Dhru Purohit Show - The Labs You Need Your Doctor to Run to Know if Your Metabolically Healthy

Episode Date: May 26, 2025

This episode is brought to you by Square, Branch Basics, and Manukora Honey. When we’re told our labs are “normal,” that doesn’t always mean they’re optimal—especially considering that over one-third of Americans are prediabetic and 47 million have metabolic syndrome. Metabolic health is the foundation of true longevity. Without actively supporting it, the risk of chronic diseases like cardiovascular disease, cancer, and type 2 diabetes increases. The good news? Prioritizing metabolic health through simple lifestyle changes can lead to long-term vitality and meaningful transformation. Today on The Dhru Purohit Show, we’re bringing you a special compilation episode featuring Dhru’s conversations with top experts on the most underrated blood tests for metabolic health and how to decode optimal lab markers. Dr. Tyna Moore breaks down the science behind metabolic dysfunction and its connection to chronic disease. She shares the essential labs to order, how often to test, and what optimal results should look like. She also offers practical tips for beginners on getting started with resistance training. Dr. Ben Bikman dives into how elevated fasting insulin contributes to insulin resistance, fat storage, and challenges in sustainable weight loss. He also explores how genetics play a role in weight gain and why lowering insulin—not just counting calories—should be the first step in any effective weight-loss strategy. Dr. Tyna Moore is a board-certified naturopathic and chiropractic physician and the founder and owner of Core Wellness Clinic in Portland, Oregon. She specializes in non-surgical pain management, natural pain solutions, and regenerative injection therapies for orthopedic and musculoskeletal conditions.  Dr. Ben Bikman is a metabolic research scientist and author of Why We Get Sick, which explores insulin resistance as a root cause of many chronic health issues. With a PhD in bioenergetics and postdoctoral work in metabolic disorders, he now serves as an associate professor at BYU, where he studies insulin’s role in obesity, diabetes, and mitochondrial health. In this episode, Dhru and his guests dive into: Metabolic health and disease pathways (2:10) Key lab tests and optimal levels (4:25) How and why to start resistance training (20:49) The most underrated blood test for metabolic health (33:57) Optimal reference ranges for fasting insulin (37:45) The two primary factors contributing to weight gain (44:22) The role of fat cells and ethnic differences (53:09) Final thoughts (1:01:34) Also mentioned: Full episode with Dr. Tyna Moore Full episode with Dr. Ben Bikman Want Dhru’s Lab Ranges Cheat Sheet? Sign up for the Try This Newsletter and we’ll send it straight to your inbox! This episode is brought to you by Square, Branch Basics, and Manukora Honey. Get everything you need to run and grow your business, without any long-term commitments with Square. Right now, you can get up to $200 off Square hardware at square.com/go/DHRU Right now, Branch Basics is offering 15% off the Premium Starter Kit; just go to branchbasics.com and use coupon code DHRU. Make 2025 your cleanest, healthiest year yet with Branch Basics! Upgrade to the creamiest honey, packed with antioxidants and prebiotics. Just go to manukora.com/dhru to get $25 off the Starter Kit and boost your energy, immunity, and digestive health today! Sign up for Dhru’s Try This Newsletter Learn more about your ad choices. Visit megaphone.fm/adchoices

Hi everyone, Drew Perot here. Every year, millions of us head to the doctor's office for our annual checkup. We get our basic labs done, maybe a couple extra tests if we're lucky, and we're told, hey, everything looks normal. Keep doing what you're doing. But here's the thing. Normal doesn't mean optimal. In fact, it doesn't even mean healthy always.

Today, more than one third of Americans are pre-diabetic, and over 47 million people are living with metabolic syndrome. Yet, so many of these people are being told. that their labs are fine or normal. So what are we missing? In today's compilation episode, we're taking a deep dive into metabolic lab markers, starting off by speaking with Dr. Tina Moore, naturopatic doctor, and chiropractor, who's been on the front lines of metabolic and chronic disease for decades.

In our conversation with Dr. Moore, she walks us through the labs that she orders personally for her patients, how often she runs them, and the actual optimal ranges she's looking for. Then I switch over to my conversation with Dr. Ben Bickman, a renowned metabolic research scientist and popular speaker on human metabolism and nutrition. And he's dedicated his career to understanding why we get sick, particularly through the lens of insulin resistance. Dr. Bickman helps us decode how hormones and fat cells interact and why lab values, especially fasting insulin, can tell you so much more about your future risk of disease than your fasting glucose or even your A1C, both. of which, of course, are very important. But first, let's listen in to my conversation with Dr. Tina Moore. It doesn't matter what drug you use, what intervention, if you are not metabolically healthy,

you are never going to be stepping into true longevity, true health, true health span, true lifespan. So first and foremost, everything comes back to metabolic health. And largely, that is lifestyle. interventions that get us there. Is that true? Yes, 100%. So let's expand on that a little bit further. What is metabolic health and how does somebody listening today know if they have it or if they don't have good quality metabolic health? Well, metabolic health, just this most simplistic definition of metabolism is that when you take in calories in whatever form in carbohydrates,

fats or proteins, that your body will hopefully metabolize them into cellular energy in its most basic form and convert them into the building blocks that we need inside our body. So some of it gets converted to energy. Some of it gets reformatted into new proteins, which is what all of our organ systems are made up of. And some of it, you know, the fat goes down the right pathways and we have myelination around our nerves. We have the building blocks of our brain and cholesterol and our steroid hormones.

