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Detecting and Managing Insulin Resistance

On-Demand Webinar

Health & Wellness

Diabetes is a significant burden on patients, physicians, and our healthcare system. Insulin resistance occurs gradually, years to decades before the diagnosis of diabetes. In this webinar, Dr Atul Sachdev will describe the prevalence of insulin-resistance and biomarkers beyond glucose and HbA1c that can be used for detection and management of insulin resistance. 


Learning objectives:

–    Explain the importance of insulin resistance across the cardiometabolic continuum
–    Identify which patients may be candidates for insulin resistance testing
–    Describe what steps to take to identify and manage insulin resistance


Atul Sachdev, MD
Clinical Assistant Professor, Department of Family and Community Medicine, Baylor College of Medicine, San Jacinto Methodist Hospital, Baytown, TX


Time of talk: 50 minutes

Apr 15, 2019

Just a little bit about myself. In the meantime, I have a membership based practice, family practice in Baytown, Texas. And I’m not saying that, so you’ll feel sorry for me, but because I want you to understand that I have a lot of experience with insulin resistance. See, Baytown is a blue collar town, and my patients love to eat. In fact, the only time they take a break from eating is to smoke. So nearly every one of my patients has insulin resistance. The ones who don’t are usually visiting from like California. As prevalent as it is here, I have no doubt that all of you have plenty of patients who have insulin resistance. In fact, it’s prevalence in the United States is increasing in epidemic proportions. So let’s take a look at some numbers. So the prevalence of obesity in America is 93 million people. That’s 40% of all adults and 18% of all children. The prevalence of insulin resistance, which of course is the main topic of the day, is 70 million people in the United States. And the important thing to know about that is this occurs 10 to 20 years before the diagnosis of diabetes. The prevalence of pre-diabetes is 84 million people. That’s one in three adults, and 90% of them don’t know that they have it. And diabetes has a prevalence of 30 million people. That’s nearly 10% of our population. And a quarter of them don’t know that they have diabetes either. Have you ever wondered how we know that they’re diabetic when they don’t know and why nobody’s telling them? That’s kind of a main secret to keep. But of course, we all know the typical complications associated with diabetes. They’re listed on the right, including blindness, renal failure, vascular disease and so on. So what exactly is insulin resistance? Insulin resistance, which I’ll refer to as IR moving forward because I’m lazy, is defined as a state of diminished cellular response to the actions of insulin. Its onset is gradual. It’s difficult to recognize clinically because of fasting glucose or in A1C will not detect it. Furthermore, you can’t trust clinical signs such as obesity to identify IR because not everyone who becomes diabetic, as you know, is overweight. Of course, left untreated, IR will progress to pre-diabetes and diabetes. But what’s important to note is that other associated diseases and conditions are occurring while the patient is insulin resistant, including hypertension, fatty liver disease, PCOS, vascular disease, and even certain cancers. So let’s take a look at the natural progression of type two diabetes. I’m a big fan of using analogies to explain concepts to my patients, so bear with me on this one. This is a new analogy I’m trying out. So if you imagine that my wife represents a beta cell function and her voice is insulin secretion, her voice that’s telling me to change the light bulbs and put weedkiller on our lawn than my ability to tune her out would be insulin resistance. So as my ability to tune her out continues to get stronger, as you see there at the beginning of the graph, she’s initially able to compensate by raising her voice until she’s practically yelling into my ear while I’m trying to watch the football game. As you can see in this example, it works for about seven years. My wife would say it’s more like seven months as I’m forced to turn off the football game and do these chores. You know, these annoying things and therefore maintaining homeostasis, which is the Latin term meaning to stay married. Now, as you see later as my ability to tune her out, get stronger, her voice, thank the Lord, gets weaker and I finally get to keep watching my football game. And her voice eventually fades to the point where she barely has enough voice left to contact her attorney. Now, here’s the problem When that happens, while I get to watch my football game, we lose homeostasis. None of our lights work. The lawn is dead and so is our marriage. That’s actually very depressing in that analogy. I probably won’t use it with patients, but what’s important here is that all of this could have been prevented in that 12 year window at the beginning. So why aren’t