Podcast 34 - Cardio Metabolic Syndrome (Part 2 of 3)

Transcription

Dr. Chad: This is Dr. Chad Edwards and you’re listening to podcast number 34 of Against the Grain.
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Welcome to Against the Grain podcast, with Dr. Chad Edwardss, where he challenges the status quo when it comes to medicine. We get into hot topics in the medical field with real stories from real patients to help you on your way to healthy lifestyle. Get ready, because we are about to go Against the Grain.
Welcome to against the grain podcast with Dr. Chad Edwards where he challenges the status quo when it comes to medicine. We get into hot topics in the medical field with real stories from real patients to help you on your way to a healthy lifestyle. Get ready, because we’re about to go against the grain Tulsa Prolotherapy.
Marshall Morris: Hello, hello, this is Marshall Morris, and today I am joined by Dr. Chad Edwards, who believes that 80% of medical recommendations are crap; technically, speaking here. He is the author of Revolutionize Your Health With Customized Supplements and he also served in the US Army for 23 years, as both an enlisted soldier and as an officer, as a physician. He graduated from Medical School at Oklahoma State University and he’s the founder of revolutionhealth.org, as well as Against the Grain podcast. Dr. Edwards, thank you so much for joining us today.
Dr. Chad: Always, always a pleasure. And I am ready to get right into it with our hot topic.
Marshall: Let’s do it. So this is the second part of a three part series, and we’re talking about insulin and a number of different things associated with it. So what is this hot topic?
Dr. Chad: Yes, so today we’re going to talk about the cardiometabolic syndrome. When I went to medical school a graduated in 2004, we actually called it syndrome X at that time, because we were just seeing a constellation of problems, and it wasn’t diabetes but we’ve got all these abnormal things, and as I’ve looked at this physiology, I’m like, “Guys, this all makes sense. It’s all part of the same thing.” We as physicians will take things and we’ll put them in this nice little box and we’ll say, “This is diabetes, and unless you qualify for the criteria that puts you in that box then there’s not a problem, there’s not a disease.” And human physiology doesn’t work that way. There’s a little physiologic difference between Hemoglobin A1c 6.4 and 6.5. It’s just a number.
We are all on this spectrum, and some people have a disease on the far end of the spectrum, and on the other end of the spectrum you have optimal physiology, and there’s a spectrum of how our physiology works. We define disease, because we see increased problems, increased negative outcomes because of certain criteria and patients that have a Hemoglobin A1c of 6.5 or greater are at increased risk of X, and you’d fill in the blanks with any disease with any metric, and that’s how we do this.
So when you look at something like metabolic syndrome, it didn’t qualify as the disease. Now we’ve come back and kind of made a disease about this. But if you look at the physiology, again, when you treat a patient if you’re all about the health and not about the disease, then — I mean the two are mutually exclusive. You can’t be healthy and have a disease. You can’t have a disease and be healthy. They’re mutually exclusive. So when you focus on the health, you don’t have to worry about the disease. Again, it’s a paradigm shift in the way that we think Tulsa Prolotherapy.
One of these days if I ever get my act together and finish my book, it’s the big one that I’m willing to write. One of the things that I talk about is ICD-9/ICD-10 coding, which stands for the International Classification of Disease. It’s how the entire medical system works. Every patient comes in, they get a diagnosis code. If you don’t have a diagnosis, there’s not a code for that. So the whole system is not a health care system, it’s a sick care system. So this is part of that 80% of crap. This is ridiculous. Focus on health, not on sickness. All right, I’m off my soapbox. [laughter]
So, we’re going to talk about metabolic syndrome. Metabolic syndrome is abnormal physiology, and let’s be clear about that. It’s a multiplex risk factor that arises from insulin resistance; we talked about insulin and the resistance of insulin, which accompanies an abnormal adipose deposition and function. So you’ve got excess fat and the fat doesn’t function normally and your physiology doesn’t function normally. And this cardiometabolic syndrome is a risk factor for several things such as diabetes. So you’re at higher risk for diabetes, you’re at higher risk for fatty liver, you’re at higher risk for a multiplex of cancers, and for cardiovascular disease, or having heart attacks and strokes and things like that, and we’ve seen that in a number of patients.
