Back Clinic Metabolic Syndrome Functional Medicine Team. This is a group of conditions that include increased blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol or triglyceride levels. These occur together, increasing an individual’s risk of heart disease, stroke, and diabetes. Having just one of these conditions doesn’t mean an individual has metabolic syndrome. However, any of these conditions increase the risk of serious disease. Having more than one of these might increase the risk even more. Most of the disorders associated with metabolic syndrome have no symptoms.
However, a large waist circumference is a visible sign. In addition, if an individual’s blood sugar is very high, they might have signs and symptoms of diabetes, including increased thirst, urination, fatigue, and blurred vision. This syndrome is closely linked to overweight/obesity and inactivity. It’s also linked to a condition called insulin resistance. Normally, the digestive system breaks down foods into sugar (glucose). Insulin is a hormone made by the pancreas that helps sugar enter the cells to fuel. People with insulin resistance their cells don’t normally respond to insulin, and glucose can’t enter the cells as easily. As a result, glucose levels in the blood rise despite the body’s attempt to control the glucose by churning out more and more insulin.
In today’s podcast, Dr. Alex Jimenez DC, Health Coach Kenna Vaughn, Truide Torres, Alexander Jimenez, and Astrid Ornelas discuss and focus on a deeper look at understanding metabolic syndrome.
Dr. Alex Jimenez DC*: It is a special day, guys. Today we’re going to be talking about metabolic syndrome. We’re going to be focusing on the sciences and the understanding of what metabolic syndrome is. Today, we’re going to be bringing out some specialists and people from all over the globe in different directions to discuss the topics of metabolic disorders and how it affects people in our local communities. The particular issue that we’re going to be talking about today is metabolic syndrome. Metabolic syndrome affects a whole lot of people now in terms of it to be diagnosed with metabolic syndrome; we have to have a couple of disorders situations that present them that are things such as blood sugar issues, high blood pressure, the ability to have triglycerides off high-density lipoproteins and also the measurements of belly fat in our diet. So today, one of the remarkable things that we’re going to be doing is bringing a panel to us to you guys to see what metabolic syndrome is now. Today is a special day because we’re going live on Facebook Live, and we’re presenting the information for the first time. So this is our first go at it, guys. So give us a thumbs up if you feel we did well. If not, let us also know because we’re learning and going through a process to get to our communities and teach them about metabolic disorders. Today, we have Astrid Ornelas, who will be talking about metabolic syndrome and specific dietary nutritional dynamics to help improve it. We also have Kenna Vaughn, which is our coach, that’s going to be discussing how we interact with patients. We also have our patient here, Trudy, a live individual who has had metabolic syndrome. And in the distance, we also have Alexander Jimenez, who’s out at the National Unity, Health Science, and Medical School, to discuss the associated and linked to metabolic disorders to give us detailed information. Detailed insights as to what metabolic syndrome is and how it affects our communities. Now what to be critical about it is, is this is a severe subject matter. It seems kind of that we chose this particular topic because that it’s affecting so many people. So many of my patients that we see today, even though I have a musculoskeletal practice, are directly related to inflammatory disorders. And when we’re dealing with inflammatory issues, we’re going to be dealing with insulin and how it affects the body. Now, as insulin goes in this process, every one of these particular dynamics that we’re going to be discussing and our future podcasts when we deal with metabolic syndrome is directly related to insulin and its effects on the body. So as we go through these dynamics, what we want to do is we want to bring out each point. I can present today Kenna Vaughn; who will be talking about what happens when we offer a patient and what we do when a patient has metabolic disorders? So we’re going to present it to Kenna. Kenna, can you tell us a bit about what happens when a patient presents with metabolic syndrome, what they look for, what we look for, how we assess it, and how we treat the issues?
Kenna Vaughn: I’d love to. So when the patient first comes in, and we see those signs of metabolic syndrome, the patient isn’t always aware because, on their own, these symptoms that make up metabolic syndrome are not necessarily a red flag. However, when we start to see them getting combined, we realize that we need to take control of this right now. So when that patient first comes in, and they’re telling us about the symptoms that they’re having, we start tracking it, and we make a detailed history on them to see if it’s something that has been going on for a long time, if it’s more recent, things like that. And then we’re going to take it from there. And we do more detailed lab work, and then we look at the kind of even their genetics. Genetics is a huge part of it. And we see what diet would best work for them and just make those realistic goals. But we also really want to make sure we give them that education they need to be successful. Education is tremendous, especially when it comes to something that can be as confusing as metabolic syndrome.
Dr. Alex Jimenez DC*: We discuss how we can give our patients take home dynamics and things of value to change the metabolic syndrome once we determine that someone has metabolic issues. Now the whole idea is to create a direct path from the kitchen to genetics. And somehow someway we have to bring science to the kitchen to understand what we can eat and what we can do and how we can avoid certain foods to change the dynamics expressed at our genetic code level. So we’re going to try to give a little bit of broad, you know, expansive understanding of the processes that can take on each of these five particular issues. One at a time. So in terms of, let’s say, the kitchen, how do we help people help themselves in the kitchen, Kenna?
Kenna Vaughn: One thing that we love to do in the kitchen is smoothies. Smoothies are so beneficial because not only are you feeding your body the proper nutrients you need. You can also provide the right nutrients to your cells, which will make the difference inside your body. And you’ll still feel satisfied and full, not going to be something that’s, you know, you’re left hungry like you just ate a little bit of birdseed. So it’s something that I recommend everybody starts with. One great thing to add to those smoothies is going to be flax seeds. So flax seeds are very high in fiber, a good fiber. So if you put those flax seeds into the blender first and blend them up, opening them up, you start adding in your healthy fats like avocados to make your smoothie nice and smooth. And the almond milk, low calorie, and low carb fruits, things like that. It’s going to just unleash a powerhouse inside that gut. So one main thing that it’s going to do is the fiber is going to stick around. So it’s going to feed your prebiotics and your probiotics every single bug in that gut. And it’s also going to help take things out of your body system that usually gets reabsorbed, such as salt, and let it be able to get excreted the way that it should be, rather than sticking around, like I said, getting reabsorbed and just causing these underlying issues.
Dr. Alex Jimenez DC*: So these dynamics and mainly when dealing with flaxseed, I know Alexander knows a bit of the flax seed dynamics in terms of how it works with cholesterol. And that’s one of the issues, the HDL component. Tell me a bit of what you’re what you’ve seen in terms of the flaxseed, Alex, in terms of our experiences with flaxseed and diminishment of cholesterol and helping out with metabolic syndrome.
Alexander Isaiah: So, flaxseeds are suitable not only for nutrients but like Kenna said, they’re outstanding in dietary fiber. So we have to ask ourselves, why is dietary fiber essential? We can’t digest it, but it can bind to other things that are within our gut. And one of the main things that it does to lower cholesterol is it binds to bile. Now, bile from our gallbladder is around ninety-five percent cholesterol. And I’m sorry, 80 percent cholesterol and ninety-five percent of it gets recycled and reused most of the time. So why have a large amount of fiber within the gut? The fiber binds to the cholesterol. The body’s mechanism to compensate for that is to pull cholesterol from other parts of the body, specifically from the serum of the blood, and pull it back in to rejuvenate those levels of bile. So not only are you forcing your gut to work properly that it is meant to, but you’re also lowering your cholesterol within the inner side of the body.
Dr. Alex Jimenez DC*: So the component of cholesterol can be assisted by fiber. Now, I know that Astrid got some ideas about lowering the blood pressure and bringing a little bit of control in nutraceuticals. And in that respect, she’s been going over some particular topics, and she’s the resident scientist that helps us see the NCBI, which is the national research center that provides daily information about what’s happening with metabolic syndrome out there. So she will be presenting a little bit of some nutraceutical topics that we can touch upon at this present time. Astrid, hello.
Astrid Ornelas: Hello. So, first of all, for those people who are barely coming into the podcast who are barely coming in to listen to us. I want to bring up again what metabolic syndrome is. So metabolic syndrome, as many of you might know, it’s not a condition or disease in itself. It’s more so a cluster of a collection of, I guess, other health issues that can increase the risk of things like heart disease, stroke, and even diabetes. So with that being said, the metabolic syndrome doesn’t have any apparent symptoms, but probably one of the most visible, I guess. You know health issues that are obvious in people with metabolic syndrome is waist fat. So with that being said, some of the nutraceuticals I want to talk about today, as you can see, I’ve listed several nutraceuticals that I discussed the last time. And these nutraceuticals can help with metabolic syndrome in a variety of ways. But I added several on here that specifically target weight loss. Since, as I mentioned, one of the apparent signs of metabolic syndrome is excess waist fat. So I want to bring in one of the nutraceuticals that is that several research studies and I’ve written articles on it that can help promote weight loss in people with metabolic syndrome is niacin. Now niacin, it’s a vitamin B3, and you can usually find it when you buy those supplements that have a kind of B-complex. It has a collection of various of the different B vitamins. So niacin, several research studies have found that it can help reduce inflammation associated with obesity people that have excess weight, of course. Usually, these people have increased blood sugar and blood sugar levels, leading to inflammation. So taking B vitamins, specifically vitamin B3, or as it’s well known for niacin, can help reduce inflammation. It can also help promote metabolism, our body’s capacity to convert carbohydrates, proteins, and fats into energy. So when we take vitamin B and specifically niacin vitamin B3, I want to emphasize that research studies have found that it can help burn calories much more efficiently.
Dr. Alex Jimenez DC*: When we’re dealing with niacin and the nutraceuticals, we are going. I know Alexander’s got some issues. Are you still with us, Alexander? Yeah, I’m here. It’s OK. It’s all good. I can see that we deal with and we’re learning about our technical issues as we go through them. I’m going to go back to Astrid, specifically about belly fat. Now she had mentioned the belly fat. Let’s be very specific when we’re dealing with belly fat. We’re dealing with issues where a male has a greater than 40-inch waist. OK. And for females, they have a greater than 35. Is that correct? Yes. So when we do the measurements, that’s one of the components. So as we discuss these particular issues, we want to make sure that when we’re talking about the belly fat and the weight gains and the BMI issues and the BIA issues, it’s the basal metabolic rate and impedance assessments that we do. We’re looking for those particular aspects. So she’s mentioning in the niacin and terms of niacin, what’s your experience with niacin, Alex with your dynamics that you have put in place?
Alexander Isiah: Niacin, or vitamin B3, is an excellent vitamin B because it is a free product. It reacts to a specific response precisely where it takes hold during glycolysis and the citric acid cycle. It plays a significant role in the citric acid cycle because it is used as the pre-product to synthesize NADH. Now, if someone has metabolic syndrome, this can upregulate that citric acid cycle. So if they’re trying to burn fat or use their carbohydrates at a more efficient rate, it will help upregulate that cycle and allow them to use their mitochondrial metabolism a lot better.
Dr. Alex Jimenez DC*: That’s awesome. Now, going back to Astrid, tell me a bit about what supplements we have here. We may not get through all of them, but little by little. We’ll break this thing down, so we’ll give you guys tidbits. So that useful information so that we can take on metabolic syndrome and change people’s lives. Go ahead.
Astrid Ornelas: OK, so the next nutraceuticals I’m going to talk about, I’m going to talk about these two together vitamin D and calcium, specifically vitamin D3. I want to emphasize that. But both of these nutraceuticals can also help promote fat mass loss. And several research studies have also found that this one, just like B vitamins, just like niacin, vitamin B3, could also help improve metabolism to make the body more efficiently burn calories. And then the next nutraceuticals I want to talk about is DHEA. Now I want to, I guess, one of the things that I want to highlight about the DHEA is that, first of all, this is a hormone. This is a hormone that is naturally produced in the body. But then, of course, you know, some people can supplement it if you talk to your health care professional. And they determined that you need more DHEA in your body because your body’s not naturally producing enough of it, then they can supplement that as well. So specifically about the DHEA, according to the Washington University School of Medicine, DHEA can also help metabolize fat much more efficiently. I guess one of the things that I wanted to discuss goes together with the DHEA. So when we consume excess calories, you know, the daily caloric intake on average, according to researchers, we need to take 2000 calories. But so what happens to the body when we eat excess calories now? These calories are stored in the body as fat. So when the body naturally produces, I guess, sufficient amounts of DHEA, our body can metabolize DHEA. I mean, metabolize fat. I’m sorry, much more efficiently so that our body gets rid of excess fat rather than storing it.
Dr. Alex Jimenez DC*: Got it! So let me ask you, DHEA is a hormone, and one of the things that I notice is that it is a hormone found over the counter. And one of the unique things with some passages of recent laws is that DHEA made it through the FDA to be used over the counter. So you’ll see the product is dispersed through all the stores and depending on the quality, you can see it more every day. And the reason you see it more common over the last couple of years is that the FDA found it, and then through a loophole, it was allowed to remain in the markets. Go ahead. Kenna wants to mention something regarding this particular component in the assessment of those specific issues.
Kenna Vaughn: I was going to add something when it comes to talking about body fat and how Astrid was saying that body fat gets stored. So what happens is when you have those excess calories, you create these things in your body called triglycerides. And triglycerides are composed of glycerol and fatty acids; and however, those in general triglycerides are too big to enter that cell membrane. So what happens is another hormone that controls almost everything, and it’s called insulin, and the insulin gets called in. And from here, we have the lipo…
Dr. Alex Jimenez DC*: Lipoprotein lipase?
Kenna Vaughn: Yes, that one. It’s a tongue twister, so that gets called in and then kind of breaks those apart. The insulin is coming in again and activating something called the glut4transporter, which will open up that cell membrane. And now we’re going to see that fat cells get stored full of glucose, triglycerides, and fat. So that’s how those fat cells go from not having anything to then having those excess calories. Now they’re being converted through this process. Now they’re getting nice and full, and they’re hanging around your belly.
Dr. Alex Jimenez DC*: I’ve noticed that certain people have more efficient LPLs, which is lipoprotein lipase. Some people may say that you know what? I gain weight by just looking at food, and it may happen more as you get older. A whole different control system controls this particular issue. What kind of control systems are the ones that control lipoprotein lips and the glut4, along with hormone-sensitive lipase, that you have there?
Kenna Vaughn: Insulin controls everything else. And it’s like I said, it’s that hormone, and it’s going to come in. And also, on top of that, we have PH that affects enzymes, temperature, and things along that line.
Dr. Alex Jimenez DC*: You know, a lot of things that when we look at enzymes, we realize that the thing that determines the enzyme’s activity or sensitivity or ability to function is encoded in the genetics in terms of lipoprotein lipase and the breakdown of the fatty acids. I know, Alex, you have some points there in terms of the fat breakdown information. What do you have there that you can help the public understand a little bit more?
Alexander Isaiah: So, without going too much into the biochemical pathways, this is just showing the mitochondria’s inner mitochondrial matrix. So after I guess you’ve been well-fed and all your cells are satisfied with energy production through ATP synthesis, if you have overconsumption of caloric intake, specifically through glucose, you end up having a large amount of acetyl-CoA being produced or hanging around in the end here. So what the body does is buy high levels of insulin. This enzyme, called citrate synthase, is induced. So what citrate synthase does is use oxygen acetate and acetyl-CoA to make citrate. Now, citrate can then exit the mitochondrial matrix, and then significant accumulations of citrate will start accumulating in the sidewall of the cell. As that happens, ATP citrate lies will break them apart again and bring acetyl-CoA and auxtyl-acetate. Because auxtyl-acetate and acetyl-CoA don’t have specific membrane transporters, they can’t cross that mitochondrial membrane. Only specific ones like citrate do so as acetyl-CoA gets taken out into the cell; taking a look over here, we have acetyl-CoA, which gets turned into methylmalonyl-CoA. And it’s actually this enzyme acetyl-CoA carboxylic is induced by insulin. So usually, acetyl-CoA carboxylic has a phosphate group on it, which inhibits its activity. But when it interacts with insulin, insulin turns on a protein phosphatase. So phosphatase are enzymes that take phosphates off, and then it becomes acetyl-CoA carboxylic. So now acetyl-CoA carboxylic is active to make methylmalonyl-CoA. Now, why is this important? So methylmalonyl-CoA is like putting the boulder on top of the hill; you’re going to start a different chemical process. So methylmalonyl-CoA inhibits fatty acid breakdown and begins fatty acid synthesis. So when you start making methylmalonyl-CoA, you’re going to, without going too much into fatty acid synthesis. The end goal is palmitate, which is the type of fatty acid. Now, palmitate chains will combine with glucose to form triglycerides. So here, we can see how a large dietary intake of carbohydrates, glucose levels, proteins, and insulin activates triglycerides. And if you have diabetes, you pretty much get halted in specific pathways. And that’s why you end up with too much acetyl-CoA. You have too many ketone bodies floating around in the blood, so you are going through without going too much in-depth; we can see that having a large number of dietary triglycerides, large amounts of glucose will force more triglycerides or try sealed glycerol within these kinds of microns within the lumen of the blood vessels. And this is going to cause a chain of reactions. So without breaking down too much here, we’re showing where it’s all going, so we have acetyl-CoA going to methylmalonyl-CoA, going to palmitate, and then we have palmitate forming these triglycerides. So like Kenna said, these triglycerides can’t enter the adipocytes. The adipocytes are fat cells without lipoprotein lipase. So with the combination of lipoprotein lipids allows these cells to get in there. You allow for the storage of the fat, so the cool part to notice is that by doing so, the first one will use fatty acids to be your heart. The heart relies on around 80 percent of its energy from fatty acids. Then it’s going to be your muscle cells. But this is in conjunction if you’re exercising regularly. If you’re not doing that, the adipose cells will favor storing the triglycerides or triglycerol more often. And then you’re also going to use more LDL, which means you have the potential to have more oxidized LDL, causing a higher event of atherosclerosis formation.
Dr. Alex Jimenez DC*: You know, as you go through this process, it seems natural, but for a lot of us, it’s a deep, deep story, and it’s far, and it’s dynamic. And what I want to do is to bring the people back to Kenna as to the diets. In terms of getting this basic understanding. How is it that we assess an individual where these particular issues? I can assure you that when we first evaluate a metabolic syndrome patient. We do a lot of blood work, blood assessment, a lot of enzyme testing. We can even do DNA testing. So we got to go back to a patient and describe precisely how we can better improve their lives by our assessments. So, Kenna, you got some cool stuff in there for us. What do you have in front of you?
Kenna Vaughn: Yes, in front of me, I have a sample report from one of our patients on who we ran the DNA blood test. And one of those things that we can see is a gene pulled up right here, and it’s called TAS1R2. And what this gene does is it’s a tissue that can be found in the gastrointestinal tract, the hypothalamus, and the pancreas. And it’s known for regulating your metabolism and energy, and homeostasis. Also affects that food intake beyond the detection of your sweet taste on the tongue. What does that mean? So what that means is it is nicknamed the sweet gene. So, somebody with this gene is more likely to be drawn to sweet foods because it’s almost like their sweetness is enhanced. So when they taste ice cream, it’s a 10 out of 10, no matter the flavor, versus someone who doesn’t have this gene. Maybe it’s more of a seven out of 10. It hits them differently.
Dr. Alex Jimenez DC*: That makes perfect sense. Or some people that, you know, they love that ice cream and that dynamics, I know that I want to take a little bit of a detour because a lot of patients will wonder, Well, what are we going to do to get into being assessed and what kind of things we can? How does someone get? Where do they go? And for that, we have our clinical liaison here, Trudy, who walks patients in and first determines that the patient is qualified because we do have questionnaires that assess the determination of if someone is a talented individual or does have presentations that are predisposing to metabolic syndrome that require further assessment. And once we do in the situation that a person does have it, they want to understand what to do. So actually, Trudy, you do us help people and guide them through the process. What do we do in the office to help guide an individual through the beginnings of metabolic assessment?
Trudy Torres: OK, well, basically, you know, when people call in, we go ahead and email them a questionnaire. It does take about 45 minutes because it’s a very in-depth questionnaire. We want to pinpoint and get to the bottom of their main concerns. The main issues that we’re going to target for the process to be successful. Once we get that questionnaire back, we set up an appointment with Dr. Jimenez and our health coach Kenna, and they will go in-depth as far as the target areas that we need to address for the process to be successful. And that’s one of the things that I wanted to ask Kenna because I know it can be a bit overwhelming as far as what is it that they get? And as far as what is the following process? So once we get the questionnaire, I know that’s when they’re going to go ahead and do the different types of lab work to determine what will be successful in the kitchen.
Dr. Alex Jimenez DC*: I know you see the patients when they walk in; how do they feel in terms of that Trudy? What is it that they typically will tell you before being further assessed?
Trudy Torres: Well, they’re tired of, you know, all the different changes that you go through as, unfortunately, as we age. You know, some of the DNA genes that we have, that they’re dormant, you know, they become active. And that’s when you start to experience a different type of bad syndromes, you know, like metabolic syndrome. And that’s one of the things that we address. You know that we go ahead and do the DNA testing and see what different genes are dormant that are not dormant.
Dr. Alex Jimenez DC*: I think that also, you know, whether you’ve noticed too and you’ve mentioned this to me, they’re just tired of feeling bad. They’re just tired of feeling like; I guess crap is a good word, right? So they’re tired of just they don’t recover. They don’t sleep well. They feel stressed. They feel like they’re being choked with high blood pressure. It’s not. Their lives are different. They’re in distress. They don’t sleep. So these are issues that the patients present to you, and I know you help them guide them. And then, Kenna, tell me a bit of the assessment you do to qualify an individual on the metabolic syndrome programs we have?
Kenna Vaughn: Like we were saying before, we go through that detailed history to look at that family history. And then we also decide, like Miss Trudy noted, the lab work gives us a lot of these underlying answers because the lab work we do is more detailed than the basic. So we get more numbers, more genetic codes, and more of all of these things. And from there, we’re able to take it and see what will be the most successful path for this patient. What supplements are they going to be able to intake better? What diet is best for them, whether it be the ketogenic diet or the Mediterranean diet? Everybody’s body is different because everybody’s insulin sensitivity is different, and everyone’s hormones change, especially for females. It’s different than male patients, and we create that individualized package for them because we want them to leave at the end of everything, not just that first visit. Still, we want them to leave feeling empowered and healthy and strong and not just they’re alive, but that they’re living. And that makes a massive difference to their families and their friends. And just everything gets impacted, all from the start of these questionnaires.
Dr. Alex Jimenez DC*: You touched on a subject matter there about being left alone. We go through a process, and we do keep connectivity with our patients. With today’s technology, there’s no reason we can’t have a person or an individual connected to our office and give us information such as BMI BIA information, which is basal metabolic stuff, the scale weight, the fat densities. We can have this information today. We have Fitbits that connect to us, and we can understand that that data is now available in a private way, and someone on the other side is reading that tell us what you do with individuals in terms of the coaching that we offer people; for specific metabolic syndrome?
Kenna Vaughn: Of course. For coaching, we have a scale. And like Dr. Jimenez was saying, this scale not only tells you your weight, but it also sends your weight, your water intake, how much of your weight is water weight, how much of your weight is lean muscle? And it also can track it and see the percentages of where you’re changing. So we can follow that maybe the number on the scale hasn’t moved. And some people might start to feel discouraged. But when we look at the numbers of what that scale tells us, we can see that you are losing body fat and being replaced by muscle. So even though that number is the same, your body inside is chemically changing. You’re making those differences you need to make to keep up with it and not to quit because, as I said, it can be discouraging for certain people.
Dr. Alex Jimenez DC*: So there’s a Mind-Body connection here. A mental component, teamwork dynamics, is essential when we’re working through metabolic syndrome. We can’t leave people here, here, take the football and run 80 plays. No, you have to huddle in each time to discuss and change the adaptive processes. Regarding the other areas with fat analysis, I know Alex has some additional areas and Astrid that will be discussing in a few minutes. But I’m going to focus on Alex right now to tell us a bit of what people can do with exercise or fitness that could stimulate or dynamically change their metabolic processes at the biochemical level.
Alexander Isaiah: Well, I would first, in all honesty, be honest with yourself; you will probably be the best observer of your situation. We all know what foods we do well with. We all know what foods we don’t do well with. We’ve always had some intuition as we’ve grown into the people we are today, knowing what foods work well for us and what foods don’t work well for us. For example, I know that if I consume a large carbohydrate consumption, I tend to put on weight pretty quickly. But I am pretty active. So the days that I have strenuous activity, I make sure that I have a balanced meal with proteins, fats, and a decent amount of carbohydrates. But the days that I’m not very active or haven’t gone to the gym. I make sure that most of my caloric intake sometimes comes from good fats or proteins. And that’s going to be the best thing is just be honest with yourself. See how you’re doing, find your BMI, find your basal metabolic rate, and then put numbers on paper. Because if you keep track of things. Odds are you’re going to do better and control the way your body’s responding. The next thing is I would find a health coach like Kenna, to stay on track and find any recommendations. The good part is that we have the internet out there and sources like yourself, Dr. Jimenez, that can provide information to the public on a new level and be able to understand and grasp the concept from a different perspective and give people more information that they didn’t know that they had at their fingertips.
Dr. Alex Jimenez DC*: I’m going to take it back to Astrid. Thank you, Alex. But one of the things is I want people to understand we’re going to assault. We’re going to assault on metabolic syndrome because this is a big problem and affects many in all communities around the United States. And we have to have an open forum to be able to open up. And sometimes, we don’t have 10 seconds, and this is not a 10 second, two-minute thing. We must understand that there needs to be a teamwork integrative medicine approach that helps the patients. So I know we’re going to go with a couple, I don’t think we make it through all of them, but we’re going to get through as best as we can because this is all recorded and can be dynamic and time purposes used later. Tell us a bit of the omega, berberine, and all the other supplements you had planned to talk about.
Astrid Ornelas: OK. Well, first of all, for those of you who are barely coming into the podcast right now, the nutraceuticals that are currently listed up there can all help improve metabolic syndrome in one way or another. The majority of these specifically target they specifically lower help lower the risk factors that can cause that could increase the risk of developing issues like heart disease, stroke, and diabetes. But I want to emphasize several of these because they do they’re more efficient at promoting weight loss associated with metabolic syndrome. You know, if you’re going to improve metabolic syndrome, you want to promote weight loss, so that the last nutraceutical we talked about that’s up there was DHEA. The next nutraceutical I want to talk about is NRF2. So just like DHEA, it is a naturally produced hormone in our body. Well, NRF2 is also found in our body naturally. But unlike DHEA, which is a hormone, NRF2’s actual name, I guess the full name is the NRF2 pathway. It’s what’s known as a transcription factor, or it’s an element that regulates several cell processes if you will. And so I’ve done quite a few articles on this myself, and there are several research studies out there, quite a few to be exact, but NFR2 can also help improve metabolism. So if you improve your metabolism, especially in people who have metabolic syndrome, your metabolism can make it much more efficient for you to burn calories and therefore burn fat more efficiently.
Dr. Alex Jimenez DC*: The Omegas and NRF2, what we’re dealing with here, along with berberine, is inflammatory issues, OK? So what we want to deal with is when someone has metabolic syndrome, we suffer from inflammation, and inflammation is rampant. And that’s what’s causing the discomfort, the joint pain, the overall swelling, the bloating. Those are the kind of things that help, and they affect the blood pressure in insulin does happen, and we haven’t talked about that yet. But we’re going to be discussing that. I know Alex has got some ideas about Nrf2 factors and Omegas and berberine, and tell me a bit of what you’ve seen in terms of the nutraceuticals, and you read in terms of its effect on metabolic syndrome.
