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Written by The Thriva Editorial Team
8th Sep 2026 • 47 minute read

Professor Naveed Sattar, one of the most cited researchers in diabetes and obesity science, explains why type 2 diabetes is really a disease of fat in the wrong places, and why the same weight gain does very different things to different people.

Show notes

Type 2 diabetes is a disease on the rise. It affects almost 6 million people in the UK, including around 1.3 million who don't yet know they have it. So how can we recognise the signs, reduce our risks, or better live with it?

This week, Greg and Charlie put these questions to Professor Naveed Sattar, Professor of Cardiometabolic Medicine at the University of Glasgow and one of the world's most cited researchers in diabetes and obesity science. With more than 1,200 peer-reviewed publications, a career spent working directly with patients, and his own first-hand experience of living with an elevated risk of diabetes, Naveed is a voice to be reckoned with on this subject.

Starting with the science, Naveed explains what happens inside the body when we develop type 2 diabetes: why it's different from type 1, and how ectopic fat (fat that gets stored around our middle and in non-fat organs like the liver or pancreas) hinders insulin production. We talk about the genetic and environmental factors that heighten our risks, and about why certain populations are more vulnerable.

You will see that when it comes to diabetes, the science has changed over the last decade: moving away from focusing on sugar, toward prioritising weight loss instead, with GLP-1 medications like Ozempic and Wegovy playing a part.

In our practice segment, Naveed, Greg, and Charlie get into what this all means for day-to-day life. Including:

  • How Naveed changed his lifestyle after being diagnosed at risk (23:21)
  • Screening and testing for diabetes (27:33)
  • The role of movement in reducing risks (30:05)
  • Where and how GLP-1 medications get factored in (33:39)

Finally, in the experience section, we turn to your listener questions. We hear from those navigating gestational diabetes, and from people who have been living with type 2 diabetes or are trying to lower their risks.

If you take only one thing away from this episode, remember that type 2 diabetes is far more than a matter of willpower. This episode is for anyone who wants to make sense of a disease shaped by genetics, environment and circumstance, and one that moves faster than most of us realise.

If you'd like to send us your health questions for future episodes, you can email us a voice note or write in at themethod@thriva.co.

Mentioned in today's episode

Transcript

Naveed: Let me compare Charlie and I. So my risk of diabetes compared to Charlie's is probably about 50 times higher, because I'm much older. But even if I was the same age as Charlie, it might be five times higher. The reason being, I've got a family history of type 2 and I'm South Asian. Being South Asian, we put fat into the liver, a key organ for breaking down excess sugar when the insulin isn't working as well, faster than white people do. Being male, males put fat in the liver faster than females. Plus I've got family history. Because my two uncles developed diabetes in their thirties, my dad in his fifties, my mum in her forties, I'm genetically loaded. But the point being is, I'm more likely to develop diabetes at a lower BMI than Charlie. The process is exactly the same, it's just that my genes, my makeup, means that I'm putting that fat in the key organs that are relevant to sugar much faster than Charlie would, for example.

Greg: Giddy Charlie.

Charlie: Oy.

Greg: With your enthusiasm.

Charlie: Excuse me.

Greg: That big beaming grin.

Charlie: I'm going to turn my camera off. How are you?

Greg: How are you? Oh, you first.

Charlie: Ah, I'm good. I'm refreshed after my two-week holiday. First time I've ever taken two weeks off in my entire working career, and I think I could do it more often, I'll be honest. Had a wonderful time.

Greg: Where did you go and what did you do?

Charlie: I went to Canada for two weeks. Well, Vancouver Island. Went hiking and kayaking and surfing and camping.

Greg: It was very passive.

Charlie: Yeah. A lot of people say to me, do you not need a holiday after your holiday? But being on a different time zone and then not having much signal. Absolute dream. No one speaks to you. It's great. In the nicest possible way, I can see why you love the nomad life so much.

Greg: I can't imagine you ever just lying by a pool.

Charlie: Maybe for like two hours, three hours I could do it, but then after that, no, it's not for me. But yeah. Back to reality.

Greg: You got a song for us this week?

Charlie: Oh, sugar. Sweet. What's that? Sugar for my honey. Sugar. That's a good one. What's the lyrics? Sweet, sweet honey. Sweet sugar for my honey. Let's go with that.

Greg: I'm impressed as always. This week we are discussing diabetes, and specifically type 2 diabetes, which is a very common problem. Going by a recent estimate, it's thought about 6% of people worldwide have diabetes, and that's about double the proportion of people that had it in 1990.

Charlie: Oh really?

Greg: Yeah, it's on the up, and a lot of people that have it have no idea that they have it.

Charlie: Hmm. I actually know someone who's got type 1 and a few people with type 2. Type 1 is quite restrictive on your life, isn't it? Whereas the people that I know with type 2 diabetes do tend to have a sweet tooth and love chocolate. I also knew someone who got it during pregnancy, which I probably wasn't really aware of, that that was such a risk factor, pregnancy.

Greg: There are lots of forms of diabetes. There's type 1, there's type 2, there's gestational diabetes, which is what you're referring to there. And people also refer to pre-diabetes. So you can go from otherwise being healthy to having pre-diabetes and then to having type 2 diabetes. And even within type 2 diabetes, there's quite large variation between people and some of the symptoms they experience.

