Insulin Resistance Uncovered The Hidden Driver Behind Heart Disease, Fatty Liver, and Dementia

Imagine being told your blood sugar is normal, your labs are "fine," and yet, beneath the surface, your body has been struggling for years with a silent metabolic dysfunction. In today's episode of Infinite Health, Dr. Arasi Maran, an interventional cardiologist, to unpacks the hidden epidemic of insulin resistance, a root cause fueling heart attacks, fatty liver, dementia, and more. Despite its impact, insulin resistance is rarely screened for and often missed until it's progressed for a decade or longer. Together, we’ll cut through the noise and reveal why traditional testing fails to catch this condition early, how it connects to nearly every chronic disease of modern life, and what practical steps you can take to detect and reverse, it before it’s too late. Get ready to shift from reactive medicine to proactive health with science-backed strategies for knowing your numbers, moving your body, eating real food, and transforming your long-term well-being.

00:00 Understanding insulin resistance early

05:24 Insulin resistance and health impacts

09:08 Early detection of insulin resistance

12:01 Understanding triglyceride to HDL ratio

14:38 Calculating and interpreting Homo IR

17:10 Exercise to combat insulin resistance

21:29 Impact of ultra processed foods

26:05 Impact of stress on visceral fat

28:11 Discussion on BMI and body composition

32:27 FDA approval for CGMs in 2024

36:11 Discussing GLP1 and diabetes treatments

39:49 Key takeaways for better health

Transcript

SPEAKER_01 0:00

Insulin resistance is upstream of almost everything we call modern disease or non-communicable chronic disease. When patients ask me what causes the heart attacks, my honest answer is not high cholesterol, it's the metabolic dysfunction driven by insulin resistance. The price you are paying is a high circulating insulin all the time. It drives inflammation, it promotes the visceral fat storage, it raises your triglycerides, it lowers your LDL. Standard medicine waits until your blood glucose rises, by which time your pancreas has given up trying. And then we call it pre-diabetes or diabetes. But by the time you get to the pre-diabetes stage, you've been sick for a decade or two. Your body has been trying to repair and repair and repair, and that mechanism is now broken down, and you're left with the byproducts of the repair, which is information.

SPEAKER_00 1:27

And then quietly knowing, because you're an interventional cardiologist who sees what comes next, that this person has actually been metabolically sick for 15 years and no one's ever told them. And that's not hypothetical. That's a routine clinic morning. And today, Dr. Miranda is going to walk us through the diseases that fuels nearly everything she treats in the cath lab. The disease almost no one screens for. Welcome back to Infinite Health. Dr. Miranda, it's great to see you as always. I think this is such an important conversation to dive into, especially because it's something not talked about enough and kind of a silent indicator that's not obvious. So great conversation.

SPEAKER_01 2:03

Absolutely. Great to see you here today, Leila.

SPEAKER_00 2:07

Absolutely. And thanks for having this conversation with us. I know that I've been hearing a lot about insulin resistance online, and there's been a lot of talk about it lately. So it's I'm happy to talk to about this with you and get the real science behind everything. So let's dive in. So most people have heard of diabetes, but far fewer have heard of insulin resistance. So what is it exactly and why should people care about it?

SPEAKER_01 2:32

Okay. Insulin resistance is the disease that becomes diabetes 10 to 20 years later. And it is the actual root cause of most of what I treat in the cat lab. So when patients ask me what causes the heart attacks, my honest answer is not high cholesterol, it's the metabolic dysfunction driven by insulin resistance with elevated cholesterol as one of its downstream consequences. Here's what's happening at a very cellular level. The job of the insulin is to take the glucose out of your blood and take it into your cells, primarily your muscle and liver. When the cells stop responding well, they become resistant. That means your pancreas thinks the blood sugars are still rising and pumps out more and more insulin to force the glucose into the cells. And if this keeps happening for years or even decades, your blood sugar stays normal because you know your pancreas is pumping a lot more insulin. But the price you are paying is a high circulating insulin all the time. And that insulin excess is not benign. It drives inflammation, it promotes the visceral fat storage, it raises your triglycerides, it lowers your LDL, it elevates your blood pressure, it accelerates atherosclerosis. So it's a metabolic emergency, but happening in slow motion. The reason most people haven't heard the term is because we don't screen for it. Standard medicine waits until your blood glucose rises, by which time your pancreas has given up trying. And then we call it pre-diabetes or diabetes. But by the time you get to the pre-diabetes stage, you've been sick for a decade or two. So the framing I want to give the listeners to walk away with today is by the time your blood sugar is high, you have been insulin resistant for years. Your body has been trying to repair and repair and repair, and that mechanism is now broken down. But you're left with the byproducts of that repair, which is inflammation.