We have criteria for metabolic syndrome. Now, again, we’ve got this box and you have to meet criteria in order to be put in the box, if that makes sense. So there are a couple of different criteria for metabolic syndrome. There’s the World Health Organization criteria and there’s the ATP III criteria or the Adult Treatment Panel III, which is the one I tend to follow. You got to have three or more of the following things: one is waist circumference. So if your waist is too big, your pant size basically. If it’s too big; for men it’s above 40 inches, for women it’s above 35 inches.
The second category is hypertriglyceridemia. Back in the part one of this three-part series we talked about triglycerides and if your fasting triglycerides are greater than 150, and again I talked about 100, because I’m looking at optimal physiology, not disease. They’re saying hypertriglyceridemia above 150 milligrams per deciliter, that would be a second criteria.
The third one is a low HDL. HDL is that High-density lipoprotein that you’ll get on a standard cholesterol test. For men it’s less than 40, for women it’s less than 50. And elevated blood pressure, greater than 135, over 85, so not qualified as hypertension, but your blood pressure is creeping up. And finally fasting glucose greater than 100. Again, not diabetic, but there’s a problem here.
We’ve put all these things together. So you’ve got five things: waist circumference, triglycerides, HDL, blood pressure, and blood sugar. Those are the criteria that we look at for metabolic syndrome. Some people may wonder why do you care about metabolic syndrome? Why should you care about metabolic syndrome? Well, some statistics on this. 20%-25% of the world’s population have metabolic syndrome.
Marshall: Wait, how many?
Dr. Chad: 20%-25%.
Marshall: So, one in four people, one in five people?
Dr. Chad: That’s correct.
Marshall: That’s crazy.
Dr. Chad: Across the globe.
Marshall: Across the globe.
Dr. Chad: Yes. There is a threefold, 300% increase in the risk of heart attacks and strokes. 300%. If you want to do something to lower risk of cardiovascular disease and strokes, then fix your blood sugar stuff. That’s where this all relates to insulin blood sugar. 300%. So it’s shocking Tulsa Prolotherapy.
200% increase in mortality, if you do have a heart attack or a stroke. So you double your risk of dying from that. And you’re five times more likely to develop diabetes. Well, duh, I mean that’s like if you’re driving from Tulsa to Oklahoma City and you’re on I44, then you’ve dramatically increased your chances of getting to Oklahoma City. This is on the same pathway as diabetes. It’s a different process, or we’re not there yet but you’re already on that process.
So why do people get cardiometabolic disease and metabolic syndrome? We always scratch our heads in traditional medicine and we try and come up with all of these fancy reasons for this, and the one that we’re going to talk about in the next series, I’ll touch on here, and it’s really interesting, and some of the research that’s coming out on this stuff is just fascinating.
The first one is that this causes “idiopathic” meaning we don’t know, but there are a number of things that play into it. Insulin resistance, we talked about insulin in the first one, and its resistance. Obesity, physical inactivity, aging, you know, the older we get, proinflammatory conditions like autoimmune diseases, and all kinds of inflammatory conditions, hormonal challenges, and gut dysbiosis. And again that’s going to be the focus of the next podcast.
All of this stuff in my opinion relates to insulin and its effectiveness in normalizing physiology. So I would argue that this is an insulin resistance problem almost exclusively.