Type 2 diabetes, which we're focusing on, accounts for about 96% of cases. So it's really very common. And part of the problem is that it's associated with lots of other health repercussions. People who have diabetes have a much higher risk of various cardiovascular diseases, and that includes problems with the heart, stroke. They have a higher risk of various different kidney disorders and peripheral artery disease too. So it comes with a big burden.

But the key is that many cases of type 2 diabetes are preventable. Arguably a lot of them are reversible as well, because nowadays we actually have quite good treatments. So Charlie, what do you know about the risk factors for diabetes? You mentioned having a sweet tooth, so that suggests that maybe nutrition is one of those risk factors, and the others.

Charlie: Risk? Do you mean as in symptoms or risks?

Greg: I mean things that people do that are going to influence their risk of developing the disease, but also demographic factors. So for example, do you know if men or women have a different risk of the disease?

Charlie: Oh gosh, you're testing me here. I don't actually know. I think weight, being overweight, I'm assuming being inactive is a bigger risk. Is it genetic? Are you more prone to it genetically?

Greg: Yeah, there certainly is a genetic contribution, and within genetics, obviously your genetics determine your biological sex. And interestingly, the most recent data from 2021, looking at lots and lots of people, suggests that the male to female ratio is about 1.14 to one. So men have a greater risk than women do, and I'm sure we'll get into that in the episode with our guest today. So who is our guest?

Charlie: Professor Naveed Sattar, who is Professor of Cardiometabolic Medicine at the University of Glasgow. Naveed is one of the world's leading researchers in diabetes, obesity, and cardiovascular disease. His work has helped shape how we think about weight in preventing and treating type 2 diabetes. He also works closely with patients and is known for making complex science much easier to understand. So fingers crossed for me that he's going to do that.

Naveed is also particularly interested in how we apply research into the real world. He's openly spoken about his own increased risk of type 2 diabetes and how this has influenced the decisions he makes about health.

Greg: It's nice to have someone who has deep expertise in the subject, but also practises what he preaches, because I think people like that are better able to empathise with people who are going through the process of trying to reduce their risk or trying to treat the disease.

And him being a medical doctor too, he'll also understand all the pitfalls of this condition and the challenges that these people face in a way that a lot of people who are pure academics might not.

Charlie: Yeah, amazing. Shall we bring you in?

Greg: Yeah, let's go for it.

Charlie: Hi Naveed. Welcome to The Method. How are you today?

Naveed: I'm very well Charlie. Nice to be here.

Charlie: Brilliant. So we're just going to start with the basics. What actually is diabetes, and what's the difference between type 1 diabetes, type 2 diabetes and gestational diabetes?

Naveed: Ah, okay. So diabetes is a condition where the sugar level goes above a certain level, and in medical terms we use what's known as HbA1c, or glucose levels. When glucose levels go above seven when you're fasting, consistently, then it's considered that your sugar levels are too high.

And what happens is when the sugar goes above that level consistently, it starts to cause damage to some of the small blood vessels in your body, and it seems to stick to proteins. So diabetes is a disease of higher sugar levels.

Type 1 happens because the hormone that we require to put sugar in the right places, to store it when we don't need it, for example in the liver, or to help put it into cells where we want to burn it to make energy, is insulin. If you cannot make insulin, then guess what? That sugar stays in the blood at very high levels and can cause huge amounts of damage, which is why people with type 1 diabetes are treated with insulin.

Type 2 is completely different. Often you can make enough insulin, but what's happened with type 2 is that you've put on weight, and that excess weight gets to a certain level where that excess adipose tissue, or fat, gets into the liver, or into the pancreas which makes insulin, or into the muscles.

And what happens then is, if you have too much fat, the cells in the liver and the muscle don't respond to the insulin in the way that they should normally do. And if you put too much fat in the pancreas, the pancreas stops making enough insulin. So effectively what we've realised now is type 2 diabetes is the disease of ectopic fat: excess fat in organ systems, which then disrupts your sugar metabolism to keep your sugar higher than it should be otherwise.

So they're completely different mechanisms, which is why type 2 diabetes is often found in older age and in more people living with excess weight, whereas type 1 diabetes can manifest at any age. The average age of type 1 diabetes is about 14, and it's because something has attacked the pancreas to stop the body making insulin. It can develop at any age, but the median age is 14, whereas type 2, because it's linked to older age and obesity, is about 50 to 60 on average. They're quite different.

Charlie: And in terms of gestational diabetes, just so we can cover that one off.

Naveed: Oh well, gestational diabetes. Pregnancy is what's known as a metabolic stress for women. When the mother is developing a growing foetus, she has to develop a placenta, she has to put a lot of metabolic resources into making a placenta and a foetus. And that means she has to move lots of energy around in different ways, which is stressing her metabolism in different ways.

Most women undergo that perfectly fine, but if you're carrying a bit of excess weight, or you have a higher genetic risk for diabetes, that stress of having to shift lots of fuels around in different ways can lead some women to develop diabetes, because it's stressing the system. And once you deliver, that stress actually goes away.