So the idea is that that system would work efficiently. But we need a couple players in place working well like insulin. insulin sensitivity, insulin signaling. We need those metabolic pathways to be optimized. And unfortunately, in U.S. adults, we're looking at, you know, 2018 data showed that 93, 94% of U.S. adults have busted metabolic health. So we're looking at a whole group of individuals in large are metabolically unhealthy. And so what that means is that they are sequestering their calories into their fat cells.

they are having hyperglycemia or high blood sugars, which is causing a lot of issues. Basically, high blood sugar will cause caramelizing. Like your cellular layers literally caramelize in the face of extreme sugars. And insulin is being cranked out of the pancreas in an attempt to regulate all this. And insulin is pro-grow, which is awesome when you're trying to build muscle. And it's not so awesome when you've got cancer happening. So it's an anabolic steroid, but it's not always. working in our favor when we are bathing in it, when we're swimming in it. So humans right now,

and we've exported this across the world, so humans are swimming in excess blood sugar and excess insulin, and it's causing them to be sick, fat, and die early from a whole variety of different disease processes. Let's talk about labs. Okay. What labs can be helpful to definitively help people know where they stand on the spectrum of metabolic health? The big one that they'll get ran on their general yearly exam is a fasting glucose because that's part of a comprehensive metabolic panel. All that looks at is a snapshot in time during the moment when they had their blood drawn. Where was their fasting glucose? And when that number gets to 120, you have magically arrived at type 2 diabetes. And they say, you know, you have type 2 diabetes. And I'm over here saying,

we could have done something 15 years ago if you ran some other labs or you just paid attention. but we've normalized it in our society. So that's the big one that most people are only looking at. That's the only one they're getting. The problem with that is if you have aberrant cortisol surges in the morning because you're stressed out or you have a very stressful life that's going to surge your glucose as well. So you can have aberrantly high fasting glucose in the morning

and it's just because your cortisol's off the charts. And so an example is I, you know, now I use a CGM or a continuous glucose monitor, but I used to prick my finger. My mentor 30 years ago was having everybody by the little home glucose monitors and pricking their finger at various times during the day, but especially in the morning. And I remember when I was in bankruptcy, single mom, trying to build my practice, stressed out of my mind. And I remember my morning glucose running at about 100 for months. I also wasn't sleeping at all because I was in such shambles financially that I couldn't sleep.

I was terrified. And I had a little girl and I was trying to keep my dogs and my family together. And it was 100 consistently. And I knew that was my cortisol, but had nothing to do with my true, you know, glucose signaling. But that cortisol, that high cortisol will drive you into insulin resistance as well. That's another factor to consider. So a morning cortisol is really helpful to look at in conjunction with a morning AM fasting glucose. What's your preferred way to look at that?

Is that like a Dutch test? No, just blood test. Blood tests. Yeah, just ask your doctor for an AM cortisol and a fasting glucose. because the glucose is going to be on there anyway because they're looking at a comprehensive metabolic panel. Ahemoglobin A1C is a three-month marker of how sugared up your red blood cells are.

So it's a nice marker to have. And let's go back to the glucose. I want that at or below 90. 90 is the number. If you're at 90, something is starting to go a little haywire. But if you have that AM cortisol, you can gauge it. And what I want that as, that depends. I'm not going to give you straight numbers on that.

But if it's high and it's on the high end of normal, you're probably driving up your AM glucose without cortisol. You're probably stressed the F out and you need to reevaluate your life. And you're probably not sleeping well. One morning, a little anecdote is my fasting insulin is usually around like three and a half, four, somewhere right around there. I think that's considered like good, optimal. Good is anything anything below five, right? Insulin, yeah.

Insulin, yeah. We'll get to that one second. But I'm bringing it up because one morning I was dealing with like all this stuff. I was running around and I went in for like my normal. normal quarterly blood work, and my fasting glucose that morning showed up as like 1-10, even though my insulin, which you're going to talk about in a second, was in a good position. So that's also just a heads up to people that, you know, it's good to have multiple markers or a continuous, you know, glucose monitor because you don't want to be making, you know,

these big recommendations or people get freaked out. And that's just one little snapshot. I know I'm going to be more of the exception to the rule in that instance, but for a lot of people that are listening to this podcast who are already thinking themselves is pretty healthy, dowing things in. I've even seen that with A1C, as you've mentioned. Some people have blood cells that stick around a little bit longer, red blood cells. And so my A1C always looks a little bit more elevated, even though my fasting insulin isn't

a good position. And I had learned through Chris Cressor, a friend of mine, that some individuals that their blood, the red blood cells stick around a little bit longer so it can look like they have elevated A1C. Have you ever seen that before? Mine runs a little bit high, but it's usually in conjunction with how stressed out I am too. So I feel like there's a cortisol player piece in there. I'm not sure exactly.

But the more stressed out I am, the higher my A1C goes. So the A1C is a more, so if we're looking at fasting glucose, that's like, okay, Susan, that's where you were that morning. And let's admit, not having any food, not having any coffee and trying to drive across town to get your blood drawn by 10 a.m. It's kind of stressful. Yeah. You know, for me, that's not like the ideal way I start my day.

Totally. So there's that. So that glucose is the snapshot in time is what I tell patients. Your A1C is the long-term marker. So folks do have, a lot of times folks will have a great normal blood glucose, fasting glucose, but their A1C's high. And I'm like, you've been cheating. You know, something is awry or something's off.

Because that's the three-month marker. It's a little bit more sensitive look into how they've been behaving. the past three months. And again, it can be off for various reasons. But I like that at or below 5.5. I think 5.5 is where I draw the line. Another marker I like to look at is fasting insulin. And not a lot of doctors will run that. In fact, a lot of doctors will give you a lot of grief if you ask for it. They're like, you're not diabetic. I'm like, yeah, but most people are on the way. So maybe we should all check that. So fasting insulin, I like between two and five. Below two or close to two is actually a sign of pretty severe burnout. And it's not great. I used to. I used to

to run at one to two when I was really, really burned out. And I've been there. It sucks. You're not even making any insulin. Were you also on like an extreme low-carb diet? Yeah. Yeah. It's it can, I'm just, that's a little bit not.

I mean, some people say, oh, that's fine. I'm like, I don't know. Most people feel like when they're down there. Like in general. Like I felt like shit all the time. And then, you know, above five, we don't want that. So we want a fasting insulin. I have seen insulin, though.

Insulin's really sensitive to where your other hormones are at. And it's sensitive to your estrogen. It's sensitive to your estrogen. it's sensitive to your cortisol. So not to say that's an excuse to ride with an elevated insulin, but we got to look further beyond that. We don't just stop there. If that's elevated, if those three things are off, yes, lifestyle interventions 100%, but also,

I think a prudent doctor should look a little further and consider how old is this person? Is it a woman who's walking into menopause? Like, what are the other factors? What are some other markers? I like. I loved running a high sensitivity C reactive protein. that just gives us, it's a non-specific marker for inflammation. It doesn't tell us where the inflammation is.