we doing that as physicians? So let’s take a look at why we’re not testing commonly in the health care field. Most health care providers don’t even test for IR because it’s an earlier indicator of risk, and they consider IR and diabetes to be similar conditions. They feel that they’re looking at IR to some extent by measuring a fasting glucose in an A1C which, as you just saw, are rather late indicators in the disease process. Health care providers often cite a lack of clinically actionable tests that quantify IR as well as a perceived high cost as reasons for not testing. Providers who are testing for IR typically looking at things like insulin, c-peptide, fasting glucose, maybe a glucose tolerance test, or certain panels such as lipid markers or a commonly used homa IR equation or score. These traditional methods for determining insulin resistance do have advantages and disadvantages. So let’s look at some of these traditional methods in more detail. The gold standard for determining IR is the hyperinsulinemic-euglycemic clamp or the HEC or the IST, which is the insulin suppression test. They do directly measure the actions of insulin, but they’re invasive, time consuming, and expensive. So if you do this in your practice, I would be impressed by you and concerned about you at the same time. How about using surrogate insulin markers like fasting insulin and fasting glucose? Insulin is specifically associated and correlated with IR, but until recently there have been no standardized insulin assays, and that prevents a quantitative comparison across platforms. In other words, tests that you might get from one lab may differ greatly from a different lab. How about using lipid markers like triglyceride HDL ratio or the LP-IR score? And until recently, this is what I was actually using to determine IR in my patients. They do correlate well with IR, but they do lack markers that are specific to IR, including insulin and c-peptide. Then there’s a multi marker approach which fails to produce an interpretive IR score that can be meaningfully tracked over time. So here’s what I use now in my practice to look at IR. This is called the Cardio IQ Insulin Resistance Panel with score available through Quest Labs or otherwise known as the IR Score. The IR score combines fasting, insulin and c-peptide measurements to evaluate the likelihood that an individual has IR. It’s the first commercially available liquid chromatography assay for either ANALYTE. It’s been validated in a Stanford University study against the IST member, the gold standard I talked about in the last slide. It’s been standardized to peptide mass measurements, meaning the reference point will not change and it enables a universally applicable quantitative assessment with well-defined cut points and reference intervals. This is that validation study that I was referring to from Stanford looking at 535 apparently healthy individuals. And you can see on the graph above that the IR score outperformed measurements of C-PEPTIDE and measurements of insulin in determining which patients actually have insulin resistance. And in the lower graph, you can see where the IR score also outperformed the triglyceride HDL ratio and the Homa IR equation. So how do you interpret this score? The IR score is reported as a number between 1 and 100, and it reports the probability of IR rather than a positive or negative result per se. The results are divided into 3 tiers or tertiles with an IR score of 1 to 33 indicating a normal insulin sensitivity. Patients with an IR score between 33 and 66 are more than 4 times more likely to have IR, and those who score in the highest tier are greater than 15 times more likely to have IR. What’s important to realize here is that this test will identify IR patients that a glucose or an A1C would miss. It will also reliably identify patients who don’t have typical clinical signs, such as metabolic syndrome or diabetes. So who should we test with this? Obviously, those with typical clinical manifestations such as your overweight patients, patients with central obesity, hypertension, acanthosis, and those with a family history of diabetes or a history of gestational diabetes. However, given the prevalence of insulin resistance like we talked about and the fact that even lean patients can have this condition, I personally feel strongly that all patients need to be tested. So in summary, the existing assays we’ve had up on up until this point cannot reliably or reproducibly assess IR knowing that IR is associated with future risk of prediabetes, diabetes, cardiovascular events, fatty liver disease and IR score like this can be useful in identifying those patients at risk even in the absence of clinical signs of IR. Therefore, it can help you identify patients who may be candidates for further evaluation, and that includes those patients, for example, who may need more intensive dietary or lifestyle intervention to prevent diabetes and diabetes, people who may need monitoring and tracking of their vascular disease to prevent heart