So gestational diabetes is effectively a stress test, and it unmasks women who are at future risk of developing diabetes by putting them under a stress during that period of nine months. That's what it is. I have friends, and lots of women who get gestational diabetes will develop diabetes in later life, because it's marked those women out as those who are at high risk of future diabetes.

And the issue now, and why it's really important that we covered gestational diabetes, is that in the UK, say 50 years ago, maybe one in a hundred pregnancies had gestational diabetes. Now it's one in six pregnancies in the UK that is affected by gestational diabetes.

Greg: We are focusing on type 2 diabetes today because it makes up so much of total diabetes. Recent estimates suggest something like 96%. And going back to something you were saying, Naveed, it's clear that when you get glucose sticking to tissues and organs that we'd rather it didn't stick to, there's dysfunction that follows that.

And associated with diabetes, there's an increased risk of things like cardiovascular disease. I read one of your recent reviews that suggested that type 2 diabetes patients have a two to four times increased risk versus people who don't have type 2 diabetes. And then there's also an increase in risk of chronic kidney disease and various other pathologies.

We don't want to fearmonger though. But it's clear that there is a genetic contribution, because it does tend to run in families a little bit. However, maybe some people might overestimate the extent of the genetic contribution. And there are lots of risk factors that are at play, including things like demographics, how old someone is, their biological sex, their race, but also lifestyle factors and various other exposures in the environment.

So it'd be great if you could put this into context and speak a bit about the relative contribution of some of the biggest risk factors.

Naveed: That's a really nice summary, Greg. So let me do it this way. There's the three of us here. I've got several risk factors compared to you two, one of which is age. I'm older than you.

But let me compare Charlie and I. My risk of diabetes compared to Charlie's is probably about 50 times higher, because I'm much older, and it's probably the age that's making it. But even if I was the same age as Charlie, it might be five times higher. The reason being, I've got a family history of type 2 and I'm South Asian. Being South Asian, we put fat into the liver faster than white people do.

The liver is a key organ for breaking down excess sugar, and if you put too much fat in the liver, that stops insulin working as well. Males put fat in the liver faster than females. Plus I've got family history. So that means, beyond just my ethnicity, because my two uncles developed diabetes in their thirties, my dad in his fifties, my mum in her forties, I'm genetically loaded. And that's partly because of where I put my fat, and there might be something else going on. But predominantly fat.

The point being, I am at this accelerated likelihood of developing diabetes for a given weight. So if I put on weight, I'm more likely to develop diabetes at a lower BMI than Charlie. Charlie might need to get to a BMI of 40 to get type 2. I probably can get it at 26.

But the process is exactly the same. It's putting fat in the liver. Ectopic tissues will eventually trigger it. It's just that my genes, my makeup, the fact that I'm male, means that I'm putting that fat in the key organs that are relevant to sugar much faster, at a lower BMI, than Charlie would.

And that's what it is. So each of us has a different gradient for when we put fat, for a given weight gain, in the wrong places where it can cause increased risk of diabetes. But the trigger, regardless of where that gradient is, is weight gain. It's just that I need to put on less weight to get it. The average man needs to put on less weight than the average woman, in fact, and the average Asian needs to put on less weight than the average white person, as an example. That's the way it works.

Greg: I just want to spell something out, which is the term ectopic fat. That is basically fat where we don't want to have fat, so in organs like the liver, the pancreas, skeletal muscle, and so on. So what we're speaking about here really is a kind of central obesity, storing fat around the viscera, which is what dramatically increases risk.

And there's this concept that was put forward by a colleague of yours, Roy Taylor, years ago: the personal fat threshold. The idea is that each of us has this personal fat threshold beyond which we start to quite quickly run into metabolic problems.

And that varies a lot between people, and part of that is related to fat distribution. So males versus females. Factors like age, older age being a risk factor. Race: anybody who is non-white relative to a Caucasian person has a higher risk associated with weight gain.

Naveed: That's exactly that. Yes. It's like your characteristics set your gradient for how quickly weight will lead to metabolic harm. As an example, the reason I knew that I had a very strong risk is that my two uncles and my mum, this is my mum's side, developed diabetes in their thirties.

And their BMIs were around about 25, an almost normal BMI for white individuals. And that's even more accelerated than the average Asian as well. And I thought, oh my goodness. And then my mum, and women obviously have a lower risk than men, she developed diabetes in her forties. So that's the way I realised it.

And younger people need more obesity to tip into diabetes than older people. If you look at both of you, you're both young, you've both got very good muscle mass, and your pancreas is younger. So you're able to make lots more insulin and you're able to burn more calories and burn more sugar in your muscles, because you've got bigger muscle mass. So you actually need more disruption of that system. You need more weight to flood into those organs to tip into diabetes.

And that matters, because we now know that younger onset type 2 diabetes is a lot more pathogenic and harmful than diabetes developing at 70 or 80.

Now if I develop diabetes eventually at 70, I don't care. Actually, I'm not too worried. First, I'm not going to live long enough for it to cause enough harm in my eyes and my kidneys. Second, I also know that developing diabetes at older age, if you look at lots of epidemiology, the sugar is going up more slowly, because it's a slow process to have got there.

Whereas if you develop diabetes at 20, it's associated with much more weight gain, much more rapid sugar rise, because you're putting fat in the wrong organs faster. And because the weight is higher, you've also got much higher blood pressure compared to your age, you've also got higher blood fat levels, and all of that begets faster damage to your key organ systems: your eyes, your kidneys, your liver, your heart, and so on.