It just tells us if they're inflamed. And I think that's nice to have. I like to run a sed rate as well because it gives us a little bit different look at inflammation. And so between those, I'll see high said rates and low C-reactive proteins or vice versa. You know, I want to know, are they inflamed? That's at the end of the day, are we dealing with an inflamed body? Are we now in bonus territory or C-reactive protein is like, you're even recommending for our audience that's listening.

Yeah, everyone should run a C-Reactive party. Sed rates are cheap. Sed rates are really cheap too. So I think that both. Okay. I run both. Yeah. Because you can miss inflammation by one being low for whatever reason.

And the other one's super high. And you're like, okay, we got a fire rate. What does sedent rate? It's sedimentation rate. So it's a marker of your red blood cells. Got it. What else? Actually, if I've ever gotten that done or not gotten it done,

Maybe it's in some of the blood work that I've done. ESR. ESR is another erythro sedimentation rate. It's cheap. I think it's a very inexpensive ad on. The other thing I'd add is get your labs ran through. I always use lab co-ops in my practice so patients could get labs. If they tried to run it through their insurance, it was going to be thousands.

And if I ran them, it was like 200 bucks. So there's so many great options now to get your blood done. There's kits you can order. There's so many things you can do at home, blood spot tests. Like, just take control of that and manage that because sending that stuff off through your insurance is potentially going to land you with a massive bill that is so much bigger than what it would have cost you to just pay out of cash. And I also have never, ever trusted using my insurance for anything.

And so I do everything I can out of pocket. Even when I was broken in bankruptcy, I was paying for things out of pocket because I just don't trust the system entirely. Yeah. They don't, my insurance doesn't need to see my lab work, you know. My lab works fine. but that's between me and the lab. That's just me putting on my tinfoil hat,

but I've been that way decades before 2020 happened. I think vitamin D is really important. Vitamin D can tell us a lot. It's really hard to get someone's vitamin D up if they have a lot of adipose tissue on them and if they're inflamed. So if they're rocking a lot of inflammation, D won't come up.

And it's the 25-OH vitamin D. It just won't come up, but they might have a high 125. So these are extra add-ons, but vitamin D can be quite inexpensive. And right now I have no idea why, but the powers that be in the medical establishment are saying we don't need to run vitamin Ds on people anymore. It's like they cannot make up their mind, but we know that people had significantly poorer outcomes with COVID when their vitamin D was low.

So really get your vitamin D ran. Pay out of pocket for that. I think it's what, like 50 bucks. It's worth it. So that's an important one just to have around because there's just so much correlation to things that we don't want happening with low vitamin D. We want to know where that's at, especially if you have, if you're a person of color and you have darker skin and you have darker melana, you're going to not probably be making as much vitamin D in that 20 minutes outside that I would be. Yeah. And we know we're not getting as much sun. And that's typically how we've always gotten

vitamin D. So if people are not making up for that with some supplementation, they're going to run into problems. Where do you like to see? You see a lot of different ranges, especially in the wellness, integrative, functional space. Some people like it higher. Some people say the body naturally down regulates to around 50. What's your goal of where you want your patients to be? I'm all about making my life as seamless as possible. And if you're a business owner like me, wanting to make your customers happy, you're going to want to hear about Square.

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at square.com slash go slash drew. That's Square, S-Q-U-A-R-E dot com slash go-G-O-D-H-R-U. It's time to run your business smarter with Square. Get started today. 50 to 80, 50 to 80, especially walking into winter. So every single late summer, early fall, my entire family started. on vitamin C, zinc, and D. I've been doing that for decades. It was really ironic because in 2020, I was not allowed to talk about that without fear of being D-platformed.

And I was like, but we've been doing this forever. Like, I'm not talking about any particular virus. Like, this is just how we don't get upper respiratory disease. So vitamin C, zinc and D. Yeah, 50 to 80, I think, is a good nice number. And I think most people taking around 5,000 I use a day depends on how much sun you get. I actually find that as my health improves, my D goes up. So again, because I think it's related to inflammation.

So I haven't really dosed vitamin D much at all in the past couple of, probably the last two winters. I've been a little lazy about it, but my D still remains in a... How much time do you spend in the sun every day? Oh, I get out in the sun every single day. Yeah. Morning sun, midday sun, and late afternoon sun, all three different types of sun. Because I'm getting different rays and having a different impact.

But I live in Oregon. So it's like only three months out of the year that I get to do that. And then I try to travel as much as I can in the winter. I actually try to bank my D. So I try to get as tan as humanly possible by the end of summer, although that is causing me some skin damage and I'm feeling it at age 50. I'm starting to see the signs. I'm like, I think I need some lasers.

I need somebody to resurface this. But I always say I'd rather die tan than die of all of the vitamin D deficiency-related cancers. Yeah, that's great. So you were continuing down the list of things that people can get done. Or if they've already gotten these done, they can do a little bit of an inventory. And generally speaking, I find that individuals have a feeling that, you know what, I don't feel my best, my body composition isn't dialed in, and I want to feel better.

And sure, if that ends up having me look better too, amazing. And they need a little bit of that reminder to go back and say, okay, I know I'm not the healthiest, but everybody's not really that healthy, but when they hear about these laps and they start to add these things together and they hear that they're not, you know, having at least some aspect of resistance training. You know, you can always even start small and work your way up. At any level, you can do resistance training. You can even do it with bands.

You could be, we interviewed the oldest female ninja warrior. Oh, awesome. She was on this podcast. Amazing. You would love her. I think everybody calls her, her friends call her Ginny. And she got diagnosed with osteopena by her doctor. And she came back and she was saying she was feeling very sorry for herself.

this was at the age of like 58. And her daughter had been getting really into CrossFit. And she was like, mom, you can reverse this. You can get stronger. And she's like, no, I'm too old. She said, no, you're not. And we go deep into her story. We'll link to it in the show notes.