SPEAKER_00 4:45

Wow. And how does this connect to diseases that people already worry about? For example, heart disease, dementia, fatty liver. Yeah.

SPEAKER_01 4:54

Insulin resistance is upstream of almost everything we call modern disease or non-communicable chronic disease. Okay. Let me walk through the connections. Cardiovascular is the most direct link. When you have hyperinsulidemia, it drives the atherogenic dyslopidemia. That is, it uh increases the lipids or the lipid dysfunction, which leads to plaque formation, which is high triglycerides, low HDL, and small dense uh LDL particles that are far more atherogenic than the fluffy ones. These are the sticky ones, okay, to make it minimalize it. A 2024 Dutch cohort of more than 6,000 patients showed that the triglycerides to HDL ratio, essentially it's a stand-in for insulin resistance, was such a strong predictor of incident cardiovascular events as direct insulin measurement. Now, example, let's go to MASLD, formerly known as non-alcoholic fatty liver disease. It roughly affects about a third of all adults and it is driven primarily by insulin resistance. Excess insulin tells your liver to store all the fat instead of burning it. So the fat starts within the intricate architecture of the liver, and your liver becomes stiffer and stiffer and stiffer, and you end up with fatty liver disease. Alzheimer's, the researchers now pretty much refer to as the type 3 diabetes. It is a diabetes affecting your brain. And the most important organ which is sensitive to insulin is your brain. So when your brain develops insulin resistance, it starts driving the central mechanism, which is essential, which is what causing Alzheimer's. Now, let's talk about PCOS. Again, driven by insulin resistance. Most of my female patients with PCOS, they also have elevated cardiovascular disease. They also have elevated cardiovascular risk for this particular reason. Now, several cancers, especially the colon, breast, endometrial, all show strong association with hyperinsulinemia than with body weight per se. So when you understand insulin resistance, you understand the engine behind chronic diseases of aging. It's the master variable. So that's why I think every adult should know their numbers.

SPEAKER_00 7:25

Absolutely. And if all of these other numbers are so important, why is the standard testing, fasting glucose and HBA1C missing for years?

SPEAKER_01 7:35

You know, because we are doing things which insurance companies want us to do. An insurance company just wants to take our money and not give us the right treatment at the right time. We spend more time treating disease than in prevention. Okay? So that's my philosophical side of it. I can't fix it right now. So I'll talk about things which we can fix. So fasting glucose, it's a snapshot of one moment. It tells you, is your pancreas currently winning the battle against insulin resistance? It does not tell you the intensity of the battle your pancreas is fighting. It just tells you pancreas is producing enough insulin to keep your blood sugars normal. But when you're insulin resistant, your pancreas is working harder and harder, producing more and more insulin to force the glucose into the cell. So your fasting glucose stays normal 15, 20 years until the day your beta cells become exhausted, can no longer compensate. Then your glucose rises. We call it prediabetes. And what is the treatment? Lifestyle and exercise. Like what is diet and exercise and lifestyle changes? It does not even break down what you need to do, right? So hemoglobin A1C is a 90-day average of glucose. Same problem, but just a different time scale. It's a downstream consequence and not an upstream marker. So let's talk about Joseph Kraft. He's a pathologist working in the 1970s, and he did something remarkable. He performed insulin tolerance tests, that is, measuring insulin levels and not just the glucose. On more than 14,000 patients, he found that you could see insulin resistance in the insulin response curves decades before glucose ever became abnormal. He called this state diabetes in situ. It was a brilliant insight, largely ignored for the past 50 years, and the mainstream is slowly catching up. So the simple takeaway is if your goal is to catch up metabolic disease at a curable stage when reversal is still possible, fasting glucose and hemoglobin A1C are too late. You need to measure insulin or a reliable proxy for it. We'll get to that in one minute.