And the way we illustrated this was looking at life losses. If you develop diabetes at 30, the average life loss in a white individual is about 15 to 20 years. If you develop type 2 diabetes at 70, it's maybe one to two years loss of life.

Charlie: You've spoken about how the modern environment can increase our risk of developing diabetes, sometimes through things that are completely out of our control. What are some of the features of modern life that are contributing to that risk?

Naveed: Well, I think it's something, Charlie, I think we all probably know them. And I've really got a bit of a, what's the word, is it a bee in my bonnet? That's not the right expression. I'm like a dog with a bone. Just to try and explain that.

It's obesity, of course. Over the last 50 years: in 1950, 1% of the population were living with obesity. In 1980, 6%. In 1980, 1% of the population had type 2, and then it went up to four or 5%, and now it's about eight to 9% in the UK. In some countries it's 20%, which are the countries where they put fat more centrally, faster, like Asia, or the Middle East as well, where food industrialisation and activity levels have substantially been altered in a really adverse way.

So there's far too many calories in society. You walk down the average high street, you can get multiple calorie sources. And of course, although there's a small proportion of people who are now more active than ever, because there's more capacity, overall commuting to work has gone down, the capacity to be physically active has diminished.

But beyond that, there's other factors as well. I think people have not recognised this thing. The humble iPhone, I think, is making life more obesogenic. What's the last thing most people do at night? Oh, I'll just check my emails, or I'll just look at something. Social media. And guess what? You're stimulating yourself and you're not going to sleep properly. And sleep affects appetite.

So basically, technological advancement improves lives, but it does make us less physically active. It does distract us in ways, and stops us getting better sleep, and stops us giving ourselves space, resting our minds. And also the capacity to buy calories, or even have them come to you, is seducing people who are vulnerable to overeating to eat too much.

And that susceptibility to weight gain is partly genetic. You two are looking really lean and healthy, so you're lucky. You've got probably good appetite genes, and you've got good life circumstances. The average person that I see in my clinic who's living with obesity, and particularly those who've been overweight all their lives, either don't have, they've obviously got a set of genes that means their appetite control is not as good.

So for a given food environment, they're going to be seduced to eat more. And or they've had psychosocial stress in their life that further compounds their lifestyle. And or they live in an area where there's more fast food and less healthy food. And or they've got parents that live with obesity that give them more food, and so on.

And guess what? Obesity is going up fastest in the poorest part of society. We're also now at a point where the environment today is much more obesogenic than it was in 1990, than it was in 1970. And guess where obesity is going up fastest? In the youngest and the poorest. And it's also going up fastest in certain people who are more susceptible. So this is not predominantly about willpower. There are multiple dimensions to this.

Greg: Thanks for that, Naveed. You've really done a good job of explaining many of the factors that are at play. Before we move to the practice section, I just wanted to try and briefly summarise what we've covered so far.

The main forms of diabetes are quite different from each other, but within them, type 2 diabetes is by far the most burdensome at the level of the general population. Type 2 diabetes is fundamentally a condition of insulin resistance, and that's driven by a range of factors. But within those, high body weight is a particularly important upstream factor, because at some point weight gain leads to deposition of fat around organs and inside organs that impairs their function, so-called ectopic fat. And that includes the pancreatic cells that make insulin.

Some of us are at much greater risk of diabetes than others, in particular people who are male, older, and who are not Caucasian. And the problem is that nowadays a lot of us live in a very obesogenic environment, and that's especially true of people who are less well off. Unfortunately a lot of those people have less access to some of the therapies that are maybe most potent.

However, we are not doomed, because if we can target the excess fat mass then we can halt the diabetes disease process. But in people who already have type 2 diabetes, there's evidence that we can actually reverse it. And I know that work by yourself and others has shown that in people who have had diabetes for years, just to give an estimate from one analysis, for every 1% weight loss from someone's baseline, the probability of complete remission of diabetes increased by over 2%. And some studies by yourself and others have shown that there's probably improvement in pancreatic function too, and that suggests that there's actually restoration of the tissue that is damaged and at the core of the diabetes disease process. So body weight is key.

Naveed: Can I just, in terms of the evidence base for reversal, the better evidence is actually reducing liver fat, Greg, than pancreatic.

Greg: Okay. Yeah.

Naveed: I think the pancreatic fat imaging is very hard and there's still a little bit of debate. I think it probably does, it is relevant. But if you cut the amount of fat within your liver from 17% in the average diabetes population down to 3%, guess what? That liver then beautifully responds to the insulin you make, to cut down production of sugar when you don't need it.

Greg: Thanks for the intervention. That's helpful. And that brings us to the practice section. Charlie, over to you.

Charlie: So now we're going to move into the practice section of the podcast. So Naveed, you've spoken openly about having an increased risk of type 2 diabetes yourself. Knowing what you know about the disease, has that changed the way that you think about your own health and the habits that you've built?

Naveed: Yeah, no, absolutely. So, knowing my family history, there was a study that was ongoing where they took blood samples from 300 people and measured various things in metabolism. And the researcher came back to me and said, Naveed, I'm sorry to say this, but your insulin level is the highest of everyone.