But she got serious and said, I want to start string training. And in the beginning, it was like she couldn't even do one pull-up. Right? And that's a lot of people. So they get intimidated. And she said, look, work with a trainer. There's plenty of things you can do. Strengthen your back.

That'll help you do pull-ups in the first place. Start off with resistance bands if the weight seemed too heavy. And little by little, she stuck with it. And by the time that she turned like 70, 72, she was competing in her first official competition as the oldest American ninja warrior. That's amazing. I think I've seen her on Instagram. She's been on all these viral wheels.

You can do it at any age. You can do it at any age. She added a ton of muscle mass and she feels amazing. And then she went back in to check because I think osteopenas on the way to osteoporosis. And they said, you must have gotten misdiagnosed because there's no evidence here that you have osteopena anymore. And obviously she knew that her lifestyle was making a difference in her body and her bones and everything were getting stronger. So wherever you're at any age, maybe you find a trainer, maybe you start the YMCA, you can get started. So these are all the things that people can do at home, right?

Yeah, and there's a few more labs. Let me just quickly mention. Well, let me say this first. Osteopenia and osteoporosis are just metabolic dysfunction of your bones. It's literally diabetes of the bones. And osteoarthritis is diabetes of the joints. So people don't realize that. That's all part of this.

So if you're suddenly plagued with a bunch of, you know, degenerative joint disease in your middle age, ironically, as your waist circumference is expanding, that is the insulin actually impacting your joints. joints and leptin and the whole signaling cascade getting screwed up. This is one of the reasons I love GLP1 so much. So that's a whole other thing. When you go in for your yearly physical, you're going to get a comprehensive metabolic panel.

So they're going to be looking at your liver enzymes. If those are elevated, it means you've got the start of fatty liver. And what often happens, it's completely been normalized and your doctor will say, you've got a little fatty liver, but that's okay. It's not okay. There's no version of fatty liver that's okay at all. So if you see elevated liver enzymes, you're having some activity in your liver. It doesn't mean your liver is diseased. It means your liver cells are active and they are

secreting this enzyme to let you know your liver's being a little, it's got a little stress on it. It's probably fatty infiltrate. That comes along with metabolic dysfunction. And then the other thing is your lipids, your cholesterol, your LDL, your HDL, your triglystorides. If your cholesterol and your triglystriads equal each other, you are in trouble. So let's say your cholesterol's creeping up at 220 and your trigs are at 120, you are in trouble and essentially your liver is pickling. it's not a good sign, your lipids are off. Now, lipids can get off because of thyroid dysfunction and because of hormonal dysfunction, but most notably, it's due to metabolic dysfunction.

So I remember I had a fellow student in chiropractic college. I was like the token naturopathic doctor in the chiropractic college, so like all the dudes would come up and be like, hey, Tina, can you explain this to me? And I understood labs really like a ninja myself. So I was like, yeah, this guy shows up and he's super fit. He's Korean and he's super fit, very well-muscled, probably the best adjuster. in our school, like fast and really into martial arts and like just so he would take his shirt off and you were like, damn, that guy's in good shape. His trigs were off the chart. His cholesterol was

creeping up and- Like off the chart, you know, like what would that look like? It was in the 200s. I mean, it was not good for him. I was look, I mean, I remember looking at his labs and him being like, what is going on here. He also had elevated LDL and low HDL, right? That's not good. We don't want high deal. I'm not worried about these lipids causing heart disease the way that we have been traditionally taught, but we still can look at them in correlation to one another and see trends. So we don't want high LDL and low HDL. And I said, what are you doing? Are you like secretly an alcoholic? And I don't know it. And he said, no, I don't drink hardly at all. And I said, well, what are you doing? And he was getting a soda every day. He was going to Carl's Jr. and getting his lunch at

Carl's Jr., which I was like, what are you doing? So back to what we were talking about, sometimes you can really mask the metabolic dysfunction. That's what I was saying. This is why waist circumference is really so important in anybody of of Asian descent because we do not want that you guys can have atrocious labs and still have really great body composition. So there's there's trouble brewing. It was soda. He was drinking soda. And so then he switched to diet because he thought I wasn't clear enough. I was like, don't drink the freaking soda. But he switches to diet. They still look bad, but they actually looked a little bit better. And not that I'm a fan of diet by any means. But yeah, so Carl's Jr. and soda every day. But he was eating well for

breakfast and dinner seemingly. So anyway, that's just a great example. So you don't want your LDL above 100 and you don't want your HDL below 45. We want these in a good ratios to one another. My LDL has always naturally been a little bit high, even with low triglycerites and high HDL. Yeah. And I've done a lot of work up and I've had my cardiologist on the podcast, Dr. Michael Twyman. Michael Twyman. And one of the things that he talked about with me is I don't have familial hyper-cholestrelemia, but I am a hyper-reabsorber of cholesterol. Yeah. So that as leads to high LDL and also my APOB traditionally has been high. Is he worried? He looks at it as these things are shots on goal. And if your goalkeeper is really strong and

which is your endothelium, if your endothelium is really strong because you have good production of nitric oxide, you don't have all this vascular inflammation through insulin resistance, and you are getting good quality sunlight. He's a big believer in photobiomodulation, and you're not super stressed, and you're not consuming alcohol all the time. These are all the things that keep an endothelium strong. Yeah, I was going to say, I think they're protective. They're all protective. And he said, because I look at the data, I know there's a lot that we don't know. So it's very clear that high APOB is atherogenic.

Is that the word? Arthrogenic, yeah. It does, it does, it is causative with vascular disease. And when these lipids are able to get into the endothelium and then you get these little pimples, that is the formation of these plaques that are there. So he said, in your case, you just have to weigh the pros and cons and the risks that are there. So after looking at all the different solutions, I said, oh, well, I wouldn't actually, I got these genetic tests done that showed me what interventions would I respond to,

what would do well. And because I'm a hyper reabsorber, one of the recommendations was, look, you can go on a Zetamide. That seems to be one of the best tolerated. And it's just blocking some of the reabsorption of these lipids. and it doesn't seem like there's a ton of side effects. And again, you got to make the decision because you're the patient, but here's the pros and cons. They are shots on goal and your endothelium is incredibly strong.