SPEAKER_00 9:58

Okay, awesome. And what labs should someone ask their doctor for at their next visit?

SPEAKER_01 10:04

Okay, here's a panel. I tell patients to request and I get them for myself. None of these are exotic, none of them are expensive. Most insurance plants cover them. And those are fasting insulin, fasting triglycerides, HDL level, fasting glucose, and hemoglobin A1C. Fasting insulin, it needs to be below seven. If it's more than 10, it's definitely concerning. Fasting triglycerides, I just say needs to be a double-digit number. If it is a triple-digit number, it's concerning. HDO, the more it is, the better. But unfortunately, we have the South Asian population who have very low HDL levels. Fasting glucose, again, a double-digit number, not a triple-digit number. Hemoglobin A1C, the standard mainstream considers 5.7, but I think 5.7 is too late. I want something below 0.4, and you need to fight to get to 5.4. So with these five numbers, you can calculate three powerful insulin resistance markers H O M A I R, HOMA IR, the triglycerides to HDO ratio, the triglyceride glucose index. These three ratios will tell you almost everything you need to know about your own personal metabolic health 10 to 20 years before any of the standard screening would catch the problem. The most important one to ask explicitly is fasting insulin. It's a $20 to $30 test. Physicians don't order it by default. You have to ask for it.

SPEAKER_00 11:40

That's so good to know. And can you walk us through the triglyceride to HDL ratio? What's a good number and what's a bad number?

SPEAKER_01 11:48

So a triglyceride to HDL ratio is the most clinically used insulin resistance proxy that I know of. And I honestly think almost every adult already has the data needed to calculate it, but it's just sitting in an old report. This is where you need to take all of these numbers and use AI to do your tasks. So take your fasting triglycerides and divide them by your HTL, and that gives you the triglyceride HDL ratio. The cutoff from the public, the cutoff for the published literature varies with ethnicities. Okay. The Caucasians under two is optimal, two to three point five borderline, more than three, you're overtly insulin resistance. For the South and the East Asians, the threshold is lower. Anything about 2.5 is concerning. And we develop Southeast Asians and South Asians and the East Asians, we develop insulin resistance at a way lower body weight. So you can't go by BMI, etc. You need to sit down and calculate it. For African Americans, actually, it becomes less reliable because their triglycerides often stays low, even though they have insulin resistance. So you may have to combine it with other markers. So you understand it's not a one cookie size cutter which fits all of it. We have to personalize it, and this is where personalized precision medicine comes into play. And honestly, the ratio works because it works on the mechanism, right? Insulin drives a specific metabolic phenotype, high triglycerides, low HDL, and small, dense etherogenic LDL particles. Two of these are already in the standard lipid panel. So this ratio captures the dysmetabolic state without requiring fasting insulin, which means anyone in this world can calculate this from their basic panel. A Dutch prospective cohort showed that the triglyceride HDL ratio actually predicted cardiovascular events more strongly than the direct measurements of insulin resistance. So this is not just a screen, this is truly a real prognostic marker.

SPEAKER_00 14:08

And what about fasting insulin and HOMAIR? Are those easy to get or are those a little bit harder?