So we talked a little bit about the physiology of insulin in the first part of this series, and again, just a brief recap as insulin goes into the cells, or it goes to the receptor, it causes blood sugar levels to come down and it changes the hormones in certain things that stores fat, it changes the way your mitochondria will perform what’s called beta-oxidation, and actually burn fat. So one of the by-products of burning fat are ketones. That’s why, on the Atkins diet they want you to measure ketones, because it tells you that you’re actually burning more fat. Type 1 diabetics are going to have higher levels of ketones. So quite interesting how this physiology works. Two other hormones I want to touch on briefly before and then we’ll take a break, Leptin. Leptin is a hormone that they identified as kind of the ‘satiety hormone’. Leptin comes from the Greek word leptos which means thin.
Marshall: What does the ‘satiety hormone’ mean?
Dr. Chad: Thank you. So satiety has to do with hunger. When you’re satiated, you’re full.
Marshall: It measures how — it sends that message to the brain?
Dr. Chad: Exactly Tulsa Prolotherapy.
Marshall: They find that when people don’t have Leptin that they don’t stop eating. They’re not getting that signal.
Dr. Chad: Sure.
Marshall: Just like with insulin resistance, there’s Leptin resistance, and we actually measure Leptin in our patients. And if you have a lot of Leptin, then there’s a high suspicion that you may have some Leptin resistance. So you’ve got the hormone, it’s just not getting to the receptor.
Leptin levels are decreased with sleep deprivation, increased testosterone, physical exercise, short-term fasting, those kinds of things. If you have too much Leptin, then all of those things can help. Leptin levels are high with sleep apnea, emotional stress, too much estrogen, dexamethasone, insulin, obesity, all those kinds of things. So Leptin also helps to regulate your fat stores.
Then you have another hormone Adiponectin. Adiponectin and Leptin are both secreted from fat cells. They are secreted from adipocytes. Adiponectin plays an important role in the action of insulin and in cardiovascular health. It can enhance beta-oxidation, that’s that burning of fat that we talked about, and it can suppress gluconeogenic enzymes. Gluconeogenic means we’re making new sugar and we are able to make our own sugar in many cells and definitely in the liver. Adiponectin counteracts that lipotoxic effects of obesity and Type 2 diabetes that leads to insulin resistance. So we want some good levels of Adiponectin.
It also enhances endothelial function. We talked a little bit about endothelial function in a previous podcast, and it inhibits atherogenesis, the development of plaque. So you can see how insulin, glucose, all of these hormones play a role in cardiovascular disease. Ideally, we want our Adiponectin levels about 14 mg/mm. And when you have low levels of Adiponectin, it increases — there’s an association with a higher risk of Type 2 diabetes. Now we can take that break.
Dr. Chad: So we’ll take a quick break and then when we come back we’re going to get into more on the cardiometabolic syndrome.
Marshall: Yes.
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Marshall: All right, we are back with Dr. Chad Edwards here and we’re talking about the cardiometabolic syndrome and as it relates to insulin and insulin resistance. Dr. Edwards, let’s get into it. You’ve mentioned a lot of these different hormones that are kind of associated with it and talked a lot about the different criteria for measuring it, the things that contribute to the precursory things that contribute to it. Let’s tie it all together for everyone.
Dr. Chad: Yes. So insulin has an effect at its receptor, which is on many, many, many cells. So fat cells, muscle cells, liver cells, hepatocytes, the main ones that we’re talking about here. And you can have insulin resistance, which means that the receptor doesn’t accept that hormone. It doesn’t have the same effect. It may only work 50% of the efficiency with which it worked before. Your body will increase the production of insulin, make more insulin, so that it kind of forces that affect. Then we see now we have higher levels of circulating insulins and we see more fat deposition. We see, you’re not burning fat as an energy source, all of these kinds of things. Then that alters in conjunction with other things high levels of blood sugar and insulin are also proinflammatory conditions, and things like stress. And stress a plays a major role in a lot of our physiologic problems in the US. Under stress you have high levels of cortisol. Cortisol induces insulin resistance, so it further plays into this. So if you are stressed out and every time you drive to work, and you’re white knuckling that steering wheel, and you got too many things going on, you just sold a house and bought land, and you just got married, and yet — I’m talking about myself about the stress. So if you’ve got all these things and you’ve got all of this stress, you probably have higher levels of cortisol, which induces insulin resistance and is the beginning steps of this whole cardiometabolic process Tulsa Prolotherapy.