Yeah. I also got a CCTV scan to look at the actual plaque in my arteries much deeper than a CT scan. And I had virtually no plaque at all whatsoever. Like he said, it was the best scan that he had seen of any male above the age of 40 years old. So that gives me peace of mind. And I know that heart disease is a big component for South Asians and skinny fat individuals who most of them are dealing with insulin resistance.

So I've chosen to take the Zetamide. And let's see, I may decide differently. But I'll tell you, it definitely lowered my ABLE B where I previously was at like 160. I've gotten down to, you know, like 90, around 90-ish, 80 around there. So again, all pros and cons that you're just trying to weigh off in your journey. of trying to decide how to make yourself healthy. Yeah, I think of it similarly. Like if something's a little off, I'm not terribly worried.

I look at trends. I'm more interested in the trend, and I'm more interested in what the other lab markers are saying in conjunction, and then I'm more interested in how that individual's living their life. So this reminds me of something I saw. It was actually during, you know, the past few years, and it was a doctor I follow who's really into metabolic health on Twitter, and he was actively seeing patients during the pandemic,

and he basically threw up some lab values, and it had like a hemoglobin A1C, a C-reactive protein, and, you know, a couple other markers. And he said, you know, you guys consider this normal, and this patient's having a really hard time in hospital with COVID. We are not the same. It was something like that. And basically what he was saying was like,

in conjunction, all of these together being a little bit off, little bit off, little bit off, little bit off, that is your typical middle-aged male in America with a little bit of belly fat, just a little bit of a dad bod, like just a little bit off is enough to put you into this really pro-inflammatory state, which would make you susceptible to all kinds of things, including what we've just been dealing with. So that was his point was like, you guys look at this and brush it off and say, oh, this is just normal because it has been normalized, right? But that doesn't mean this is ideal or optimal. And he's like, we are not the same because all of that looks like a hot mess.

It's so true. Yeah. And I remember like turning to my husband and I was like, your lips look a little bit like this. Maybe you should listen to me. You know, like that middle age, you know, it's easy to neglect it. But it's hard to see it, especially as a man, because you can really sort of pack it on throughout that torso, especially guys that are taller.

You don't see it as much. You wear it well, right? But it's, I'm telling you that waist circumference is the truth. Well, you were talking about HDL, triglycerides, LDL, and where you look at that, is there anything else that you want to say on the lab conversation? No, because all that's really inexpensive and really easy to get a hold of. Like you're talking about more advanced lipid panels and some other fancy stuff, but just for your average American, you're going to get a comprehensive metabolic panel, which is going

to have your lipid, I'm sorry, your liver enzymes, and you're going to have your cholesterol and lipids done. That's just part of annual physical exam. So you can easily just ask, hey, can we add on the D? Can we add on the C reactive protein? Can we add, you know, you don't necessarily need the CED rate, but it's nice to have in conjunction so you don't miss the inflammation. And you can add on the serum fasting insulin. That's a pretty complete package.

It's not a terribly huge expense. It's something that people can do because I think people get intimidated. And this, I see this all the time in my community. They're looking at the biohackers and the influencers online. And it's hardcore. You know, there's a lot of guys that are young and a lot of women. that are young, that are kind of sitting in your age group, that are starting to dabble with this and taking their health really seriously. But a lot of this feels really hardcore to a lot of

people. And I'm over here dealing with patients who just more in reality, like, these folks just want to live well and they're not necessarily concerned about having like a perfect body composition. They just want to be happy and healthy. And so like take what you have already that your insurance is covering on your annual. And like, let's just add a few factors and learn how to use it. Yeah. Next up, while conventional medicine primarily focuses on glucose levels and A1C to assess metabolic health, Dr. Ben Bickman explains why he calls fasting insulin the most underrated blood tests for accessing metabolic health. He talks about fasting insulin and how it can serve as the canary in the

coal mine for metabolic dysfunction, silently increasing while glucose sometimes for people can remain normal, often coinciding with weight gain, fatigue, migraines, and other symptoms of insulin resistance. Dr. Bickman also explains why fat cells play a central role in metabolic health, especially in how they grow. Let's listen in to this fascinating conversation with Dr. Ben Bickman. If people care about losing weight and they care about reducing their risk of chronic disease, talk to us about the number one most underrated blood tests that they should be getting, which is fasting insulin. Yeah, there are a lot of ways we could define. metabolic health and even overall health, for me, it is a matter of insulin resistance.

The problem with defining a lot of cardiometabolic outcomes is that we have a very glucose-centric paradigm. And this has led conventional clinical care to focus almost exclusively on glucose as the primary metabolic marker. And yet underlying the changes in glucose that could be happening over time is the humble little hormone insulin who's just overlooked. just kind of crying out for some attention sitting in the corner. But to sort of bring these ideas together, we look at glucose all the time. And any blood tests when someone goes into the clinic, they're going to measure glucose and they're going to measure hemoglobin A1C.

And it could be normal and normal and normal for years, but the person has high blood pressure. They're gaining weight. They have migraine headaches. And so there's no even suspicion that the glucose could not only be contributing to these problems, but that there is any problem, metabolically speaking. But while the glucose levels have stayed at a normal range during all these years, decades even, the hormone insulin has been the canary in the coal mine. It has been increasing steadily year over year, over year. And so to answer your question explicitly, if I were to say, is there a marker that has been overlooked,

it is fasting insulin completely, full stop, because it is the early-estead. It is the early sign of metabolic disruption, that if we could shift from the glucose-centric paradigm away from the glucose and have an insulin-centric paradigm, by measuring insulin, we can not only detect the problems decades before they manifest, in other words, insulin would be elevated potentially 10 or 20 years before the glucose ever starts to change, so we detect it at its earliest stages. But by focusing on the insulin, we also, embrace more effective strategies because with a glucose-centric paradigm, conventional clinical care will say we need to lower the glucose at all costs, even at the expense of increasing insulin.