SPEAKER_01 14:15

You know, it's easier than people think. Fasting insulin, you know, if you choose to pay, it's a $20 to $30 test. The challenge is not the test. It's the physicians who don't honor it. So patients need to ask for it. So let's say you have your fasting insulin level and you have your fasting glucose. Homo IR is a simple calculation. Fasting glucose times fasting insulin divided by four or five. Again, use your AI tools and plug in your numbers and it will tell you. So HOMO IR interpretation is pretty easy. If you're less than one, you have excellent insulin sensitivity, one to 1.9 normal. But if you hit 2 or above, you have early insulin resistance. And if you're 2.5 and above, you have overt insulin resistance. But if you're 2.5 or above, you invariably have other things also, which would be obvious. The advantage of OMOHIR over triglyceride HDL ratio, it's slightly more direct. The disadvantage is the fasting insulin assays vary from lab to lab. So the number, absolute numbers, can drift. You can use both and they triangulate each other. And there's also on the newer marker, triglyceride glucose index, and that's gaining traction because it's calculated from fasting triglycerides and fasting glucose. So no insulin is needed. And the recent NHANES study data suggests that it may actually predict heart failure or risk better than HOMO IR. And it's the kind of the marker that could be reasonably easily done and it might be a part of a routine practice in the next few years.

SPEAKER_00 15:54

And if someone does find out that they're insulin resistant, what's the most powerful thing that they should do or that they can do?

SPEAKER_01 16:01

Do you really want me to answer this? Because I think I've beaten this to its death. So let me beat this again. Move your muscles. Of every intervention I have as a physician, including medications, including my rotational atherectomy, intravascular lithotripsy, the stents, impellers, including all of that. The single most powerful tool for reversing insulin resistance is exercise. And specifically the right kind of exercise. Here's the physiology, and this is why I'm gonna nod out. Bear with me. It's beautiful and it's worth understanding. Your skeletal muscles, your biceps and your triceps and your quads and your hamstrings and your glutes, it's the largest glucose disposal organ in your body. So after a meal, somewhere between 70 to 80 percent of your glucose, which goes into your bloodstream, is taken up by the muscle, not by your liver or your fat. It is your muscle. So when your muscle is metabolically healthy and well-trained, it pulls the glucose right out of your blood with very little insulin. And your muscle is sedentary and it is small, it doesn't pull insulin well. And your pancreas has to now overproduce the insulin to push it in. So muscle health is insulin sensitivity. Okay? And I mean, I can't just say generic exercise. That'll be like generic prescription. Let me consolidate it even more. There are two specific tools that have the strongest evidence. Strength training, resistant training increases the size and the number of glucose uptake transporters, the molecular machines that literally pull the glucose into the muscle. Glucose uptake transporters, right? A single resistant session improves insulin sensitivity for up to two days. So if you do three sessions a week over a month, you can reduce your HOMO IR by 30 to 40% in some patients. Now, the next category, cardio, builds mitochondrial density, which allows the muscle to oxidize fat as a fuel source. So the more mitochondria you have, the more metabolically flexible you become. The diabetes prevention program on landmark NIH trial showed that lifestyle intervention reduced progression to diabetes from insulin resistance by 58%. Metformin reduced it by 31%. So lifestyle was nearly twice as effective as medication. Let that sit there for a minute. The most powerful drug we have for diabetes is not metformin, it's exercise. So when patients ask me whether to start lifestyle change first or the medication, my answer is almost always lifestyle, but with a proper structure, properly monitored to give it a real chance to work.

SPEAKER_00 19:02

Absolutely. And speaking about lifestyle, diet obviously plays a significant role too. So what does the evidence actually say? Is it sugar, refined carbs, is it ultra-processed food? Uh is there an option for all of the above?