That basically meant that my pancreas was working really, really hard to keep my sugar normal. That probably meant I had a bit of ectopic fat. And I was probably about a stone and a half heavier in my twenties and thirties, as a junior doctor running around and not eating so well. We had family, we had kids, and your ability to be active obviously when you have kids is limited.

So when I got to about 40, again, it became evident that my family history was even stronger. It wasn't just in diabetes, it was in cardiovascular disease. So I was starting to think I really need to improve my health. My lipid levels were okay, but my HDL was low, which means I probably wasn't as active.

I got into biking and cycling, just as you have, Charlie. And so for the last probably 15 years I've commuted to work on the bike. I go cycling every weekend with friends. Any time I get an opportunity to bike, I'm good.

So I'm lucky I've got that agency. I biked from a young age. I'm able to afford a really nice gravel bike. I'm able to store it properly. I'm able to take it into work and have a shower. I've got all of those agencies that helped me. And the other thing, 10 years ago we got a dog, for the same reason.

Charlie: I would strongly recommend everyone does get a dog though, Naveed.

Naveed: Yeah. And so my step count probably went from an average of about five or 6,000, and now I'm doing about 11,000 a day. And I'm approaching my sixties and my muscle mass is great.

My HDL is a biomarker of activity. It used to be one. It always tends to be low in South Asians. I bet you Greg's is about 1.6 and yours is probably about two, Charlie, because you look pretty active to me. So I realised that needed to go up, and my HDL has gone up to 1.6 now. And I can see that in clinic: when people become more active, the HDL goes up. So it's a good biomarker of activity.

Anyway. So by that process, I'm still in the pre-diabetes range, but I'm at the very, very bottom of that. So I'm likely to get diabetes, but probably when I'm 70. So I've probably delayed it by 30 years compared to my uncles, by 20 years compared to my mum, by 15 years compared to my dad. And as I've said to you, if I get diabetes at 70, I'm not really that worried, because the damage to eyes and kidneys probably won't happen, because we'll have better drugs by then anyway.

So that's the way. But again, this is not to say I'm better than other people. I'm not. I have been lucky. I've got that agency. I've got that ability, I've got that understanding, and I've got all these opportunities around me, because I live in an affluent area, I've been educated, and all these things. I don't have the barriers. What we now need to do is help other people overcome barriers to be more physically active, to enjoy physical activity, eat better.

The other thing I've learned to do is, as part of my eating, I always try and bring a piece of fruit to work, and I didn't do that 20 years ago. I've retrained my palate to enjoy more fruit and vegetables. I still have some chocolate, but I have half of what I used to.

So again, maybe I'm lucky, maybe I've got better genes, genetic willpower, to be able to do that. But I've retrained my palate to enjoy more fibre-rich foods. I have people in my clinic who have never really eaten salad. Again, it's not their fault, but they say, oh no, I'm repulsed by that. Well, they've never really tried it. And be satisfied by eating chocolate slower. It's those small tips that we need to help people with.

Because what happens in clinics, and actually you'll like this, in clinics we give them booklets, or we give them diet sheets. Do you know where that goes? Mostly in the bin.

It's not enough anymore to say, Mr Smith, you're overweight, come back when you're five kilograms lighter. Well, for frick's sake, if he knew how to do that, he would have.

Charlie: Yeah, it wouldn't be sat in your office.

Naveed: Would he be sat in my office? Do you think he wants to be a BMI 32? Come on.

Charlie: Yeah.

Naveed: So we have to make lifestyle advice much simpler. We're developing something, I think we're going to do it with the Scottish government, which is going to go out to all clinicians in Scotland. Three or four of my colleagues in the NHS in primary care love it. They said, this really helps. We explain to people how to eat fewer calories, what the simple tips are. And we give them the agency to fail, to try one of those things.

So that's how we need to improve the lifestyle part. I think we've improved, but we can improve it a lot further. And I also think with those 10 or so different choices, all evidence-based, you could also give people a 30-second TikTok video. This is what we mean by how you make that change. Because if you don't explain how to make that change, you're not empowering them enough.

Greg: If we speak about screening and testing, which you've already mentioned, Naveed, you touched on screening very briefly early on. If someone listening thinks that he or she might be at increased risk based on some of the things that we've spoken about so far, is there a free screening tool that you would recommend to help them approximate their risk?

And then secondarily, when it comes to testing, you've spoken there about things like HbA1c. You also mentioned HDL. Both of those are available through Thriva. If people want to get tested at home, which tests do you pay most attention to clinically when you're trying to get an overall assessment of somebody's metabolic health and risk?

Naveed: Again, it's a great question, Greg. So for the vast majority of people, I think HbA1c is really good actually, because it's an average of your sugar levels over the last three months. Diabetes is when HbA1c gets to a level of 48 millimoles per mole, which is the kind of units we use.

Pre-diabetes, so you're at risk of diabetes, in the UK is when you're 42 to 47, and normal sugar levels are below 42. So 41 and under. And HbA1c can be done any time of the day, whether you're fasting or non-fasting. I've helped change the guidelines to remove the need for fasting for lipids as well, because most of the lipids that we measure are pretty accurate when you're non-fasting. So in the clinics that I do, we measure non-fasting lipids, if I'm worried about their diabetes risk, because I can see it, their age and their ethnicity and their weight.