attacks, strokes, Alzheimer’s disease and patients who may have fatty liver disease, which may require further evaluation. So let’s take a look at an actual clinical application of this score in my practice. This is a patient of mine named James. Obviously, I’m not using his real name in order to protect his identity because his real name is Mark. So, Mark, I mean, James came in in July of last year with in A1C, sorry, a fasting glucose that was elevated at 115. His fasting insulin was elevated at 24.3 and his A1C was for the first time elevated above 6.5, which is in the diabetic range. Now, we would technically need to repeat this test on another day to confirm the result to officially diagnose him with diabetes. But he doesn’t know that. The next few numbers are associated more with insulin resistance, including the LDL particle count, which was elevated, his oxidized LDL, which is associated both with vascular disease and his risk for future metabolic syndrome, was 37, which is technically within the normal range, and his weight was 230 pounds, which would have been just fine if he was six foot ten, but instead he was five foot eight. So I told him that we could start medication for his diabetes and vascular risk, but I usually like to give my patients the option to try a trial of lifestyle changes first, which is what he opted to do. We discussed dietary and exercise changes, which I’ll talk more about later, and he agreed to come back in 3 months, which ended up being 7 months later, and his numbers looked very different. I intentionally showed him these 3 numbers first. Why do you ask? Well, if you calm down and quit interrupting, I’ll tell you in a minute. So I said, James, your fasting sugar is lower, your fasting insulin is lower and your A1C is now normal. Does this make sense to you? And as I expected, he had this puzzled look on his face and he said, to be honest, Doc, I expected the numbers to be worse because I just spent 2 months at home in the Philippines and my diet was horrible. I drank a lot of coke, ate a lot of desserts, and hardly exercised at all. I then told him that I already knew that. But if you’re a physician who happens to be listening today and you’re looking only at these markers of glycemic control, you would have missed this. So how did I know? Because his insulin markers, the markers more specific to his insulin and insulin resistance were higher than last time. His LDL particle count, for example, was up, his oxidized LDL was up, and of course, his weight was up an additional 10 pounds from last time. Unfortunately, he was still five foot eight inches tall. But here’s what really stood out. Now, we didn’t have the IR-score when we last checked him back in July because it was offered to us after that point. But we did this time when he came in last month and it was very telling he was in the highest tier because his c-peptide level was so elevated at 3.66. Upper limit of normal is 2.16. This is a good example of an IR-score telling you something that the other typical parameters did not. Well, we often assume that the insulin and sugar traveled together. I see this commonly in my practice. In fact, I often see the opposite situation where the A1C and fasting glucose are temporarily higher when the patient has lost weight and insulin parameters are much better. If you’re not looking at IR then you might end up negatively reinforcing the patients who are actually doing much better with diet and lifestyle. So how do we help our patients address this problem once it’s identified? I educate them. I tell them what’s responsible for this pandemic and what’s driving their insulin up. Causing obesity, IR, prediabetes, diabetes, vascular disease and all the things we just talked about. And the answer is sugar in particular, fructose. If we understand that sugar is responsible for this pandemic of IR we understand that sugar is by far the biggest threat to the health of our population because it’s IR that drives the vast majority of vascular disease and even infections and cancers. I found it interesting that CVS announced in October of 2014 that it had decided to stop the sale of tobacco at their stores. The president and CEO of CVS Caremark, Larry J. Merlo, said, quote, Put simply, the sale of tobacco products is inconsistent with our purpose. End quote. But apparently, Larry, the sale of M&M, Snickers and Butterfinger bars place at eye level of all of our children is consistent with their purpose. I’m not saying that addressing tobacco is a bad thing, but today, if you just look at the statistics, 14% of the population smoke cigarettes well, compared with 42% in the 1960s. But what percentage of our patient population do you think consumes candy bars and sodas? Sugar is just a different but far more prevalent drug that is equally, if not more devastating than tobacco. Even with regard to vascular disease, CVS would have done us a much bigger favor if they removed all of the candy and soda and continued selling cigarettes. And I’m not singling out CVS by any means. They