And that is a way to make people fatter and sicker, which is why people with type 2 diabetes who are given insulin therapy to correct their glucose, because it's only seen as a glucose disease, do in fact get fatter and die faster. They're twice as likely to die from cancer, three times as likely to die from heart disease, twice as likely to develop Alzheimer's disease, because those chronic diseases are not problems of hyperglycemia, per se. They're problems of hyperinsulinemia. So focus on the insulin. We can detect problems sooner, and we can treat them better because it's the high insulin that's contributing, not the high glucose. The high glucose is a symptom. Before we pull on some threads that are there, I always love when you come on the podcast and you give people tangible,

practical things that they should be paying attention to. So when it comes to fasting, insulin and the fact that it's one of the most underrated tests out there and that often doctors don't order it unless if they suspect that something might be wrong with the patient but you're saying basically that your fasting insulin could be out of whack years ahead of time before you are diagnosed with something and it could look like excess weight it could look like low energy it could feel like being tired all the time so what are the optimal numbers and what are the ranges when it comes to fasting insulin. And of course, this is not medical advice. Everybody's got to talk to their doctor, but I do think that there is medical literacy. And people should be literate when it comes

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That's a good thing, Manuka Honey, travel honey sticks, a wooden spoon, and a guidebook. To get this offer, just head over to Manukora.com slash Drew to grab yours. That's Manukora, M-A-O-R-A-com slash D-H-R-U. Seriously, if you're looking to upgrade your honey to the best that's out there, all you have to do is head over to manukora.com slash drew to get $25 off their amazing starter kit today. Yeah, and I wish that there were firm consensus with regards to fasting insulin like we have with so many other markers.

There isn't. And the ranges will vary almost from lab to lab. Someone could, if they convince their clinician to get their fasting insulin measured, it's entirely possible that the lab will say anything under 15 microunits per mill is normal. And I blanche at that idea. I think that's way too high. So with a little bit of scrutiny in the evidence, digging through the evidence, my conclusion is that if someone has a fasting insulin of six microunits per mil or less,

it's a very, very good sign that the body is insulin sensitive. In other words, you only need a modest amount of insulin to get the job. done, you know, whatever insulin needs to do. And insulin does a lot of things, because as a reminder to the audience, literally every single cell of the body is responsive to insulin, or to say that another way, every cell has insulin receptors, these little docking sites for insulin to come and dock onto the cell, and then tell the cell to do something. And there are all kinds of somethings that insulin will tell the cell to do, depending on the cell. So measure the fasting insulin, hopefully less than six micro units per mil.

That to me is a very, very good sign. If it's up, if it's above, if it's around, say, 7 to 17 or so, that's a warning. And I know that's a bit of a big range, but it's just hard to know in that range whether you are consistently at, say, 15 or whether you are consistently at 5, and you just happen to have a peak in your insulin at that moment when you measured. And then anything above the high teens in insulin, I would say, is almost guaranteed to be a problem. But in that kind of middle range to the mid to low teens, it might be a problem, but again, it might be that you just caught the peak of insulin's natural circadian rhythm.

And that's why, as much as I am a great advocate of measuring insulin, I also don't ever mean to imply that it's the only marker that I think there are other scores, like, for example, the triglystic the triglyceride to HDL ratio, take triglycerides fasted, divide by HDL fasted, and that number, it varies a little bit across ethnicities, but the kind of average point appears to be around 1.5. So get your fasting insulin measured, absolutely, but also couple that with your triglyceride to HDL ratio. And if that number is less than 1.5, it's a very good sign that you're insulin sensitive, even if your insulin creeped up into the teens, don't lose hope. Look at that number and that'll help fill in some details.

And the value of that number is in the event that anyone listening is not able to convince their clinician to measure their insulin because, let's face it, it's not easy to do. It's often a bit of a battle to get it done. You will always get your triglyceride to HDL ratio measured or not even the ratio, but those two numbers. Every blood test will include triglycerides. Every blood test will include HDL cholesterol. So take that ratio, just compute it on your own.

And if it's less than 1.5, then you can be really confident that your fasting insulin is also going to be good. Yeah, and I want to add a little caveat that fasting insulin is generally considered an inexpensive test, right? So there's the whole medical bureaucracy for good reasons, you can say, where you have to get your doctor to order it. So there's the whole convincing side that's there. And if you generally ask nicely, I find that, that people are willing. Some doctors don't like to be told what to do, just like some people don't like to be told what to do. And in that case, remember, you know, you are a client of theirs. You're a patient. So go shop around and find somebody else. And, you know, in some instances,

you might be able to use some direct-to-consumer services. We can list some of those below. There's a bunch of them that are out there. But let's continue. So we mentioned that, and I appreciate that caveat, that by no means is fasting insulin the only thing you're telling people they should be paying attention to. We're just saying why it's one of the most underrated markers to pay attention to both for short-term health and long-term health. Now, in the short-term health side, there's this whole category. We've been doing this summer weight loss series that I've invited you to be a part of for your deep knowledge and expertise when it comes to the topic of insulin and energy expenditure inside the body. You made a video recently that was fantastic, and you said, really when it comes to weight gain,

we need two things to come in unison together to basically start that process of significantly starting to gain weight. Can you explain what those two things are and how they work together? Yeah, we can start with the one that appears to have the greater mass appeal, which would be calories or what I would like to refer to as just energy. sufficient energy. So you must have sufficient energy in the body coming into the body in order to provide the fuel for the growth of the fat cell. So that is pretty easy. That's very palatable because we have such a calorie-centric idea or view of obesity and weight gain, weight loss.

However, what is too often overlooked is the absolute requirement of elevated insulin. A fat cell does not inherently know what to do with the energy that it has surrounding it. And let me just refer to my own lab. Here I am at my university, right across the hallway in my building, is my laboratory. And we are regularly growing fat cells on little petri dishes. And it is so stark to look at the difference in the way the fat cells behave in the absence or later the presence of insulin. So as we are growing the fat cells out across this little plate, they are surrounded with energy, calories.