Alexander Isaiah: So the way we need to look at the different types of fatty acids is that most of the surface of each cell is composed of a fatty acid. It depends on what type gets incorporated based on the consumption or dietary intake that you have daily. So the main two components that your body’s going to use is cholesterol. That’s why we still need cholesterol and healthy fats that we get. But at the same time, if you’re taking in a lot of red meats, you’re also going to use arachidonic acid, which makes different types of fatty acids. And it also makes a transcription factor called PGE two, which is known for its very informative process or aspects. So what fish oils do, specifically EPA and DHEA, are by incorporating these into the cell membrane. You upregulate NRF2 and downregulate NF Kappa B, which is the inflammatory response. And not only by doing that, but as we talked about before with green tea extract and turmeric, otherwise known as curcumin. These also inhibit the pathways for inflammation. Now there could be the argument Well, do these pathways inhibit the inflammation? So let’s say I get sick or something, right? Well, the cool part is that two different pathways are stimulating the same response. By doing the dietary regimen of curcumin, fish oils, or even green tea, you’re inhibiting it from the body overexpressing these genes. Now, suppose you still get sick in a sense, right. In that case, you could still allow these cells to proliferate, specifically your macrophages, to do their job correctly, so you’re not inhibiting them by overstimulating them. You’re allowing them to be more proficient in their job. And suppose you are virally infected or with some unknown pathogen or let’s say. In that case, a cell decides to go rogue and start producing cancer cells, allowing the body to be more proficient in extracting these pathogens.
Dr. Alex Jimenez DC*: In essence, we’ve learned that if we try to suppress inflammation, we create a huge problem. The question is, let’s stop inflammation from progressing to be too extreme. So, in essence, to keep it at a workable dynamics, and that’s what these curcumins and the green teas do. I know Astrid has something to mention in terms of this particular concept. Tell me a bit about what you’re thinking.
Astrid Ornelas: Yeah. So as Alex mentioned, green tea is a fantastic drink. It’s actually in my nutraceutical list that’s up there, and I wanted to talk about green tea because it’s a very easily accessible drink, you know, for those of you who like tea. Green tea is delicious as well. And green tea has a variety of research studies demonstrated to be super beneficial for people with metabolic syndrome. So as many of you know, green tea contains caffeine. Of course, it has much less caffeine than a cup of coffee, for example, but it still does have caffeine, and green tea is also a powerful antioxidant. That’s another of the things that it’s very well known for. But just like NF2, you know that the interruptive pathway, green tea, has been demonstrated to help improve metabolism tremendously. You see, it promotes the body’s ability to burn calories, to burn fat. And because of its caffeine, I guess amount because even though it is less than a cup of coffee, but it’s just enough, it can help improve exercise performance. And you know, for those people who are looking to lose weight because of the, you know, the issues that they have associated with metabolic syndrome. Drinking green tea can help promote and improve their exercise performance so that they’re more able to engage and participate more efficiently in their exercise and physical activity to burn fat.
Dr. Alex Jimenez DC*: So basically, you’re indicating that as a good option instead of, let’s say, a whatever kind of drink or a juicy drink, it’s wise to keep sort of in the background green tea throughout the day. Is that correct? Or how much the water is good? The green tea’s good; a little bit of coffee and a little bit of this fluid is essential to keep our bodies hydrated through the process. Since it’s already available, green tea is a great option not only for metabolic processes to stop inflammation but also to help with the burning of the fat too?
Astrid Ornelas: Yeah, definitely. Green tea is a great drink. You can pretty much have it throughout your day. You know it has less caffeine than, say, you know, coffee, as I mentioned. And it will, you know, for those who have green tea, I love green tea, and I will have it. And you do get that little, that extra amount of energy. You feel it when you have green tea. But, yeah, you can have it throughout your day. And you know, it’s essential to stay hydrated, drink plenty of water. And you just want to make sure that if you do exercise enough, you don’t want to lose your electrolytes. So, you know, drink plenty of water and just stay hydrated.
Dr. Alex Jimenez DC*: I know that we’re going over there. I know that Kenna wants to speak something, and we’re going to go in that direction right now because Kenna wants to talk about specific dietary changes and things that we can do from a health coach’s point of view.
Kenna Vaughn: I just wanted to say that green tea is super beneficial from Astrid’s point. But I don’t particularly appreciate drinking green tea, which means that all hope is lost. They do have green tea and capsules as well, so you can still get all of those great benefits without actually drinking it because, for some people, it’s, you know, their coffee over tea. So you don’t have to drink the tea. You can still get all those great benefits that attitude was talking about but through capsules.
Dr. Alex Jimenez DC*: yeah, we got exciting, sneaky ways to help people. To help people understand and to come into our office. What can they do, Trudy, in terms of being facilitated in the office if they want to make, if they’re going to have questions or for any doctor, they have out wherever they may be because this is reaching far.
Trudy Torres: I know this can be very overwhelming to just the regular population. You see, we went in too deep, you know, as far as all the physiology behind it and everything else. One of the things that I can tell you is that when you call our office, we’re going to walk you step by step. You’re not going to be alone. You’re going to walk out with a lot of information and know what works for you. Like Kenna was saying, everybody’s different. This is not a cookie-cutter program. We take the time and talk one on one with everybody who walks in and make sure that when they walk out and have a lot of information with them, they also walk out with just the lab work; they will walk out with recipes. Kenna is going to be constantly following up with you. It’s a highly successful approach when you have accountability from a health coach. So you’re not going to be by yourself.
Dr. Alex Jimenez DC*: You know again where our goal is to make the kitchen to the genes and from the genes to the kitchen, we got to give the understanding maybe not of the deep biochemistry as Alex has taken us into or the nutraceutical dynamics, just know that there are ways that we can monitor. We can assess; we can periodically evaluate. We have diagnostic tools to determine blood assessments that are way beyond what was done ten years ago. We have dynamic metabolic testing in our office to determine fundamental critical aspects of weight density, the limb way to the body, and how much water you have. We use things like phase angle to assess the health of the cells and how they’re functioning. So there’s a lot that goes on in this process. So I want to take the opportunity to thank my guests today because from Alexander, all the way far on the north side of the United States, to Astrid, who assesses things at the NCBI because we need to have our finger right on the research that has been done. To our clinical liaison, which is Trudy, and one of our dynamic health coaches. I can be a health coach, but sometimes I’m with a patient, but she’s really with you all the time, and she can connect with you via email, which is Kenna. So together, we have come with an intention, and our purpose is to understand what the process is. A metabolic syndrome to break it down to deep levels will get down to them as you can see, to the genes, to the kitchen. And that’s what our goal is to educate people on how to feed our children. We intuitively know how to feed our families. Moms know what to do. However, today’s technology and research offer us the ability to break it down and specific to the sciences. And sometimes, when we get a little older, we realize that our bodies change and our genetics change, and that’s preordained based on our past, our peoples, our ontogeny, which is the generations in the past. But we have to realize that we can make a change and we can stimulate. We can activate genetic codes. We can suppress genes that want to get active if you improperly diet or do a proper diet. So our goal today is to bring this awareness, and I want to thank you guys for allowing us to listen in. We look forward to getting different subjects, maybe not as intense or dynamic, but this was our first run at the process. And we’re going to learn, and please ask questions so that we can kind of make it better for you and give you the information you need. So we thank you very much, and I want to tell you from all of us out here in El Paso that we look forward to offering the world information into metabolic syndrome that affects so many people. So thank you, guys. Thank you for everything.
In today’s podcast, Dr. Alex Jimenez, health coach Kenna Vaughn, chief editor Astrid Ornelas discuss about metabolic syndrome from a different point of view as well as, different nutraceuticals to combat inflammation.
Dr. Alex Jimenez DC*: Welcome, guys, welcome to the podcast for Dr. Jimenez and crew. We’re discussing today’s metabolic syndrome, and we’re going to be discussing it from a different point of view. We will give you excellent, useful tips that can make sense and are easily doable at home. Metabolic syndrome is a very vast concept. It contains five major issues. It has high blood glucose, it has belly fat measurements, it has triglycerides, it has HDL issues, and it pretty much has a whole conglomeration of dynamics that have to be measured in the whole reason we discuss metabolic syndrome because it affects our community very much. So, we’re going to be discussing these particular issues and how we can fix them. And give you the ability to adapt your lifestyle so that you don’t end up having. It’s one of the most important disorders affecting modern medicine today, let alone once we understand it. Everywhere you go, you’re going to see a lot of people having metabolic syndrome. And it’s part of a society, and that’s something you see in Europe as much. But in America, because we do have a lot of foods and our plates are usually bigger, we have the ability to adapt our bodies differently by just what we eat. No disorder will change so quickly and fast as a good mechanism and a good protocol to help you with metabolic disorders and metabolic syndrome. So having said that, today, we have a group of individuals. We have Astrid Ornelas and Kenna Vaughn, who will discuss and add information to help us through the process. Now, Kenna Vaughn is our health coach. She’s the one who works in our office; when I’m a practicing physician on physical medicine and when I’m working with people one on one, we have other people working with dietary issues and dietary needs. My team here is very, very good. We also have our top clinical researcher and the individual who curates much of our technology and is at the cutting edge of what we do and our sciences. It’s Mrs. Ornelas. Mrs. Ornelas or Astrid, as we call her, she’s ghetto with the knowledge. She gets nasty with science. And it’s really, really where we are. Today, we live in a world where research is coming and spitting out of the NCBI, which is the repository or PubMed, which people can see we use this information and we use what works and what does it. Not all information is accurate in PubMed because you have different points of view, but it’s almost like a finger on a pulse when we have our finger in. We can see the things that affect it. With certain keywords and certain alerts, we get notified of changes for, let’s say, dietary sugar issues or triglyceride issues with fat issues, anything about metabolic disorders. We can kind of come up with a treatment protocol that is live adapted from doctors and researchers and PhDs around the world almost instantaneously, literally even before they’re published. For example, today happens to be February 1st. It’s not, but we’ll be getting results and studies presented by the National Journal of Cardiology that will come out in March if that makes sense. So that information is early hot off the press, and Astrid helps us figure these things out and sees, “Hey, you know, we found something really hot and something to help our patients” and brings the N equals one, which is patient-doctor equals one. A patient and therapist equal one that we don’t do specific protocols for everyone in general. We do specific protocols for each person as we go through the process. So as we do this, the journey of understanding metabolic syndrome is very dynamic and very deep. We can start from just looking at someone to the bloodwork, all the way to dietary changes, to metabolic changes, all the way down to the cellular activity that it’s actively working. We measure issues with BIAs and BMI, which we have done with previous podcasts. But we can also get into the level, the genomics and the changing of the chromosomes and the telomeres in the chromosomes, which we can affect by our diet. OK. All roads lead to diets. And what I say in some weird way, all roads lead to smoothies, OK, smoothies. Because when we look at smoothies, we look at the components of smoothies and come up with dynamics that are abilities to change now. What I look for is when I look for treatments, I look at things that make people’s lives better, and how can we do this? And for all those mothers, they understand that they may not realize that they do this, but a mom doesn’t wake up saying, I’m going to give my kid food. No, she’s kind of doing a mental lavage of bringing the whole kitchen because she wants to infuse the best nutrition for their child and offer their best kind of options for their baby to go through the world or daycare or elementary school, through middle school, through high school so that the child can develop well. Nobody goes out thinking that I’m going to give my kid just junk and. And if that’s the case, well, that’s probably not good parenting. But we won’t talk about that well; we will talk about good nutrition and adapting those things. So I’d like to introduce Kenna right now. And she’s going to be discussing a little bit of what we do when we see someone with metabolic disorders and our approach to it. So as she goes through that, she’s going to be able to understand how we evaluate and assess a patient and bring it in so that we can start getting a little bit of control for that individual. Kenna, it’s all yours.
Kenna Vaughn: All right. So first, I just want to talk about the smoothies a little bit more. I am a mom, so in the morning time, things get crazy. You never have as much time as you think you do, but you need those nutrient nutrients and so do your kids. So I love smoothies. They’re super fast. You get everything you need. And most people think that when you’re eating, you’re eating to fill your stomach, but you’re eating to fill your cells. Your cells are what need those nutrients. That’s what carries you on with the energy, the metabolism, all of that. So those smoothies are a super great option, which we give our patients. We even have a book with 150 smoothie recipes that are great for anti-aging, helping diabetes, lowering cholesterol, controlling inflammation, and things like that. So it’s one resource we give to our patients. But we do have multiple other options for the patients who come in with metabolic disease.
Dr. Alex Jimenez DC*: Before you go in there, Kenna. Let me just kind of add that what I’ve learned is that we have to make it simple. We got to take homes or takeaways. And what we’re trying to do is we’re trying to give you the tools that can help you in that process. And we’re going to take you to the kitchen. We’re going to grab you by the ear, so to speak, and we’re going to show you the areas where we need to look at. So Kenna is about to give us the information in terms of smoothies that will assist us with dietary changes that we can provide our families and change its metabolic disaster that affects so many people called metabolic syndrome. Go ahead.
Kenna Vaughn: OK, so like he was saying with those smoothies. One thing that you should add to your smoothie is, which what I love to add in mine is spinach. Spinach is an excellent choice because it gives your body more nutrients. You are getting an extra serving of vegetables, but you can’t taste it, especially when it gets covered up by the natural sweetness that you find in fruits. So that’s a great option when it comes to the smoothies. But another thing that Dr. Jiménez was mentioning is other things in the kitchen. So there are other substitutes that we’re kind of wanting our patients to use and implement. You can start small, and it’ll make a huge difference just by switching out the oils you’re cooking with. And you’ll begin to see an improvement in your joints, your kids, and everyone will just improve immensely. So one thing we want to get our patients into using is those oils, such as avocado oil, coconut oil, and… Olive oil? Olive oil. Yes, thank you, Astrid.
Dr. Alex Jimenez DC*: That was olive oil. That was Astrid in the background. We’re getting the facts out excellent and continue.
Kenna Vaughn: When you switch those out, your body breaks things down differently with those unsaturated fats. So that’s just another option that you have in that kitchen besides making those smoothies. But like I said before, I’m all about quick, easy, simple. It’s way easier to change your lifestyle when you have a whole team around you. And when it’s easy, you don’t. You don’t want to go out and make everything super difficult because the chances of you sticking to it aren’t very high. So one thing we want to do is make sure that everything that we’re giving our patients is easy to do and it’s attainable for everyday life.
Dr. Alex Jimenez DC*: I’m very visual. So when I go to the kitchen, I like making my kitchen look like the cocina or whatever they call it in Italy, the cucina and I have three bottles there, and I have an avocado oil one. I have the coconut oil one, and I have the olive oil right there. There are big bottles there. They make them pretty, and they look Tuscan. And, you know, I don’t care if it’s an egg, I don’t care. Sometimes, even when I’m having my coffee, I grab the coconut oil one, and I pour that one in and make myself a java with coconut oil in it. So, yeah, go ahead.
Kenna Vaughn: I was going to say that’s a great option too. So I drink green tea, and I also add coconut oil in that green tea to help boost everything and give my body another dose of those fatty acids that we want.
Dr. Alex Jimenez DC*: I got a question for you when you have your coffee like that; when you have the oil in it, does it kind of lubricate your lips.
Kenna Vaughn: It does a little bit. So it’s also like chapstick.
Dr. Alex Jimenez DC*: Yeah, it does. It’s like, Oh, I love it. OK, go ahead.
Kenna Vaughn: Yeah, I also have to stir a little bit more just to make sure everything gets it right. Yeah. And then another thing just talking about something our patients can do when it comes to at home, there are tons of different options with eating fish. Increasing your good fish intake throughout the week, that’s going to help also. And just because fish provides so many great things like omegas, I know Astrid also has some more information on omegas.
Dr. Alex Jimenez DC*: I got a question before Astrid gets in there. You know, look, when we talk about carbohydrates, people, is it what a carbohydrate is? Oh, people say an apple, banana, candy bars, and all kinds of stuff people can rattle off carbohydrates or proteins. Chicken, beef, whatever they can rile up. But one of the things I found that people have a difficult time with is what good fats are? I want five. Give me ten good fats for a million dollars. Give me ten good fats like lard, like meat. No, this is what we’re talking about. Because the simple fact that we use and we’re going to add more to it relative bad is going to be avocado oil. Olive oil. Is it coconut oil? We can use things like butter oils, different types of margins, and not margins, but kinds of butter that are from, you know, grass-fed cows. We basically can run out of creamers, you know, non-nondairy creams, very specific creamers, those we run out of it, right? Real fast. So it’s like, what else is fat, right? And then we search for it. So one of the best ways to do it is that we’re not going to always put creamer on top or our butter on top, which by the way, some coffees they have, they put butter in it and blend it, and they make a fantastic little java hit. And everyone comes with their little ginger and oils and their coffee and makes espresso from heaven, right? So what else can we do?
Kenna Vaughn: We can, like I said, adding those fish in, which is going to help to give our bodies more of those omegas. And then we can also do more purple vegetables, and those are going to provide your body with more antioxidants. So that’s a good option when it comes to the grocery store. A rule of thumb that I love and heard a long time ago is to not shop in the aisles is to try to shop on the edges because the edges are where you’re going to find all that fresh produce and all those lean meats. It’s when you start to get into those aisles, and that’s where you’re going to start finding, you know, the cereal, those bad carbohydrates, those simple carbohydrates that the American diet has come to love but does not necessarily need. The Oreos?
Kenna Vaughn: Yes.
Dr. Alex Jimenez DC*: The candy aisle that every kid knows. OK, yes.
Kenna Vaughn: So that’s just another great point there. So when you come into our office, if you’re suffering from metabolic syndrome or just anything in general, we make your plans super personalized and give you so many tips. We listen to your lifestyle because what works for one person might not work for another. So we make sure that we provide you with information that we know you’ll be successful with and provide education because that’s another huge part of it.
Dr. Alex Jimenez DC*: All roads lead to the kitchen, huh? Right? Yes, they do. OK, so let’s zoom on precisely for the fat and the nutraceuticals. I want to give you an idea as to what type of nutraceuticals are appropriate for us because we want to bust down these five issues affecting metabolic syndrome that we discussed. What are the five guys? Let’s go ahead and start them up. It’s high blood sugar, right?
Kenna Vaughn: High blood glucose, low HDLs, which will be that good cholesterol everyone needs. Yes. And it’s going to be the high blood pressure, which is not considered high from a doctor’s standard, but it is deemed to be elevated. So that’s another thing; we want to ensure that this is metabolic syndrome, not a metabolic disease. So if you go to the doctor and your blood pressure is 130 over eighty-five, that’s an indicator. But yet your provider might not necessarily say your blood pressure is super high.
Dr. Alex Jimenez DC*: None of these disorders here by themselves are clinical states, and, individually, they’re pretty much just things. But if you combine all these five, you have metabolic syndrome and feel like not too good, right?
Astrid Ornelas: Yeah, yeah.
Kenna Vaughn: Another one is going to be the excess weight around the belly and the higher triglycerides.
Dr. Alex Jimenez DC*: Easy to see. You can see when someone has a belly that’s hanging over like a fountain, right? So we can see that you can go to it sometimes Italian restaurants and see the great cook. And he sometimes I got to tell you, sometimes it’s just, you know, we talked to Chef Boyardee wasn’t a thin guy. I think that Chef Boyardee, you know what? And the Pillsbury guy, right? Well, it wasn’t very healthy, right? Both of them suffer from metabolic syndrome just from the outset. So that’s an easy one to see. So these are the things we’re going to be reflecting on. Astrid will go over some nutraceuticals, vitamins, and some foods that we can improve things. So here’s Astrid, and here’s our science curator. But here’s Astrid, go ahead.
Astrid Ornelas: Yeah, I guess before we get into the nutraceuticals, I want to make something clear. Like we were talking about metabolic syndrome. Metabolic syndrome is not a, and I guess per se, a disease or a health issue itself. Metabolic syndrome is a cluster of conditions that can increase the risk of developing other health issues like diabetes, stroke, and heart disease. Because metabolic syndrome is not, you know, an actual health issue itself, it’s more so this group, this collection of other conditions, of other problems that can develop into much worse health issues. Just because of that fact, metabolic syndrome has no apparent symptoms itself. But of course, like we were talking about, five risk factors are pretty much the ones we discussed: excess waist fat, high blood pressure, high blood sugar, high triglycerides, low HDL, and according to health care professionals. To doctors and researchers, you know you have metabolic syndrome if you have three out of these five risk factors.
Dr. Alex Jimenez DC*: Yes. Three. Now, that doesn’t mean that if you have it, you have symptoms. As I see it was evident on. But I got to tell you in my experience when someone has more than three or three. They’re starting to feel crummy. They don’t feel right. They just feel like, you know, life’s not good. They have just an overall. They don’t look it right. So and I don’t know them, maybe. But their family knows that they don’t look good. Like mom doesn’t look good. Dad does look good.
Astrid Ornelas: Yeah, yeah. And metabolic syndrome, as I said, it has no apparent symptoms. But you know, I was kind of going with one of the risk factors with waist fat, and this is where you will see people with what you call the apple or pear-shaped body, so they have excess fat around their abdomen. And although that’s not technically considered a symptom, it is a factor that can; I guess it can give an idea to doctors or other health care professionals that this person who is, you know, they have prediabetes or have diabetes. And, you know, they have excess weight and obesity. They could have an increased risk of metabolic syndrome and therefore developing, you know, if it’s left untreated, developing other health issues like heart disease and stroke. I guess with that being said; then we’ll get into the nutraceutical.
Dr. Alex Jimenez DC*: I love this, I love this. We’re getting some good stuff, and we’re getting some information.
Astrid Ornelas: And I guess with that being said, we’ll get into the nutraceuticals. Kind of like, how Kenna was talking about what’s the takeaway? You know, we’re here talking about these health issues, and we’re here talking about metabolic syndrome today. But what’s the takeaway? What can we tell people? What can they take home about our talk? What can they do at home? So here we have several nutraceuticals, which I’ve written several articles in our blog and looked at.
Dr. Alex Jimenez DC*: You think, Astrid? If you look at 100 articles written in El Paso, at least in our area, they were all curated by somebody. Yes. All right.
Astrid Ornelas: Yes. So we have several nutraceuticals here that have been researched. Researchers have read all these research studies and found that they can help in some way and some form improve, you know, metabolic syndrome and these associated diseases. So the first one I want to discuss is the B vitamins. So what are the B vitamins? These are the ones that you can usually find them together. You can find them in the store. You’ll see them as B-complex vitamins. You’ll see like a little jar, and then it comes with several of the B vitamins. Now, why do I bring up B vitamins for metabolic syndrome? So one of the reasons like researchers has found that one of them, I guess, one of the causes of metabolic syndrome could be stress. So with that being said, we need to have B vitamins because when we get stressed when we have a hard day at work when we have, I guess a lot of you know, a lot of stressful things at home or with family, our nervous system will use these B vitamins to support our nerve function. So when we have a lot of stress, we will use up these vitamins, which increases stress; you know, our body will produce cortisol. You know, which serves a function. But we all know that too much cortisol, too much stress can actually. It can be harmful to us. It can increase our risk of heart disease.
Dr. Alex Jimenez DC*: You know, as I remember when we did this, all roads lead to the kitchen in terms of getting the food back in your body. All roads lead to the mitochondria when it comes to the area of the breakdown. The world of ATP energy production is surrounded and wrapped around with nicotinamide, NADH, HDP, ATPS, ADP. All these things have a connection with vitamin B of all sorts. So the vitamin B’s are at the engine in the turbine of the things that help us. So it makes sense that this was the top of the vitamin and the most important one. And then she’s got some other endpoints here on niacin. What is with niacin? What have you noticed there?
Astrid Ornelas: Well, niacin is another B vitamin, you know, there are several B vitamins. That’s why I have it there under its plural and niacin or vitamin B3, as it’s more well known. A lot of several are so clever. Many research studies have found that taking vitamin B3 can help lower LDL or bad cholesterol, help lower triglycerides, and increase HDL. And several research studies have found that niacin, specifically vitamin B3, can help increase HDL by 30 percent.
Dr. Alex Jimenez DC*: Incredible. When you look at NADP and NADH, These are the N is the niacin, the nicotinamide. So in the biochemical compound, niacin is the one that people have known that when you take it the good one or the one that’s supposed to be, you get this flushing feeling and it makes you scratch all your part of your body, and it feels good when you scratch because it makes you feel that way. Right, so lovely. And this huge.
Astrid Ornelas: Yes. Yes, and also, I just want to highlight a point about B vitamins. B vitamins are essential because they can help support our metabolism when we eat, you know, carbohydrates and fats, good fats, of course, and proteins. When the body goes through the metabolism process, it converts these carbohydrates, fats, and protein. The proteins turn into energy, and B vitamins are the main components in charge of doing that.
Dr. Alex Jimenez DC*: Latinos, in our general population, know that we have always heard of the nurse or the person who gives vitamin B injection. So you heard of those things. Right. Because you’re depressed, you’re sad, what would they do? Well, you know what would inject them with B12, right? Which are the B vitamins, right? And the person would come out like, Yeah, and they’d be excited, right? So we’ve known this, and this is the elixir of the past. Those traveling salesmen, who had the potions and lotions, made a living off of giving B vitamin complex. The first energy drinks were first designed with a B complex, you know, packing of them. Now here’s the deal. Now that we’ve learned that energy drinks cause so many issues, that we’re heading back to the B complexes to help people better. So the following vitamin we have there is that one that we have the D, we have the vitamin D.
Astrid Ornelas: Yeah, the next one I wanted to talk about is vitamin D. So there are several research studies on vitamin D and the benefits, the benefits of vitamin D for metabolic syndrome, and just how I discussed how B vitamins are beneficial for our metabolism. Vitamin D is also helpful for our metabolism, and it can help regulate our blood sugar, essentially our glucose. And that in itself is very important because, like one of the predisposing factors of metabolic syndrome, high blood sugar. And you know, if you have uncontrolled high blood sugar, it can lead to, you know, it can lead to prediabetes. And if that is left untreated, it can lead to diabetes. So research studies have also found that vitamin D itself can also improve insulin resistance, which is pretty much one that can lead to diabetes.
Dr. Alex Jimenez DC*: You know, I just wanted to put out the vitamin D is not even a vitamin; it’s a hormone. It was discovered after C by Linus Pauling. When they found it, they just kept on naming the following letter. OK, so since it is a hormone, you just have to look at it. This particular vitamin D or this hormone tocopherol. It basically can change so many metabolism issues in your body. I’m talking about literally four to five hundred different processes that we’re finding. Last year was 400. We’re now almost 500 other biochemical processes that are affected directly. Well, it makes kind of sense. Look, our most significant organ in the body is our skin, and most of the time, we ran around in some sort of skimpy clothes, and we were in the sun a lot. Well, we didn’t stand to reason that that particular organ can produce a tremendous amount of healing energies, and vitamin D does that. It is produced by the sunlight and activated. But today’s world, whether we’re Armenian, Iranian, different cultures in the north, like Chicago, people don’t get as much light. So depending on cultural changes and closed people living and working in these fluorescent lights, we lose the essence of vitamin D and get very sick. The person who takes vitamin D is much healthier, and our goal is to raise the vitamin D is a fat-soluble vitamin and one that embeds itself by it and is saved in the liver along with the fat in the body. So you can raise it slowly as you take it, and it’s tough to get toxic levels, but those are at about one hundred twenty-five nanograms per deciliter that are too high. But most of us run around with 10 to 20, which is low. So, in essence, by raising that, you’re going to see that the blood sugar changes are going to happen that Astrid is speaking about. What are some of the things that we notice about, particularly vitamin D? Anything?
Astrid Ornelas: I mean, I’ll get back to vitamin D in a bit; I want to discuss some of the other nutraceuticals first. OK. But pretty much vitamin D is beneficial because it helps improve your metabolism, and it helps improve your insulin resistance, at least towards metabolic syndrome.
Dr. Alex Jimenez DC*: How about calcium?
Astrid Ornelas: So calcium goes hand-in-hand with vitamin D, and the thing that I wanted to talk about with vitamin D and calcium together. We often think about these five factors that we mentioned before that could cause a metabolic syndrome. Still, there’s, you know, if you want to think about it, like what are the underlying causes for a lot of these risk factors? And like, you know, obesity, a sedentary lifestyle, people who don’t engage in an exercise or physical activity. One of the things that can predispose a person or increase their risk of metabolic syndrome. Let me put the scenario. What if a person has a chronic pain disease? What if they have something like fibromyalgia? They’re constantly in pain. They don’t want to move, so they don’t want to exercise. They don’t want to aggravate these symptoms. Sometimes, some people have chronic pain or things like fibromyalgia. Let’s go a little bit more basic. Some people just have chronic back pain, and you don’t want to work out. So just you’re not choosing like some of these people aren’t choosing to be inactive because they want to. Some of these people are legitimately in pain, and there are several research studies, and this is what I was going to tie in vitamin D and calcium with that vitamin D and calcium. You know, we can you can take them together. They can help improve chronic pain in some people.