at least tried to do something. The entire food industry is in on this because sugar is highly addictive and they’re in the business of creating lifelong customers. This is the slide I borrowed from Dr. Lustig, who I’ll introduce to you later. This is called the Coca-Cola Conspiracy, and it shows how the standard serving size of a soda has changed dramatically over time. The average serving size of a Coke in 1915 was six and a half ounces. I don’t know if any of you remember that. I certainly don’t because I’m in my twenties. But the number below the container size, by the way, in this picture indicates the amount of weight gain that one can expect in a year by consuming one container per day. So the serving size increased to ten ounces in 1955 with the advent of vending machines, and five years later in 1960, the ubiquitous 12 ounce can made its first appearance. Then in 1988 came the super sized sodas of various names, including Big Gulps, King Size and Thirst Busters. And finally, in 1992 came what is still considered a standard sized soda today, the 20 ounce bottle, which is actually 2 1/2 servings and 3 times the size of a Coke from 1915. The other important change with soda came in the 1980s when the industry switched to using high fructose corn syrup as a sweetener instead of sugar because it was not only cheaper but also sweeter and more addictive than sugar. As it turns out, it was much more devastating from an insulin perspective than sugar was. As time goes by, we’re drinking more and more of our sugar in the form of high fructose corn syrup which there are even sneaking into drinks that are presented as healthy alternatives to sodas such as Gatorade, VitaminWater and Orange Juice. And when your insulin is sky high from drinking all of these sweetened beverages, so is your appetite. And a regular Big Mac just doesn’t cut it anymore. So why not deep fry it to make it more satisfying? I have no doubt that this was invented in Baytown, Texas. So a lot of people point to a lack of exercise to explain this epidemic of obesity and IR in the United States. While it’s true that this is a factor and that there are certainly clear benefits with exercise, it’s also clear that exercise does not make up for a bad diet. If you subscribe to the calories in, calories out train of thinking, you would have to swim for about an hour and 12 minutes to make up for one medium order of French fries. The problem is generally not as simple as we’re not burning enough calories as many would like to think. For example, we currently have an epidemic of obese six month olds. Is this baby obese because he’s not exercising enough? There are certainly maternal and gestational factors, but the sugar problem affecting a lot of our children starts as babies with the formula we’re feeding them. These are the ingredients in Isomil formula. And the number one ingredient is corn syrup solids, which is basically just sugar. And it makes up 39% of the formula. And if that’s not enough sugar, added sugar in the form of sucrose makes up an additional 10% of the ingredients. So from day one, many of our babies are practically drinking milkshakes all day, every day. If you haven’t done so already, I highly recommend that you check out Dr. Robert Lustig on YouTube. He’s a pediatric endocrinologist at UCSF, and he has a video entitled The Bitter Truth About Sugar and Fructose. He makes the point that the obesity epidemic coincides with the introduction of high fructose corn syrup to our society in 1975 and the fact that we now consume 63 pounds of it per person per year. He calls fructose a metabolic disaster in the body, and I couldn’t agree any more. Another thing worth checking out is this documentary available on Netflix called Fed Up. It’s narrated by Katie Couric, and it chronicles the history of this obesity epidemic that we’re dealing with, as well as the lives of a few children who are battling their obesity, often unsuccessfully. Just a little tidbit. One of the few kids chronicled in this movie is actually from Baytown, Texas. No joke. Anyways, we played this movie from time to time in our waiting room, and I recommend it to all my patients as I’m recommending it to you. There are 600,000 food items in America, 80% of which have added sugar. To confuse the public even more, the food industry has numerous different names for sugar, and here’s 56 of them on this slide alone. The patients who are making an effort to decrease or eliminate their consumption of sugar and who are reading nutritional labels may not fully understand that Dexedrine and cane juice crystals are alternative words for sugar. So how do we guide our insulin resistant patients when this addictive and metabolically disastrous substance is so ubiquitous in our society? What’s work best for me and my patients has been a ketogenic diet. Now I realize that diets are very controversial and that most experts don’t even agree on what diet is the best. I also realize that there is not one specific diet that works for all patients and that it has to be individualized. My