There's fat and there's glucose, which are the two building blocks for triglycerides within the fat cell itself, the triglycerides, which are kind of giving the fat cell its big fat blob, or what we call a lipid droplet. And so again, the fat cells are surrounded by calories, an abundance of energy, and yet they're small. There's no changes on those fat cells until we start sprinkling in insulin into the culture, into the bath, the medium we call it, the liquid that the cells are bathing in. Once we start putting in insulin, now the fat cells know what to do, which is store the energy. So that's a part that's so often overlooked. And this doesn't apply to all metabolism in all cells, but it is a pretty central theme that cells need to be told what to do with the energy they have available,

whether it's energy available on the outside to come in, or whether it's energy that the cell already has available within itself. It's the hormones, it's hormones like insulin or glucagon or epinephrine, adrenaline, and others, growth hormone, that signal to the cell what to do with the energy that it has access to. The cell doesn't just know what to do with the energy. energy. The hormones are what's sort of sampling the entire body, understanding what's going on in the entire body, and then dictating individual cells. You know, it's like the hormones are the

conductor to the orchestra. Any individual section, the brass, the woodwinds, the percussion, they don't know what notes to play on their own. They need something to tell them when to come in, the pace, the volume. The hormones are the conductors of the orchestra. And when it comes to fat, growth, you have on one side the hormone insulin, which is overwhelmingly promoting the growth of the fat cell, and it is so powerful in its own right that it is offset by multiple other hormones that tend to have a catabolic effect to insulin's anabolic effect, like some of the other ones I mentioned, glucagon and epinephrine most obviously, and growth hormone. There are a handful of hormones that are trying to get the fat cell to shrink and share its energy,

all to try to offset the incredible power of insulin, which is telling the fat cell to store energy. But insulin goes even further than that. As much as insulin has a very pronounced central effect on or directed effect on fat cells to stimulate their growth, insulin also has effects at the brain, stimulating to a degree, some degree of appetite or satiety in various instances, not to mention the effect that insulin has on leptin levels from the fat cells, again, a direct effect at the fat cell. But insulin will also elicit a whole body effect to slow metabolic rate. We have known that for decades. Indeed, over 100 years ago, two famous Harvard scientists, Elliot P. Jocelyn and Francis G. Benedict,

Jocelyn kind of being the father of modern endocrinology, Benedict being the father of modern metabolism, they came together to try to understand the metabolism in what they called severe diabetes, which we would just say kind of uncontrolled type 1 diabetes, that they noted in these individuals who have no insulin, their metabolic rate was 20 to 30 percent higher than it should be. there was something uncontrolled, this fire just raging through their body. And you see this in people with type 1 diabetes. In fact, it's so obvious that some type 1 diabetics are tempted to capitalize on it

and engage in a pattern of disordered eating, which is commonly called diabolemia. In other words, the type 1 diabetic learns that if they can eat whatever they want and enjoy it, eat it, swallow it, and keep it in their stomach and digest it, and they can be as skinny as they want to by simply deliberately underdosing their insulin. That is the most powerful evidence of the absolute requirement of insulin in telling fat cells to grow or to shrink. Because they learn, again, just if they skip their injections, they will be as skinny as they want. Now, there is metabolic mayhem in the body in that instance. Their glucose levels are 10 times higher than they should be.

Their ketones are 10 or 20 times higher than it should be. and they're dying, but they look as lean as they want to be. And that is because they have learned that insulin, injecting insulin is like injecting fat shots as one type one diabetic referred to it, that they learn that it's the insulin that's making them gain weight, whether they want to or not. So insulin tells the fat cells what to do with the energy that it has available, namely grow, but insulin also helps that growth by enriching the availability of total energy by reducing overall metabolic rate.

And we even see this in people with type 2 diabetes. People with type 2 diabetes who go on insulin therapy, taking their already kind of high insulin and putting it even higher, their metabolic rate slows at the moment the therapy begins. And it's no surprise that diabetics around the world, type 1 or type 2, when they begin their insulin therapy, they gain weight. In a type 1 diabetic, it's often essential because they've been losing so much weight that the insulin hopefully will just get them back to where they should be. But in a type 2 diabetic, who's often already overweight, once they start insulin therapy,

it's guaranteed they're going to gain more weight, and so up they go. And so within this long-winded answer, Drew, I've touched on a lot of points. If I were to sort of bring it together, I would present what I hope is a unifying hypothesis, which is that, there are two camps, and I don't want to straw man any one of them and speak for either of them, but you would have the kind of pure caloric theorists who would say, no, it's purely a matter of calories in calories out, hormones be damned, or you have the other camp, which they would say it's purely a matter of insulin and it's pure hormones. I might have misspoke earlier, but then in that case, calories don't matter, whereas the other group would say hormones don't matter.

But in reality, both do. You must, to put it in a distinct sort of a thesis statement, you must have elevated insulin to signal the growth of fat cell, and you must have sufficient energy to fuel the growth of the fat cell. Either is insufficient. You need both. I simply harp more on the insulin because it's the one that's so much more readily overlooked. The caloric-centric view of obesity has so enamored the world that there's almost no room intellectually to consider that there's another facet to this, namely hormones. But let me just revisit the role of the fat cell very briefly. And this is a particular interest with two guys like me and you. You have Ben Bickman, who is kind of European, Northern European descent,

and I have Drew, Drew, I think you're South Asian. Indian, yep. Yep. So these are two remarkably comparable ethnicities. When I did my postdoctoral work in Singapore, one of the reasons, Singapore was so interested in partnering with Duke University, which is where I was, was to understand these ethnic differences on how you can take ethnicities, particularly in Singapore, with both Chinese, South Asian, Malaysian, and European. And you have these four different guys who are best drinking buddies, and they're all gaining weight, and yet they start to suffer the consequences of that weight gain at very different rates. But a study done in Caucasians compared to South Asians, not only,

do we know that the average South Asian Indian has a fasted insulin that is more than double what his Caucasian counterpart is, but also even at the same body weight, his fat cells are about three to four times larger than his Caucasian counterpart. And there, so there are these, and this could explain why partly India has more people with type 2 diabetes. The absolute numbers more than anyone, but of course India's population is so massive. Even per capita, it's approaching the number one spot in the world, being truly the diabetes capital of the world. And a part of it is this combination, yes, environment, diet matters, but also genetics. And so that is, it's very much important for us to understand what we could call the personal

fat threshold that based on our genetics and partly our diet, certain bodies have the potential to store fat in their fat cells to varying levels. And, and, just Caucasians in the case of this example appear to have the higher threshold. But basically, as long as you can continue to store fat in fat cells, the body stays metabolically sound. And that it's once the fat cells start to reach a point of maximum dimension. And by that, I mean, every individual fat cell is getting too big. Now the body has reached its threshold. And if insulin is attempting to still tell the body to store energy, now you have a war, a metabolic mutiny, where the fat cell starts to rebel. So we gain fat through two different processes.