Dr. Alex Jimenez DC*: Incredible. And we all know that calcium is one of the causes of muscle spasms and relaxers. Tons of reasons. We’re going to go into each one of these. We’re going to have a podcast on just vitamin D and the issues in calcium because we can go deep. We’re going to go deep, and we’re going to go all the way to the genome. The genome is genomics, which is the science of understanding how nutrition and the genes dance together. So we’re going to go there, but we’re kind of like we’re penetrating slowly in this process because we have to take the story slowly. What’s up next?
Astrid Ornelas: So next, we have omega 3s, and I want to specifically highlight that we’re talking about omega 3s with EPA, not DHA. So these are EPA, which is the one that’s listed up there, and DHA. They are two essential types of omega 3s. Essentially, they’re both very important, but several research studies and I’ve done articles on this as well have found that I guess taking omega 3s specifically with EPA, it’s just more superior in its benefits than DHA. And when we talk about the omega 3s, these can be found in fish. Most of the time, you want to take omega 3s; you see them in the form of fish oils. And this is going back to what Kenna discussed before, like following a Mediterranean diet, which mainly focuses on eating a lot of fish. This is where you get your intake of omega 3s, and research studies have found that omega 3s themselves can help promote heart health, and they can help lower bad cholesterol to your LDL. And these can also improve our metabolism, just like vitamin D.
Dr. Alex Jimenez DC*: Want to go ahead and blanket all these things under the fact that we’re also looking, and when we’re dealing with metabolic syndrome, we’re dealing with inflammation. Inflammation and omegas have been known. So what we need to do is to bring out the fact that omegas have been in the American diet, even in a grandma’s diet. And then, like again, we hear back in the day when grandma or great-grandma would give you cod liver oil. Well, the highest omega-carrying fish is the herring, which is at about 800 milligrams per serving. The cod is next when it’s around 600. But because of the availability, the card’s much more available in certain cultures. So everybody would have cod liver oil, and they’d make you close your nose and drink it, and they knew that it correlated. They would think it’s a good lubricant. Still, it was an anti-inflammatory specifically with people, and usually, grandmothers who knew about this right helps with the intestines, helps the inflammation, helps with the joints. They knew the whole story behind that. So we’ll go deep into the Omegas in our later podcast. We have another one that’s here. It’s called berberine, right? What’s the story on berberine?
Astrid Ornelas: Well, pretty much the next set of nutraceuticals that are listed here, berberine, glucosamine, chondroitin, acetyl L-carnitine, alpha-lipoic acid, ashwagandha, pretty much all of these have been tied into what I talked before about chronic pain and all of these health issues. I listed them up here because I’ve done several articles. I’ve read various research studies that have covered these in different trials and across multiple research studies with numerous participants. And these have pretty much found, you know, this group of nutraceuticals here that are listed; these have also been tied in to help reduce chronic pain. You know, and as I discussed before, like chronic pain, you know, people who have fibromyalgia or even like, you know, let’s go a little bit simpler people who have back pain, you know, these inactive people who have sedentary lifestyles simply because of their pain and they can be at risk of metabolic syndrome. A lot of these research studies have found these nutraceuticals themselves can also help reduce chronic pain.
Dr. Alex Jimenez DC*: I think the new one is called alpha-lipoic acid. I see acetyl L-carnitine. We’re going to have our resident biochemist on the following podcast to go deep into these. Ashwagandha is a fascinating name. Ashwagandha. Say it. Repeat it. Kenna, can you tell me a bit about ashwagandha and what we’ve been able to discover about ashwagandha? Because it is a unique name and a component that we look at, we will talk about it more. We’re going to get back to Astrid in a second, but I’m going to give her a little break and kind of like, let Kenna tell me a bit of ashwagandha.
Kenna Vaughn: I was going to add in something about that berberine.
Dr. Alex Jimenez DC*: Oh, well, let’s go back to berberine. These are berberine and ashwagandha.
Kenna Vaughn: OK, so that berberine has also been shown to help decrease the HB A1C in patients with blood sugar dysregulation, which will come back to the whole prediabetes and type two diabetes situations that can occur in the body. So that one is also has been shown to decrease that number to stabilize the blood sugar.
Dr. Alex Jimenez DC*: There’s a whole thing we’re going to have on berberine. But one of the things that we did in terms of metabolic syndrome definitely made the top list here for the process. So there’s ashwagandha and berberine. So tell us all about ashwagandha. Also, ashwagandha is the one. So in terms of blood sugar, the A1C is the blood sugar calculation that tells you exactly what the blood sugar does over about three months. The glycosylation of the hemoglobin can be measured by the molecular changes that happen within the hemoglobin. That’s why the Hemoglobin A1C is our marker to determine. So when ashwagandha and berberine come together and use those things, we can alter the A1C, which is the three-month kind of like the historical background of what is going on. We’ve seen changes on that. And that’s one of the things that we do now in terms of the dosages and what we do. We’re going to go over that, but not today because that’s a little bit more complex. Soluble fibers have also been a component of things. So now, when we deal with soluble fibers, why are we talking about soluble fibers? First of all, it is food for our bugs, so we have to remember that the probiotic world is something we cannot forget. People need to understand that, though, that probiotics, whether it’s the Lactobacillus or Bifidobacterium strains, whether it’s a small intestine, large intestine, early on the small intestine, there are different bacteria to the very end to see come to the back end. So let’s call that the place that things come out. There are bacteria everywhere at different levels, and each one has a purpose of discovering that. There’s vitamin E and green tea. So tell me, Astrid, about these dynamics in terms of green tea. What do we notice as it pertains to metabolic syndrome?
Astrid Ornelas: OK. So green tea has a lot of benefits, you know? But, you know, some people don’t like tea, and some are more into coffee, you know? But if you want to get into drinking tea, you know, definitely because of its health benefits. Green tea is an excellent place to start and in terms of metabolic syndrome. Green tea has been demonstrated to help improve heart health, and it can help lower these risk factors that pertain to metabolic syndrome. It can help, you know, several research studies that have found that green tea can help lower cholesterol, bad cholesterol, LDLs.
Dr. Alex Jimenez DC*: Does green tea help us with our belly fat?
Astrid Ornelas: Yeah. There’s one of the benefits of green tea that I’ve read about. Pretty much one of the ones that probably that it’s most well known for is that green tea can help with weight loss.
Dr. Alex Jimenez DC*: Oh my gosh. So basically water and green tea. That’s it, guys. That’s all. We limit our lives that are also, I mean, we forgot even the most powerful thing. It takes care of those ROSs, which are reactive oxygen species, our antioxidants, or oxidants in our blood. So it just basically squelch them and takes them out and cools their cool and prevents even the normal deterioration that happens or the excessive deterioration that occurs in the breakdown of normal metabolism, which is a byproduct which is ROS, reactive oxygen species are wild, crazy oxidants, which we have a neat name for the things that squashes them and calms them and puts them in the order they call antioxidants. So the vitamins that are antioxidants are A, E, and C are antioxidants, too. So those are potent tools that we deal with as we lower body weight. We free up a lot of toxins. And as the green tea goes into squirt, squelch them, cools them, and gets them out of gear. Guess where the other organ that helps with the whole insulin production is, which is the kidneys. The kidneys are flushed out with green tea and then also helps. I notice that one thing that you haven’t done, Astrid, is done articles on turmeric, right?
Astrid Ornelas: Oh, I’ve done a lot of articles on turmeric. I know because, from the list that’s up there, turmeric and curcumin are probably like one of my favorite nutraceuticals to talk about.
Dr. Alex Jimenez DC*: Yeah, she’s like gnawing on a root and a couple of times.
Astrid Ornelas: Yeah, I have some in my fridge right now.
Dr. Alex Jimenez DC*: Yeah, you touch that turmeric, and you can lose a finger. What happened to my finger? Did you get near my turmeric? The root, right? So. So tell us a bit about the properties of turmeric and curcumin in terms of metabolic syndrome.
Astrid Ornelas: OK. I’ve done several, you know, a lot of articles on turmeric and curcumin. And we’ve also discussed that before, and several of our past podcasts and turmeric is that it’s that yellow yellowish could look orange to some people, but it’s usually referred to as a yellow root. And it’s very popular in Indian cuisine. It’s what it’s one of the main ingredients that you’ll find in curry. And curcumin, pretty sure some of you people have heard of curcumin or turmeric, you know? What’s the difference? Well, turmeric is the flowering plant, and it’s the root. We eat the root of turmeric, and curcumin is just the active ingredient in turmeric that gives it a yellow color.
Dr. Alex Jimenez DC*: Guys, I will not let anything but the top type of curcumin and turmeric products be available to their patients because there’s a difference. Certain ones are produced with literally, I mean, we got solvents, and with the way we get things out and of curcumin and turmeric or even stuff like cocaine, you have to use a distillate. OK? And whether it’s water, acetone, benzene, OK, or some sort of a byproduct, we know today that benzene is used to process many types of supplements, and certain companies use benzene to get the best out of turmeric. The problem is benzene is cancer-producing. So we’ve got to be very careful which companies we use. Acetone, imagine that. So there are processes that are in place to extract the turmeric properly and that are beneficial. So finding suitable turmeric, all turmerics are not the same. And that’s one of the things that we have to assess since it has so many products in the world is running real crazy to try to process turmeric and precisely, even if it’s the last thing that we’re discussing today on our subject matter. But it’s one of the most important things today. We don’t even understand aspirin. We know it works, but the total magnitude of it is yet to be told. However, turmeric is in the same boat. We’re learning so much about it that every day, every month, studies are being produced on the value of turmeric into the natural diet, so Astris is in tune in on the target on that. So I’m sure she’s going to bring more of that to us, right?
Astrid Ornelas: Yes, of course.
Dr. Alex Jimenez DC*: So I think what we can do today is when we look at this, I’d like to ask Kenna, when we look at a metabolic syndrome from the presentations of symptoms or even from laboratory studies. The confidence of knowing that N equals one is one of the essential components that we have now in functional medicine and functional wellness practices that a lot of physical medicine doctors are doing in their scope of practice. Because in metabolic issues, you can’t take metabolic away from the body. Does the metabolism happen in a back problem? We notice a correlation with back injuries, back pain, back issues, chronic knee disorders, chronic joint musculoskeletal disorders, and metabolic syndrome. So we can’t tease it. So tell us a bit, Kenna, as we close out today a bit of what a patient can expect when they come to our office, and they get kind of put in the “Oops, you got metabolic syndrome.” So boom, how do we handle it?
Kenna Vaughn: We want to know their background because, as you said, everything is connected; everything is in-depth. There are details we want to get to know all so we can make that personalized plan. So one of the first things we do is a very lengthy questionnaire by Living Matrix, and it’s a great tool. It does take a little while, but it gives us so much insight into the patient, which is great because it allows us to, like I said, dig deep and figure out, you know, traumas that might have happened that are leading to inflammation, which how Astrid was saying then leads that sedentary lifestyle, which then leads to this metabolic syndrome or just kind of down that road. So one of the first things we do is do that lengthy questionnaire, and then we sit down and talk to you one on one. We build a team and make you part of our family because this stuff isn’t easy to go through alone, so the most success is when you have that close-knit family, and you have that support, and we try to be that for you.
Dr. Alex Jimenez DC*: We have taken this information and realized it was very complex five years ago. It was challenging. 300 300-page questionnaire. Today we have software that we can figure out. It is backed by the IFM, the Institute of Functional Medicine. The Institute of Functional Medicine had its origin over the last decade and became very popular, understanding the whole person as an individual. You can’t separate an eyeball from kind of the body as you can’t separate the metabolism from all effects that it has. Once that that body and that food, that nutraceutical that nutrient enters our body. On the other side of our mouth is these little weighting things called chromosomes. They’re spinning, and they’re churning, and they’re creating enzymes and proteins based on what we feed them. To find out what’s going on, we have to do an elaborate questionnaire about mental body spirituality. It brings in the mechanics of normal digestion, how the entanglement works, and how the overall living experience happens in the individual. So when we take into consideration Astrid and Kenna together, we kind of figure out the best approach, and we have a tailor-made process for each person. We call it the IFM one, two, and three, which are complex questions that allow us to give you a detailed assessment and an accurate breakdown of where the cause can be and the nutraceuticals the nutrient nutrients that we focus on. We push you right direction to the place where it matters into the kitchen. We end up teaching you and your family members how to feed so that you can be good to those genetic genomes, which you’re, as I always say, ontogeny, recapitulates phylogeny. We are who we are from the past to the people, and those people have a thread between us and my past, and everyone here’s past. And that is our genetics, and our genetics responds to the environment. So whether it goes in the south fast or exposed or predisposed, we’re going to discuss those, and we’re going to enter the world of genomics soon in this process as we go deeper into the metabolic syndrome process. So I thank you all for listening in on us and know that we can be contacted here, and they’re going to leave you the number. But we have Astrid here that’s doing research. We have a team established by many individuals who can give you the best information that applies to you; N equals one. We got Kenna here that there’s always available and we’re here taking care of people in our beautiful little town of El Paso. So thank you again, and look forward to the following podcast, which will probably be within the next couple of hours. Just kidding. All right, bye, guys.
In today’s podcast, Dr. Alex Jimenez, health coach Kenna Vaughn, Astrid Ornelas, Truide Torres, and biochemist Alexander Isaiah Jimenez discuss what is metabolic syndrome and the steps to fix it.
Dr. Alex Jimenez DC*: All right, guys, we’ve come to another podcast, and welcome to Dr. Jimenez and Crew podcast. Welcome, and you have a family here. We’re going to go over metabolic syndrome today. Metabolic syndrome is a disorder that ultimately affects a whole lot of people. And what happens is, is it affects one of the largest populations in affecting El Paso, pretty much in this region. And what we have is it’s not a disease, OK? First of all, it’s a combination of presentations that medical doctors and the World Health Organization have determined high-risk factors to have a stroke, kidney disorders, and even problems with dementia. But overall, it’s pretty much if you have metabolic syndrome, you feel crummy. So today, what are we going to do is we’re going to discuss the issues, and we’d like to at least present it to you so that it becomes useful for you and the information provided by us is going to be helpful for you or a family member. So if you have the opportunity and something that you enjoy, please go ahead and at the bottom area. There’s a little bell to subscribe to. And a little belt in markets so that you could be the very first person to get information in the future when we ever posted. And also allows you to present or ask us for things that are important to you in the health-related realm. Now, what are we going to do today? My name is Dr. Alex Jimenez. I have my entire staff here. We’re going to go, and we’re going to present each one of them in different moments. And we’re going to do some fascinating dynamics. We will also have our resident biochemist at the National University of Health Science, who’s going to chime in and give us a little bit of foundational biochemistry. This information is going to be helpful. We’re going to try to make it as simple but as useful as possible. Now, bear in mind everything that we’re going to be talking about in and today revolves around the metabolic syndrome. Metabolic syndrome is what the health care organizations have determined, and the cardiac departments have five major symptoms. Now you have to have three of them, at least to be classified as metabolic syndrome. OK, now the first thing is to ask… What do you feel? Pretty much you feel like crap, OK? And it’s not a good feeling to feel this way, but you’ll see that if you have of these presentations, you’re going to notice that your doctor may give you a diagnosis of metabolic syndrome. Now, the first thing that happens is you usually have a bit about belly fat. Now, the belly fat that people have, people measure it. For men, it’s a belly kind of like the lonja, the belly that hangs over, and it’s about a good, I’d say, about 40 inches or greater in the male. In women is 35 inches or more. Now that’s one of the first presentations. Now the other presentation is high blood pressure. Now that high blood pressure that they use is 135 milligrams over deciliter. Sorry, yeah. Miller Mercury’s millimeters of mercury over these leaders to determine exactly on the diastolic and the systolic. So the diastolic is going to the systolic is going to be 135, the diastolic is going to be over 85. Now that doesn’t happen again; you’re going to notice something. These aren’t extreme ranges from OK. Metabolic syndrome has high triglycerides. Now the high triglycerides are going to be noted in the blood. OK, now one of the things that can be determined early on is high blood pressure, which is also so associated with metabolic syndrome. So the other final one is the elevation of or decrease actually of HDL. HDL or the good fragments of cholesterol. Alexander will be a resident biochemist and talk to us more about that in the latter part of the show. Now, bear in mind, I’ve given five things a. the fat, b. the high blood pressure, c. the blood glucose levels, and also the triglycerides, along with the lowering of the HDLs. The question is, how are we going to be able to control this now? I’m going to give you some real good basic ways that you can control metabolic syndrome. And by the time we’re done today, we’re going to be able to assess the situation. And even if you have it, you basically will be able to control it. There are rare diseases that you can be disordered. And again, this is not a disease; it’s a combination of syndromes or symptoms to be called a syndrome collectively. So metabolic syndrome can be construed. Now you’ll notice that the blood glucose level will be elevated, usually over 100; these are relatively average numbers people have. But if they’re higher than that, they do create issues now. Also, when you have the belly fat 40, and it’s not that much, many people have it. People also have blood glucose levels that are higher than 5.6 on their blood glucose A1C. These numbers and the 150 mg per deciliter of triglycerides are all normal but in combination. Together, they do ultimately create a scenario that is not favorable to cardiac issues. Cardiovascular issues do present as a result. So what we’re going to try to do is try to bring down and control these issues. Now, what are the things that cause metabolic syndrome? One of the things is stress, smoking, a sedentary lifestyle, and even sleep problems and disturbances. We can be elaborating on each of these we can we’re going to be elaborating on in the future podcasts. Still, we’re going to be able to tell exactly what’s going on in a better way. We also have issues with inflammation and processed foods. At the core metabolic syndrome, the main issue is insulin sensitivity issues and high blood pressure issues, and inflammation. So what are we going to do to control that? I want you to know that every single one of these five issues, whether it’s blood glucose, high triglycerides, low HDL counts, or blood glucose, they’re all relatable to one disorder. It’s insulin sensitivity. Insulin sensitivity controls every one of these factors from raising high blood pressure. The kidneys are controlled by insulin, causing an increase in blood pressure, and we’ll discuss that issue and its correlation. So if we can control the blood glucose, we ultimately have the fastest and the surest way to provide the fastest route to heal and fix an individual with metabolic syndrome. So let’s go ahead about the issues that are going to result from that. Now, as I’ve got this, we’re going to notice that if over some time you continue to have a lifestyle that has high levels of these particular five factors, you’re going to notice that you’re going to tend to have high cardiac risks. Now we have a team here, and I want to introduce each one. We have Kenna Vaughn, who is our health coach. Our health coach is the one that’s going to be the one that explains to our patients what is going on. I’ll bring her in. We also have the clinical liaison, which is Trudy. Trudy is the individual who will be able to bring out the questions and determine what kind of issues are appropriate for you. So we’ll be discussing those. And we have our resident chief editor, Astrid Ornelas, who will be the one that explains the studies on it. From Illinois, we also have Alexander, which we have right in the back where you can’t see him, but he’s presenting and say, Hello, Alex, can you get them there? Hello. All right. So he’s out there, and he’s going to discuss the issues and the biochemistry side of things, and we’re looking forward to explaining those issues. Now, one of the things we have to do is go back to the issue of insulin sensitivity. Insulin sensitivity is at the root of all these issues. So what we’re going to do is discuss exactly how insulin can be controlled. But what we’ve learned through these studies, and I’m going to bring in Mrs. Ornelas, is here to discuss the studies on how to control blood glucose and blood sensitivity. Astrid, what did you find out recently that shows the proof and presents the easiest way to control blood insulin and elevate HDL?
Astrid Ornelas: OK, well, first of all, just as you know, as you mentioned, metabolic syndrome, it’s a collection of health issues that can increase the risk of developing heart disease, stroke, and diabetes. It’s basically like, you know, it can affect our overall health and wellness. And I’ve done quite some research, and I’ve found them through the National Center of Biotechnology Information, the NCBI. A variety of research states that metabolic syndrome or people with metabolic syndrome, one of the easiest, you know, quote-unquote easiest or one of the best ways out there that can be used to help… Restore? Yeah, to help restore or reverse all metabolic syndrome would be through the ketogenic diet. So the ketogenic diet or the keto diet is a low carbohydrate, high-fat diet, which, according to research studies, offers many benefits towards people with metabolic syndrome. It can help improve or promote weight loss, and it can help reduce diabetes.
Dr. Alex Jimenez DC*: You know, I want to mention right there, I have found nothing faster to lower the blood glucose and reverse triglycerides issues and HDL issues than the ketogenic diet. So, in essence, if you want to do it fast, it’s incredible the speed at which it restores the body to what it is. What else is there?
Astrid Ornelas: Yeah. So, like the human body, usually, we use glucose or sugar. It is supposed to be our primary source of fuel, our main source of energy. But of course, for people who have metabolic syndrome, people who have obesity, insulin resistance, diabetes, or the increased risk of diabetes. The ketogenic diet can be very beneficial because it is a low carbohydrate diet, carbohydrates essentially turn into sugar or glucose, and we don’t want that. Like if people have metabolic syndrome, they have, you know, diabetes and insulin resistance. You don’t want sugar in your body because they produce too much of it. They have too much blood sugar. And but by increasing your height, by increasing the number of fats that you eat, and decreasing the number of carbohydrates, you keep a low amount. You keep insulin low, and you, by eating more fats, basically what you would do is make the body go into a state of ketosis.
Dr. Alex Jimenez DC*: You know what? Let me ask you something. I’m going to feed this over right now to Kenna, and I’m going to ask Kenna in your experiences with the blood sugar issues. How is it that we contain and we learn to be able to manage someone’s blood sugar? The quick is the fastest. What is it that you do in terms of coaching individuals, helping them back?
Kenna Vaughn: For coaching individuals. I always evaluate their diet, and the main thing I like to focus on is education because so many people are not educated about, as Astrid was saying, carbs and how they fuel your body. A Big Mac might have 54 carbs, and a sweet potato might have 30 carbs, and people don’t realize that they’re that different, and they only see 20 points or something like that. But the way that the carbohydrate breaks down in the body is enormous. And that’s why the ketogenic diet works so well because you’re using those good whole carbs that are going actually to contain protein as well. And so it’s going to help to break it down slower versus a Big Mac, which is just going to spike your insulin way up.
Dr. Alex Jimenez DC*: And what part of the Big Mac is the thing that spikes the sugar? I mean, in terms of that?
Kenna Vaughn: Right. So the bread, the carbs in the bread, actually breaks down differently in your body than a sweet potato would. And so that’s what’s going to give you that high glucose level. And then after that, you’re going to have the fall of the glucose level, which is your blood sugar going up and down does not feel great. So it’s something you want to avoid.
Dr. Alex Jimenez DC*: I have a question for you. For the sugars. When you asked the types of sugars you have, you just mentioned that the variety of carbohydrates matters. Yes. Tell me a bit of that.
Kenna Vaughn: The quality, like I was saying, sweet potatoes, avocados, things like that. They’re going to have the carbohydrates that are better for you, meaning you break them down differently than you would. Faster sugars like sucrose and things like that.
Dr. Alex Jimenez DC*: So simple sugars are out, basically, which is why, first of all, metabolic syndrome did not even exist before the advent of refined foods. So refined sugars have caused this problem. So what we want to do is sugar leads to inflammation. Sugar leads to triglyceride issues. Sugar or insulin sensitivity issues are the things that are the basis of this process. All roads lead to insulin sensitivity in this process. And the organ that provides us with insulin, the most significant amount is is the pancreas. The pancreas is nonstop. And depending on how the pancreas responds to this blood sugar drama, it determines the fate of the individual. It will alter the triglycerides. It will transform the blood pressure by directly holding sodium in the kidneys, the kidneys the body prepares. It retains the sodium, and by the nature of sodium, the blood pressure soars. So the fastest way to lower your blood pressure is a ketogenic diet. And this is amazing because it is simple. It’s not that complex. We can go extreme. And I know that Astrid had an excellent research document on that. Tell me a bit of what you noticed.
Astrid Ornelas: Yeah, basically, like, what Kenna was saying. Before, many people didn’t know the difference between what type of carbohydrates they want to eat, like, for example, as you said, you know, a lot of people will eat a Big Mac, and they’ll eat that sweet potato, and they don’t know the difference between a good carbohydrate; basically, we want to eat what you call complex carbohydrates, which is it’s more like we want to eat like whole wheat or we want to eat like like good starches because those there break in the body breaks them down into glucose, into sugar. But they’re used much more slowly to where it won’t. The body won’t directly use them. And then you’ll get that crash, that sugar crash.
Dr. Alex Jimenez DC*: Because of the insulin spike, right? It controls the insulin spike. You know what? I want to bring in our resident biochemist here. OK, so our brilliant biochemist is Alexander. He’s got a presentation here, actually, if I can see it there and see if I pop up here. And there he is. Alex, can you tell us a bit about what you’re trying to explain here on the biochemistry side of things?
Alexander Isaiah: As you guys mentioned, just in general, glucose is the primary energy source in the way that we use it for the breakdown. Its breakdown on energy consumption is called glycolysis. So without getting too much into it, our end goal here is pyruvate, which then goes into the citric acid cycle to be turned into acetylcholine. In normal conditions, this is good to have a carbohydrate meal, but when in excess, do you produce too much acetylcholine? When is too much acetylcholine used? You end up inducing fatty acid synthesis, which is induced by significant levels of insulin. So by doing so, you have acetylcholine, which ends up turning into palmitate. And one thing that Kenna mentioned is that not all foods are of equal quality. So here, we can see all the different types of fatty acids. So without going too much into biochemistry, but just giving you an idea of what’s going on here? These numbers on the left side represent the number of carbons in a row, and then the numbers to the right of the semicolon are the number of double bonds. And usually, double bonds don’t play a significant role until you get into digestion and the way the body uses these. So by having more double bonds, it’s more fluid. So you notice the difference between a piece of lard and olive oil. What’s the difference? The only difference is the number of carbons and the number of double bonds. So here we have oleic acid, olive oil, and then we have some saturated fat. We can see that the difference is prominent in the number of carbons and double bonds. Double bonds allow for a lower melting point. That’s why olive oil is a liquid at room temperature versus fatty acids, and this plays a significant role in how the body uses these types of things.
Dr. Alex Jimenez DC*: Alex, are you saying that? We all know that the excellent work of olive oil, avocado oil, and coconut oil is the best thing is, this is why this happens.
Alexander Isaiah: Exactly. So the more double bonds they have, the more fluid it will be within the body and allow the body to use those fats on time versus clogging up artery arteries and creating plaques within those arteries.
Dr. Alex Jimenez DC*: Excellent. You know what? One of the things that insulin does, it pack away carbohydrates in energy in the cell. If you do that, what happens with this blood sugar? Eventually, insulin spikes it and puts it in the cells. Finally, the cell grows, hence the belly fat. Ultimately, The belly starts green and gains the fat cells, and they start getting bigger, bigger, bigger because they get injected in there. That stuff starts seeping out, and once it can’t go in anymore, it ends up in the places like the pancreas. It ends up in the places like the liver. It ends up in the intramuscular into the muscular tissue. And that’s why we have the accumulation. And when you have a big belly, that’s what tips off the doctor, not only with the triglycerides in the blood glucose levels but also the belly fat. And that’s one of the things we have to kind of assess. So are these now these fatty acids? What are fatty acids used for, typically, Alexander?