SPEAKER_01 19:16

Then that's what I'm going to choose. It's all of the above, truly, but there is a specific order of importance. We talked about sugar. Fiber is sugar, refined carbs is sugar, beetroot is sugar, carrots is sugar, but it's not the same as pizza, pasta, candy, etc. So the most important dietary lever, supported by the strongest evidence, is reducing ultra-processed food intake. The 2019 Hall study at NIH again put adults in a metabolic ward, fed them either ultra-processed or whole food diet batched for calories, sugar, fat, and fiber and macronutrients. The ultra-processed group ate 500 more calories spontaneously. They gained weight and showed worse metabolic markers. Same calories on paper, but they had different physiological responses. Ultraprocessed food is a metabolic event and not just a nutrient delivery system. So after that, in the order of impact, comes your refined carbs and your added sugar. Beverages are the worst offenders. They bypass satiety mechanisms, which are built in by million years of evolution and delivers glucose fructose load directly to the liver, driving fatty liver and insulin resistance. The fructose pathway specifically promotes hepatic insulin resistance. Now, moving on to excess refined seed oils relative to whole fat food. This one is more debated than the influenza ecosystem suggests. The strongest evidence is for the total ultra-processed food intake, with industrial oils being a component. So I tell patients cook with olive oil, butter, or ghee, use whole foods. Don't fall into the seed oil. Panic without context. Now, ultimately, you need adequate proteins. Insulin sensitivity depends on muscle. Muscles require protein. Most adults under eat protein, especially women. We are such big culprits of this. So aim for 1.2 to 1.6 grams per kilogram of your ideal body weight, not your actual body weight. What I tell my patients not to do is don't chase diets, okay? Mediterranean diet, DASH diet, low carb, whole 30, all of them work because they reduce the ultra processed food intake. The pattern matters more than the label. So don't get fixated on the oh, I'm on a Mediterranean diet. I'm on low carb. Nothing matters. Just if you avoid ultra processed food and eat real food, then you're Doing all of these diets.

SPEAKER_00 22:01

Absolutely. And how does sleep and stress and visceral fat all feed in?

SPEAKER_01 22:07

Uh, they're all parts of the same loop. So ignoring them is why so many of my motivated patients can't seem to move their numbers despite exercising and eating well. So we seem to think that if I do one, everything else will change. But sometimes, in some people, that might be enough. But in some patients, you need to independent study and also do tutoring. And some people, independent study alone is enough. And some people need independent study, tutoring, and they have to sit down and auditorily listen or do practical things. So it's again, one thing alone is not enough. It's a package deal. So sleep, five days of restricted sleep. You know, if you just have six hours a night, that produces measurable insulin resistance even in young, healthy adults. The classic speech will study from 1999 in Lancet, you know, it showed it. Subsequent work from Van Quarter from the University of Chicago confirmed it many times over. Sleep is your think of your body's reset. It resets your cortisol, your growth hormone, your autonomic system, your brain lymph clears it out. Without it, your next morning, you are functionally insulin resistant, even if you weren't the day before. So if you keep piling it on, it's going to show. The same way with chronic stress. If you had a one stressful day, sure, your body could catch up. Sustained cortisol level elevates both visceral fat accumulation and insulin resistance. And the mechanism is very direct. Cortisol signals the liver to release insulin to your tissues. And your tissues learn to resist the insulin because it wants the blood glucose levels to be high. So even if your pancreas is pumping out insulin, the cortisol prevents your tissues from seeing it. So that's why people in high stress environments, even thin people, can develop metabolic syndrome. Visceral fat, the fat around your organs, differs completely different from your fat in your thighs and fat in your arms because visceral fat is metabolically active. It releases pro-inflammatory cytokines, free fatty acids, directly into your portal circulation, which hits your liver first and creates insulin resistance right at the source. You can have a normal BMI and still be visceral fat dominant. This is what we call thin on the outside, fat on the inside phenotype. The honest message I give patients is you can out-exercise some of this, but you cannot outrun bad sleep, chronic stress, excess visceral fat. All three need to be addressed. They are not soft factors. It's hard biology at play here.

SPEAKER_00 24:52

Absolutely. And what about certain populations, which you kind of touched on earlier? For example, South Asians, East Asians, and certain populations seem to develop this at a lower BMI. So why is that?