purpose for presenting this to you is not to stir up a debate on which diet is the best. Rather, I’m showing you what I found to be the most effective in the most patients with regard to addressing IR in my practice. So this is what I tell them. I tell them for three weeks or longer if they have a lot of weight to lose, don’t consume any grains. That’s breads, pasta, cereals, chips, tortillas, bagels. No what we call bad carbs, rice, potatoes, corn, carrots, peas and even fruit? No dairy. That includes milk, cheeses, creams, yogurts and no caffeine. Coffees, teas, sodas, energy drinks, etc.. Now, I know a few of you have probably already taken exception to some of these items such as fruit, maybe cheese, caffeine. There are a lot of versions of the ketogenic diet, for example, that include cheese and caffeine. And I do believe that a number of patients will have great success even including those items. But I’ve found that if you want 100% success, eliminating even those items will basically lead to a more rapid improvement in insulin status. What can you eat on this diet? Basically, meats, vegetables. Remember, corn is not a vegetable. We tell patients it’s a grain, eggs, nuts, seeds and of course, primarily water to drink or decaffeinated tea. It’s important to forewarn your patients about the keto flu. Not all patients will experience this, but most will. It’s basically a sugar withdrawal phenomenon and it does resolve on its own after about 5 to 10 days on the average. After that, the patient becomes what we call keto adapted to enough of a degree where they’re not experiencing the flu symptoms and they begin to lose weight rapidly. They feel much more energy, experience mental clarity that they probably haven’t had in years. So I tell patients, if you feel miserable, you’re probably doing it right. What’s important to note here, though, is that there’s a lot more freedom in this diet after those initial few weeks of strict carb restriction. Many patients, for example, if they can maintain that eating for long enough, can later reintroduce a modest intake of fruit, complex carbohydrates, etc.. In other words, the total elimination of carbs is not permanent nor sustainable, in my opinion. So let’s look at a case where we used that particular intervention with one of our patients. Sandy came to me frustrated because she wasn’t able to lose any weight. I always ask them to take me through a typical day with regard to what they normally eat for breakfast, lunch, dinner, as well as any snacks. And this is what she told me for breakfast. She’ll typically have a spinach and kale fruit smoothie, or on some days she might have oatmeal, steel cut. She drinks black coffee. She takes care not to add any sweetener or cream. For lunch she would typically have a turkey sandwich on whole grain bread. The beverage would be either iced tea unsweetened with or water and lemon. The formula for dinner is typically a meat, vegetable. She did admit that occasionally when circumstances arose that she would have fast food. And it is very important to ask your patients what they mean by occasionally. For some patients, that means every day. But she seemed to indicate that this would happen maybe once every 1 to 2 months. Her beverage again would be unsweetened iced tea or water with lemon. And then this took a little prying, but we found out that her evening ritual was to have a small cup of bluebell ice cream. They make bluebell ice cream just 2 hours away from us. So for some reason, a lot of my patients feel obligated to eat it. So this was our intervention. We wanted her to replace her kale and fruit smoothie with or oatmeal with eggs, bacon, sausage, ham, vegetables, any combination of those things. I also tell my patients that there’s no law saying that they have to eat breakfast food for breakfast. They can eat lunch or dinner items at that time. The beverage again, water with lemon or decaf tea for lunch. She would typically have, let’s say, a chicken breast salad, roll, deli meat, vegetables. There are a lot of very creative options for ketogenic meals on Pinterest and other websites like that. Again, the beverage. water with lemon or decaf tea. Dinner, the formula was to be meat, vegetables, salad and same beverages and the evening snack instead of bluebell ice cream, nuts. And she thought I was nuts, by the way. So this is what happened. So after years of being relatively stagnant in terms of her weight loss efforts, she ended up dropping close to 50 pounds. Her A1C again, after years of being essentially in a pre-diabetic range, dropped from 6.0 down to 5.2. I check F2-IsoProstanes in my practice. I do a lot of heart attack and stroke prevention and this is an indicator of vascular risk, but it also tracks nicely with lifestyle changes. And you can see here that it improved dramatically. Her LDL cholesterol decreased modestly, so it dropped from 130 to, let’s say, around 107 or so. But what’s even more important than that is that her particle count decreased significantly. This is what’s most