Alexander Isaiah: Fatty acids are used almost for everything within the body, especially for energy consumption. It’s like saying, would you rather be able to go five miles or 10 miles? You always want to go 10 miles, right? So gram for gram fat as an energy source is much more fuel-efficient than glucose or carbs. So carbs provide our four grams of four calories per gram and fats are around nine. So it’s almost it’s more than double the amount of energy that you’re producing from these fatty acids. The tricky part is just knowing which ones are good. So going into the good fatty acids, which will be the ones with the double bonds. So I mean, any plant oils, animal fats, depending on which ones, we tend to want to stay away from large amounts of wretched ionic acid, as they tend to cause inflammation responses through the inflammation pathway. But the rest of these are good, especially EPA and DHEA. So DHEA is used within the nervous system. It’s turned into neurotic acid and EPA as well. So getting these marine oils is going to be suitable for your system just in general.
Dr. Alex Jimenez DC*: You know what, as I understand these processes and start realizing the biochemistry behind it, bringing it home to this process down to the cellular component it honors. It shows appreciation in terms of what creates the fatty acid excess. Now again, what happens due to too much of these fatty acids or carbohydrates in the bloodstream? The body tries to store it. It tries to store in the form of fat, and it’s shoved into the pancreas. So you get this fat inside the pancreas. If it can’t do it there, it eventually puts it in the liver. And like we mentioned, it gets it in the stomach, or that’s when we see it as a final thing. So then I like to take the explanation and break apart one other point, the high blood pressure component. Insulin has a direct effect on the kidneys. Insulin tells the kidneys, Look, we need to pack this stuff into the fat. And without getting beyond too much of the chemistry dynamics, you can see that what’s going to occur is that the kidneys will be commanded to hold more sodium. In chemistry, biochemistry, and clinical science, we learned that the more sodium you retain, the blood pressure rises. In essence, that’s how quick the blood pressure goes. So you do that for some time, and then you force the collection of atherosclerotic plaques because that fat is in there, and it can’t go anywhere. You’re going to have a problem in the long term, in the long term future. So speaking about the oils, as Alexander just did, one of the things we ask is, Well, what oils cannot we should know? We use canola oil, corn oil, sesame seed oil. I love sesame seeds. But the problem is that sesame seed oil causes inflammation, as Alex said, with arachidonic acids. So what we have to do is figure out precisely what types of oils we can do and avocados, as Kenna had mentioned, are a great source of fats that we can use and make things more processed. Our bodies and the old pyramid of diet are really bad because it’s heavy on carbohydrates. So one of the things that we look at is maintaining all those components. So we talked about triglycerides, the belly fat, how it’s put together. And each one of these, I want to point this out again. The high blood pressure, which is 135 high blood pressure, is not considered at 135. Usually, it’s at 140. OK. So if so, why are we using triglycerides at 150 are not regarded as excessive. You know, HDL is lower than 50 is not considered horrible, but in combination together, if you have one at all, these three of these components are the five. That’s what leads to a pre-position of of of being sick and feeling crummy, let alone any prolonged period of this will end up leading to metabolic disorders, heart problems, stroke problems, dementias that occur as a result of protracted metabolic syndrome states that are within the individual. I want to ask Alexander. He’s got some fascinating dynamics, as I want to present right now, and we’re going to show his screen right here because he’s got some exciting components on what also affects metabolic syndrome. Alexander.
Alexander Isaiah: So kind of going into what it is, I guess ketosis, because everyone wonders what goes on. So I kind of got this diagram here that I drew out for you guys. We’re ignoring the ephedrine pathway over here, but just in general. So what’s going to happen first is you’re going to deplete any glucose that you have. So the body typically stores around 100 grams of glucose in the liver and around 400 grams within the muscle components of the entire body. So if you times 500 times for, that’s about 2000 calories, which is your daily limit, so you’ve got almost a day’s worth of glucose always stored within your body. But once you deplete that, your body’s going to start looking for other things. In the meantime, it takes a few days for your body to switch over from burning sugar, which is glucose, to burning ketone bodies from fat. So what’s going to happen? Your, first of all, your adrenals are going to start releasing epinephrine, its precursors, norepinephrine. And this is because of a couple of different things. You’re going to get a bit jittery first, and you’re going to feel bad for the first couple of days, but then your body and starts switching over as your brain starts to begin using these ketone bodies as an energy source. So as you’re producing norepinephrine, these are just like, this is the cell surface here. These are just different precursor markers. So we have B1, B2, B3, and A2. Doing these will mark and signal to the gas protein, which will allow aminoglycosides to activate ATP into cyclic AMP. Now, cyclic AMP is an essential component of the degradation of fatty acids. The cool part is it’s inhibited by phosphodiesterase. So when people come in and say, why is caffeine a good fat burner? The main reason why is because caffeine inhibits phosphodiesterase to a certain extent. You don’t want to go too crazy with the caffeine and start doing lots of cups of coffee.
Dr. Alex Jimenez DC*: Should I have eight glasses of coffee, or how many cups?
Alexander Isaiah: I think one glass of coffee is more than enough. So by having cyclic amp be more active, you activate the thing called protein kinase A, which activates ATP, and then it starts a hormone-sensitive life base. Once hormone-sensitive lipase is activated, it begins to degrade. It begins to break down fatty acids. Once these fatty acids enter and are broken down, they then enter into the mitochondria, and the mitochondria will then produce heat from this. So that’s why people who are ketosis are always really warm. So what do I recommend when people are starting to do a ketosis diet? Water? Keto diet, definitely water and as well as, I would say, L-carnitine. So as we’re looking at L-carnitine here, we could see that during fatty acid degradation, you use L-carnitine as the primary transporter between the outer mitochondrial membrane and the inner mitochondrial membrane. So by using fatty acids, here’s fatty asceloca; after we’ve broken down these fatty acids, it’s going to enter CPT one, which is carnitine, a seal translocated want or poly transferase one. It’s going to enter and interact with carnitine, and then it’s going to turn into seal carnitine. Once seal carnitine turns into it, it can enter the inner mitochondrial membrane through these two enzymes translocation and CPT two to be broken down back into a seal code, which does the same byproduct as glucose eventually. Also, then, your mitochondria can use these in beta-oxidation. One thing to know is you have to drink a lot of water because people going through ketosis will be upregulating the urea cycle. So you need to make sure that you pull a lot of water or drink a lot of water throughout the day. Anyone doing a keto diet today has a minimum of a gallon of water throughout the day, not all at once, but throughout the day.
Dr. Alex Jimenez DC*: It’s incredible, Alex, that you put that together because that makes perfect sense to me and also explains why people do say when we put them on the ketogenic diet, that they do increase body temperature and the water helps you kind of keep the whole system pumping because that’s what we’re pretty much made of. And also, the pathways that you indicated the hydrogen in the water are necessary for the process to occur.
Alexander Isaiah: Yes. Certain aspects within each of these fuel each other; it’s all an interconnected pathway. But you will upregulate the urea cycle during ketosis much more than when you’re not. For example, everyone’s notorious or cats are notoriously known for having a rotten urine smell. And we have to take a look at that from the reason why right? So general in humans there, urea content in the urine is three percent. In cats, on the other hand, it’s anywhere between six to nine percent. So you have to think about it. What is the only mammal on the planet that is a carnivorous animal that only eats meat? Since they only eat meat, the feline family upregulates their urea cycled, thus having more urea in their urine. So if you’re only a meat-eater, you’re going to have more urea. Therefore you need to drink more water to flush it out through your kidneys.
Dr. Alex Jimenez DC*: That’s amazing because it explains why we make sure that everybody drinks a lot of water, and then they feel better. And I guess if we don’t monitor it correctly, if we don’t do it right, we get that thing called the ketogenic flu, right? And then the body feels kind of crummy until it restores and it stabilizes the blood glucose through ketones. Now, the body can use ketones for sugar, as it’s known. So one of the things that we do is teach the people exactly how to go through the process. And I know we got some research articles here, and Astrid wants to discuss a bit of that.
Astrid Ornelas: So basically, like, as Alex mentioned, when people start going, they start following the ketogenic diet, we do want to, you know, as he said, we want to make sure that they stay hydrated, but more so than that. I guess another thing that we want to educate people on is that not many people know, you know, we need to store up the body with good fats so that as the body adjusts, it starts burning fat as a fuel than sugar or glucose. So we want to teach people, what are the good fats that we want them to like to eat, you know, because like, we need to store up in these fats of that the body can go into ketosis and we can go through the whole process that Alex just explains.
Dr. Alex Jimenez DC*: You know what? I would like to bring Trudy here because she’s the one that connects with the patients at the moment. We do assess someone to have metabolic syndrome. In terms of the resources, how do you go through the process of presenting? Hello, Trudy. Trudy, what are we going to do there? I’m going to ask you, how do you bring that? Because she’s our clinical liaison, our wellness liaison, and she’s the one that basically will give us the information that helps the patient in the right direction.
Trudy Torres: Well, hello. And I, you know, this is all excellent information, which is fantastic that we can provide this to the public. And I know this can be very overwhelming for people that are not don’t have this information. So that’s where I come in when people come, you know, either call us or come in inquiring about their different symptoms. They don’t necessarily know that they’re experiencing the metabolic syndrome. But you know, one of their main concerns is they’re waking. Based on their concerns, I connect them to our primary is with Kenna, and they go ahead and say, OK, well, what are the steps that we have to take and Kenna certainly educate them as far as, OK, this is the lab work that you’re going to have to take. We connect them with Dr. Jimenez after we know exactly their primary concern, and we’re going to start peeling things apart like an onion to get to the bottom of things and get them feeling better. They’re not only going to walk away with the specific results, but they’re also going to walk away with, like Astrid said, what are the good fats to have? What should I be eating? So they’re going to be walking away with a lot of information, but also structure. Another thing that we’re offering is that Kenna is always going to be there, you know, to answer any questions and also Dr. Jimenez, so they don’t have to feel overwhelmed with the process as they’re going through a better, healthy lifestyle.
Dr. Alex Jimenez DC*: You know, that one of the things is there’s a lot of confusion out there, and I’ve got to be honest with you. There’s a lot of misinformation out there. This misinformation can be categorized as intentional or old, or it’s just not up to date, with these five elements and an individual having three of them. It’s essential to repeat precisely how to fix this issue with the individual and change their lives because there’s nothing quicker to change the body than the ketogenic diet. We also have to monitor the individuals and monitor them through the process. Now we have Kenna Vaughn that she’s got some methods that we employ in the office and are helpful to her. Doctors do this around the country, but it’s beneficial in helping guide and allow for interaction and communication between us, the providers, and the patient. What kind of things do we offer, Kenna?
Kenna Vaughn: We have one-on-one coaching, which is great for when you’re just starting something out. Like they were talking about the ketogenic diet. You might be confused, and there is misinformation. So with this one-on-one coaching, it’s great because we can connect through an app that we have, and you pull out your phone. You can send a quick text message; hey, I saw one website said that I could eat this, but another said, this, can I have this? Things like that. We can clear up that confusion fast, which can keep you on track rather than doing that guessing game. We also have scales that connect to this app, which allows us to monitor the water weight they have and the fat that they have. And we can also monitor their activity through a wristband to constantly track the steps they’re taking. Ensure that they’re doing exercise because exercise is also great to help lower that blood glucose level.
Dr. Alex Jimenez DC*: You know, you mentioned that about the monitoring. We do that in the office along where we send the patients home with actual scales that are the mini BIAs and their hands and wrist. We can do pretty much for patients who want to connect with our office. We can directly get the information downloaded, and we can see their BIAs changing. We also use the in-body system, in which we do a deep analysis of the baseline basal metabolic rate, along with other factors that we’ve discussed prior podcast. This allows us to put together a quantifiable method to assess how the body is changing and rapidly restoring the body to or away from a metabolic syndrome episode. It’s a very uncomfortable feeling it really can. There’s nothing that destroys the body in these combinations of issues at one time. However, it’s easy to see that the body does everything quickly. It fixes a ketogenic diet, removes body weight, decreases the fat in the liver, decreases the intramuscular fat, restores blood sugar. It gets the mind working better. It helps the HDLs through some studies, and I know that Astrid knows there’s a study out there that pulls the information upon how the HDL are elevated with and with a ketogenic diet. We have a study here. You can put it on the screen right there that I think you found that shows the HDLs. Am I correct? And the apolipoprotein, the lipid part of the HDL, also is raised and activates the genetic component. Tell me about that.
Astrid Ornelas: So basically something that a lot of researchers, many health care professionals out there, doctors, they often say, is that when people have high cholesterol, you know, and we’re usually talking about the bad cholesterol. According to several research articles, it’s generally associated with a genetic predisposition when they have bad high cholesterol or the LDL fragment. If your parents, if your grandparents had high cholesterol, there is also an increased risk of you having a genetic predisposition to already having high cholesterol plus like add that like your diet. And if you follow a sedentary lifestyle and you know you don’t do enough exercise or physical activity, you have an increased risk of having higher bad cholesterol.
Dr. Alex Jimenez DC*: You know, I’m going to pull the information from I’ve noticed that Alexander’s pulling something information up here on the screen. He’s presenting the monitor where you can see his blood glucose and the screens that he’s going ahead and putting that up there for him. There you go. Alex, tell me what you’re talking about right there because I see that you’re talking about the apolipoprotein, the lipoproteins, and the HDL fragments there.
Alexander Isaiah: So kind of going into a little bit of everything here. So what happens when you eat something that is going to cause an increase in cholesterol? So first of all, you have these genes called Callum microns within the intestinal lumen or your GI tract, and they have apolipoprotein B 48. They have a B 48 because it’s 48 percent of apolipoprotein B 100, so it’s just a little different variation. These microns will bring these through the body and transfer them into the capillaries using apolipoprotein C and apolipoprotein E. Once they enter the capillaries, they’re going to degrade and allow for different aspects of the body to use them. So I have three tissues. We have adipose tissue, cardiac tissue, and skeletal muscle. So cardiac tissue has the lowest KM, and adipose tissue has the highest KM. So what is KM? KM is just a measurement of the way that the enzymes are used. So a low KM means a high specificity for binding to these fatty acids, and a high Km means low specificity for them. So what are the three parts of the body? They use the most energy. It’s the brain, the heart, and the kidneys. Those are the most caloric consumption parts of the body to stay alive. So, first of all, the heart relies large amounts on these fatty acids here, and transferring them to the heart uses mostly fatty acids. I think it’s about 80 percent; 70 to 80 percent of its fuel comes from fatty acids. And to deliver these, your body uses these Callum microns. So once the Callum microns exit the capillaries, it’s already an LDL. It has two choices: the LDL, It can be taken back to the liver or can switch its contents with HDL, and the seals can deliver them correctly to the proper places. So that’s why HDL is so important because they deliver them to the appropriate places if these Callum microns or these LDLs aren’t transferred correctly back to the liver. So why is LDL so detrimental to the system of our body? So here’s a couple of reasons why. So as LDL scavenges throughout the body, they are seen as a foreign object by our macrophages, and our macrophages are our cells used for immune response. So the macrophages end up engulfing these LDLs, and they turn into these things called foam cells. Foam cells become atherosclerotic plaque eventually. But what they do is they embed themselves within or under the surface of the epithelial lining, causing a buildup of these foam cells here and eventually blocking the pathways, causing a plaque. So by eating better fats, having a higher amount of HDL, you can avoid these plaques and avoid atherosclerotic plaques, which clog up your arteries.
Dr. Alex Jimenez DC*: You know what, actually, the link between atherosclerotic plaques and metabolic syndrome you’ve made very, very clear at this point, and that is the reason why prolonged states of the metabolic syndrome do create these disorders. I want to take a moment to thank the entire crew here because what we’re doing is we’re bringing in a lot of information and a lot of teams. And if someone has an issue, I want them to meet the face they’re going to see when they walk into the office. So, Trudy, tell them how we greet them and what we do with them when they walk in if they feel they may be a victim of metabolic syndrome.
Trudy Torres: Well, we’re very blessed to have a very exciting and energized office. You’re always going to feel at home. If we don’t have the correct answer at that moment, we’re certainly going to research. We’re not going to toss your side. We’re always going to get back to you. Everybody gets treated as an individual. You know, each vessel that we have, it’s unique in its way. So we certainly don’t create a cookie-cutter approach. We’re always going to make sure that, as I said, you walk away with the most and valuable, informed option for yourself. We’re just a phone call away. We’re just a click away. And, you know, don’t ever feel that there’s not a reasonable question. We always want to make sure that all the questions and concerns you have always get the best answer possible.
Dr. Alex Jimenez DC*: Guys, I want to tell you, thank you. And I want to also share with you that we happen to be in the fantastic facilities when we do; there’s exercise involved with returning the body to a normal state. We function out of the PUSH Fitness Center. We’re doing the podcast from the fitness center. And you can see the information herewith Danny Alvarado. And he’s the one that or Daniel Alvarado, the director of Push Fitness who we work with a bunch of therapies and physical therapists to help you restore your body to where it should be. We look forward to coming back, and as I said, if you appreciate, are you like what we have here, reach down on the little bottom, hit the little button, and hit subscribe. And then make sure you hit the bell so you can be the first to hear what we got to go on. OK, thank you, guys, and we welcome you again. And God bless. Have a good one.
The body’s metabolism along with body composition go hand in hand. The higher the metabolism the faster the body burns calories. The slower the metabolism the longer it takes and leads to fat storage as well as other issues, which include:
Metabolism is linked with weight gain and loss because it is a biological process involved with energy and calories. The process of the body converting food and drink into energy. The process involves the calories in food and drinks that get combined with oxygen to release energy that the body needs to operate.
Body Composition Linked To Body’s Metabolism
Metabolism varies for every individual. Here are two body composition profiles.
Individual A has a much smaller Basal Metabolic Rate than Individual B. This means individual B needs more calories than individual A to provide the body with the proper energy to function without losing weight. Because the Basal Metabolic Rate is bigger, the metabolism is bigger. The most important factor playing into Basal Metabolic Rate is the amount of Lean Body Mass every individual has.
The more Lean Body Mass the greater the Basal Metabolic Rate will be. Strength training for muscle gain will increase lean body mass and is recommended to increase metabolism. For example: Take a look at Jane and Sarah, two individuals who are similar in age, height, weight, and gender.
Despite being similar in age, height, weight, and gender, these two individuals have very different body compositions, as well as have different Basal Metabolic Rates.
Metabolism and Weight Gain
Take a deeper look at slow metabolism. It is not about being fast or slow but weight gain is almost always the result of caloric imbalance that goes on over a period of time. Two major factors are:
An individual’s energy level and how active they are
The thermic effect of food or the energy the body uses when digesting food
To take a closer look into the body’s metabolism and weight gain, take the two individuals above, Jane and Sarah, and see what could happen in real treatment development that includes diet and exercise. First, the TDEE for Jane and Sarah needs to be estimated, using their BMRs as a guide. Based on their compositions, it’s fair to assume that Jane is involved in less physical activity/exercise than Sarah. So an activity level of sedentary for Jane will be assigned and light activity will be assigned for Sarah.
Using these numbers and multiplying them by the appropriate activity factor, Jane�s TDEE can be estimated to be 1573 calories and Sarah�s 1953 calories, a difference of 380 calories. When activity levels are factored in, the difference in actual caloric needs gets magnified. This is an estimate of the calories Jane and Sarah will need to burn in a day. The nutritionist and/or health coach place both of them on a diet of 1,800 calories a day. This is the estimated calorie intake recommended by the USDA for sedentary women between 26-30 years of age.
Let’s say they both follow the diet perfectly without any extra, high-calorie snacks/treats. Jane will end each day with a surplus of 227 calories, while Sarah ends each day with a slight calorie deficit of 153 calories a day. When in a calorie surplus taking more calories and living a sedentary lifestyle, weight gain, specifically, fat storage will be experienced. 227 extra calories a day doesn’t seem like a lot, but that is a single soda. However, over time, 227 calories a day becomes 1,589 extra calories a week and 7,037 extra calories a month, which is around 2 pounds of fat gain every month.
So despite the same height, gender, similar weight, and similar ages, the difference between Jane and Sarah is their body compositions. Jane will experience weight gain over time while Sarah might experience some weight loss because of the calorie deficit, even though the diets are the same. This is because each individual’s caloric needs are different and may seem small at first, but increases to significant differences over time.
Making The Body’s Metabolism Work
With the correct exercise and dietary plan, an individual can make their metabolism work for them. Because the body needs more energy to support itself when it has more Lean Body Mass, working to increase Lean Body Mass will increase Basal Metabolic Rate. Avoiding a decrease in metabolism can be done by maintaining the Lean Body Mass that is already present and also means maintaining Skeletal Muscle Mass. Skeletal Muscle Mass is not the same as Lean Body Mass but is the overall largest contributor. It is the muscles that will grow and develop through exercise.
Skeletal Muscle Mass is effectively developed through strength training, resistance exercise, and a healthy diet. This will help maintain Skeletal Muscle Mass. This is especially important as the body ages. Activity levels tend to drop and a healthy diet can become harder to maintain as responsibilities increase. Poor nutrition can lead to loss of Lean Body Mass over time, which leads to a decrease in overall metabolism. Balancing diet and metabolism. The example of Jane shows a well-intentioned dietary plan that does not match the metabolism of the person practicing it.
Even though Jane was told that 1,800 calories are right for her based on age and gender, her metabolism does not require that calorie intake. This will cause weight gain despite any efforts to eat a healthy diet. This is where a health coach and nutritionist come in. The first step is to get the information needed to get the answers by getting an accurate body composition analysis.
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The scope of our information is limited to chiropractic, musculoskeletal, physical medicines, wellness, and sensitive health issues and/or functional medicine articles, topics, and discussions. We use functional health & wellness protocols to treat and support care for injuries or disorders of the musculoskeletal system. Our posts, topics, subjects, and insights cover clinical matters, issues, and topics that relate and support directly or indirectly our clinical scope of practice.*
Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. We understand that we cover matters that require an additional explanation as to how it may assist in a particular care plan or treatment protocol; therefore, to further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900. The provider(s) Licensed in Texas& New Mexico*
Westerterp, Klaas R. �Exercise, energy balance, and body composition.��European journal of clinical nutrition�vol. 72,9 (2018): 1246-1250. doi:10.1038/s41430-018-0180-4
Mazzoccoli, Gianluigi. �Body composition: Where and when.��European journal of radiology�vol. 85,8 (2016): 1456-60. doi:10.1016/j.ejrad.2015.10.020
Metabolic syndrome is the term for a group of risk factors like heart disease, diabetes, along with other health issues. The number of individuals dealing with the condition could be as high as 1 in 4. An individual can have one risk factor but most have several in combination. When there are three of these risk factors it becomes metabolic syndrome. The syndrome is a collection of conditions, that culminate in a correlative diagnosis. Risk factors/Symptoms include some or all of the following:
If left untreated and continued poor life choices that include unhealthy diet, lack of physical activity/exercise, and habit formation an individual can die from complications of the syndrome. The condition requires clinical treatment and medical assistance, however, chiropractic has been seen as a viable way to help treat the syndrome.
The syndrome can have several causes that progress together:
Age the risk goes up as an individual gets older
Genetics and family history
Insulin resistance, a condition where the body can’t use insulin properly
The resistance can lead to high blood sugar levels
Individuals with metabolic syndrome tend to have excessive blood clotting and inflammation throughout the body. However, research has not shown whether these conditions cause the syndrome or worsen it.
Chiropractic�s role is to stabilize the spine and the body. Too much weight leads to spinal dislocation and vertebral compression issues. This can lead to nerve impingement and disc problems. Even a small subluxation can turn into an extreme condition/s with widespread symptoms. Individuals that are overweight require a spinal realignment in order to gain proper stability. A chiropractor will administer corrective adjustments to generate the body’s natural healing process in the affected areas.
Restoring the nerve pathways will promote better blood flow and nutrient delivery to and through the spine. Chiropractic will set the tone for a metabolic syndrome reversal. The second phase of treatment will look at diet and exercise. This serves a dual purpose of introducing proper nutrition to the body, encouraging weight loss, and conditioning the individual’s mindset for the lifestyle adjustments/changes. A healthy/balanced spine will help those with metabolic syndrome get a proper foothold on turning their poor lifestyle into a healthy one.
The syndrome can be reversed with the right treatment approach. Usually, this begins with weight loss. Once the weight begins to reduce the secondary benefits kick in. This includes a reduction in blood pressure and a decrease in triglycerides. Once an individual’s spine is stable, they will then be educated on how to adapt and apply a long-term plan to maintain healthy habits for diet, physical activity, sleep, and stress relief strategies. As chiropractors focus on whole-body wellness, treatment plans will also look at:
Remember, the spine is the root of the body. The key to wellness is total body balance. All-natural chiropractic medicine can help achieve optimal health.
Weight Loss Doctor of Chiropractic
Dr. Alex Jimenez�s Blog Post Disclaimer
The scope of our information is limited to chiropractic, musculoskeletal, physical medicines, wellness, and sensitive health issues and/or functional medicine articles, topics, and discussions. We use functional health & wellness protocols to treat and support care for injuries or disorders of the musculoskeletal system. Our posts, topics, subjects, and insights cover clinical matters, issues, and topics that relate and support directly or indirectly our clinical scope of practice.*
Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. We understand that we cover matters that require an additional explanation as to how it may assist in a particular care plan or treatment protocol; therefore, to further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900. The provider(s) Licensed in Texas& New Mexico*
Samson, Susan L, and Alan J Garber. �Metabolic syndrome.��Endocrinology and metabolism clinics of North America�vol. 43,1 (2014): 1-23. doi:10.1016/j.ecl.2013.09.009
Fructose is one of the main components of added sugar. It is a simple type of sugar that makes up about 50 percent of table sugar or sucrose. Table sugar is also made up of glucose or the main energy source of the human body. However, fructose needs to be turned into glucose by the liver before it can be used as fuel for energy by our cells. Fructose, sucrose, and glucose are all naturally found in fruits, vegetables, dairy products, and whole grains as well as in many processed foods. The effects of this simple sugar on our health have been a controversial topic for many years. Research studies are starting to demonstrate the connection between fructose and obesity, diabetes, and even cancer.
What is Fructose?
Fructose, also referred to as fruit sugar, is a monosaccharide or simple sugar like glucose. It’s naturally found in fruits, most root vegetables, agave, and honey. Moreover, it’s commonly added to processed foods as high-fructose corn syrup. The fructose used in high-fructose corn syrup mainly comes from corn, sugar beets, and sugar cane. High-fructose corn syrup is made from cornstarch and it has more of this simple sugar than glucose, compared to regular corn syrup. Fructose has the sweetest taste of the three sugars. It is digested and absorbed differently by the human body. Because monosaccharides are simple sugars, they don’t need to be broken down to be used as fuel for energy by our cells.
Natural foods that are high in fructose can include:
Similar to glucose, fructose is absorbed directly into the bloodstream through the small intestine. Healthcare professionals have found that fructose has the least impact on blood sugar levels. It increases blood sugar levels much more gradually than glucose does and it doesn’t seem to immediately affect insulin levels. However, although this simple sugar has the least impact on blood sugar levels than any of the other simple types of sugars, it may ultimately cause more long-term negative effects on the human body. Fructose needs to be turned into glucose by the liver before it can be used as fuel for energy by our cells. Eating excess fructose can increase triglycerides and lead to metabolic syndrome.
Why is Fructose Bad for You?
When people eat a diet that is high in calories and processed foods with lots of high-fructose corn syrup, the liver can become overwhelmed and start turning fructose into fat. Research studies are starting to demonstrate the connection between this simple sugar and an increased risk of developing a variety of health issues, including obesity, type 2 diabetes, and even cancer. Many healthcare professionals also believe that eating excess fructose is one of the main causes of metabolic disorders. However, there currently isn’t enough evidence to demonstrate the full extent to which fructose can contribute to these health issues. Nevertheless, numerous research studies have justified these controversial concerns.
Research studies have demonstrated that eating excess fructose can increase LDL or bad cholesterol which may lead to fat accumulation around the organs and heart disease. As a result, evidence showed that the deposition of fat in the liver due to the negative effects of this simple sugar can also result in non-alcoholic fatty liver disease. Eating excess fructose may also affect body fat regulation. Other research studies have demonstrated that because fructose doesn’t suppress appetite as much as other types of sugars do, it can promote overeating which may lead to obesity, insulin resistance, and type 2 diabetes. Furthermore, evidence has demonstrated that fructose can increase uric acid levels and cause gout.