You know, you have two buddies, you drew and Ben, we're going on vacation, hanging out together, and we both come back from our trip 10 pounds fatter. Because of our unique ethnicity and the genetics that come with that, some of my weight gain potentially would have happened through some modest degree of hyperplasia, where when my fat cell started to get a little big, I would simply create some new fat cells. Whereas Drew, with South Asian ethnicity, your fat cells, you have a very limited potential for hyperplasia. In other words, you're not going to multiply your fat cells.

The number of fat cells is pretty set. So then what happens is the fat cells each just get bigger and bigger and bigger. So each fat cell is carrying a bigger metabolic load than it would normally. Whereas again, in another body that can undergo hyperplasia, the fat cell gets a little big, and it recruits a new fat cell, which gets a little big. So more important than the mass of fat we have on our body is the size of each individual fat cell, which of course is impossible to measure outside of a lab. We can do that thing here in my lab by taking biopsies of people's fat tissue,

but even still, it's not something you're going to really do. That's why you start to look at these other markers that we mentioned. But to sort of wrap through this idea quickly, when the fat cell gets really, really, big, two problems start to happen. One, it starts to reach a point of maximum dimension that it can't grow anymore. Otherwise, the cell membrane starts to lose its integrity and literally start to pop, which would be a very messy inflammatory process. And at the second, the fat cell, as it's swollen up to 10 or 20 times bigger than it used to be, is now suffocating. It's getting pushed too far from capillaries, in other words, blood vessels where it can get oxygen and give its CO2 and get nutrients.

So the fat cell starts to get too big and it starts to suffocate. This elicits two responses. When the fat cell starts to get so big, it starts to tell insulin, insulin, you are trying to make me big and yet I can't grow anymore. And so while you are trying to block me from breaking down my fat, I'm not listening. and I'm going to start leaking fats. To say that in a more precise term, insulin normally inhibits lipolysis,

which is the term for breaking down fat. That's the primary mechanism whereby insulin promotes the growth of a fat cell, not necessarily force-feeding it, but preventing it from breaking it down. So the fat cell says insulin, fats are still coming in, or glucose is still coming in, but now I'm going to start breaking down fat, even though you're trying to tell me not to.

So one, the fat cell, the hypertrophic or swollen fat cell, becomes insulin resistant to prevent further growth, leaking free fatty acids into the blood in the midst of elevated insulin, and those two things should not be high at the same time. High insulin and high free fatty acids now means you're going to start storing fat in other places throughout the body, most especially the liver, getting fatty liver and excess fat in the pancreas, creating insulin resistance in those tissues.

But the second problem, as I mentioned, is that the fat cell becomes hypoxic. It starts to suffocate, if you will, as it's gotten pushed too far from the capillary. The fat cell has a potential solution for that, too, and that is by secreting a bunch of pro-inflammatory cytokines into the bloodstream. So the hypertrophic fat cell becomes very pro-inflammatory because some of those cytokines that it's secreting have the ability to promote the growth of new capillaries. And so it starts to correct its hypoxia by stimulating the growth of new fat. cells, which is a better outcome than suffocating and becoming necrotic.

You know, once again, a very messy, inflamed death, if that were to happen. So the hypertrophic fat cell, in order to ensure its own survival, becomes insulin-resistant to prevent further growth, inadvertently thereby flooding the body with free fatty acids to be stored elsewhere, and two, becomes very prone inflammatory in order to correct its own hypoxia, but in the process, flooding the body. body with pro-inflammatory cytokines, things like C-reactive protein, for example, which is increasingly measured on blood tests. But the combination of these two things, high free fatty acids and high inflammation, is a wicked combination because now you start promoting the accumulation of these

other types of fats in the body called seramides within the cells. And when these two signals come to a cell promote seramide development or accumulation, now those cells become insulin-resistant as well, whether it's the brain, whether it's the muscle, whether it's the liver, or the blood vessels, you know, promoting hypertension, this is why I have a fat first focus, that fat cells are the first domino to fall, that when the fat cells become insulin resistant, that's that earliest stages where the insulin's going up, but it's all still enough to keep glucose in check. You know, the muscles are still responding to the insulin, pulling in glucose, the liver is still responding to the insulin, pulling in and storing glucose, helping blood glucose levels stay low.

But once the fat cells have become insulin resistant and now pro-inflammatory, they start spreading that insulin resistance to, like, for example, muscle and liver, now you have the glucose levels start to climb. So where you have other people who may promote or advocate an idea that the muscle becomes insulin resistant first or the liver, I don't agree with that because of that were the case, then glucose levels would start to climb immediately. They don't. glucose levels stay low because insulin resistance starts in the very low metabolic rate fat cells and then it spreads to the higher metabolic rate, higher glucose consuming tissues, you know, like the muscle, for example.

Whether you're looking to optimize your health, lose weight, or simply better understand your lab results, I hope you're walking away from today's episode with helpful insights and information to help you decode the often confusing world of laboratory markers and especially metabolic health. And by the way, if you enjoyed this episode and want to dive deeper into any one of these conversations featured today, I highly recommend checking them out. You can check out both of these conversations with Dr. Tina Moore and Dr. Ben Bickman in the show notes below. And as always, if you found this episode valuable, do me a huge favor in my team as well.

Share this episode with someone who's thinking about how to improve their metabolic health or how to address their prediabetes or why they should be paying attention to this, especially if they have people in their family who've dealt with any chronic disease. Well, until next time, thanks for tuning in to today's compilation episode. Drew Prod's signing off. I'll see you next week.