associated with insulin resistance. Our goal is to try to get a particle count to less than 1000. Less than 850 is ideal and you can see that she’s well on her way. As I mentioned earlier, I was typically using an LP-IR score to help determine insulin status because we didn’t have this IR score that I just described to you back then. But you can see it moved from a highly abnormal range down into the normal range. This is one of the vascular markers that’s very closely associated with the risk of heart attacks and strokes called the Lp-PLA2. And after years of progressively increasing, you can see that this diet addressing her insulin resistance caused her to turn the corner. And a very similar story with myeloperoxidase again, vascular risk marker went from abnormal back down into the normal range. So in summary, I’m hoping that you’ve learned the following things. Number one, don’t tune out your wife. Number two, the prevalence of insulin resistance is epidemic. It’s likely extremely prevalent in your practice, whether you realize it or not. Insulin resistance is directly or indirectly associated with many important diseases. Again, not just a progression to prediabetes and diabetes, but fatty liver disease, obesity, cardiovascular disease, stroke and many others. And if you identify this early and treat it, we can actually prevent and even reverse a lot of these adverse outcomes. Thank you for your attention. Thank you so much, Dr. Sachdev. That was fabulous. Really appreciate it. We have we’re now at the time where we can take your questions. I do see them coming in on the chat. But before we get to some of those, Amber, our operator is there and she’s going to review the instructions for a live question. Thank you. So now begin the question and answer session. And to ask a question on following, you may press star 1 and record your name slowly and clearly when prompted. To withdraw, you may dial star 2. One moment as we wait for the questions. Well, they’re flying in through the chat. So we’ll start with Gillian’s question. What are your thoughts on the carcinogenic effects or cardiovascular effects of processed meat such as deli meats? I do think that’s an important thing to consider. I do generally try to tell my patients to, avoid processed meat. And so I think it’s certainly a good idea to consider that in your recommendations. But again, one of the main goals here is to eliminate the things that are driving insulin up when it comes to insulin resistance. But that’s a very good point. Dr. Sachdev, you were talking about your your case study. So when asked could you can you reiterate again why James Mark’s fasting insulin went down on the recent testing? So I cannot but I can tell you that I see it quite commonly when everything points to a situation where you would think the fasting insulin would be much higher for some reason it’s not. I suspect, you know, since there are so many factors that can impact a fasting insulin level, um, could maybe even be rather than a long term marker, something that he had done just the night before. Maybe some elements of cortisol stress. So what I found over time is that fasting insulin can be used perhaps as a general guidepost, but it’s not, for example, as reliable as, let’s say an A1C, which gives us a pretty reliable indicator of an average sugar over the previous 60 to 90 days. So, um, I can just tell you that I’ve learned not to rely too, too much on a fasting insulin. And this is a case where the fasting insulin clearly didn’t match up with what he had been doing in the preceding months. Thank you. We’re going to check with the operator to see if there’s any live questions. Yes, we have two questions on queue and first will be coming from James Davis. New line is now open. James, your line is open. You may proceed for the question. Good morning, Doctor. Thank you for the thorough briefing on IR I just wanted to ask you, you had mentioned that the test is standardized for this, Quest has this standardized. And I wanted to find out, is it standardized for adult patients only or is it standardized for adolescents and children as well as far as the measures and the levels? My understanding is that it is standardized using adult patients based on that Stanford study. But that is something that, uh, can be clarified. Yeah, I just got word that it is for adult patients. Um, nobody under 18 apparently was in that study. Okay. Thank you for the clarification. Thank you. Good point. Thank you. The next question will be coming from Dr. is I heard. Your line is open. Hello. Good morning, Doctor. My question is related to a recent. Over the past few years, there have been a lot of discussions about the impact of vitamin K2 on this insulin resistance or sensitivity at the cellular level. Have you come across anything that either endorse or confirms or actually deny if there is any impact of vitamin K2 on insulin sensitivity? I can tell you that I’ve heard the same information in the past. I do happen to use a lot of vitamin K2 because of its role in vitamin D