For information regarding if fructose is bad for your health, please review the following article:
AS PREVIOUSLY MENTIONED IN THE FOLLOWING ARTICLE, FRUCTOSE IS ONE OF THE MAIN COMPONENTS OF ADDED SUGAR. IT IS A SIMPLE SUGAR THAT MAKES UP APPROXIMATELY 50 PERCENT OF TABLE SUGAR OR SUCROSE. TABLE SUGAR ALSO CONSISTS OF GLUCOSE OR THE MAIN ENERGY SOURCE OF THE HUMAN BODY. HOWEVER, FRUCTOSE NEEDS TO BE CONVERTED INTO GLUCOSE BY THE LIVER BEFORE IT CAN BE UTILIZED AS FUEL FOR ENERGY BY OUR CELLS. FRUCTOSE, SUCROSE, AND GLUCOSE ARE ALL NATURALLY FOUND IN SEVERAL FRUITS, VEGETABLES, DAIRY PRODUCTS, AND WHOLE GRAINS AS WELL AS IN MANY PROCESSED FOODS. THE EFFECTS OF THIS SIMPLE SUGAR ON OUR HEALTH HAVE BEEN A CONTROVERSIAL TOPIC FOR MANY YEARS. RESEARCH STUDIES ARE STARTING TO DEMONSTRATE THE CONNECTION BETWEEN FRUCTOSE AND OBESITY, DIABETES, AND EVEN CANCER. IN THE FOLLOWING ARTICLE, WE DISCUSS IF FRUCTOSE IS BAD FOR YOUR HEALTH. DRINKING SMOOTHIES ADD A HEALTHY NUTRITIONAL BOOST.� -�DR. ALEX JIMENEZ D.C., C.C.S.T. INSIGHTS
Sweet and Spicy Juice
Servings: 1 Cook time: 5-10 minutes
� 1 cup honeydew melons
� 3 cups spinach, rinsed
� 3 cups Swiss chard, rinsed
� 1 bunch cilantro (leaves and stems), rinsed
� 1-inch knob of ginger, rinsed, peeled, and chopped
� 2-3 knobs whole turmeric root (optional), rinsed, peeled, and chopped
Juice all ingredients in a high-quality juicer. Best served immediately.
Red peppers have almost 2.5 times more vitamin C than oranges
Citrus fruits like oranges are a great source of vitamin C, however, there are other fruits and vegetables that offer an even better boost of this essential nutrient. Just half a red pepper, eaten raw, offers more than your requirement of vitamin C for the day, according to healthcare professionals. Cut it into crudit�s for a healthy mid-morning or afternoon snack. Red peppers are also rich in a variety of other essential nutrients, including vitamin A, B6, folate, and antioxidants!
The scope of our information is limited to chiropractic, musculoskeletal, physical medicines, wellness, and sensitive health issues and/or functional medicine articles, topics, and discussions. We use functional health & wellness protocols to treat and support care for injuries or disorders of the musculoskeletal system. Our posts, topics, subjects, and insights cover clinical matters, issues, and topics that relate and support directly or indirectly our clinical scope of practice.* Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. We understand that we cover matters that require an additional explanation as to how it may assist in a particular care plan or treatment protocol; therefore, to further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900. The provider(s) Licensed in Texas*& New Mexico*�
Curated by Dr. Alex Jimenez D.C., C.C.S.T.
Gunnars, Kris. �Is Fructose Bad for You? The Surprising Truth.� Healthline, Healthline Media, 23 Apr. 2018, www.healthline.com/nutrition/why-is-fructose-bad-for-you#section1.
Nall, Rachel. �Is Fructose Bad for You? Benefits, Risks, and Other Sugars.� Medical News Today, MediLexicon International, 28 Nov. 2018, www.medicalnewstoday.com/articles/323818.
Groves, Melissa. �Sucrose vs Glucose vs Fructose: What’s the Difference?� Healthline, Healthline Media, 8 June 2018, www.healthline.com/nutrition/sucrose-glucose-fructose.
Rizkalla, Salwa W. �Health Implications of Fructose Consumption: A Review of Recent Data.� National Center for Biotechnology Information, BioMed Central, 4 Nov. 2010, www.ncbi.nlm.nih.gov/pmc/articles/PMC2991323/.
Daniluk, Julie. �5 Health Benefits of Red Peppers. Plus, Our World’s Healthiest Pizza Recipe.� Chatelaine, 26 Feb. 2016, www.chatelaine.com/health/healthy-recipes-health/five-health-benefits-of-red-peppers/.
If you are experiencing any of these situations, then you might want to try astaxanthin.
The body needs specific vitamins, minerals, and supplements from food, in order to function correctly. The variety of these nutrients can be found in healthy foods like fruits, vegetables, lean meats, and whole grains are precisely what the body needs. One of the essential nutrients that the body needs is antioxidants. Antioxidants help the body get rid of free radicals that can cause the body to become overly stressed and leading it to develop chronic illnesses. There is an antioxidant that can help the body and can be found in berries and pomegranates, and it is called astaxanthin.
Astaxanthin is a xanthophyll carotenoid that can be found in various microorganisms and marine animals. Astaxanthin is common for humans to apply and consume into the body while also being different. This red, fat-soluble pigment is quite different from the other kinds of food that contain carotenoids. Astaxanthin surprising does not contain vitamin A like all the other food containing carotenoids, and astaxanthin is an impressive antioxidant. Studies have shown that astaxanthin can not only be beneficial for the eyes but can provide nutritional support as well as having potential health-promoting effects in preventing and treating various diseases that can harm the body. Some of the various diseases that can harm the body when there is an excessive amount of free radicals can include:
Chronic inflammatory diseases
Another study found that astaxanthin was superior to fish oil due to astaxanthin having the ability to enhance the body’s immune response and thus lowering the risk of vascular and infectious diseases that can harm the body, causing it to dysfunction.
A Powerful Antioxidant
There are some fantastic beneficial properties that astaxanthin can provide for the body and help improve the body�s systems as well.
Astaxanthin is a powerful antioxidant since various chronic diseases are rooted in a disproportionate balance of reactive oxygen and nitrogen species to antioxidants. Studies have shown�that astaxanthin has been known to scavenge free radicals more effectively out of the body than beta-carotene. There was another study showing how the body�s DNA was damage due to low plasma 8 -OHdG (8-hydroxy-2′-deoxyguanosine) levels.
Boosts the Immune System
The publication of the immunomodulatory effects of astaxanthin is not getting enough attention as they should be. A test study has reported that dietary astaxanthin was able to stimulate mitogen-induced lymphocyte proliferation. This will help increase the natural killer cell cytotoxicity and even delay the hypersensitivity response in the body while also increasing the numbers of total T and B cells in the peripheral blood in the body. Another study showed how astaxanthin could help significantly enhanced lymphocyte proliferation in vitro and ex vivo. The studies also found that astaxanthin can be consumed in high concentrations without the risk of cytotoxicity.
Controls Glucose and Lipids
Surprisingly there has been new research that has been revealing about another unique but vital role that astaxanthin has. The studies show that it can modulate peroxisome proliferator-activated receptors or PPARs. What this function does is that it may have various applications in human health, including producing glucose and lipid homeostasis. Since PPARs are members of the nuclear hormone receptors in the body, they are a superfamily that plays roles in the expression of many genes that are regulating cellular differentiation and many other functions in the body.
There are at least three subtypes of PPARs that helps the major organs and help the metabolism of glucose and lipids. PPAR? can primarily be expressed in the liver, kidney, heart, and skeletal muscle, where it can be involved in lipid metabolism and insulin sensitivity to the body. Another subtype of PPARs is PPAR?, which plays a role in glucose and lipid homeostasis but also is the site of action in the adipose tissue in the body. When astaxanthin is being involved, astaxanthin is a PPAR? agonist but can act as either an agonist or antagonist to PPAR? receptors. Studies have found that PPAR? agonist and PPAR? antagonist in astaxanthin can decrease cholesterol and triglycerides in loaded HepG2 cells, while changing several enzymes expressions that are being involved in lipid and glucose metabolism pathways, thus resulting in a hypolipidemic effect in the body.
Surprisingly astaxanthin can be used to prevent exercise-induced free radical production and is a lesser-known application. Astaxanthin can enhance exercise performance and even improve the recovery process. The increase in the reactive oxygen and nitrogen species or RONS are being produced during an exercise regime is deleterious to the health. It is often combated with a matching increase in the endogenous antioxidant enzymes. However, when a person is doing excessive exercises, it can cause RONS to rise above the body’s natural capacity to eliminate them. This will cause an increased risk of oxidative damage in lipids, protein, and DNA molecules. In a review study, it showed the ability of astaxanthin to squelch the RONS generating during exercising. It reported that the antioxidant effects of astaxanthin could provide a variety of benefits to athletes.
Astaxanthin is a powerful immunomodulatory antioxidant that can support numerous biological pathways that are in the body. It can dampen the effects of a variety of chronic diseases and illnesses that can harm the body. Astaxanthin is useful for being a therapeutic and powerful nutraceutical while also being an excellent addition for someone who needs supplements to support their general health and well-being. Some of the products here are beneficial to the body as they help support the immune system while providing more excellent stability.
The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.
Ambati, Ranga Rao, et al. �Astaxanthin: Sources, Extraction, Stability, Biological Activities and Its Commercial Applications–a Review.� Marine Drugs, MDPI, 7 Jan. 2014, www.ncbi.nlm.nih.gov/pmc/articles/PMC3917265/.
Brown, Daniel R, et al. �Astaxanthin in Exercise Metabolism, Performance and Recovery: A Review.� Frontiers in Nutrition, Frontiers Media S.A., 18 Jan. 2018, www.ncbi.nlm.nih.gov/pmc/articles/PMC5778137/.
Brown, Daniel R, et al. �Astaxanthin in Exercise Metabolism, Performance and Recovery: A Review.� Frontiers in Nutrition, Frontiers Media S.A., 18 Jan. 2018, www.ncbi.nlm.nih.gov/pmc/articles/PMC5778137/.
Choi, Chang-Ik. �Astaxanthin as a Peroxisome Proliferator-Activated Receptor (PPAR) Modulator: Its Therapeutic Implications.� Marine Drugs, MDPI, 23 Apr. 2019, www.ncbi.nlm.nih.gov/pmc/articles/PMC6521084/.
Lin, Kuan-Hung, et al. �Astaxanthin, a Carotenoid, Stimulates Immune Responses by Enhancing IFN-? and IL-2 Secretion in Primary Cultured Lymphocytes in Vitro and Ex Vivo.� International Journal of Molecular Sciences, MDPI, 29 Dec. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4730289/.
Park, Jean Soon, et al. �Astaxanthin Decreased Oxidative Stress and Inflammation and Enhanced Immune Response in Humans.� Nutrition & Metabolism, BioMed Central, 5 Mar. 2010, www.ncbi.nlm.nih.gov/pmc/articles/PMC2845588/?report=reader.
Team, DFH. �Applications of the Antioxidant, Astaxanthin.� Designs for Health, 27 June 2019, blog.designsforhealth.com/node/1047.
Yuan, Jian-Ping, et al. �Potential Health-Promoting Effects of Astaxanthin: a High-Value Carotenoid Mostly from Microalgae.� Molecular Nutrition & Food Research, U.S. National Library of Medicine, Jan. 2011, www.ncbi.nlm.nih.gov/pubmed/21207519.
The University offers a wide variety of medical professions for functional and integrative medicine. Their goal is to inform individuals who want to make a difference in the functional medical fields with knowledgeable information that they can provide.
The ketogenic diet also referred to as the keto diet, is a low-carbohydrate, high-fat diet that has been demonstrated to have a variety of health benefits, especially for people with metabolic syndrome. Several research studies found that the ketogenic diet can help promote weight loss and improve overall wellness. Researchers also found that the keto diet may even be beneficial against diabetes, epilepsy, Alzheimer’s disease, and cancer, among others.
What is the Ketogenic Diet?
As previously mentioned, the keto diet is a low-carb, high-fat diet similar to the Atkins diet, as well as other low-carbohydrate diets. The primary goal of the ketogenic diet is to considerably decrease the consumption of carbohydrates and replace them with “good” fats. Reducing carb intake will allow the body to enter a metabolic state, known as ketosis. During ketosis, the body becomes tremendously efficient at burning fat in order to turn it into energy for fuel. It will also produce ketones in the liver to be used as energy by the brain. The ketogenic diet can greatly improve high blood sugar levels and insulin resistance.
Metabolic syndrome is commonly characterized by 5 risk factors. People with 3 our of 5 risk factors may have metabolic syndrome, including:
Excess waist fat (> 40 inches in men, and > 35 inches in women)
High blood pressure (130/85 mm Hg)
Hight blood sugar or glucose levels (100 mg/dL or greater)
High triglyceride levels (150 mg/dL or greater)
Low HDL cholesterol (< 40 mg/dL in men or < 50 mg/dL in women)
Metabolic syndrome can increase the risk of a variety of health issues, including diabetes, stroke, and heart disease. Fortunately, the keto diet can help improve the risk factors associated with metabolic syndrome, such as increased HDL cholesterol as well as decreased blood pressure and blood sugar levels. In a controlled 12-week research study, people with metabolic syndrome following a calorie-restricted ketogenic diet lost 14 percent of their body fat. The research study also found that the participants had decreased triglycerides by more than 50 percent and experienced several other health benefits.
How the Keto Diet Helps Improve Metabolic Syndrome
The ketogenic diet has been demonstrated to help improve the risk factors associated with metabolic syndrome. As a low-carbohydrate, high- fat diet, the keto diet is effective in decreasing high blood sugar levels and improving insulin resistance by having the body break down body fat into ketones for energy. Metabolic syndrome is a cluster of signs that are associated with various health issues, including diabetes, stroke, and heart disease. The signs of metabolic syndrome include excess waist fat, high blood pressure, high blood sugar, high triglyceride levels, and low HDL or “good” cholesterol.
A research study conducted by researchers at Bethel University, Minnesota, USA, compared the health of three groups of adults with metabolic syndrome. The first group followed the ketogenic diet without exercise, the second group followed the standard American diet without exercise, and the third group followed the standard American diet with 30 minutes of exercise or physical activity for three to five days per week. The findings showed that the ketogenic diet without exercise was much more effective than the other groups at promoting weight loss, decreasing body fat and reducing HbA1c.
According to a variety of other research studies like the one above, the ketogenic diet may help improve a variety of other health issues, including:�
Type 2 Diabetes
Although there’s a variety of research studies on what is the best type of diet for people with type 2 diabetes to promote weight loss and improve insulin resistance, healthcare professionals recommend following the keto diet. The keto diet lowers carb intake which causes high blood glucose levels to drop, producing less insulin, burning fat, and potentially improving insulin sensitivity. Research studies suggest that the keto diet may be helpful for people with type 2 diabetes. Several hospitals have comprehensive programs dedicated to using the nutritional approach to help treat type 2 diabetes.
Excess weight and obesity increase the risk of developing type 2 diabetes. A small research study published in December 2016 in the journal Endocrine involved 45 obese participants either on a very-low-calorie ketogenic diet or a standard low-calorie diet. After two years, the participants following the keto diet lost approximately 27 pounds on average compared with less than 10 pounds in the low-calorie participants. The participants following the keto diet also lost more belly fat. The ketogenic diet also helped keep lean body mass during weight loss which prevented a metabolic slowdown.
Metabolic syndrome is a collection of risk factors, including excess waist fat, high blood pressure, high blood sugar, high triglyceride levels, and low HDL cholesterol, according to the American Heart Association. Improving insulin resistance may also reduce the risk of developing metabolic syndrome. One small research study on 30 adults found that adults with metabolic syndrome who followed the ketogenic diet for 10 weeks lost more weight and body fat as well as lowered their A1C levels compared with participants who followed a standard American diet, even with or without exercise.
About 23 percent of adults in the United States have metabolic syndrome. Although the risk factors for developing the collection of signs are significant, there are good news. Many of the risk factors associated with metabolic syndrome can be addressed through diet and lifestyle modifications, such as the ketogenic diet as well as exercise and physical activity. By making these changes, people can considerably reduce their risks of developing a variety of other health issues, including diabetes, stroke, and heart disease. Although metabolic syndrome can be a serious health issue, people can reduce their risks by reducing their weight; increasing exercise and physical activity; eating a heart-healthy diet that’s rich in fruits, vegetables, whole grains, and fish; as well as working with a healthcare professional to regulate blood pressure, blood sugar, blood cholesterol. In the following article, we will discuss how the ketogenic diet can help improve metabolic syndrome and its risk factors. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
The ketogenic diet also referred to as the keto diet, is a low-carbohydrate, high-fat diet that has been demonstrated to have a variety of health benefits, especially for people with metabolic syndrome. Several research studies found that the ketogenic diet can help promote weight loss and improve overall wellness. Researchers also found that the keto diet may even be beneficial against diabetes, epilepsy, Alzheimer’s disease, and cancer, among others.
The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.�
Curated by Dr. Alex Jimenez
Mawer, Rudy. �The Ketogenic Diet: A Detailed Beginner’s Guide to Keto.� Healthline, Healthline Media, 30 July 2018, www.healthline.com/nutrition/ketogenic-diet-101#weight-loss.
Spritzler, Franziska. �15 Health Conditions That May Benefit From a Ketogenic Diet.� Healthline, Healthline , 12 Sept. 2016, www.healthline.com/nutrition/15-conditions-benefit-ketogenic-diet.
Migala, Jessica. �Can Keto Cure You? 11 Conditions It May Help and 6 It Won’t: Everyday Health.� Everyday Health, Everyday Health Media, 28 Dec. 2018, www.everydayhealth.com/ketogenic-diet/diet/health-conditions-it-may-help-and-definitely-wont/.
Dr. Alex Jimenez Podcast: Metabolic Syndrome
Metabolic syndrome is a cluster of risk factors that can ultimately increase the risk of developing a variety of health issues, including heart disease, stroke, and diabetes, among other problems. Central obesity, high blood pressure, high blood sugar, high triglycerides, and low HDL or good cholesterol levels are the 5 risk factors associated with metabolic syndrome. Having at least three of the five risk factors may suggest the presence of metabolic syndrome. Dr. Alex Jimenez, Alexander Jimenez, Truide Torres, Kenna Vaughn, and Astrid Ornelas explain the 5 risk factors associated with metabolic syndrome, in further detail, as they recommend diet and lifestyle modification advice and guidelines, such as the ketogenic diet or the keto diet, as well as demonstrate the biochemical and chemical pathways that the body goes through during ketosis to help people with metabolic syndrome improve their overall health and wellness. From eating good fats and staying hydrated to exercise and better sleep, Dr. Alex Jimenez, Alexander Jimenez, Truide Torres, Kenna Vaughn, and Astrid Ornelas discuss how diet and lifestyle modifications, such as the ketogenic diet or keto diet, can help improve the 5 risk factors associated with metabolic syndrome to prevent the risk of developing a variety of other health issues, including heart disease, stroke, and diabetes. – Podcast Insight
Neural Zoomer Plus for Neurological Disease
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention.
Food Sensitivity for the IgG & IgA Immune Response
Dr. Alex Jimenez utilizes a series of tests to help evaluate health issues associated with a variety of food sensitivities and intolerances. The Food Sensitivity ZoomerTM is an array of 180 commonly consumed food antigens that offers very specific antibody-to-antigen recognition. This panel measures an individual�s IgG and IgA sensitivity to food antigens. Being able to test IgA antibodies provides additional information to foods that may be causing mucosal damage. Additionally, this test is ideal for patients who might be suffering from delayed reactions to certain foods. Utilizing an antibody-based food sensitivity test can help prioritize the necessary foods to eliminate and create a customized diet plan around the patient�s specific needs.
Gut Zoomer for Small Intestinal Bacterial Overgrowth (SIBO)
Dr. Alex Jimenez utilizes a series of tests to help evaluate gut health associated with small intestinal bacterial overgrowth (SIBO). The Vibrant Gut ZoomerTM offers a report that includes dietary recommendations and other natural supplementation like prebiotics, probiotics, and polyphenols. The gut microbiome is mainly found in the large intestine and it has more than 1000 species of bacteria that play a fundamental role in the human body, from shaping the immune system and affecting the metabolism of nutrients to strengthening the intestinal mucosal barrier (gut-barrier). It is essential to understand how the number of bacteria that symbiotically live in the human gastrointestinal (GI) tract influences gut health because imbalances in the gut microbiome may ultimately lead to gastrointestinal (GI) tract symptoms, skin conditions, autoimmune disorders, immune system imbalances, and multiple inflammatory disorders.
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Modern Integrated Medicine
The National University of Health Sciences is an institution that offers a variety of rewarding professions to attendees. Students can practice their passion for helping other people achieve overall health and wellness through the institution’s mission. The National University of Health Sciences prepares students to become leaders in the forefront of modern integrated medicine, including chiropractic care. Students have an opportunity to gain unparalleled experience at the National University of Health Sciences to help restore the natural integrity of the patient and define the future of modern integrated medicine.
Eating sweets does not relieve the craving for sugar?
If you are experiencing any of these situations, then you might be experiencing an imbalance of your blood glucose. Why not try adding berberine into your daily diet and lifestyle.
For many individuals reclaiming their health, the incidence of metabolic syndrome, and type 2 diabetes along with many other conditions that can be related to insulin resistance. Many local healthcare practitioners need all the tools to inform their patients as a powerful supplement that has been receiving recognition for its efficacy in improving the multiple parameters for metabolic health and improving glycemic control. This supplement is known as berberine, and the studies have shown that berberine is as effective as metformin and can help patients who have type 2 diabetes.
What Is Berberine?
Berberine is an alkaloid compound that is found in several plants like goldenseal, barberry, and tree turmeric. When berberine is crushed, it has a yellow color hue that is similar to curcumin and has been part of Chinese and Ayurvedic traditional medicine that has been used for thousands of years. Surprisingly berberine has worked in multiple ways and has been able to make some changes within the body�s cells and metabolic system. There has been research showing that berberine can transport in the bloodstream once it has been ingested and can activate the AMPK (AMP-activated protein kinase) enzyme. Once this happens, the enzyme is referred to as a “metabolic master switch” and can help regulate the significant organs and regulating the body’s metabolism.
The Health Benefits from Berberine
Research shows that berberine can provide many health benefits to the body, especially those who have been affected with type 2 diabetes and have metabolic syndrome. Here are some of the health benefits that berberine has to offer.
Studies have found that berberine is an active antimicrobial agent. Studies have shown that berberine can enhance the inhibitory efficacy of antibiotics against the bacteria Staphylococcus aureus. This type of bacteria can cause many health problems in the body, like sepsis, pneumonia, and meningitis. There is even another study that shows that when a person consumes a high concentration of berberine could kill the Staphylococcus aureus bacteria more quickly. The berberine effects can dissociate the bacteria protein into individual chains and separate them into their molecular weight.
Regulates Blood Glucose
Type 2 diabetes is a common disease that can make a person’s blood sugar to either rise or fall, causing them to DKA (diabetic ketoacidosis). With berberine, it can help regulate blood glucose in the body. Studies have shown that type 2 diabetes has become a worldwide health threat for people, and finding treatment for this disease is limited due to the availability of effective medications that can help control the blood glucose levels. With berberine, it can help reduce insulin resistance and surprisingly, regulate the blood glucose to healthy levels like metformin. The research even shows that berberine can also help regulate the body�s lipid metabolism as well.
More results showed that berberine could do the following:
Lower the insulin resistance to make the blood sugar to lower the hormone insulin more effectively.
It helps increase the glycolysis so the body can break down the sugars.
Decease the sugar produced in the liver.
It helps break down the carbohydrates in the gut microbiome.
It helps increase the beneficial bacteria in the gut to prevent inflammation.
Help Losing Weight
Studies have shown that berberine is an effective weight loss supplement for anyone who may be obese. There was a twelve-week study that showed that the participates took about 500 mg of berberine, and they lost about five pounds of body fat. While another study stated that about 37 participants that have metabolic syndrome took about 300 mg of berberine, and the results showed that the participants have dropped their BMI (body mass index) levels go from obese to overweight in three months. The participants even improved many of their health markers and lose their belly fat.
Many researchers believed that when people take berberine and see that they are losing their excess weight, it can help improve their fat-regulating hormones like insulin, adiponectin, and leptin in their body. There is still more research being done about berberine and how its beneficial weight loss effects can help anyone with metabolic syndrome and might be overly obese.
Berberine is a compound that is found in plants like tree turmeric, goldenseal, and barberry. It has a yellow color cue and has many beneficial properties. Berberine can help anyone who has type 2 diabetes and metabolic syndrome. For the beneficial properties, berberine can help regulate the body�s glucose hormones and has the same effects as the pharmaceutical drug, metformin. When people consume berberine, their metabolic system will begin to function correctly and begun to live a healthier life. Some products can help the metabolic system and the immune system by supporting sugar metabolism as well as reducing the glutathione for providing more excellent stability, bioavailability, and digestive comfort in the body.
The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.
Berry, Jennifer. �Everything You Need to Know about Berberine.� MedicalNewsToday, 19 July 2019, www.medicalnewstoday.com/articles/325798.php.
Chu, Ming, et al. �Role of Berberine in the Treatment of Methicillin-Resistant Staphylococcus Aureus Infections.� Scientific Reports, Nature Publishing Group, 22 Apr. 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC4840435/.
Gunnars, Kris. �Berberine � A Powerful Supplement With Many Benefits.� Healthline, 14 Jan. 2017, www.healthline.com/nutrition/berberine-powerful-supplement.
Hu, Yueshan, et al. �Lipid-Lowering Effect of Berberine in Human Subjects and Rats.� Phytomedicine, Urban & Fischer, 25 June 2012, www.sciencedirect.com/science/article/abs/pii/S0944711312001870.
Li, Zheng, et al. �Antioxidant and Anti-Inflammatory Activities of Berberine in the Treatment of Diabetes Mellitus.� Evidence-Based Complementary and Alternative Medicine, Hindawi, 11 Feb. 2014, www.hindawi.com/journals/ecam/2014/289264/.
Peng, Lianci, et al. �Antibacterial Activity and Mechanism of Berberine against Streptococcus Agalactiae.� International Journal of Clinical and Experimental Pathology, e-Century Publishing Corporation, 1 May 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4503092/.
Team, DFH. �Berberine: Boon for Metabolic Syndrome.� Designs for Health, 5 Jan. 2018, blog.designsforhealth.com/berberine-boon-for-metabolic-syndrome.
Yang, Jing, et al. �Berberine Improves Insulin Sensitivity by Inhibiting Fat Store and Adjusting Adipokines Profile in Human Preadipocytes and Metabolic Syndrome Patients.� Evidence-Based Complementary and Alternative Medicine: ECAM, Hindawi Publishing Corporation, 2012, www.ncbi.nlm.nih.gov/pmc/articles/PMC3310165/.
Yin, Jun, et al. �Efficacy of Berberine in Patients with Type 2 Diabetes Mellitus.� Metabolism: Clinical and Experimental, U.S. National Library of Medicine, May 2008, www.ncbi.nlm.nih.gov/pmc/articles/PMC2410097/.
The University offers a wide variety of medical professions for functional and integrative medicine. Their goal is to inform individuals who want to make a difference in the functional medical fields with knowledgeable information that they can provide.
Metabolic syndrome is caused by having more than one condition. Metabolic syndrome often leaves individuals with headaches, joint pain, fatigue, and more! Metabolic syndrome is an epidemic all over the world, but in the US, we are seeing this condition all too often.
Metabolic Syndrome can be defined as having two or more of the conditions listed below:
Women with abdominal fat or a waistline greater than 35
Men with abdominal fat or a waistline greater than 40
Individuals with high blood pressure ( 130/85 or higher)
Patients with triglycerides higher than 150
A fasting glucose of 100 or greater
Low HDL ( good cholesterol ) less than 40 in men and 50 for women
These symptoms are often associated with inflammation. Many people believe inflammation is just something that occurs in the joints and on the skin, but inflammation can occur to the organs inside the body and create havoc.