The other thing we measure is often liver function. Because one of the liver tests, called ALT, is basically an enzyme that's produced within the cells of the liver, and it goes up when there's too much fat within the cells of the liver. So we've now realised, and not always, it can go up in many other things, but in the vast majority of people, when you see people who've got slightly higher ALT along with blood triglycerides, which is again a form of ectopic fat, excess fat in the circulation. So ALT, triglycerides, so lipids, liver function and HbA1c are the three tests that we commonly measure in the clinic.

If someone out there is worried about their diabetes risk, they can go online first, Greg. They can use the diabetes risk score from Diabetes UK. There's also what's known as the QDiabetes risk score, which includes things like some drugs that you're on, and that's available online. And there's a few other diabetes risk scores, there's the Leicester Diabetes Risk Score.

And then if you do that diabetes risk score, putting a few factors in, and it comes up as moderate to high, you can go to your GP, or you can go online as you say and get some of these tests, and tell your GP, listen, I've got this high diabetes risk score, would you please measure my HbA1c? And they should do that. It should be an easy test to do.

Charlie: I know we briefly just touched on your cycling habits, to help with your higher risk of diabetes, but what about exercise to prevent and manage diabetes? For other listeners, do you think there are any key types of exercise or goals of exercise that people should pay attention to?

Naveed: So I don't even like the term exercise anymore. But actually that's not true, I'm changing that, I'm changing my views slightly. One of the things I have an opportunity to do is to reflect on evidence all the time.

So there are barriers toward using the word exercise for lots of our patients. Three of us have got huge agency. Charlie, you've got beautiful bikes behind you. Greg, you look fit and athletic. But listen, I see patients who are in their thirties who have obesity, psoriasis, sleep apnoea, who are not working, who are demotivated, who are depressed.

So depending on where people are at, the key thing is, can we help them work out what the barriers to physical activity are? How many steps are they walking a day? And if so, can they increase the number of steps even by 500 a day, which equates to five minutes extra walking? Can they start to measure it systematically, so that they know what they're doing, and can they use that as a biomarker, which is what I do?

If I look at the end of the day, I think, oh my God, I've only walked 4,000 steps, and I did that a couple of days ago. I better go and do another walk. Put my podcast on, or maybe take the dog for a walk. Just to, and consistent activity is really good. Mind, sleep, activity.

So just giving people, and saying, look, well, how would I get more activity? Well, just maybe walk a bit more. Maybe walk with a friend. Maybe listen to a podcast. Maybe is there a friend that you can join a walking club with? Instead of taking your car to the shops, maybe you should, it's only 15 minutes' walk. That'll get you about 1,500 steps. And if you do it back and forth, that's 3,000 steps more. That's fantastic. That's about 120 calories that you've burned.

Explaining it in the way that people resonate with, or maybe getting into the habit that after your main meal at night, rather than jumping in front of the TV, to develop that habit. Like, okay, I'll go for a 10-minute walk around the block. It's those kinds of things.

Once they've achieved that, I completely agree, exercise is important. If you can get to a point where you're a bit fitter, maybe you could then start thinking, but find an activity that gets your heart rate going a little bit. Because as you put your heart rate up, you're making your blood vessels more pliable. You are pushing blood through your blood vessels, and you are keeping your pumps and your pipes and your filters more efficient, is the way I try and explain it. So how we explain these things to people really matters, I think.

Greg: And on that note, I think something people miss, who maybe don't share some of those features, is that exercise can be really aversive for a lot of people. And it's very different if you are carrying a lot of body weight that you have to lug around. The amount of inertia that's involved is nothing like what the three of us here experience.

And so sometimes, rather than starting with exercise, it makes sense to actually start with something pharmacological, a drug medication that can help kickstart the process. And then if somebody can lose weight first, they start to adopt healthier lifestyle habits because they become less aversive.

So on that note, when it comes to type 2 diabetes, how do you decide which medications are best for a patient of yours, as well as when to start said medications? I realise that this is a massive subject.

Naveed: I can summarise it really easily, Greg. The simple summary is the following. 15, 20 years ago we had drugs that lowered sugar, didn't often lower weight by very much, did it by different mechanisms, and very few of them affected major outcomes.

Now we've got two classes of drugs. One that seems to get rid of excess volume in the system, which is the SGLT2 inhibitors. They lower sugar and they protect the pumps, pipes and filters, particularly for kidney and heart failure. And they're now almost first line in diabetes, because they really reduce those hard outcomes. And they reduce sugar in diabetes and they help a little bit with weight loss, two to three or four kilograms.

The other class is the incretins, or weight loss drugs, and they're now being used much, much more, because it's targeting the primary cause of diabetes in the vast majority of type 2. And the vast majority was ectopic fat, excess weight that led to ectopic fat.

And the most recent guidance, so those used to be third or fourth line, after insulin, with insulin, now before insulin, now after other drugs. Now they're starting to become almost first line in some countries. In fact, they're too expensive to be first line. But the new guidelines, like those coming from the American and European diabetes associations, are likely to push them much higher up in their algorithm.