SPEAKER_01 25:04

So, you know, this is very personal for me, okay. As a South Asian woman, I see this in my community every day. And I see it in my patient panel as well. South Asians develop insulin resistance type 2 diabetes, atherospherosis at a lower BMI than Caucasian populations. The reason is body composition. Just because you have a normal BMI by Western standards, it does not matter for South Asians because at 22 or 23, we tend to carry more visceral fat, less skeletal muscle relative to our body size. That's the worst possible body composition for insulin sensitivity. The classic name, again, thin on the outside, fat on the inside phenotype. And they, these patients, but they just have really brittle coronary artery disease even by the time they are 40s. So the BMI the South Asians need to look at is 23 and not 27 for the Caucasians. So having said that, we've talked about BMI and we've beaten that horse to its death also. BMI is a tool created by the insurance companies. So I would not focus on BMI, but rather work on body composition. So again, what we talked about in our previous episode, you don't need to go to a fancy lab to get your VO2 max. You don't need to go to a fancy lab and expose yourself to radiation to figure out what your BMI is. You can calculate it, you can measure it. Yes, it's not 100%, but it's enough. You have in-body scales right now, and there are so many of them, which tells your body composition. Again, don't look at the number, look at the trend. Look at your muscle mass. Your muscle mass should be going up and your fat percentage should be going down. That's how I would look at it, rather than focusing on a single number.

SPEAKER_00 26:56

And what are some of the biggest mistakes that you see patients make when they try to interpret this on their own?

SPEAKER_01 27:02

One, trusting your normal lab ranges as if they were optimal. Okay, so normal versus optimal. When your lipid triglyceride says it's under 150, that's the clinical cutoff for treatment, but that's not the optimal. Remember, I told you your triglycerides needs to be a double-digit number and not a triple-digit number. Same way for fasting glucose. Under 100 is normal, but it's not optimal. I want it under 95. The labs were built for diagnosing and population-based, but it was not meant to define metabolic health. So most of the patients who think they are fine, they're kind of sitting on the upper edge of normal, but at the lower end of the disease. And number two is chasing single numbers in isolation. I talked about this earlier, right? Body composition, not a single number of fat composition. You need fat and muscle and the trend of it. But don't get obsessed just with your LDL. You want your trichylesterite HDL ratio, or you have a great cholesterol on paper, but your fasting insulin is 18. That's the insulin-resistant pattern. So you have to put it all together. And then finally, uh, my favorite and something which I love to hate and truly hate is supplements. If you really think one supplement or tons of supplements is going to fix all your metabolic problems, it's just not going to happen. Like berberine, it's an alpha lipoic acid, chromium cinnamon. Yes, they all have small effects on insulin sensitivity. Small, but none of that comes close to regular exercise, sleep, and not eating ultra-processed food. I am anti-supplement, but I also believe in supplements which can actually be of benefits. But I am anti-illusion. You know, spend $40 and $50 or $100 on different supplements, but skip on the work that actually works, or skip on the labs which gives you more meaning. You know, that's not, that's just not going to overall get you to your goal, which is a healthy, meaningful quality and quantity of life. The shift I want the listeners to make is from what number is wrong or what pill I can take is what is the pattern showing me and what is it asking me to do differently. That's what I want the listeners to take from this.

SPEAKER_00 29:30

And what about glucose monitors? So continuous glucose monitors are now something that's available over the counter. Do you think that every adult should be wearing one?

SPEAKER_01 29:39

Honest answer, no, but also qualified yes for right reasons. It's a nuanced topic, okay? So in 2024, FTA approved the first over-the-counter continuous glucose monitors for non-diabetic. Stello by Dexcom, Lingo by Abbott, the wellness industry just pounced on it, and every podcast is telling you to watch your blood sugar post-meal spikes, okay? But here's what the real evidence shows. A 2025 study from Mass General Brigham Hospital looked at nearly 1,000 adults wearing continuous glucose monitors and found that in non-diabetic individuals, CGM metrics largely don't correlate with hemoglobin AM and C, meaning that they're not measuring what they think they're measuring. The Harvard Health Review the same year concluded there is no evidence that healthy non-diabetics derive any long-term benefit from continuous glucose monitoring. That said, here is the qualified yes. There is one use case where CGMs are genuinely valuable. Wearing one for 14 days can be used as a learning tool, not a chronic monitor, as an experiment. You can see how rice affects versus oatmeal. You can see how a bad night of sleep elevates your glucose the next day. And you can also see how a 15-minute walk after dinner blunts your post-meal spike. That kind of personal data can change your behavior. But do you need to wear it to actually change your behavior? Because we already know that if you eat ultra-processed food, you're gonna get a blood sugar spike. If you don't have a good night's sleep, you're gonna have a blood glucose spike. You know, any sort of movement after a meal plants your post-meal spike. You know all of this, but if believing is the kind of person you are, then go for it, do it for 14 days, learn the tools, learn all the things, and use it to change your behavior. But what I don't want to happen, and what is actually happening, this continuous obsession with physiological spikes and ending up with restricting food in unhelpful ways and just going like Nazi about it. It's just increasing your stress and then ultimately increasing information in your body.