Metabolic syndrome does not target a specific population but can affect anyone who has an overlap of the factors listed above. Those who have an “apple” or “pear” body shape, are likely to have higher abdominal fat, and therefore are more at risk.
As individuals age, their chances of developing metabolic syndrome increases. On top of age, previously having or having a history of diabetes in one’s family also increases their risk of developing metabolic syndrome.
Speaking from personal experience, and having Type 1 Diabetes myself, I can say that metabolic syndrome really takes a toll on one’s body. With experiencing these symptoms first hand, it can leave your body feeling exhausted. When the blood glucose level in the body rises, it causes the blood to become thick due to the excess sugar in the blood. This then causes the heart to work harder and raise the body’s blood pressure due to the effort needed to pump. From here, the body responds with a hard and heavy headache, nausea, occasional vomiting, increased thirst, increased urination, and blurred vision. Recovering from a day of high blood sugars can leave you feeling defeated and similar to feeling like you are recovering from the flu.
One of the things that occur within the body when an individual has metabolic syndrome is their insulin sensitivity decreases. Insulin is the hormone produced that helps to turn the food you eat into fuel for the body or store it as fat. When the insulin sensitivity becomes decreased, it means not enough glucose in the body is being absorbed.� Leading to high blood glucose levels and increases the risk for Type 2 Diabetes.
For those who are suffering from metabolic syndrome, or have one or more of the above risk factors there are ways to take charge. The benefits of taking charge and preventing metabolic syndrome from getting worse or returning means getting back the energy you thought was lost. By decreasing your symptoms and increasing your energy, you could be feeling better than you remembered.
The best diet to quickly gain control of blood sugars and raise HDL is the ketogenic diet. This diet works by eating low carb, high-fat foods. In turn, this makes the body burn fat as fuel rather than carbohydrates. It starts by burning the fat around the pancreas and liver and then starts to burn the intramuscular fat ( excess abdominal weight ). By eliminating most carbs and increasing water intake, individuals can see a decrease in depression, brain fog, their risk of stroke, and blood pressure. All while seeing an increase in sleep and energy.
One of the best ways to reach your goals and stay healthy is to work with a team who understands them and is willing to educate you. We provide 1:1 coaching, scales to track weight that also reports the water weight and BMI of the individual, wrist bands to track caloric activity, and education. The education will help you understand why you are following a specific diet or food guidelines, how that food is breaking down to help you, and what foods to avoid. We will never leave a patient confused or with unanswered questions.
Speaking from personal experience, it is best to get a handle on these symptoms before they cause permanent damage. There are ways and things to do to help reduce your risk. I highly recommend seeing us, or a local doctor to start to build your plan. We can create personalized plans that will help you reach your goals, lower your risk, and work with your lifestyle. Take it from me, you do not want to be stuck feeling the side effects metabolic syndrome comes with.� -Kenna Vaughn, Senior Health Coach
The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.
We usually talk of energy in general terms, as in �I don�t have a lot of energy today� or �You can feel the energy in the room.� But what really is energy? Where do we get the energy to move? How do we use it? How do we get more of it? Ultimately, what controls our movements? The three metabolic energy pathways are the�phosphagen system, glycolysis�and the�aerobic system.�How do they work, and what is their effect?
Albert Einstein, in his infinite wisdom, discovered that the total energy of an object is equal to the mass of the object multiplied by the square of the speed of light. His formula for atomic energy, E = mc2, has become the most recognized mathematical formula in the world. According to his equation, any change in the energy of an object causes a change in the mass of that object. The change in energy can come in many forms, including mechanical, thermal, electromagnetic, chemical, electrical or nuclear. Energy is all around us. The lights in your home, a microwave, a telephone, the sun; all transmit energy. Even though the solar energy that heats the earth is quite different from the energy used to run up a hill, energy, as the first law of thermodynamics tells us, can be neither created nor destroyed. It is simply changed from one form to another.
The energy for all physical activity comes from the conversion of high-energy phosphates (adenosine�triphosphate�ATP) to lower-energy phosphates (adenosine�diphosphate�ADP; adenosine�monophosphate�AMP; and inorganic phosphate, Pi). During this breakdown (hydrolysis) of ATP, which is a water-requiring process, a proton, energy and heat are produced: ATP + H2O ���ADP + Pi�+ H+�+ energy + heat. Since our muscles don�t store much ATP, we must constantly resynthesize it. The hydrolysis and resynthesis of ATP is thus a circular process�ATP is hydrolyzed into ADP and Pi, and then ADP and Pi�combine to resynthesize ATP. Alternatively, two ADP molecules can combine to produce ATP and AMP: ADP + ADP ���ATP + AMP.
Like many other animals, humans produce ATP through three metabolic pathways that consist of many enzyme-catalyzed chemical reactions: the phosphagen system, glycolysis and the aerobic system. Which pathway your clients use for the primary production of ATP depends on how quickly they need it and how much of it they need. Lifting heavy weights, for instance, requires energy much more quickly than jogging on the treadmill, necessitating the reliance on different energy systems. However, the production of ATP is never achieved by the exclusive use of one energy system, but rather by the coordinated response of all energy systems contributing to different degrees.
1. Phosphagen System
During short-term, intense activities, a large amount of power needs to be produced by the muscles, creating a high demand for ATP. The phosphagen system (also called the ATP-CP system) is the quickest way to resynthesize ATP (Robergs & Roberts 1997). Creatine phosphate (CP), which is stored in skeletal muscles, donates a phosphate to ADP to produce ATP: ADP + CP ���ATP + C. No carbohydrate or fat is used in this process; the regeneration of ATP comes solely from stored CP. Since this process does not need oxygen to resynthesize ATP, it is anaerobic, or oxygen-independent. As the fastest way to resynthesize ATP, the phosphagen system is the predominant energy system used for all-out exercise lasting up to about 10 seconds. However, since there is a limited amount of stored CP and ATP in skeletal muscles, fatigue occurs rapidly.
Glycolysis is the predominant energy system used for all-out exercise lasting from 30 seconds to about 2 minutes and is the second-fastest way to resynthesize ATP. During glycolysis, carbohydrate�in the form of either blood glucose (sugar) or muscle glycogen (the stored form of glucose)�is broken down through a series of chemical reactions to form pyruvate (glycogen is first broken down into glucose through a process called�glycogenolysis). For every molecule of glucose broken down to pyruvate through glycolysis, two molecules of usable ATP are produced (Brooks et al. 2000). Thus, very little energy is produced through this pathway, but the trade-off is that you get the energy quickly. Once pyruvate is formed, it has two fates: conversion to lactate or conversion to a metabolic intermediary molecule called acetyl coenzyme A (acetyl-CoA), which enters the mitochondria for oxidation and the production of more ATP (Robergs & Roberts 1997). Conversion to lactate occurs when the demand for oxygen is greater than the supply (i.e., during anaerobic exercise). Conversely, when there is enough oxygen available to meet the muscles� needs (i.e., during aerobic exercise), pyruvate (via acetyl-CoA) enters the mitochondria and goes through aerobic metabolism.
When oxygen is not supplied fast enough to meet the muscles� needs (anaerobic glycolysis), there is an increase in hydrogen ions (which causes the muscle pH to decrease; a condition called acidosis) and other metabolites (ADP, Pi�and potassium ions). Acidosis and the accumulation of these other metabolites cause a number of problems inside the muscles, including inhibition of specific enzymes involved in metabolism and muscle contraction, inhibition of the release of calcium (the trigger for muscle contraction) from its storage site in muscles, and interference with the muscles� electrical charges (Enoka & Stuart 1992; Glaister 2005; McLester 1997). As a result of these changes, muscles lose their ability to contract effectively, and muscle force production and exercise intensity ultimately decrease.
3. Aerobic System
Since humans evolved for aerobic activities (Hochachka, Gunga & Kirsch 1998; Hochachka & Monge 2000), it�s not surprising that the aerobic system, which is dependent on oxygen, is the most complex of the three energy systems. The metabolic reactions that take place in the presence of oxygen are responsible for most of the cellular energy produced by the body. However, aerobic metabolism is the slowest way to resynthesize ATP. Oxygen, as the patriarch of metabolism, knows that it is worth the wait, as it controls the fate of endurance and is the sustenance of life. �I�m oxygen,� it says to the muscle, with more than a hint of superiority. �I can give you a lot of ATP, but you will have to wait for it.�
The aerobic system�which includes the�Krebs cycle�(also called the�citric acid cycle or TCA cycle) and the�electron transport chain�uses blood glucose, glycogen and fat as fuels to resynthesize ATP in the mitochondria of muscle cells (see the sidebar �Energy System Characteristics�). Given its location, the aerobic system is also called�mitochondrial respiration.�When using carbohydrate, glucose and glycogen are first metabolized through glycolysis, with the resulting pyruvate used to form acetyl-CoA, which enters the Krebs cycle. The electrons produced in the Krebs cycle are then transported through the electron transport chain, where ATP and water are produced (a process called�oxidative phosphorylation) (Robergs & Roberts 1997). Complete oxidation of glucose via glycolysis, the Krebs cycle and the electron transport chain produces 36 molecules of ATP for every molecule of glucose broken down (Robergs & Roberts 1997). Thus, the aerobic system produces 18 times more ATP than does anaerobic glycolysis from each glucose molecule.
Fat, which is stored as triglyceride in adipose tissue underneath the skin and within skeletal muscles (called�intramuscular triglyceride), is the other major fuel for the aerobic system, and is the largest store of energy in the body. When using fat, triglycerides are first broken down into free fatty acids and glycerol (a process called�lipolysis). The free fatty acids, which are composed of a long chain of carbon atoms, are transported to the muscle mitochondria, where the carbon atoms are used to produce acetyl-CoA (a process called�beta-oxidation).
Following acetyl-CoA formation, fat metabolism is identical to carbohydrate metabolism, with acetyl-CoA entering the Krebs cycle and the electrons being transported to the electron transport chain to form ATP and water. The oxidation of free fatty acids yields many more ATP molecules than the oxidation of glucose or glycogen. For example, the oxidation of the fatty acid palmitate produces 129 molecules of ATP (Brooks et al. 2000). No wonder clients can sustain an aerobic activity longer than an anaerobic one!
Understanding how energy is produced for physical activity is important when it comes to programming exercise at the proper intensity and duration for your clients. So the next time your clients get done with a workout and think, �I have a lot of energy,� you�ll know exactly where they got it.
Energy System Characteristics
Energy System Workouts
Have clients warm up and cool down before and after each workout.
An effective workout for this system is short, very fast sprints on the treadmill or bike lasting 5�15 seconds with 3�5 minutes of rest between each. The long rest periods allow for complete replenishment of creatine phosphate in the muscles so it can be reused for the next interval.
2 sets of 8 x 5 seconds at close to top speed with 3:00 passive rest and 5:00 rest between sets
5 x 10 seconds at close to top speed with 3:00�4:00 passive rest
This system can be trained using fast intervals lasting 30 seconds to 2 minutes with an active-recovery period twice as long as the work period (1:2 work-to-rest ratio).
8�10 x 30 seconds fast with 1:00 active recovery
4 x 1:30 fast with 3:00 active recovery
While the phosphagen system and glycolysis are best trained with intervals, because those metabolic systems are emphasized only during high-intensity activities, the aerobic system can be trained with both continuous exercise and intervals.
60 minutes at 70%�75% maximum heart rate
15- to 20-minute tempo workout at lactate threshold intensity (about 80%�85% maximum heart rate)
5 x 3:00 at 95%�100% maximum heart rate with 3:00 active recovery
Brooks, G.A., et al. 2000.�Exercise Physiology: Human Bioenergetics and Its Applications.Mountain View, CA: Mayfield.
Enoka, R.M., & Stuart, D.G. 1992. Neurobiology of muscle fatigue.�Journal of Applied Physiology, 72�(5), 1631�48.
Glaister, M. 2005. Multiple sprint work: Physiological responses, mechanisms of fatigue and the influence of aerobic fitness.�Sports Medicine, 35�(9), 757�77.
Hochachka, P.W., Gunga, H.C., & Kirsch, K. 1998. Our ancestral physiological phenotype: An adaptation for hypoxia tolerance and for endurance performance?�Proceedings of the National Academy of Sciences, 95,�1915�20.
Hochachka, P.W., & Monge, C. 2000. Evolution of human hypoxia tolerance physiology.�Advances in Experimental and Medical Biology, 475,�25�43.
McLester, J.R. 1997. Muscle contraction and fatigue: The role of adenosine 5′-diphosphate and inorganic phosphate.�Sports Medicine, 23�(5), 287�305.
Robergs, R.A. & Roberts, S.O. 1997.�Exercise Physiology: Exercise, Performance, and Clinical Applications.�Boston: William C. Brown.
Abstract: Metabolic syndrome (MetS) is established as the combination of central obesity and different metabolic disturbances, such as insulin resistance, hypertension and dyslipidemia. This cluster of factors affects approximately 10%�50% of adults worldwide and the prevalence has been increasing in epidemic proportions over the last years. Thus, dietary strategies to treat this heterogenic disease are under continuous study. In this sense, diets based on negative-energy-balance, the Mediterranean dietary pattern, n-3 fatty acids, total antioxidant capacity and meal frequency have been suggested as effective approaches to treat MetS. Furthermore, the type and percentage of carbohydrates, the glycemic index or glycemic load, and dietary fiber content are some of the most relevant aspects related to insulin resistance and impaired glucose tolerance, which are important co-morbidities of MetS. Finally, new studies focused on the molecular action of specific nutritional bioactive compounds with positive effects on the MetS are currently an objective of scientific research worldwide. The present review summarizes some of the most relevant dietary approaches and bioactive compounds employed in the treatment of the MetS to date.
It was during the period between 1910 and 1920 when it was suggested for the first time that a cluster of associated metabolic disturbances tended to coexist together . Since then, different health organisms have suggested diverse definitions for metabolic syndrome (MetS) but there has not yet been a well-established consensus. The most common definitions are summarized in Table 1. What is clear for all of these is that the MetS is a clinical entity of substantial heterogeneity, commonly represented by the combination of obesity (especially abdominal obesity), hyperglycemia, dyslipidemia and/or hypertension [2�6].
Obesity consists of an abnormal or excessive fat accumulation, for which the main cause is a chronic imbalance between energy intake and energy expenditure [7,8]. The excess of energy consumed is primarily deposited in the adipose tissue as triglycerides (TG) .
Dyslipidemia encompasses elevated serum TG levels, increased low density lipoprotein- cholesterol (LDL-c) particles, and reduced levels of high density lipoprotein-cholesterol (HDL-c) . It is associated with hepatic steatosis , dysfunction of pancreatic ?-cells  and elevated risk of atherosclerosis , among others.
Another main modifiable MetS manifestation is hypertension, which is mainly defined as a resting systolic blood pressure (SBP) ? 140 mmHg or diastolic blood pressure (DBP) ? 90 mmHg or drug prescription to lower hypertension . It usually involves narrowed arteries and is identified as a major cardiovascular and renal risk factor, related to heart and vascular disease, stroke and myocardial infarction [13,15�17].
Hyperglycemia, related insulin resistance and type 2 diabetes mellitus are characterized by an impaired uptake of glucose by the cells, that lead to elevated plasma glucose levels, glycosuria and ketoacidosis . It is responsible for different tissue damage that shortens the life expectancy of diabetics, involving cardiovascular diseases (CVD), atherosclerosis, hypertension , ?-cell dysfunction , kidney disease  or blindness . Currently, diabetes is considered the leading cause of death in developed countries .
Moreover, oxidative stress and low grade inflammation are two important mechanisms implicated in the etiology, pathogenesis, and development of MetS . Oxidative stress is defined as an imbalance between the pro-oxidants and antioxidants in the body . It plays a key role in the development of atherosclerosis by different mechanisms such as the oxidation of LDL-c particles  or impairment of HDL-c functions . Inflammation is an immune system response to injury hypothesized to be a major mechanism in the pathogenesis and progression of obesity related disorders and the link between adiposity, insulin resistance, MetS and CVD .
Although the prevalence of the MetS varies broadly around the word and depends on the source used for its definition, it is clear that over the last 40�50 years the number of people presenting with this syndrome has risen in epidemic proportions . Moreover, the frequency of this syndrome is increased in developed countries, sedentary people, smokers, low socioeconomic status population, as well as in individuals with unhealthy dietary habits [29,30].
For all of this, there is currently a wide concern to find effective strategies to detect, treat and control the comorbidities associated with MetS. This is a complex challenge as MetS is a clinical entity of substantial heterogeneity and therefore, the different cornerstones implicated in its development should be addressed. In this review we compiled and examined different dietary patterns and bioactive compounds that have pointed out to be effective in MetS treatment.
2. Dietary Patterns
Several dietary strategies and their potential positive effects on the prevention and treatment of the different metabolic complications associated to the MetS, are described below and summarized in Table 2.
2.1. Energy-Restricted Diet Strategies
Energy restricted diets are probably the most commonly used and studied dietary strategies for combating excess weight and related comorbidities. They consist in personalized regimes that supply less calories than the total energy expended by a specific individual .
A hypocaloric diet results in a negative energy balance and subsequently, in body weight reduction . Weight loss is achieved via fat mobilization from different body compartments as a consequence of the lipolysis process necessary to provide energy substrate [32,33]. In people who are overweight or suffering from obesity, as is the case of most people with MetS, weight loss is important as it is associated with improvement of related disorders such as abdominal obesity (visceral adipose tissue), type 2 diabetes, CVD or inflammation [32�36].
Moreover, as described above, low grade inflammation is associated with MetS and obesity. Therefore, of particular importance is the fact that in obese individuals following a hypocaloric diet, a depletion of plasma inflammatory markers such as interleukin (IL)-6 has been observed . Thus, caloric restriction in obese people suffering MetS may improve the whole-body pro-inflammatory state.
At the same time, body weight reduction is associated with improvements in cellular insulin signal transduction, increments in peripheral insulin sensitivity and higher robustness in insulin secretory responses [32,36]. People with excess body weight who are at risk of developing type 2 diabetes, may benefit from a hypocaloric regime by improving plasma glucose levels and insulin resistance.
In addition, different intervention trials have reported a relationship between energy restricted diets and lower risk of developing CVD. In this sense, in studies with obese people following a hypocaloric diet, improvements in lipid profile variables such as reductions of LDL-c and plasma�TG levels, as well as improvements in hypertension via depletion of SBP and DBP levels have been observed [35,37].
Among the different nutritional intervention trials, a reduction of 500�600 kcal a day of the energy requirements is a well-established hypocaloric dietary strategy, which has demonstrated to be effective in weight reduction [38,39]. However, the challenge lies in maintaining the weight loss over time, as many subjects can follow a prescribed diet for a few months, but most people have difficulty in maintaining the acquired habits over the long term [40,41].
2.2. Diets Rich in Omega-3 Fatty Acids
The very long-chain eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are essential omega-3 polyunsaturated fatty acids (n-3 PUFAs) for human physiology. Their main dietary sources are fish and algal oils and fatty fish, but they can also be synthesized by humans from ?-linolenic acid .
There is a moderate body of evidence suggesting that n-3 PUFAs, mainly EPA and DHA, have a positive role in the prevention and treatment of the pathologies associated to MetS .
In this context, it has been described that EPA and DHA have the ability to reduce the risk of developing CVD and cardiometabolic abnormalities as well as CVD-related mortality . These beneficial effects are thought to be mainly due to the ability of these essential fatty acids to reduce plasma TG levels .
Moreover, different studies have shown that people following an increased n-3 PUFA diet have reduced plasma levels of the pro-inflammatory cytokines IL-6 and tumor necrosis factor-alpha (TNF?), as well as plasma C-reactive protein (CRP) . These effects are probably mediated by resolvins, maresins and protectins, which are EPA and DHA metabolic products with anti-inflammatory properties .
There are some studies that have observed an association between n-3 ingestion and improvements or prevention of type 2 diabetes development. However, other studies found opposite results . Thus, it cannot be made any specific affirmation in this respect.
The European Food Safety Authority recommends and intake of 250 mg EPA + DHA a day, in the general healthy population as a primary prevention of CVD . These amounts can be achieved with an ingestion of 1�2 fatty fish meals per week .
2.3. Diets Based on Low Glycemic Index/Load
Over the last ten years, the concern about the quality of the carbohydrates (CHO) consumed has risen . In this context, the glycemic index (GI) is used as a CHO quality measure. It consists in a ranking on a scale from 0 to 100 that classifies carbohydrate-containing foods according to the postprandial glucose response . The higher the index, the more promptly the postprandial serum glucose rises and the more rapid the insulin response. A quick insulin response leads to rapid hypoglycemia, which is suggested to be associated with an increment of the feeling of hunger and to a subsequent higher caloric intake . The glycemic load (GL) is equal to the GI multiplied by the number of grams of CHO in a serving .
There is a theory which states that MetS is a consequence of an elevated intake of high GI foods over time, among others unhealthy dietary habits . In this sense, following a diet rich in high GI CHO has been associated with hyperglycemia, insulin resistance, type 2 diabetes, hypertriglyceridemia, CVD, and obesity [47,50,51], abnormalities directly related to MetS.
On the contrary, a low GI diet has been associated with slower absorption of the CHO and subsequently smaller blood glucose fluctuations, which indicate better glycemic control . In patients with type 2 diabetes, diets based on low GI are associated with reductions in glycated hemoglobin (HbA1c) and fructosamine blood levels, two biomarkers used as key monitoring factors in diabetes management [52,53].
For all of this, it is common to find the limitation of CHO at high GI among the advice for MetS treatment , in particular with respect to �ready-to-eat processed foods� including sweetened beverages, soft drinks, cookies, cakes, candy, juice drinks, and other foods which contain high amounts of added sugars .
2.4. Diets with High Total Antioxidant Capacity
Dietary total antioxidant capacity (TAC) is an indicator of diet quality defined as the sum of antioxidant activities of the pool of antioxidants present in a food . These antioxidants have the capacity to act as scavengers of free radicals and other reactive species produced in the organisms . Taking into account that oxidative stress is one of the remarkable unfortunate physiological states of MetS, dietary antioxidants are of main interest in the prevention and treatment of this multifactorial disorder . Accordingly, it is well-accepted that diets with a high content of spices, herbs, fruits, vegetables, nuts and chocolate, are associated with a decreased risk of oxidative stress-related diseases development [58�60]. Moreover, several studies have analyzed the effects of dietary TAC in individuals suffering from MetS or related diseases [61,62]. In the Tehran Lipid and Glucose Study it was demonstrated that a high TAC has beneficial effects on metabolic disorders and especially prevents weight and abdominal fat gain . In the same line, research conducted in our institutions also evidenced that beneficial effects on body weight, oxidative stress biomarkers and other MetS features were positively related with higher TAC consumption in patients suffering from MetS [63�65].
In this sense, the World Health Organization (WHO) recommendation for fruit and vegetables consumption (high TAC foods) for the general population is a minimum of 400 g a day . Moreover, cooking with spices is recommended in order to increase the TAC dietary intake and, at the same time, maintain flavor while reducing salt .
2.5. Moderate-High Protein Diets
The macronutrient distribution set in a weight loss dietary plan has commonly been 50%�55% total caloric value from CHO, 15% from proteins and 30% from lipids [57,68]. However, as most people have difficulty in maintaining weight loss achievements over time [69,70], research on increment of protein intake (>20%) at the expense of CHO was carried out [71�77].
Two mechanisms have been proposed to explain the potential beneficial effects of high-moderate protein diets: the increment of diet-induced thermogenesis  and the increase of satiety . The increment of the thermogenesis is explained by the synthesis of peptide bonds, production of urea and gluconeogenesis, which are processes with a higher energy requirement than the metabolism of lipids or CHO . An increment of different appetite-control hormones such as insulin, cholecystokinin or glucagon-like peptide 1, may clarify the satiety effect .
Other beneficial effects attributed to moderate-high protein diets in the literature are the improvement of glucose homeostasis , the possibility of lower blood lipids , the reduction of blood pressure , the preservation of lean body mass  or the lower of cardiometabolic disease risk [84,85]. However, there are other studies that have not found benefits associated to a moderate-high protein diet . This fact may be explained by the different type of proteins and their amino acid composition , as well as by the different type of populations included in each study . Therefore, more research in the field is needed in order to make these results consistent.
In any case, when a hypocaloric diet is implemented, it is necessary to slightly increase the amount of proteins. Otherwise it would be difficult to reach the protein energy requirements, established as 0.83 g/kg/day for isocaloric diets and which should probably be at least 1 g/kg/day for energy-restricted diets .
2.6. High Meal Frequency Pattern
The pattern of increasing meal frequency in weight loss and weight control interventions has currently become popular among professionals [87,88]. The idea is to distribute the total daily energy�intake into more frequently and smaller meals. However, there is no strong evidence about the efficacy of this habit yet . While some investigations have found an inverse association between the increment of meals per day and body weight, body mass index (BMI), fat mass percentage or metabolic diseases such as coronary heart disease or type 2 diabetes [71,88,90�92], others have found no association [93�95].
Different mechanisms by which high meal frequency can have a positive effect on weight and metabolism management have been proposed. An increment of energy expenditure was hypothesized; however, the studies carried out in this line have concluded that total energy expenditure does not differ among different meal frequencies [96,97]. Another postulated hypothesis is that the greater the number of meals a day, the higher the fat oxidation, but again no consensus has been achieved [89,98]. An additional suggested mechanism is that increasing meal frequency leads to plasma glucose levels with lower oscillations and reduced insulin secretion which is thought to contribute to a better appetite control. However, these associations have been found in population with overweight or high glucose levels but in normal-weight or normoglycaemic individuals the results are still inconsistent [93,99�101].
2.7. The Mediterranean Diet
The concept of the Mediterranean Diet (MedDiet) was for the first time defined by the scientific Ancel Keys who observed that those countries around the Mediterranean Sea, which had a characteristic diet, had less risk of suffering coronary heart diseases [102,103].
The traditional MedDiet is characterized by a high intake of extra-virgin olive oil and plant foods (fruits, vegetables, cereals, whole grains, legumes, tree nuts, seeds and olives), low intakes of sweets and red meat and moderate consumption of dairy products, fish and red wine .
There is a lot of literature supporting the general health benefits of the MedDiet. In this sense, it has been reported that a high adherence to this dietary pattern protects against mortality and morbidity from several causes . Thus, different studies suggested the MedDiet as a successful tool for the prevention and treatment of MetS and related comorbidities [106�108]. Moreover, recent meta-analysis concluded that the MedDiet is associated with less risk of developing type 2 diabetes and with a better glycemic control in people with this metabolic disorder [107,109,110]. Other studies have found a positive correlation between the adherence to a MedDiet pattern and reduced risk of developing CVD [111�114]. In fact, many studies have found a positive association between following a MedDiet and improvements in lipid profile by reduction of total cholesterol, LDL-c and TG, and an increase in HDL-c [111�115]. Finally, different studies also suggest that the MedDiet pattern may be a good strategy for obesity treatment as it has been associated with significant reductions in body weight and waist circumference [108,116,117].
The high amount of fiber which, among other beneficial effects, helps to weight control providing satiety; and the high antioxidants and anti-inflammatory nutrients such as n-3 fatty acids, oleic acid or phenolic compounds, are thought to be the main contributors to the positive effects attributed to the MedDiet .
For all these reasons, efforts to maintain the MedDiet pattern in Mediterranean countries and to implement this dietary habits in westernized countries with unhealthy nutritional patterns should be made.
3. Dietary: Single Nutrients and Bioactive Compounds
New studies focused on the molecular action of nutritional bioactive compounds with positive effects on MetS are currently an objective of scientific research worldwide with the aim of designing more personalized strategies in the framework of molecular nutrition. Among them, flavonoids and antioxidant vitamins are some of the most studied compounds with different potential benefits such as antioxidant, vasodilatory, anti-atherogenic, antithrombotic, and anti-inflammatory effects . Table 3 summarizes different nutritional bioactive compounds with potential positive effects on MetS, including the possible molecular mechanism of action involved.