Guess what. Why? Because if you help an individual reduce that food noise, which is what these drugs do, cut the caloric intake by 200 to 400 calories, lose 15 to 20 kilograms, reduce your liver fat from 17% to 3%, guess what? And you do it quite early on after they develop diabetes, their sugar levels normalise or get much better, and you reduce their blood pressure and you improve their blood lipids.

And a side effect, or what we didn't anticipate, the drugs also seem to have direct effects in slowing up blockage of your arteries as well, protecting your kidneys.

So if we could afford it, if these drugs were really cheap, they would be first line everywhere in the world for type 2 diabetes. So it's a huge revolution. Huge revolution.

And if you go back to the earlier conversation, they are now first line in a group of people with type 2 diabetes who are at the highest risk and who've got the highest levels of obesity: young onset type 2 diabetes. More of my colleagues are now using these drugs, because nothing else really touches them.

But if you could tackle the weight and the food noise in people who've got a BMI of 40 at the age of 25 with type 2, that's the way to treat the diabetes. And that individual's got the highest risk of the worst complications, because guess what? It's the obesity and the food noise that's the primary culprit leading to everything else for that individual. That's where we're heading, Greg.

Greg: Let's just hope that the price of them continues to come down.

Naveed: Yes, absolutely. And the safety elements continue to be good.

And you made a really important point. People living with obesity are not greedier or lazier than other people. If you're carrying excess weight in your arms and legs, it's much harder to move. And my colleagues actually proved, using genetics, that being heavier leads to lower activity levels.

So once you're on these drugs, what we need to do is help people overcome barriers. Once they've lost 15, 20 kilograms, help them imagine a new life, to either re-engage in an activity they did when they were 20 years younger, or to find new activities to capitalise on the new way that they feel, the new weight that they're at, to really give them an even greater improvement in their quality of life. If we can.

Greg: Charlie, sing the sentence.

Charlie: Before we move on to the next section, just a quick break to talk about Thriva.

Greg: That's got to be used. We have to use that.

Charlie: It was so good.

Greg: So what is Thriva? Well, it's a platform to support healthy longevity. It provides at-home blood testing that helps you understand what's going on in your body. And with their tests, you can establish a baseline for your health and take steps to sustainably improve it.

Charlie: You order your test online, do it at home, post it back, and within a few days you get your doctor's report explaining where all your levels are. We've done it and I can confirm, it's super easy to do at home. Also, I'm a picture of health and have more vitamin D than Dr P.

Greg: Yeah, not anymore, mate. Sorry about that. So if you're interested in learning more about your health, or you just want to show off like Charlie does all the time, you can order your kit online at thriva.co.

Charlie: That's thriva dot co.

Greg: All right, should we get to these questions then?

Charlie: Let's.

Charlie: So we now move on to the experience section of the podcast, which is where we're going to put some listener questions to you, Naveed. So the first question is from Helen in Norfolk, and she has asked: I have a family history of type 2 diabetes and had gestational diabetes during both my pregnancies. How does this affect my risk factors for type 2 later in life? And is there anything I can do to prevent onset?

Naveed: So I guess that individual should have been checked. If you've had gestational diabetes, the policy in the NHS is that you should be checked regularly by your practitioner for diabetes risk. So if she's had gestational diabetes in two pregnancies, that individual should get their HbA1c checked by the GP to know where she's at.

And it might be that, because she's now fine and she's lost weight, and she might have had a much bigger rise in the metabolic risk during pregnancy than most, it may be that HbA1c is normal, in which case she can relax a little bit. Or it may be that she's got pre-diabetes, in which case she can get a sense of what weight she's at, what's the HbA1c, and how much weight she needs to maybe lose to reduce that risk, or how urgent is that risk for diabetes.

Because if the HbA1c is like 46, she's close to developing diabetes, then that's a reason to perhaps think about lifestyle and reducing weight by four or five kilograms. Or she may have undiagnosed diabetes, in which case then clearly. So for that individual, get the HbA1c, because that is the measure that tells that individual where they're at in terms of diabetes risk.

Charlie: Hmm. The next question is from Richard in Edinburgh, and he has asked: I had an HbA1c that crept up to 67. However, after starting on Mounjaro, it dropped to 31. I've since, eight months ago, stopped Mounjaro, and it's heading back to around 40. Would you recommend restarting on a low or maintenance dose?

Naveed: Ah, so that's an individual choice. But what's happened there is exactly what you would expect. So with tirzepatide, which is the proper name, Mounjaro is obviously the name that Richard and many of the listeners, and all of us, will hear in the media, how it's marketed. It has shown evidence in people living with obesity that if you start Mounjaro and you've got pre-diabetes, it reduces the risk of developing diabetes by 93%.

Charlie: Gosh.

Naveed: That tells you it's huge. Exactly. And the 7% who did develop it probably had a different form of diabetes, to do with maybe the insulin not working as well.

So the answer is, if Richard is willing to pay for that and he wants to not get diabetes, the answer is yes. If he stays on Mounjaro at low dose, he's likely to keep his sugar levels down. The reason the HbA1c is going back up is he's probably putting weight back on again.

