest position is in the middle, a real signal, just drawn
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with a slightly blunt pencil.
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Jamie: A blunt pencil.
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I'm having that.
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Jen: You can have that one for free.
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Chris: So while you're talking about your pencils, for whatever reason, um, I
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can take us down a, a kind of genuinely upbeat route, because after all the
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uncertainty, this is actually one of the most changeable situations in medicine,
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and the s- the evidence is in- unusually deep when it comes to prediabetes.
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Jen: Yeah, it's decades deep.
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So there was a landmark prevention trial that took a few thousand
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high-risk people and split them up.
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So the group making modest changes, you know, a bit of weight loss and a bit
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more movement, they cut their chance of developing diabetes by getting on
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for, like, 60% over about three years.
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Clearly better than the medication group in the same trial.
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Jamie: Hang on, so the walking and eating group beat the drug?
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That's not how these stories usually go.
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Jen: I know, and it surprised everyone at the time, too.
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Um, and there was a clear dose, so roughly every kilogram lost lowered the risk
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by about a sixth, and people c- who hit all their targets cut it by nearly 90%.
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Chris: And the important thing is, is it lasts, doesn't it?
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Mm. Which is actually quite moving when you think about it.
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Yeah.
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So there was one big study that followed people for 30 years after
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a six-year program, and they still had a death rate about a quarter
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lower and had gained, on average, like, well over a year of extra life.
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Jen: Mm.
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Jamie: Now, I can feel everyone bracing for the part where we say- … "Overhaul
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your entire existence by Monday." In my experience, that's usually
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exactly where these things fall down.
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Jen: It is, and the number that matters isn't the perfect plan, it's the one
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that you'll still be doing this time next year, because real-life results are
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always smaller than trials pres- precisely because, well, life happens, doesn't it?
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Chris: It does, and the actual levers here are reassuringly dull, I can promise you.
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So the trials aimed at about 7% weight loss, which is not that high, is it?
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Mm. And roughly 150 minutes of movement a week, which is two and a half hours.
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Which sounds a lot until you actually cut it down and it
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becomes the equivalent of l- like a brisk 20 to 25-minute walk daily.
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Jamie: Mm. A 20-minute walk, not a personality transplant, not a
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wardrobe of new gym kit, a walk.
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Yeah.
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Chris: That's it.
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And the, the bit I like is that the movement helps on its own.
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So people that miss that weight target but- kind of kept moving,
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they still cut their risk by over 40%, which is huge, isn't it?
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Jen: Mm.
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Chris: So even if the scales aren't budging, the
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walking's doing the real work.
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Jen: And there's good evidence for how you eat, too, not just how much.
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So if you follow a Mediterranean-style diet, uh, which, you know, consists
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of lots of veg, beans, whole grains, olive oil, um, that cut new diabetes
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meaningfully in one big trial, even when people barely lost weight.
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Mm.
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Jamie: So nobody has to live on dry crackers and willpower.
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That's the version that usually dies by Wednesday.
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Jen: Everyone's cheering
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Chris: now.
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Yeah, absolutely.
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Now, two, um, honest caveats.
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So the first one, and is the responsible one, so do forgive me.
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So if your blood sugar is in the pre-diabetic range- Mm … and
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that's typically, um, an HbA1c
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result of 42 to 47, where anything below 42 is considered normal, by the
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way, please don't treat a podcast as your cue to self-diagnose- No, don't
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or start doing anything drastic.
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It's a good reason to have a decent chat with your doctor,
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though, but just don't panic.
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Jamie: And there it is.
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Chris cannot get through a podcast without doing a safety briefing.
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Chris: Yeah.
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Tray tables away- … seats in the upright position, please.
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Someone's gotta do the safety briefing, haven't they?
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Yeah.
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Um, and the second caveat is the science.
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So for most people, making the weight and movement changes powerfully delay
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diabetes rather than cancel it forever.
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Jen: Mm.
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Chris: So with the long kind of follow-up studies showing the gap does narrow
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over about 15 years or so, but let's be honest, delaying something by years when
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it comes to health is a prize that- Yeah
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shouldn't be underestimated.
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Jen: Yeah, definitely.
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And there's also some genuinely powerful medical options, too, for people with a
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lot of weight to lose, but that's, like, doctor's office territory, not ours.
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Um, but the honest thing to know is that several mainly work while
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you're taking them, and you stop, and the benefits do tend to drift back.
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Jamie: So no magic wand, but a lot of leverage, and most of it the unglamorous
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stuff you already know how to do.
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Jen: What strikes me is this isn't really a standalone thing.
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It sits downstream of all the ordinary stuff, isn't it?
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You know, how you sleep, how much you move, even how stressed you are.
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They all feed the same picture.
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Chris: They do, and a rough night nudges your blood sugar the wrong way
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the next day- Mm … and bumps up the stress hormones, and the problems build.
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So the body doesn't fit these as separate kind of problems the way
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our health checks try to, does it?
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Jen: Yeah.
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Jamie: Yeah, that's the bit that gets me.
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We get a separate appointment and leaflet for each as if the body is posting
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out individual health memos- … when really it's all one long conversation.
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Mm.
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Jen: And I'll, I mean, I'll confess, I do treat my own health like
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a to-do list of unrelated jobs.
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You know, if I'm not sleeping it's like, "Sort my sleep, move my body", and then
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that you think about your foods, as though they aren't all the same drawing.
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Chris: No, that's right.
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Uh, but they are really very much the same drawing, aren't they?
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Mm. So wh- which is why, um, pre-diabetes is best thought of
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less as a verdict and more as the, the foundations of a house sh, uh,
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showing their first hairline cracks.
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Yeah.
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So it's easily enough to do something about long before they reach the walls.
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Jen: Yeah.
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Jamie: So then why do we get pre-diabetes?
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Jen: Because two things slowly drift out of step over years, so your cells
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stop responding to insulin as well as they should, and the cells that
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make insulin gradually go quiet, and underneath both very often is fat
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overflowing its normal cupboard into organs that don't usually hold it.
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Chris: Yep, and it builds in kind of near silence for a decade or more,
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which is why a, like, a warning that lands while you feel perfectly fine
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is so easy to wave away, isn't it?
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Jen: Mm.
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Jamie: So that pre that spooked us at the start turns out to be good news.
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Yeah.
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It's the chapter where the ending isn't written yet.
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Blunt pencil and all, you're handed the warning while you
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can still do something about it.
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Jen: Yeah.
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So that's why we develop pre-diabetes, not a sentence, but a signpost, the
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body flagging early and quietly that the conditions have tipped while there's
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plenty of road left to change the course.
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That's it from us this week.
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Make sure you hit that subscribe button.
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We're unpacking the science behind everyday questions each week.
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Tell us in the comments what you'd like us to explore next.
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Thanks for geeking out with us, but for now, that's it from me.
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Jamie: That's it from me.
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Chris: And that's it from me.
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Jen: Bye for now.