Vitamin C, ascorbic acid or ascorbate is an essential nutrient as human beings cannot synthesize it. It is a water-soluble antioxidant mainly found in fruits, especially citrus (lemon, orange), and vegetables (pepper, kale) . Several beneficial effects have been associated to this vitamin such as antioxidant and anti-inflammatory properties and prevention or treatment of CVD and type 2 diabetes [121�123].
This dietary component produces its antioxidant effect primarily by quenching damaging free radicals and other reactive oxygen and nitrogen species and therefore preventing molecules such as LDL-c from oxidation . It can also regenerate other oxidized antioxidants like tocopherol .
Moreover, it has been described that ascorbic acid may reduce inflammation as it is associated with depletion of CRP levels . This is an important outcome to take in consideration in the treatment of MetS sufferers, as they usually present low grade inflammation .
Supplementation with vitamin C have also been associated with prevention of CVD by improving the endothelial function  and probably by lowering blood pressure . These effects are thought to be exerted by the ability of vitamin C to enhance the endothelial nitric oxide synthase enzyme (eNOS) activity and to reduce HDL-c glycation .
Additionally, several studies have attributed to ascorbate supplementation an antidiabetic effect by improving whole body insulin sensitivity and glucose control in people with type 2 diabetes . These antidiabetic properties are thought to be mediated by optimization of the insulin secretory function of the pancreatic islet cells by increasing muscle sodium-dependent vitamin C transporters (SVCTs) .
Despite all of this, it should be taken into account that most people reach ascorbic acid requirements (established at 95�110 mg/day in the general population) from diet and do not need supplementation [122,129]. Besides, it should be considered that an excess of vitamin C ingestion leads to the opposite effect and oxidative particles are formed [130,131].
Hydroxytyrosol (3,4-dihydroxyphenylethanol) is a phenolic compound mainly found in olives .
It is considered the strongest antioxidant of olive oil and one of the main antioxidants in nature . It acts as a powerful scavenger of free radicals, as a radical chain breaker and as metal chelator . It has the ability of inhibiting LDL-c oxidation by macrophages . In this sense, it is the only phenol recognized by the European Food Safety Authority (EFSA) as a protector of blood lipids from oxidative damage .
Hydroxytyrosol has also been reported to have anti-inflammatory effects, probably by suppressing cyclooxygenase activity and inducing eNOS expression . Thus, enhancement of olives/olive oil intakes or hydroxytyroxol supplementation in people suffering from MetS may be a good strategy in order to improve inflammatory status.
Another beneficial effect attributed to this phenolic compound is its cardiovascular protective effect. It presents anti-atherogenic properties by decreasing the expression of vascular cell adhesion protein 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) [132,137], which are probably the result of an inactivation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF?B), activator protein 1 (AP-1), GATA transcription factor and nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase [138,139]. Hydroxytyrosol also provides antidyslipidemic effects by lowering plasma levels of LDL-c, total cholesterol and TG, and by rising HDL-c .
Despite the beneficial effects attributed to hydfroxytyrosol as an antioxidant, for its antiinflamatory properties and as cardiovascular protector, it should be taken into account that most studies focused on this compound have been performed with mixtures of olive phenols, thus a synergic effect cannot be excluded .
Quercetin is a predominant flavanol naturally present in vegetables, fruits, green tea or red wine. It is commonly found as glycoside forms, where rutin is the most common and important structure found in nature .
Many beneficial effects that can contribute to MetS improvement have been attributed to quercetin. Among them, its antioxidant capacity should be highlighted, as it has been reported to inhibit lipid peroxidation and increase antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT) or glutathione peroxidase (GPX) .
Moreover, an anti-inflammatory effect mediated via attenuation of tumor necrosis factor ? (TNF-?), NF?B and mitogen-activated protein kinases (MAPK), as well as depletion of IL-6, IL-1?, IL-8 or monocyte chemoattractant protein-1 (MCP-1) gene expression has also been attributed to this polyphenol .
As most people with MetS are overweight or obese, the role of quercetin in body weight reduction and obesity prevention has been of special interest. In this sense, it stands out the capacity of quercetin to inhibit adipogenesis through inducing the activation of AMP-activated protein kinase (AMPK) and decreasing the expression of CCAAT-enhancer-binding protein-? (C/EBP?), peroxisome�proliferator-activated receptor gamma (PPAR?), and sterol regulatory element-binding protein 1 (SREBP-1) [141,144].
According to the antidiabetic effects, it is proposed that quercetin may act as an agonist of peroxisome proliferator-activated receptor gamma (PPAR?), and thus improve insulin-stimulated glucose uptake in mature adipocytes . Moreover, quercetin may ameliorate hyperglycemia by inhibiting glucose transporter 2 (GLUT2) and insulin dependent phosphatidylinositol-3-kinase (PI3K) and blocking tyrosine kinase (TK) .
Finally, different studies observed that quercetin has the ability to reduce blood pressure [146�148]. However, the mechanisms of action are not clear, since some authors have suggested that quercetin increases eNOS, contributing to inhibition of platelet aggregation and improvement of the endothelial function [146,147], but there are other studies that have not come across these results .
Resveratrol (3,5,4?-trihidroxiestilben) is a phenolic compound mainly found in red grapes and derived products (red wine, grape juice) . It has shown antioxidant and anti-inflammatory activities, and cardioprotective, anti-obesity and antidiabetic capacities [150�156].
The antioxidant effects of resveratrol have been reported to be carried out by scavenging of hydroxyl, superoxide, and metal-induced radicals as well as by antioxidant effects in cells producing reactive oxygen species (ROS) .
Moreover, it has been reported that the anti-inflammatory effects of resveratrol are mediated by inhibiting NF?B signaling . Furthermore, this polyphenol reduces the expression of proinflammatory cytokines such as interleukin 6 (IL-6), interleukin 8 (IL-8), TNF-?, monocyte chemoattractant protein-1 (MCP-1) and eNOS . In addition, resveratrol inhibits the cyclooxygenase (COX) expression and activity, a pathway involved in the synthesis of proinflammatory lipid mediators .
Concerning the effects of resveratrol against development of type 2 diabetes, it has been reported that treatment of diabetes patients with this polyphenol provides significant improvements in the status of multiple clinically relevant biomarkers such as fasting glucose levels, insulin concentrations or glycated hemoglobin and Homeostasis Model Assessment Insulin Resistance (HOMA-IR) [153,154].
Additionally, cardioprotective effects have been attributed to resveratrol. In this sense, it is suggested that resveratrol improves the endothelial function by producing nitric oxide (NO) through increasing the activity and expression of eNOS. This effect is thought to be conducted through activation of nicotinamide adenine dinucleotide-dependent deacetylase sirtuin-1 (Sirt 1) and 5? AMP-activated protein kinase (AMPK) . Besides, resveratrol exerts endothelial protection by stimulation of NF-E2-related factor 2 (Nrf2)  and decreasing the expression of adhesion proteins such as ICAM-1 and VCAM-1 .
Finally, it has been described that resveratrol may have a role in preventing obesity as it has been related with energy metabolism improvement, increasing lipolysis and reducing lipogenesis . However, more studies are needed in order to corroborate these findings.
Tocopherols, also known as vitamin E, are a family of eight fat-soluble phenolic compounds whose main dietary sources are vegetable oils, nuts and seeds [130,158].
For a long time, it has been suggested that vitamin E could prevent different metabolic diseases as a potent antioxidant, acting as scavenger of lipid peroxyl radicals by hydrogen donating . In this sense, it was described that tocopherols inhibit peroxidation of membrane phospholipids and prevent generation of free radicals in cell membranes .
Moreover, it has been shown that supplementation with ?-tocopherol or ?-tocopherol, two of the different isoforms of vitamin E, could have an effect on inflammation status by reducing CRP levels . Additionally, inhibition of COX and protein kinase C (PKC) and reduction of cytokines�such as IL-8 or plasminogen activator inhibitor-1 (PAI-1) are other mechanisms that may contribute to these anti-inflammatory effects [162,163].
However, the beneficial effects attributed to this vitamin previously have lately became controversial as different clinical trials have not come across such benefits, but ineffective or even harmful effects have been observed . It has been recently suggested that this may be explained by the fact that vitamin E may lose most of the antioxidant capacity when ingested by human beings through different mechanisms .
Anthocyanins are water-soluble polyphenolic compounds responsible for the red, blue and purple colors of berries, black currants, black grapes, peaches, cherries, plums, pomegranate, eggplant, black beans, red radishes, red onions, red cabbage, purple corn or purple sweet potatoes [165�167]. Actually, they are the most abundant polyphenols in fruits and vegetables . Moreover, they can also be found in teas, honey, nuts, olive oil, cocoa, and cereals .
These compounds have high antioxidant capacity inhibiting or decreasing free radicals by donating or transferring electrons from hydrogen atoms .
Regarding clinical studies, it has been shown that these bioactive compounds may prevent type 2 diabetes development by improving insulin sensitivity . The exact mechanisms by which anthocyanins exert their antidiabetic effect are not yet clear, but an enhancement of the glucose uptake by muscle and adipocyte cells in an insulin-independent manner has been suggested .
Moreover, it has been shown that anthocyanins may have the capacity to prevent CVD development by improving endothelial function via increasing brachial artery flow-mediated dilation and HDL-c, and decreasing serum VCAM-1 and LDL-c concentrations [170�173].
Finally, these polyphenolic compounds may exert anti-inflamatory effects via reducing proinflamatory molecules such as IL-8, IL-1? or CRP [172,174].
However, most studies have used anthocyanin-rich extracts instead of purified anthocyanins; thus, a synergic effect with other polyphenols cannot be discarded.
Catechins are polyphenols that can be found in a variety of foods including fruits, vegetables, chocolate, wine, and tea . The epigallocatechin 3-gallate present in tea leaves is the catechin class most studied .
Anti-obesity effects have been attributed to these polyphenols in different studies . The mechanisms of action suggested to explain these beneficial effects on body weight are: increasing energy expenditure and fat oxidation, and reducing fat absorption . It is thought that energy expenditure is enhanced by catechol-O-methyltransferase and phosphodiesterase inhibition, which stimulates the sympathetic nervous system causing an activation of the brown adipose tissue . Fat oxidation is mediated by upregulation of acyl-CoA dehydrogenase and peroxisomal b-oxidation enzymes [178,179].
Moreover, catechin intake has also been associated with lower risk of CVD development by improving lipid biomarkers. Thus, it has been reported that consumption of this kind of polyphenols may increase HDL-c and decrease LDL-c and total cholesterol .
Finally, and antidiabetic effect has also been related to catechin comsumption, lowering fasting glucose levels  and improving insulin sensitivity .
As the prevalence of MetS reaches epidemic rates, the finding of an effective and easy-to-follow dietary strategy to combat this heterogenic disease is still a pending subject. This work recompiled different dietary nutrients and nutritional patterns with potential benefits in the prevention and�treatment of MetS and related comorbidities (Figure 1) with the aim of facilitating future clinical�studies in this area. The challenge now is to introduce precision bioactive compounds in personalized�nutritional patterns in order to gain the most benefits for prevention and treatment of this disease�through nutrition.
Conflicts of Interest: The authors declare no conflict of interest.
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Abstract Objective: This article presents an overview of metabolic syndrome (MetS), which is a collection of risk factors that can lead to diabetes, stroke, and heart disease. The purposes of this article are to describe the current literature on the etiology and pathophysiology of insulin resistance as it relates to MetS and to suggest strategies for dietary and supplemental management in chiropractic practice.
Methods: The literature was searched in PubMed, Google Scholar, and the Web site of the American Heart Association, from the earliest date possible to May 2014. Review articles were identified that outlined pathophysiology of MetS and type 2 diabetes mellitus (T2DM) and relationships among diet, supplements, and glycemic regulation, MetS, T2DM, and musculoskeletal pain.
Results: Metabolic syndrome has been linked to increased risk of developing T2DM and cardiovascular disease and increased risk of stroke and myocardial infarction. Insulin resistance is linked to musculoskeletal complaints both through chronic inflammation and the effects of advanced glycosylation end products. Although diabetes and cardiovascular disease are the most well-known diseases that can result from MetS, an emerging body of evidence demonstrates that common musculoskeletal pain syndromes can be caused by MetS.
Conclusions: This article provides an overview of lifestyle management of MetS that can be undertaken by doctors of chiropractic by means of dietary modification and nutritional support to promote blood sugar regulation.
Introduction: Metabolic Syndrome
Metabolic syndrome (MetS) has been described as a cluster of physical examination and laboratory findings�that directly increases the risk of degenerative metabolic disease expression. Excess visceral adipose tissue, insulin resistance, dyslipidemia, and hypertension are conditions that significantly contribute to the syndrome. These conditions are united by a pathophysiological basis in low-grade chronic inflammation and increase an individual’s risk of cardiovascular disease, type 2 diabetes mellitus (T2DM), and all-cause mortality.1
The National Health and Nutrition Examination Survey (NHANES) 2003-2006 estimated that approximately 34% of United States adults aged 20 years and more had MetS.2 The same NHANES data found that 53% had abdominal adiposity, a condition that is closely linked to visceral adipose stores. Excess visceral adiposity generates increased systemic levels of pro-inflammatory mediator molecules. Chronic, low- grade inflammation has been well documented as an associated and potentially inciting factor for the development of insulin resistance and T2DM.1
NHANES 2003-2006 data showed that 39% of subjects met criteria for insulin resistance. Insulin resistance is a component of MetS that significantly contributes to the expression of chronic, low-grade inflammation and predicts T2DM expression. T2DM costs the United States in excess of $174 billion in 2007. 3 It is estimated that 1 in 4 adults will have T2DM by the year 2050.3 Currently, more than one third of US adults (34.9%) are obese, 4 and, in 2008, the annual medical cost of obesity was $147 billion.4,5 This clearly represents a health care concern.
The pervasiveness of MetS dictates that doctors of chiropractic will see a growing proportion of patients who fit the syndrome criteria.6 Chiropractic is most commonly used for musculoskeletal complaints believed to be mechanical in nature;6 however, an emerging body of evidence identifies MetS as a biochemical promoter of musculoskeletal complaints such as neck pain, shoulder pain, patella tendinopathy, and widespread musculoskeletal pain. 7�13 As an example, the cross-linking of collagen fibers can be caused by increased advanced glycation end-product (AGE) formation as seen in insulin resistance.14 Increased collagen cross-linking is observed in both osteoarthritis and degenerative disc disease, 15 and reduced mobility in elderly patients with T2DM has also been attributed to AGE-induced collagen cross-linking. 16,17
A diagnosis of MetS is made from a patient having 3 of the 5 findings presented in Table 1. Fasting hyperglycemia is termed impaired fasting glucose and indicates insulin resistance. 18,19 An elevated hemoglobin A1c (HbA1c) level measures long-term blood glucose�regulation and is diagnostic for T2DM when elevated in the presence of impaired fasting glucose. 3,18
The emerging evidence demonstrates that we cannot view musculoskeletal pain as only coming from conditions that are purely mechanical in nature. Doctors of chiropractic must demonstrate prowess in identification and management of MetS and an understanding of insulin resistance as its main pathophysiological feature. The purposes of this article are to describe the current literature on the etiology and pathophysiology of insulin resistance as it relates to MetS and to suggest strategies for dietary and supplemental management in chiropractic practice.
PubMed was searched from the earliest possible date to May 2014 to identify review articles that outlined the pathophysiology of MetS and T2DM. This led to further search refinements to identify inflammatory mechanisms that occur in the pancreas, adipose tissue, skeletal muscle, and hypothalamus. Searches were also refined to identify relationships among diet, supplements, and glycemic regulation. Both animal and human studies were reviewed. The selection of specific supplements was based on those that were most commonly used in the clinical setting, namely, gymnema sylvestre, vanadium, chromium and ?-lipoic acid.
Insulin Resistance Overview
Under normal conditions, skeletal muscle, hepatic, and adipose tissues require the action of insulin for cellular glucose entry. Insulin resistance represents an inability of insulin to signal glucose passage into insulin-dependent cells. Although a genetic predisposition can exist, the�etiology of insulin resistance has been linked to chronic low-grade inflammation.1 Combined with insulin resistance-induced hyperglycemia, chronic low-grade inflammation also sustains MetS pathophysiology.1
Two thirds of postprandial blood glucose metabolism occurs within skeletal muscle via an insulin-dependent mechanism.18,19 Insulin binding to its receptor triggers glucose entry and subsequently inhibits lipolysis within the target tissue.21,22 Glucose enters skeletal muscles cells by way of a glucose transporter designated Glut4. 18 Owing to genetic variability, insulin-mediated glucose uptake can vary more than 6-fold among non-diabetic individuals. 23
Prolonged insulin resistance leads to structural changes within skeletal muscle such as decreased Glut4 transporter number, intramyocellular fat accu- mulation, and a reduction in mitochondrial con- tent.19,24 These events are thought to impact energy generation and functioning of affected skeletal mus- cle.24 Insulin-resistant skeletal muscle is less able to suppress lipolysis in response to insulin binding.25 Subsequently, saturated free fatty acids accumulate and generate oxidative stress. 22 The same phenomenon within adipose tissue generates a rapid adipose cell expansion and tissue hypoxia.26 Both these processes increase inflammatory pathway activation and the generation of proinflammatory cytokines (PICs).27
Multiple inflammatory mediators are associated with the promotion of skeletal muscle insulin resistance. The PICs tumor necrosis factor ? (TNF-?), interleukin 1 (IL- 1), and IL-6 have received much attention because of their direct inhibition of insulin signaling.28�30 Since cytokine testing is not performed clinically, elevated levels of high- sensitivity C-reactive protein (hsCRP) best represent the low-grade systemic inflammation that characterizes insulin resistance.31,32
Insulin resistance�induced hyperglycemia can lead to irreversible changes in protein structure, termed glycation, and the formation of AGEs. Cells such as those of the vascular endothelium are most vulnerable to hyperglycemia due to utilization of an insulin-independent Glut1 transporter. 33 This makes AGE generation responsible for most diabetic complications, 15,33,34 including collagen cross-linking.15
If unchanged, prolonged insulin resistance can lead to T2DM expression. The relationship between chronic low-grade inflammation and T2DM has been well characterized. 35 Research has demonstrated that patients with T2DM also have chronic inflammation within the pancreas, termed insulitis, and it worsens hyperglycemia due to the progressive loss of insulin- producing ? cells.36�39
Visceral Adiposity And Insulin Resistance
Caloric excess and a sedentary lifestyle contribute to the accumulation of subcutaneous and visceral adipose tissue. Adipose tissue was once thought of as a metabolically inert passive energy depot. A large body of evidence now demonstrates that excess visceral adipose tissue acts as a driver of chronic low-grade inflammation and insulin resistance.27,34
It has been documented that immune cells infiltrate rapidly expanding visceral adipose tissue. 26,40 Infil- trated macrophages become activated and release PICs that ultimately cause a phenotypic shift in resident macrophage phenotype to a classic inflammatory M1 profile.27 This vicious cycle creates a chronic inflam- matory response within adipose tissue and decreases the production of adipose-derived anti-inflammatory cytokines.43 As an example, adiponectin is an adipose- derived anti-inflammatory cytokine. Macrophage- invaded adipose tissue produces less adiponectin, and this has been correlated with increasing insulin resistance. 26
Hypothalamic Inflammation And Insulin Resistance
Eating behavior in the obese and overweight has been popularly attributed to a lack of will power or genetics. However, recent research has demonstrated a link between hypothalamic inflammation and increased body weight.41,41
Centers that govern energy balance and glucose homeostasis are located within the hypothalamus. Recent studies demonstrate that inflammation in the hypothalamus coincides with metabolic inflammation and an increase in appetite.43 These hypothalamic centers simultaneously become resistant to anorexigenic stimuli, leading to altered energy intake. It has been suggested that this provides a neuropathological basis for MetS and drives a progressive increase in body weight. 41
Central metabolic inflammation pathologically activates hypothalamic immune cells and disrupts central insulin and leptin signaling.41 Peripherally, this has been associated with dysregulated glucose homeostasis that also impairs pancreatic ? cell functioning.41,44 Hypothalamic inflammation contributes to hypertension through similar mechanisms, and it is thought that central inflammation parallels chronic low-grade systemic inflammation and insulin resistance.41�44
Feeding generally leads to a short-term increase in both oxidative stress and inflammation. 41 Total�calories consumed, glycemic index, and fatty acid profile of a meal all influence the degree of postprandial inflammation. It is estimated that the average American consumes approximately 20% of calories from refined sugar, 20% from refined grains and flour, 15% to 20% from excessively fatty meat products, and 20% from refined seed/legume oils.45 This pattern of eating contains a macronutrient composition and glycemic index that promote hyperglycemia, hyperlipemia, and an acute postprandial inflammatory response. 46 Collectively referred to as postprandial dysmetabolism, this pro-inflammatory response can sustain levels of chronic low-grade inflammation that leads to excess body fat, coronary heart disease (CHD), insulin resistance, and T2DM.28,29,47
Recent evidence suggests that several MetS criteria may not sufficiently identify all individuals with postprandial dysmetabolism. 48,49 A 2-hour oral glucose tolerance test (2-h OGTT) result greater than 200 mg/dL can be used clinically to diagnose T2DM. Although MetS includes a fasting blood glucose level less than 100 mg/dL, population studies have shown that a fasting glucose as low as 90 mg/dL can be associated with an 2-h OGTT level greater than 200 mg/dL.49 Further, a recent large cohort study indicated that an increased 2-h OGTT was independently predictive of cardiovascular and all-cause mortality in a nondiabetic population. 48 Mounting evidence indicates that post- prandial glucose levels are better correlated with MetS and predicting future cardiovascular events than fasting blood glucose alone.41,48
Fasting triglyceride levels generally correlate with postprandial levels, and a fasting triglyceride level greater than 150 mg/dL reflects MetS and insulin resistance. Contrastingly, epidemiologic data indicate that a fasting triglyceride level greater than 100 mg/dL influences CHD risk via postprandial dysmetabolism. 48 The acute postprandial inflammatory response that contributes to CHD risk includes an increase in PICs, free radicals, and hsCRP.48,49 These levels are not measured clinically but, monitoring fasting glucose, 2-hour postprandial glucose and fasting triglycerides can be used as correlates of postprandial dysmetabolic and low-grade systemic inflammation.
MetS And Disease Expression
Diagnosis of MetS has been linked to an increased risk of developing T2DM and cardiovascular disease over the following 5 to 10 years. 1 It further increases a patient’s risk of stroke, myocardial infarction, and death from any of the aforementioned conditions.1
Facchini et al47 followed 208 apparently healthy, non-obese subjects for 4 to 11 years while monitoring the incidence of clinical events such as hypertension, stroke, CHD, cancer, and T2DM. Approximately one fifth of participants experienced clinical events, and all of these subjects were either classified as intermediately or severely insulin resistant. It is important to note that all of these clinical events have a pathological basis in chronic low-grade inflammation,50 and no events were experienced in the insulin-sensitive groupings. 47
Insulin resistance is linked to musculoskeletal com- plaints both through chronic inflammation and the effects of AGEs. Advanced glycation end-products have been shown to extensively accumulate in osteoarthritic cartilage and treatment of human chondrocytes with AGEs increased their catabolic activity. 51 Advanced glycation end-products increase collagen stiffness via cross-linking and likely contribute to reduced joint mobility seen in elderly patients with T2DM.52 Com- pared to non-diabetics, type II diabetic patients are known to have altered proteoglycan metabolism in their intervertebral discs. This altered metabolism may pro- mote weakening of the annular fibers and subsequently, disc herniation.53 The presence of T2DM increases a person’s risk of expressing disc herniation in both the cervical and lumbar spines.17,54 Patients with T2DM are also more likely to develop lumbar stenosis compared with non-diabetics, and this has been documented as a plausible relationship between MetS risk factors and physician-diagnosed lumbar disc herniation. 55�57
There are no specific symptoms that denote early skeletal muscle structural changes. Fatty infiltration and decreased muscle mitochondria content are observed within age-related sarcopenia 58 ; however, it is still being argued whether fatty infiltration is a risk factor for low back pain. 59,60
Clinical management of MetS should be geared toward improving insulin sensitivity and reducing chronic low-grade inflammation. 1 Regular exercise without weight loss is associated with reduced insulin resistance, and at least 30 minutes of aerobic activity and resistance training is recommended daily. 61,62 Although frequently considered preventative, exercise, dietary, and weight loss interventions should be considered alongside pharmacological management in those with MetS. 1
Data regarding the exact amount of weight loss needed to improve chronic inflammation are inconclusive. In overweight individuals without diagnosed MetS, a very-low-carbohydrate diet (b 10% calories from carbohydrate) has significantly reduced plasma inflammatory markers (TNF-?, hsCRP, and IL-6) with�as little as 6% reduction in body weight.63,64 Individuals who meet MetS criteria may require 10% to 20% body weight loss to reduce inflammatory markers. 65 Interestingly, the Mediterranean Diet has been shown to reduce markers of systemic inflammation independent of weight loss65 and was recommended in the American College of Cardiology and American Heart Association Adult Treatment Panel 4 guidelines.66
A growing body of research has examined the effects of the Spanish ketogenic Mediterranean diet, including olive oil, green vegetables and salads, fish as the primary protein, and moderate red wine consumption. In a sample of 22 patients, adoption of the Spanish ketogenic Mediterranean diet with 9 g of supplemental salmon oil on days when fish was not consumed has led to complete resolution of MetS.67 Significant reductions in markers of chronic systemic inflammation were seen in 31 patients following this diet for 12 weeks.68
A Paleolithic diet based on lean meat, fish, fruits, vegetables, root vegetables, eggs, and nuts has been described as more satiating per calorie than a diabetes diet in patients with T2DM.69 In a randomized crossover study, a Paleolithic diet resulted in lower mean HbA1c values, triglycerides, diastolic blood pressure, waist circumference, improved glucose tolerance, and higher high-density lipoprotein (HDL) values compared to a diabetes diet.70 Within the context of these changes, a referral for medication management may be advisable.
Irrespective of name, a low-glycemic diet that focuses on vegetables, fruits, lean meats, omega-3 fish, nuts, and tubers can be considered anti-inflammatory and has been shown to ameliorate insulin resistance. 49,71�73 Inflammatory markers and insulin resistance further improve when weight loss coincides with adherence to an anti-inflammatory diet.70 A growing body of evidence suggests that specific supplemental nutrients also reduce insulin resistance and improve chronic low-grade inflammation.
Key Nutrients That Promote Insulin Sensitivity
Research has identified nutrients that play key roles in promoting proper insulin sensitivity, including vitamin D, magnesium, omega-3 (n-3) fatty acids, curcumin, gymnema, vanadium, chromium, and ?-lipoic acid. It is possible to get adequate vitamin D from sun exposure and adequate amounts of magnesium and omega-3 fatty acids from food. Contrastingly, the therapeutic levels of chromium and ?-lipoic acid that affect insulin sensitivity and reduce�insulin resistance cannot be obtained in food and must be supplemented.
Vitamin D, magnesium, and n-3 fatty acids have multiple functions, and generalized inflammation reduction is a common mechanism of action.74�80 Their supplemental use should be considered in the context of low-grade inflammation reduction and health promotion, rather than as a specific treatment for MetS or T2DM.