So Mounjaro is working in two ways to improve the sugar. One, big weight loss, getting rid of fat in the liver and so on. And two, because the incretin, which is what the drug is, also helps the pancreas make more insulin. So it's got a direct effect on sugar, because of the molecule that helps the pancreas make more insulin, and an indirect one through weight loss.

So the answer is yes. And I've written a paper recently that says we should be using these drugs right at the diagnosis to reverse diabetes, exactly as Richard has done. And if you keep on that drug, he may be able to delay his diabetes by 10 to 15 years, and that will reduce his future risk of many complications.

Charlie: Thank you. The next question is from Ali, and they have asked: I am South Asian and I have a family history of diabetes. I had gestational diabetes three years ago. My HbA1c is 32, which is good, but my fasting glucose level is 5.9 to six on waking. My GP isn't concerned and said he will help if the fasting glucose gets higher, but I don't want it to. I'd rather act now. What can I do to help myself now?

Naveed: I would just reassure Ali, an HbA1c of 32 is completely normal. I would get that rechecked just to double check that's accurate. We have published papers that show that in South Asians, and not actually generally in white, but it applies for many, that HbA1c is the best marker for the complications of diabetes.

And 32 is so far away from diabetes, which is 48. I would be delighted if I had an HbA1c of 32. And fasting sugar is neither here nor there. The HbA1c is a marker of the average exposure to sugar levels over three months, 24 hours a day, over three months. So that's the thing that matters the most. And it's the marker that best predicts eye disease, best predicts heart disease in diabetes.

If you get diabetes, they're miles away from diabetes. Just double check that that's accurate. Just non-fasting. Forget the fasting, double check the HbA1c is accurate, and then if it is, then be reassured. And I suspect Ali is relatively lean. And then forget about doing fasting glucose. And even the fasting glucose is completely normal, it's well below seven. Keep doing the HbA1c.

Greg: Thanks, Naveed. I think Ali will find that very reassuring.

To close, what's one thing that you'd like our listeners to take away from this conversation today?

Naveed: There's a couple. One is that we have realised that it's getting harder to maintain a healthy lifestyle because of the environment. Do the best you can. Try and learn some simple tips. Choose one goal. Maybe just one simple tip would be, for me, try and eat more salad with your main meal would be my major tip. And walk an extra 500 steps.

And you can get to a point where you start to enjoy salad. Trust me. Or eating fruit. It just takes a bit of pressure to retrain the palate.

And the other big thing is, for health professionals and all of us, and for governments, and we are all starting to realise this: obesity is the major driver of type 2 diabetes. By far. It's ectopic fat. We have different susceptibilities, but if the obesity prevalence goes up, we will see more diabetes. As night follows day, diabetes follows obesity. And it's the obesity that's the major driver, not only of the sugar, but of many other risk factors that also lead to the other complications.

So we are moving towards attacking obesity, probably first and foremost in diabetes, beyond any other condition, with the new drugs, which is what we want to do to help more people and have less suffering. But in the future, the big picture is, hopefully we can change the environment so future generations don't need these drugs in four or five generations. But it's going to be a long journey.

So that's the one thing. Let's remove the stigma about obesity. Let's try and help people in the best possible way, explain things in the best possible way, use the right tools in the best possible way, and really have advocacy to change the food environment and policy. That's the direction of travel, and that hopefully is an optimistic viewpoint in the future. Let's see.

Greg: Thanks so much, Naveed. We really appreciate you sharing your expertise.

Charlie: Thank you.

Naveed: Absolute pleasure. Yeah.

Greg: Charlie, hit me with the key takeaways.

Charlie: Oh, I thought you were going to say hit me with your rhythm stick. That as well as my key takeaways. What were my key takeaways from today? I probably didn't realise how much genetics played such a part in type 2 diabetes. That was quite interesting.

And the differences between my chance of getting diabetes as a 35-year-old female versus Naveed's as a nearly 60 South Asian male. Yeah, really actually quite surprised about those stats. What about yours? What are your takeaways from today?

Greg: One of them is that he really emphasises the importance of ectopic fat, much more so than insulin resistance, which traditionally most people discuss. Another is just that body fat is such a huge factor, and it's amazing how when people lose it, their risk of diabetes goes down.

And just to give an example of this, there's a programme, the Diabetes Prevention Programme, a very widely cited study that found that for every one kilogram of weight that people lost, there was a 16% lower risk of going on to develop type 2 diabetes.

Charlie: For one kilogram.

Greg: Every kilo, yeah. And I wonder, with these new medications, how the landscape is going to shift over time. Naveed has spoken previously at length about the fact that cardiovascular disease has come down over time, in part due to better stopping people from smoking, but also lipid-lowering drugs like statins.

Meanwhile, obesity has carried on going up, as has type 2 diabetes. But now that we've got these new medications that are really effective, are we going to see a shift in that trajectory? In the US, for example, obesity has actually started declining, but it's carried on rising globally, just because most of us don't have access to these medications.

So hopefully, if prices carry on coming down, they get in the hands of more people that need them, we'll start to see a shift. And based on the data so far, it seems like the proportion of people with type 2 diabetes will potentially drop dramatically. So fingers crossed.

Disclaimer: This information is for general educational purposes only and isn't a substitute for professional medical advice, diagnosis, or treatment. Always speak with a qualified healthcare professional first if you have concerns about your health.

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