absorption, and we’re very aggressive about vitamin D replacement here for vascular reasons and a number of other reasons. But I’m not aware of any specific studies that I guess have been definitive in that area either supporting or refuting that concept. All right. Thank you. Sure. Thank you. Thank you. We have a few more questions on queue. The next one will be coming from Dr. Ariana Bender. Your line is open. Yes. Thank you for the presentation. My question is, in a seemingly healthy person, how often do you check for IR and what is the ICD-10 code which would make it covered for the insurance? Who is the insurance? So my practice is an M.D. VIP affiliated practice. So we are able to do that testing at least once a year outside of insurance. So unfortunately I don’t know that I would be able to help you with a specific ICD-10 code for that. And again, Cleveland HeartLab can give you some more information. But generally speaking, ICD-10 codes related to diabetes or diabetes risk should work for that. But again, our patients typically get this testing under a panel that we order annually through M.D. VIP. Well, I’m in the M.D. VIP doctor as well, and I don’t know which panel contains it. I’m looking at the Cleveland HeartLab M.D. VIP panel. Yeah, for the annual wellness panel. Yeah. So they we actually I think you’re you’re correct about that because we put that on the third party rec and I don’t know if you’re familiar with the CHL program that they told us about it. Yes. M.D. VIP, where there’s a limited additional cost if it is not, you know, covered under a commercial plan. But I’m told that the IR score is actually pretty well covered under just about any ICD-10 codes related to diabetes risk. Hmm. Okay. My other question was what does caffeine do wrong? Yeah. Yeah. So, again, we have plenty of cases where the patients do consume caffeine. There’s this whole concept of bulletproof coffee out there. The theory with that approach is that the problem isn’t the caffeine itself, but the various mold spores that are present in a majority of our coffee in the United States. So they say if you get a mold free coffee, you don’t have that issue with insulin. But there are some genetics involved. There’s a certain gene anomaly that some people have where caffeine does seem to directly interfere with glycemic control in diabetics and metabolic syndrome. But the theory there is that caffeine tends to be associated with increased cortisol levels. And then the idea is that the higher cortisol levels lead to more dumping of sugar into the system by the liver, which therefore interferes with insulin. But again, I do think a majority of patients will still enjoy great success, even including the caffeine. But I have had a number of patients report that their weight loss and their ability to meet their health goals was increased markedly when they quit coffee. Mm hmm. Okay. Thank you. You’re welcome. Thank you. Thank you. Another question on queue coming from Dr. David DiPietro. Your line is open. Yeah, hello. The question would be, you know, say you have a person who has done lifestyle modifications other than metformin. Do you find any medications that can be used to decrease insulin sensitivity and perhaps, you know, decrease their particle number such as Actos, etc.? Absolutely. Yeah. I feel there are several things we do aside from lifestyle changes to help certain patients. GLP-1 therapy, for example, just by virtue of its association with weight loss and to some degree even the SGLT2 agents, anything basically that leads to weight loss will of course end up addressing insulin resistance. I do use Pioglitazone quite a bit, especially if there’s a lot of vascular inflammation. However, I tend to use only 15 milligrams of pioglitazone. As you know, there’s a lot of controversy out there now around these TZD agents and but I feel like you get plenty of effect with regarding regarding a reducing insulin resistance with even a small dose like 15 milligrams and to boot less swelling and weight gain. Find that changes the particle number? I do yeah. So generally speaking, whatever intervention ends up leading to a decrease in insulin resistance will essentially, by default, address the particle number. If I find that hard to push with a statin alone. That is absolutely right, yeah, because the statin, of course, is very good at reducing LDL, but the particle number seems much more tied in to insulin resistance. So you can have somebody with a very reasonable LDL, but a bad particle count. Turning out some studies on particle number, you have the cardiologist in the area saying all that doesn’t mean anything. You know, particle number means nothing, which makes me look bad. Right. Yes. I don’t know that I can quote him at the moment, but I do know there’s some data out there supporting that for sure. Particle number and cardiovascular risk. Okay. Thank you. Thank you. Thank you. No, we’re going to jump back. Operator, we’re going to jump back to some of the chat questions if there’s no more live questions. Yes, no