So in treating our patients we have to mitigate each one of those, and again stress plays a big role. But measuring Leptin levels, measuring Adiponectin levels, we’re looking at risk. How does your physiology work? Properly identifying the true problem, which is the underlying physiology, and then focusing on lifestyle changes, supplements, and if we need to, medications, to minimize the risks of this getting worse while we’re working on the underlying problem to normalize that physiology so that we don’t go down this pathway. Did that kind of give a good recap?
Marshall: Yes, absolutely. So it sounds like there’s a lot of things that kind of — it’s a domino effect.
Dr. Chad: Absolutely.
Marshall: Stress, just a very superficial level one, is most people think, “Oh, well, it’s just a little bit of stress. It’s just a tough part of my job. It’s not going to affect the hormones and lead to syndromes, and lead to even following things,” diabetes in a number of these different things. But it starts at that very first level, and that’s what addressing the overall health of a patient really is, is reducing those precursor stress levels, or diets, or nutrition, or like you said the optimal physiology of the body.
Dr. Chad: Absolutely, without question. All of those things without question play a role in this whole physiologic process. I’d like to mention two more hormone pathways and then we’ll talk about some things that we can kind of do to help mitigate — specifically to help mitigate this stuff.
So the first one. Well, these two together are called incretins, and they are hormones that — when you eat and you’re eating glucose — before the break we talked about how your body is able to make glucose on its own, a process called gluconeogenesis. When you eat, you don’t need to make your own glucose. Especially if you’re eating carbohydrates. So you have this hormone path we call the incretins that helps regulate when you eat, are you making glucose, are you not.
One of the things that we see with Type 2 diabetics is even though they’re eating a carbohydrate meal, their physiology still produces — it makes its own glucose further driving up insulin. More stuff that your system has to deal with, producing more fats, all of these kinds of things.
So there’s a problem with these incretins, so this is a target for Type 2 diabetes management from the pharmacologic perspective. The first one is Glucagon-like peptide-1 or GLP-1. These are medication — well, they’re hormones, but from the medication sense, they’re subcutaneous injections. The first one that came out I think was BYETTA, and you got these injections which helps regulate the system. We see naturally these hormones that are produced in the enteroendocrine cells, which is throughout the small and large intestines. So entero meaning the gut, basically, and endocrine meaning that they are the hormones released from these cells, enteroendocrine cells. We also make these things in the brainstem. We see these incretins increase with carbs, protein, and fat. So when you eat higher levels of these things come out. Type 2 diabetics don’t have as much. This stuff increases insulin, decreases glucagon, and there are decreased levels in obese patients. That’s kind of that whole thing. So we don’t have enough of them, so in response to this stuff, your physiology is messed up and it further exacerbates that condition.
So you can give patients these GLP-1s analogs like BYETTA, the other names are — Victoza is one of them. With those medications we’ll often see some weight loss, because, again, we’re targeting the underlying physiology. So from a medication perspective I would far rather have a medication like this than one like sulfonylurea, which is our class of medications that just simply squeezes your pancreas and kicks out more insulin. Some patients need something like that, but I want to target that physiology. Some patients don’t want to take an injection and they can take an oral medication which is a DPP-4 inhibitor and that’s a certain protein that breaks down the GLP-1 chemical. One you’re giving the chemical, the other one you’re preventing breaking it down.
These DPP-4 inhibitors are oral medications and we see that the DPP-4 proteins, or the action of this is decreased in bariatric patients, so patients that have had gastric bypass and things like that. It’s one of the ways that that surgery helps the physiology. To be clear, I am not an advocate for that procedure. I think it’s awful and barbaric, but we do see improvement in physiology. I think you can get there with aggressive lifestyle management.