SPEAKER_00 32:01

Absolutely. And what is the future of insulin resistance detection and management? Where do you think about that?

SPEAKER_01 32:08

The future of insulin resistance detection and management is moving really fast. The first place I will look at is the multi-omic risk scoring. AM models are combining variable data, lab values, genetic risk, metabolic markers to predict insulin resistance before it shows up clinically. A 2025 paper out of Stanford uses variable data plus routine blood work and was able to predict insulin resistance very accurately in healthy individuals. This is the direction, not one number, but a predicted metabolic trajectory. Number two is early pharmacological intervention, the GLP1 revolution. We can't talk about insulin resistance without talking about GLP1. So the semaglutide and trisepatide, they were designed for semaglutide and trisepatide. They were designed for diabetes and obesity. The 2023 select trial showed semaglutide reduced major adverse cardiovascular events by 20% in non-diabetic adults with diabetes, with obesity and existing cardiovascular disease. So we are going to see these drugs move earlier into the disease into people with insulin resistance whose diabetes hasn't set in as yet because the cardiovascular outcomes are too compelling to ignore. Then finally, personalized nutrition algorithms. The 2015 Weisman study by Segel and LNF showed that two healthy people can have wildly different glucose responses to the same meal. And that machine learning can predict an individual response with a high degree of accuracy. This is going to mature into routine clinical practice. Imagine a patient walking into my clinic with a six-month CGM trace plus their genome and an AI, which gives me a list of specific foods that drive that personal insulin spikes. That will pretty much change how I prescribe from eat better to eat this specific carbohydrate in this specific proportion at this specific time of the day. The future of metabolic medicine isn't about catching disease earlier with the same blunt tools. It's about a completely different resolution of signal. And insulin resistance is the most actionable upstream variable we have access to.

SPEAKER_00 34:28

Absolutely. And if listeners can take one thing from this episode, what would it mean?

SPEAKER_01 34:33

By the time your blood sugar becomes high, you have been sick for over a decade. So insulin resistance is the upstream cause of most of what we treat in the hospital. Heart attacks, strokes, fatty liver, cognitive decline, several cancer. And unfortunately, it is invisible to standard screening for years. So the fix, frankly, not glamorous, like everything I usually say, move your body, sleep enough, get real food, manage your stress, know your numbers with the basic tests you've already done in sort of fancy schmancy laboratory testing. That's the prescription from Dr. R.C. Marin. There is no pill that beats exercise. There is no supplement that replaces real food. But I hope people get empowered by it and not discouraged by the unglamorous part of what I am telling you.

SPEAKER_00 35:31

Absolutely. Thank you so much, Dr. Man. This was a really good episode and really informative as always. And I think another takeaway that I know I learned from this is what gets measured early can be changed early. So insulin resistance often develops quietly for years, but it becomes a diagnosis. But it's also one of the most reversible drivers of chronic disease when it's caught in time. So I think it's important for everyone to know your numbers, make sure you build the muscle, sleep well, eat real food, move daily, manage stress, and small habits now really do become major outcomes later. So a lot of good key takeaways from this episode. Thank you so much. As always, it was a great episode of Infinite Health. And until next time, invest in your health before you're forced to fight for it. And make sure you follow and subscribe to the show and share with someone who it resonates with. And it was great speaking with you as always, and I can't wait for our next episode. Same your Leila.