further questions on queue. Okay. So, Dr. Sachdev, lots and lots of questions about the keto diet, questions about can you can you would quinoa be restricted because it’s a seed? Is there a way to measure the actual carbohydrate content of foods? Is the keto diet worth the risk of? And I’m not familiar with this word keto. Ketonuria? Any Can you give us a little bit more on the keto diet? Yeah, I think quinoa is a reasonable choice actually, so I don’t have a major problem with that. Nuts and seeds are technically included in in this diet that we profess. And again, the strict restriction is mostly in the first few weeks or so to get them to that adapted state and essentially detox them from sugar. And after that, certainly I wouldn’t worry a whole lot about quinoa. But again, as far as measuring carbohydrates in food, you know, it’s you have nutritional labels and things like that, but this is really more about the hormonal impact from insulin. In other words, the carbs, not a carb necessarily. So I would look more at the source of the carbohydrates. And when you pick sources that contain fiber, generally speaking, the impact on insulin goes down dramatically. So that’s why fruit, for example, if you do consume fruit later, is a lot better than getting your carbs from Oreo cookies. You know, even if you have the an equal carb load between the two, the effect on insulin is very, very different. Thank you. So, yeah, go ahead. Another question, can you re-introduce calcium people are worried about the effects of no calcium in the diet. Sure. Yeah. We often recommend calcium and magnesium. You know, they come often together as a supplement because one of the complications that can happen with a keto diet is electrolyte changes, imbalances. You end up releasing a lot of retained water in the process of going through all of this. So constipation can become an issue. So when you add calcium slash magnesium, you often end up addressing that pretty well as well. Thank you so much. I’m going to turn back to some questions about the testing. How often do you follow up IR testing after you’ve initially diagnosed someone with it? So I think a lot of it depends on for me, you know, again, one of my big focuses is in preventing heart attacks and strokes. So we watch vascular disease very, very closely. So if I have somebody with a bad insulin situation, you know, a lot of insulin resistance, but their vascular inflammation is still reasonably controlled, I’ll usually do a six month interval. And on the other hand, if they have a concerning level of vascular inflammation, then we’ll typically see them back in 3 months and we’ll look at that again because, again, this is generally going to be one of the bigger driving forces of vascular disease. Thank you so much. Again, a couple of questions about the Ketonuria. I’m sorry. Biggest concern on the keto diet, I guess it’s a ketone in the urine. So is that something you worry about? I don’t, honestly. We’ve had many, many patients go through this over many years and I haven’t really seen that to be an issue. Generally speaking, the ketones in the urine happen for about a month as they become keto adapted. Then the ketones generally quit appearing in the urine. Thank you. How. How much do you use insulin resistance to guide medications? I do. I do use it again. If we ultimately you know, we’re we are worried about the progression to pre-diabetes and diabetes. But again, in my mind, the biggest deal is its dramatic effect on vascular inflammation. Mm hmm. So if you have somebody with quite a bit of vascular inflammation, then you know, other than diet and lifestyle, like the previous caller mentioned, that’s a situation where I might bring in pharmaceutical agents and, you know, things like that to address it more aggressively. And like I said, we’ll typically monitor more aggressively as well. So GLP-1s, TZDs, low dose, you know, things like that. Thank you. Do you see an elevation in total cholesterol in LDL with the higher fat ketogenic diet? You see it at first and 9 times out of 10, that’s because they’re losing a lot of weight. So it’s it’s what we call the LDL bump and it scares people at first. You’ll see in some cases the LDL will jump 50, 60, 70 points when their baseline was much lower. And it’s basically the fat leaving the body. It’s on the way out. It’s being transported through the blood. So, yes, you do see it at first, but if you hang in there and check it again, a few months later, you often see that it stabilizes and normalizes at a much lower level. But the fat in the blood isn’t from the fat you’re eating. The fat in the blood is typically made out of fructose. So I’ve seen situations where people are on, let’s say, an extreme version of a ketogenic diet like the Atkins diet, and they eat nothing but butter and lard and bacon and all those things. And conversely, as you might not expect, their cholesterol levels plummet because they’re cutting out sugar, which is really what drives the cholesterol upward.

Page Published: October 17, 2023