So those are two other hormones that I think it’s important to understand and it’s a target for Type 2 diabetes. We will give these medications. I would argue that they maybe beneficial earlier before you actually have a disease. To be clear, insurance most certainly will not cover these medications. They’re more expensive, you don’t have a diagnosis of diabetes so the insurance company is going to say, “You don’t need them.” That’s why you need to be an advocate for your own health and not wait on the insurance company to save you, and we’ll talk about that more on some other day.
So with this cardiometabolic syndrome, we’re talking about higher levels of insulin, insulin resistance, how this whole thing comes together, you got too much fat, because of this insulin, all of those things. Touch on one more component of this and then we’ll tie it altogether. Adipose tissue itself it’s — if you see people with the belly rolls, that’s excess fat tissue. Adipose tissue, certainly, it has several functions, and the first one that we would I think probably all understand is that it’s an energy storage. It’s a forum where we store those fats.
But it is also a very active endocrine organ. So it has a lot of endocrine function. It has hormones. We’ve talked about Leptin and Adiponectin and all those kinds of things. That helps coordinate the hormonal metabolic inflammatory and neurohumoral activities. That’s a big way of saying, it controls a lot of stuff. Fat tissues’ certain components are proinflammatory and it’ll secrete certain hormones like Interleukin 6, TNF-alpha, monocytes, chemoattractant protein-1, Interleukin 8, all those kinds of things. It does have some anti-inflammatory effect and it secretes some chemicals interleukin 1 RA, interleukin 10, and Adiponectin, we talked on that a minute ago. But he proinflammatory component is dominant in whole body metabolism.
Omental fat, so inside the lining. If you see a guy with a beer belly and he’s got an outie. his belly button is pushing out, that’s because he’s got increased intra-abdominal fat, and that is what we call omental fat, and it is particularly inflammatory. That is why one of the criteria for metabolic syndrome is waist circumference. Because if you’re depositing most of your fat in that omental area, we know that that’s an increased risk. So this helps explain why.
So what do we do about this? Well, again, go look at the underlying physiology, lifestyle, lifestyle, lifestyle, reduce stress, increase your exercise. I would argue that lower carbohydrate diets tend to help quite a bit more, but I would say clean nutrition. And we’re going to touch specifically on some components of nutrition in a minute, or in the next podcast on what we can do and why some of the stuff takes place. And then there are certainly some supplements that can help. We mentioned in the first podcast, chromium. If you’re chromium deficient, insulin doesn’t work as efficiently at the receptor.
And there are a number of herbal medic aid or herbal supplements like GYMNEMA, Senulin, I mean there’s all kinds of things that can be very beneficial at reducing that insulin resistance, optimizing the function of insulin, and those kinds of things. We can always use medications if we’re failing at those.
If your blood sugar levels are rising your insulin resistance is increasing or doing all these other things, then you may need medications to manage your blood sugar. High levels of insulin are problematic, but high levels of glucose are more problematic. It’s choose the lower poison.
Marshall: Sure. So this is the second part of a three-part series. The first part we’re talking about what is insulin and what’s the function of insulin, and began to get in some insulin resistance. The second part really covers the cardiometabolic syndrome. What are we talking about in the third part for the listeners following along?
Dr. Chad: Yes, we’re going to talk about the gut microbiome, and that means the bacteria in your gut. It’s really interesting, some of the research that’s out on this stuff and what changes the gut microbiome. Really, really interesting stuff. I did a presentation in November of 2015 at a medical conference on this topic and it’s just really, really interesting stuff.
Marshall: Cool. Thank you so much for today Dr. Edwards and I appreciate you coming in.
Dr. Chad: Thanks, man. Well, see you soon.
Announcer: Thanks for listening to this week’s podcast with Dr. Chad Edwards. Tune in next week where we’ll be going against the grain.