Evidence pertaining to the precise role of vitamin D in MetS and insulin resistance is inconclusive. Increas- ing dietary and supplemental vitamin D intake in young men and women may lower the risk of MetS and T2DM development,81 and a low serum vitamin D level has been associated with insulin resistance and T2DM expression. 82 Supplementation to improve low serum vitamin D (reference range, 32-100 ng/mL) is effective, but its impact on improving central glycemia and insulin sensitivity is conflicting. 83 Treating insulin resistance and MetS with vitamin D as a monotherapy appears to be unsuccessful. 82,83 Achieving normal vitamin D blood levels through adequate sun exposure and/or supplementation is advised for general health. 84�86
The average American diet commonly contains a low magnesium intake.80 Recent studies suggest that supple- mental magnesium can improve insulin sensitivity. 81,82 Taking 365 mg/d may be effective in reducing fasting glucose and raising HDL cholesterol in T2DM,83 as well as normomagnesemic, overweight, nondiabetics. 84
Diets high in the omega-6 fat linoleic acid have been associated with insulin resistance85 and higher levels of serum pro-inflammatory mediator markers including IL-6, IL-1?, TNF-?, and hsCRP.87 Supplementation to increase dietary omega-3 fatty acids at the expense of omega-6 fatty acids has been shown to improve insulin sensitivity. 88�90 Six months of omega-3 supplementation at 3 g/d with meals has been shown to reduce MetS markers including fasting triglycerides, HDL cholesterol, and an increase in anti-inflammatory adiponectin. 91
Curcumin is responsible for the yellow pigmentation of the spice turmeric. Its biological effects can be characterized as antidiabetic and antiobesity via down- regulating TNF-?, suppressing nuclear factor ?B activation, adipocytokine expression, and leptin level modulation,. 92�95 Curcumin has been reported to activate peroxisome proliferator-activated receptor-?, the nuclear target of the thiazolidinedione class of antidiabetic drugs,93 and it also protects hepatic and pancreatic cells. 92,93 Numerous studies have reported�weight loss, hsCRP reduction, and improved insulin sensitivity after curcumin supplementation.92�95
There is no established upper limit for curcumin, and doses of up to 12 g/d are safe and tolerable in humans. 96 A randomized, double-blinded, placebo- controlled trial (N = 240) showed a reduced progression of prediabetes to T2DM after 9 months of 1500 mg/d curcumin supplementation.97
Curcumin, 98 vitamin D, 84 magnesium, 91 and omega-3 fatty acids80 are advocated as daily supplements to promote general health. A growing body of evidence supports the views of Gymnema sylvestre, vanadium, chromium, and ?-lipoic acid should as therapeutic supplements to assist in glucose homeostasis.
Gymnemic acids are the active component of the G sylvestre plant leaves. Gymnemic acids are the active component of the G sylvestre plant leaves. Studies evaluating G sylvestre’s effects on diabetes in humans have generally been of poor methodological quality. Experimental animal studies have found that gymnemic acids may decrease glucose uptake in the small intestine, inhibit gluconeogenesis, and reduce hepatic and skeletal muscle insulin resistance.99 Other animal studies suggest that gymnemic acids may have comparable efficacy in reducing blood sugar levels to the first-generation sulfonylurea, tolbutamide.100
Evidence from open-label trials suggests its use as a supplement to oral antidiabetic hypoglycemic agents. 96 One quarter of patients were able to discontinue their drug and maintain normal glucose levels on an ethanolic gymnema extract alone. Although the evidence to date suggests its use in humans and animals is safe and well tolerated, higher quality human studies are warranted.
Vanadyl sulfate has been reported to prolong the events of insulin signaling and may actually improve insulin sensitivity.101 Limited data suggest that it inhibits gluconeogenesis, possibly ameliorating hepatic insulin resistance. 100,101 Uncontrolled clinical trials have reported improvements in insulin sensitivity using 50 to 300 mg daily for periods ranging from 3 to 6 weeks. 101�103 Contrastingly, a recent randomized, double-blind, placebo-controlled trial found that 50 mg of vanadyl sulfate twice daily for 4 weeks had no effect in individuals with impaired glucose tolerance. 104 Limited clinical and experimental data exist supporting the use of vanadyl sulfate to improve insulin resistance,�and further research is warranted regarding its safety and efficacy.
Diets high in refined sugar and flour are deficient in chromium (Cr) and lead to an increased urinary excretion of chromium. 105,106 The progression of MetS is not likely caused by a chromium deficiency, 107 and dosages that benefit glycemic regulation are not achievable through food. 106,108,109
A recent randomize, double-blind trial demonstrated that 1000 ?g Cr per day for 8 months improved insulin sensitivity by 10% in subjects with T2DM.110 Cefalu et al110 further suggested that these improvements might be more applicable to patients with a greater degree of insulin resistance, impaired fasting plasma glucose, and higher HbA1c values. Chromium’s mechanism of action for improving insulin sensitivity is through increased Glut4 translocation via prolonging insulin receptor signaling.109 Chromium has been well tolerated at 1000 ?g/d,105 and animal models using significantly more than 1000 ? Cr per day were not associated with toxicological consequences.109
Humans derive ?-lipoic acid through dietary means and from endogenous synthesis. 111 The foods richest in ?-lipoic acid are animal tissues with extensive metabolic activity such as animal heart, liver, and kidney, which are not consumed in large amounts in the typical American diet. 111 Supplemental amounts of ?-lipoic acid used in the treatment of T2DM (300-600 mg) are likely to be as much as 1000 times greater than the amounts that could be obtained from the diet.112
Lipoic acid synthase (LASY) appears to be the key enzyme involved in the generation of endogenous lipoic acid, and obese mice with diabetes have reduced LASY expression when compared with age-and sex- matched controls.111 In vitro studies to identify potential inhibitors of lipoic acid synthesis suggest a role for diet-induced hyperglycemia and the PIC TNF- ? in the down-regulation of LASY.113 The inflammatory basis of insulin resistance may therefore drive lowered levels of endogenous lipoic acid via reducing the activity of LASY.
?-Lipoic acid has been found to act as insulin mimetic via stimulating Glut4-mediated glucose trans- port in muscle cells. 110,114?-Lipoic acid is a lipophilic free radical scavenger and may affect glucose homeostasis through protecting the insulin receptor from damage114 and indirectly via decreasing nuclear factor ?B�mediated TNF-? and IL-1 production. 110 In�postmenopausal women with MetS (presence of at least 3 ATPIII clinical criteria) 4 g/d of a combined inositol and ?-lipoic acid supplement for 6 months significantly improved OGTT scores by 20% in two thirds of the subjects. 114 A recent randomized double-blinded placebo-controlled study showed that 300 mg/d ?- lipoic acid for 90 days significantly decreased HbA1c values in subjects with T2DM.115
Side effects to ?-lipoic acid supplementation as high as 1800 mg/d have largely been limited to nausea. 116 It may be best to take supplemental ?-lipoic acid on an empty stomach (1 hour before or 2 hours after eating) because food intake reportedly reduces its bioavailability.117 Clinicians should be aware that ?-lipoic acid supplementation might increase the risk of hypoglycemia in diabetic patients using insulin or oral antidiabetic agents.117
This is a narrative overview of the topic of MetS. A systematic review was not performed; therefore, there may be relevant information missing from this review. The contents of this overview focuses on the opinions of the authors, and therefore, others may disagree with our opinions or approaches to management. This overview is limited by the studies that have been published. To date, no studies have been published that identify the effectiveness of a combination of a dietary intervention, such as the Spanish ketogenic diet, and nutritional supplementation on the expression of the MetS. Similarly, this approach has not been studied in patients with musculoskeletal pain who also have the MetS. Consequently, the information presented in this article is speculative. Longitudinal studies are needed before any specific recommendations can be made for patients with musculoskeletal that may be influenced by the MetS.
Conclusion: Metabolic Syndrome
This overview suggests that MetS and type 2 diabetes are complex conditions, and their prevalence is expected to increase substantially in the coming years. Thus, it is important to identify if the MetS may be present in patients who are nonresponsive to manual care and to help predict who may not respond adequately.
We suggest that diet and exercise are essential to managing these conditions, which can be supported with key nutrients, such as vitamin D, magnesium, and�omega-3 fatty acids. We also suggest that curcumin, G sylvestre, vanadyl sulfate chromium, and ?-lipoic acid could be viewed as specific nutrients that may be taken during the process of restoring appropriate insulin sensitivity and signaling.
David R. Seaman DC, MS,?, Adam D. Palombo DC
Professor, Department of Clinical Sciences, National University of Health Sciences, Pinellas Park, FL Private Chiropractic Practice, Newburyport, MA
Funding Sources and Conflicts of Interest
No funding sources were reported for this study. David Seaman is a paid consultant for Anabolic Laboratories, a manufacturer of nutritional products for health care professionals. Adam Palombo was sponsored and remunerated by Anabolic laboratories to speak at chiropractic conventions/meetings.
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The increased prevalence of obesity and related comorbidities is a major public health problem. While genetic factors undoubtedly play a role in determining individual susceptibility to weight gain and obesity, the identified genetic variants only explain part of the variation. This has led to growing interest in understanding the potential role of epigenetics as a mediator of gene-environment interactions underlying the development of obesity and its associated comorbidities. Initial evidence in support of a role of epigenetics in obesity and type 2 diabetes mellitus (T2DM) was mainly provided by animal studies, which reported epigenetic changes in key metabolically important tissues following high-fat feeding and epigenetic differences between lean and obese animals and by human studies which showed epigenetic changes in obesity and T2DM candidate genes in obese/diabetic individuals. More recently, advances in epigenetic methodologies and the reduced cost of epigenome-wide association studies (EWAS) have led to a rapid expansion of studies in human populations. These studies have also reported epigenetic differences between obese/T2DM adults and healthy controls and epigenetic changes in association with nutritional, weight loss, and exercise interventions. There is also increasing evidence from both human and animal studies that the relationship between perinatal nutritional exposures and later risk of obesity and T2DM may be mediated by epigenetic changes in the offspring. The aim of this review is to summarize the most recent developments in this rapidly moving field, with a particular focus on human EWAS and studies investigating the impact of nutritional and lifestyle factors (both pre- and postnatal) on the epigenome and their relationship to metabolic health outcomes. The difficulties in distinguishing consequence from causality in these studies and the critical role of animal models for testing causal relationships and providing insight into underlying mechanisms are also addressed. In summary, the area of epigenetics and metabolic health has seen rapid developments in a short space of time. While the outcomes to date are promising, studies are ongoing, and the next decade promises to be a time of productive research into the complex interactions between the genome, epigenome, and environment as they relate to metabolic disease.
Keywords: Epigenetics, DNA methylation, Obesity, Type 2 diabetes, Developmental programming
Obesity is a complex, multifactorial disease, and better understanding of the mechanisms underlying the interactions between lifestyle, environment, and genetics is critical for developing effective strategies for prevention and treatment .
In a society where energy-dense food is plentiful and the need for physical activity is low, there is a wide variation in individuals� susceptibility to develop�obesity and metabolic health problems. Estimates of the role of heredity in this variation are in the range of 40�70 %, and while large genome-wide association studies (GWAS) have identified a number of genetic loci associated with obesity risk, the ~100 most common genetic variants only account for a few percent of variance in obesity [2, 3]. Genome-wide estimates are higher, accounting for ~20 % of the variation ; however, a large portion of the heritability remains unexplained.
Recently, attention has turned to investigating the role of epigenetic changes in the etiology of obesity. It has been argued that the epigenome may represent the mechanistic link between genetic variants and environmental�factors in determining obesity risk and could help explain the �missing heritability.� The first human epigenetic studies were small and only investigated a limited number of loci. While this generally resulted in poor reproducibility, some of these early findings, for instance the relationship between PGC1A methylation and type 2 diabetes mellitus (T2DM)  and others as discussed in van Dijk et al. , have been replicated in later studies. Recent advances and increased affordability of high- throughput technologies now allow for large-scale epigenome wide association studies (EWAS) and integration of different layers of genomic information to explore the complex interactions between the genotype, epigenome, transcriptome, and the environment [6�9]. These studies are still in their infancy, but the results thus far have shown promise in helping to explain the variation in obesity susceptibility.
There is increasing evidence that obesity has develop mental origins, as exposure to a suboptimal nutrient supply before birth or in early infancy is associated with an increased risk of obesity and metabolic disease in later life [10�13]. Initially, animal studies demonstrated that a range of early life nutritional exposures, especially those experienced early in gestation, could induce epigenetic changes in key metabolic tissues of the offspring that persisted after birth and result in permanent alterations in gene function [13�17]. Evidence is emerging to support the existence of the same mechanism in humans. This has led to a search for epigenetic marks present early in life that predict later risk of metabolic disease, and studies to determine whether epigenetic programming of metabolic disease could be prevented or reversed in later life.
This review provides an update of our previous systematic review of studies on epigenetics and obesity in humans . Our previous review showcased the promising outcomes of initial studies, including the first potential epigenetic marks for obesity that could be detected at birth (e.g., RXRA) . However, it also highlighted the limited reproducibility of the findings and the lack of larger scale longitudinal investigations. The current review focuses on recent developments in this rapidly moving field and, in particular, on human EWAS and studies investigating the impact of (pre- and postnatal) nutritional and lifestyle factors on the epigenome and the emerging role of epigenetics in the pathology of obesity. We also address the difficulties in identifying causality in these studies and the importance of animal models in providing insight into mechanisms.
Epigenetic Changes In Animal Models Of Obesity
Animal models provide unique opportunities for highly controlled studies that provide mechanistic insight into�the role of specific epigenetic marks, both as indicators of current metabolic status and as predictors of the future risk of obesity and metabolic disease. A particularly important aspect of animal studies is that they allow for the assessment of epigenetic changes within target tissues, including the liver and hypothalamus, which is much more difficult in humans. Moreover, the ability to harvest large quantities of fresh tissue makes it possible to assess multiple chromatin marks as well as DNA methylation. Some of these epigenetic modifications either alone or in combination may be responsive to environmental programming. In animal models, it is also possible to study multiple generations of offspring and thus enable differentiation between trans-generational and intergenerational transmission of obesity risk mediated by epigenetic memory of parental nutritional status, which cannot be easily distinguished in human studies. We use the former term for meiotic transmission of risk in the absence of continued exposure while the latter primarily entails direct transmission of risk through metabolic reprogramming of the fetus or gametes.
Animal studies have played a critical role in our current understanding of the role of epigenetics in the developmental origins of obesity and T2DM. Both increased and decreased maternal nutrition during pregnancy have been associated with increased fat deposition in offspring of most mammalian species studied to date (reviewed in [11, 13�15, 19]). Maternal nutrition during pregnancy not only has potential for direct effects on the fetus, it also may directly impact the developing oocytes of female fetuses and primordial germ cells of male fetuses and therefore could impact both the off- spring and grand-offspring. Hence, multigenerational data are usually required to differentiate between maternal intergenerational and trans-generational transmission mechanisms.
Table 1 summarizes a variety of animal models that have been used to provide evidence of metabolic and epigenetic changes in offspring associated with the parental plane of nutrition. It also contains information pertaining to studies identifying altered epigenetic marks in adult individuals who undergo direct nutritional challenges. The table is structured by suggested risk transmission type.
(i) Epigenetic Changes In Offspring Associated With Maternal Nutrition During Gestation
Maternal nutritional supplementation, undernutrition, and over nutrition during pregnancy can alter fat deposition and energy homeostasis in offspring [11, 13�15, 19]. Associated with these effects in the offspring are changes in DNA methylation, histone post-translational modifications, and gene expression for several target genes,�especially genes regulating fatty acid metabolism and insulin signaling [16, 17, 20�30]. The diversity of animal models used in these studies and the common metabolic pathways impacted suggest an evolutionarily conserved adaptive response mediated by epigenetic modification. However, few of the specific identified genes and epigenetic changes have been cross-validated in related studies, and large-scale genome-wide investigations have typically not been applied. A major hindrance to comparison of these studies is the different develop mental windows subjected to nutritional challenge, which may cause considerably different outcomes. Proof that the epigenetic changes are causal rather than being associated with offspring phenotypic changes is also required. This will necessitate the identification of a parental nutritionally induced epigenetic �memory� response that precedes development of the altered phenotype in offspring.
(ii)Effects Of Paternal Nutrition On Offspring Epigenetic Marks
Emerging studies have demonstrated that paternal plane of nutrition can impact offspring fat deposition and epigenetic marks [31�34]. One recent investigation using mice has demonstrated that paternal pre-diabetes leads to increased susceptibility to diabetes in F1 offspring with associated changes in pancreatic gene expression and DNA methylation linked to insulin signaling . Importantly, there was an overlap of these epigenetic changes in pancreatic islets and sperm suggesting germ line inheritance. However, most of these studies, although intriguing in their implications, are limited in the genomic scale of investigation and frequently show weak and somewhat transient epigenetic alterations associated with mild metabolic phenotypes in offspring.
(iii)Potential Trans-generational Epigenetic Changes Promoting Fat Deposition In Offspring
Stable transmission of epigenetic information across multiple generations is well described in plant systems and C. elegans, but its significance in mammals is still much debated [36, 37]. An epigenetic basis for grand- parental transmission of phenotypes in response to dietary exposures has been well established, including in livestock species . The most influential studies demonstrating effects of epigenetic transmission impacting offspring phenotype have used the example of the viable yellow agouti (Avy) mouse . In this mouse, an insertion of a retrotransposon upstream of the agouti gene causes its constitutive expression and consequent yellow coat color and adult onset obesity. Maternal transmission through the germ line results in DNA methylation�mediated silencing of agouti expression resulting in wild-type coat color and lean phenotype of the offspring [39, 40]. Importantly, subsequent studies in these mice demonstrated that maternal exposure to methyl donors causes a shift in coat color . One study has reported transmission of a phenotype to the F3 generation and alterations in expression of large number of genes in response to protein restriction in F0 ; however, alterations in expression were highly variable and a direct link to epigenetic changes was not identified in this system.
(iv) Direct Exposure Of Individuals To Excess Nutrition In Postnatal Life
While many studies have identified diet-associated epigenetic changes in animal models using candidate site-specific regions, there have been few genome-wide analyses undertaken. A recent study focussed on determining the direct epigenetic impact of high-fat diets/ diet-induced obesity in adult mice using genome-wide gene expression and DNA methylation analyses . This study identified 232 differentially methylated regions (DMRs) in adipocytes from control and high-fat fed mice. Importantly, the corresponding human regions for the murine DMRs were also differentially methylated in adipose tissue from a population of obese and lean humans, thereby highlighting the remarkable evolutionary conservation of these regions. This result emphasizes the likely importance of the identified DMRs in regulating energy homeostasis in mammals.
Drawing on the evidence from animal studies and with the increasing availability of affordable tools for genome- wide analysis, there has been a rapid expansion of epigenome studies in humans. These studies have mostly focused on the identification of site-specific differences in DNA methylation that are associated with metabolic phenotypes.
A key question is the extent to which epigenetic modifications contribute to the development of the metabolic phenotype, rather than simply being a con- sequence of it (Fig. 1). Epigenetic programming could contribute to obesity development, as well as playing a role in consequent risk of cardiovascular and metabolic problems. In human studies, it is difficult to prove causality , but inferences can be made from a number of lines of evidence:
(i) Genetic association studies. Genetic polymorphisms that are associated with an increased risk of developing particular conditions are a priori linked to the causative genes. The presence of differential�methylation in such regions infers functional relevance of these epigenetic changes in controlling expression of the proximal gene(s). There are strong cis-acting genetic effects underpinning much epigenetic variation [7, 45], and in population-based studies, methods that use genetic surrogates to infer a causal or mediating role of epigenome differences have been applied [7, 46�48]. The use of familial genetic information can also lead to the identification of potentially causative candidate regions showing phenotype-related differential methylation .
(ii)Timing of epigenetic changes. The presence of an epigenetic mark prior to development of a phenotype is an essential feature associated with causality. Conversely, the presence of a mark in association with obesity, but not before its development, can be used to exclude causality but would not exclude a possible role in subsequent obesity-related pathology.
(iii)Plausible inference of mechanism. This refers to epigenetic changes that are associated with altered expression of genes with an established role in regulating the phenotype of interest. One such example is the association of methylation at two CpG sites at the CPT1A gene with circulating triglyceride levels . CPT1A encodes carnitine palmitoyltransferase 1A, an enzyme with a central role in fatty acid metabolism, and this is strongly indicative that differential methylation of this gene may be causally related to the alterations in plasma triglyceride concentrations.
Epigenome-Wide Association Studies: Identifying Epigenetic Biomarkers Of Metabolic Health
A number of recent investigations have focused on exploring associations between obesity/metabolic diseases�and DNA methylation across the genome (Table 2). The largest published EWAS so far, including a total of 5465 individuals, identified 37 methylation sites in blood that were associated with body mass index (BMI), including sites in CPT1A, ABCG1, and SREBF1 . Another large-scale study showed consistent associations between BMI and methylation in HIF3A in whole blood and adipose tissue , a finding which was also partially replicated in other studies [9, 51]. Other recently reported associations between obesity-related measures and DNA methylation include (i) DNA methylation differences between lean and obese individuals in LY86 in blood leukocytes ; (ii) associations between PGC1A promoter methylation in whole blood of children and adiposity 5 years later ; (iii) associations between waist-hip ratio and ADRB3 methylation in blood ; and (iv) associations between BMI, body fat distribution measures, and multiple DNA methylation sites in adipose tissue [9, 56]. EWAS have also shown associations between DNA methylation sites and blood lipids [55, 57�59], serum metabolites , insulin resistance [9, 61], and T2DM [48, 62, 63] (Table 2).
From these studies, altered methylation of PGC1A, HIF3A, ABCG1, and CPT1A and the previously described RXRA  have emerged as biomarkers associated with, or perhaps predictive of, metabolic health that are also plausible candidates for a role in development of metabolic disease.
Interaction Between Genotype And The Epigenome
Epigenetic variation is highly influenced by the underlying genetic variation, with genotype estimated to explain ~20�40 % of the variation [6, 8]. Recently, a number of studies have begun to integrate methylome and genotype data to identify methylation quantitative trait loci (meQTL) associated with disease phenotypes. For instance, in adipose tissue, an meQTL overlapping�with a BMI genetic risk locus has been identified in an enhancer element upstream of ADCY3 . Other studies have also identified overlaps between known obesity and T2DM risk loci and DMRs associated with obesity and T2DM [43, 48, 62]. Methylation of a number of such DMRs was also modulated by high-fat feeding in mice  and weight loss in humans . These results identify an intriguing link between genetic variations linked with disease susceptibility and their association with regions of the genome that undergo epigenetic modifications in response to nutritional challenges, implying a causal relationship. The close connection between genetic and epigenetic variation may signify their essential roles in generating individual variation [65, 66]. However, while these findings suggest that DNA methylation may be a mediator of genetic effects, it is also important to consider that both genetic and epigenetic processes could act independently on the same genes. Twin studies [8, 63, 67] can provide important insights and indicate that inter-individual differences in levels of DNA methylation arise predominantly from non-shared environment and stochastic influences, minimally from shared environmental effects, but also with a significant impact of genetic variation.
The Impact Of The Prenatal And Postnatal Environment On The Epigenome
Prenatal environment: Two recently published studies made use of human populations that experienced �natural� variations in nutrient supply to study the impact of maternal nutrition before or during pregnancy on DNA methylation in the offspring [68, 69]. The first study used a Gambian mother-child cohort to show that both seasonal variations in maternal methyl donor intake during pregnancy and maternal pre-pregnancy BMI were associated with altered methylation in the infants . The second study utilized adult offspring from the Dutch Hunger Winter cohort to investigate the effect of prenatal exposure to an acute period of severe maternal undernutrition on DNA methylation of genes involved in growth and metabolism in adulthood . The results highlighted the importance of the timing of the exposure in its impact on the epigenome, since significant epigenetic effects were only identified in individuals exposed to famine during early gestation. Importantly, the epigenetic changes occurred in conjunction with increased BMI; however, it was not possible to establish in this study whether these changes were present earlier in life or a consequence of the higher BMI.
Other recent studies have provided evidence that prenatal over-nutrition and an obese or diabetic maternal environment are also associated with DNA methylation changes in genes related to embryonic development, growth, and metabolic disease in the offspring [70�73].
While human data are scarce, there are indications that paternal obesity can lead to altered methylation of imprinted genes in the newborn , an effect thought to be mediated via epigenetic changes acquired during spermatogenesis.
Postnatal environment: The epigenome is established de novo during embryonic development, and therefore, the prenatal environment most likely has the most significant impact on the epigenome. However, it is now clear that changes do occur in the �mature� epigenome under the influence of a range of conditions, including aging, exposure to toxins, and dietary alterations. For example, changes in DNA methylation in numerous genes in skeletal muscle and PGC1A in adipose tissue have been demonstrated in response to a high-fat diet [75, 76]. Interventions to lose body fat mass have also been associated with changes in DNA methylation. Studies have reported that the DNA methylation profiles of adipose tissue [43, 64], peripheral blood mononuclear cells , and muscle tissue  in formerly obese patients become more similar to the profiles of lean subjects following weight loss. Weight loss surgery also partially reversed non-alcoholic fatty liver disease-associated methylation changes in liver  and in another study led to hypomethylation of multiple obesity candidate genes, with more pronounced effects in subcutaneous compared to omental (visceral) fat . Accumulating evidence suggests that exercise interventions can also influence DNA methylation. Most of these studies have been conducted in lean individuals [80�82], but one exercise study in obese T2DM subjects also demonstrated changes in DNA methylation, including in genes involved in fatty acid and glucose transport . Epigenetic changes also occur with aging, and recent data suggest a role of obesity in augmenting them [9, 84, 85]. Obesity accelerated the epigenetic age of liver tissue, but in contrast to the findings described above, this effect was not reversible after weight loss .
Collectively, the evidence in support of the capacity to modulate the epigenome in adults suggests that there may be the potential to intervene in postnatal life to modulate or reverse adverse epigenetic programming.
Effect Sizes And Differences Between Tissue Types
DNA methylation changes associated with obesity or induced by diet or lifestyle interventions and weight loss are generally modest (<15 %), although this varies depending on the phenotype and tissue studied. For instance, changes greater than 20 % have been reported in adipose tissue after weight loss  and associations between HIF3A methylation and BMI in adipose tissue were more pronounced than in blood .
The biological relevance of relatively small methylation changes has been questioned. However, in tissues consisting of a mixture of cell types, a small change in DNA methylation may actually reflect a significant change in a specific cell fraction. Integration of epigenome data with transcriptome and other epigenetic data, such as histone modifications, is important, since small DNA methylation changes might reflect larger changes in chromatin structure and could be associated with broader changes in gene expression. The genomic context should also be considered; small changes within a regulatory element such as a promotor, enhancer, or insulator may have functional significance. In this regard, DMRs for obesity, as well as regions affected by prenatal famine exposure and meQTL for metabolic trait loci have been observed to overlap enhancer elements [8, 43, 68]. There is evidence that DNA methylation in famine-associated regions could indeed affect enhancer activity , supporting a role of nutrition-induced methylation changes in gene regulation.
A major limitation in many human studies is that epigenetic marks are often assessed in peripheral blood, rather than in metabolically relevant tissues (Fig. 2). The heterogeneity of blood is an issue, since different cell populations have distinct epigenetic signatures, but algorithms have been developed to estimate the cellular composition to overcome this problem . Perhaps more importantly, epigenetic marks in blood cells may not necessarily report the status of the tissues of primary interest. Despite this, recent studies have provided clear evidence of a relationship between epigenetic marks in blood cells and BMI. In the case of HIF3A for which the level of methylation (beta-value) in the study population ranged from 0.14�0.52, a 10 % increase in methylation was associated with a BMI increase of 7.8 %�. Likewise, a 10 % difference in PGC1A methylation may predict up to 12 % difference in fat mass .
The study of the role of epigenetics in obesity and metabolic disease has expanded rapidly in recent years, and evidence is accumulating of a link between epigenetic modifications and metabolic health outcomes in humans. Potential epigenetic biomarkers associated with obesity and metabolic health have also emerged from recent studies. The validation of epigenetic marks in multiple cohorts, the fact that several marks are found in genes with a plausible function in obesity and T2DM development, as well as the overlap of epigenetic marks with known obesity and T2DM genetic loci strengthens the evidence that these associations are real. Causality has so far been difficult to establish; however, regardless of whether the associations are causal, the identified epigenetic marks may still be relevant as biomarkers for obesity and metabolic disease risk.
Effect sizes in easily accessible tissues such as blood are small but do seem reproducible despite variation in ethnicity, tissue type, and analysis methods . Also, even small DNA methylation changes may have biological significance. An integrative �omics� approach will be crucial in further unraveling the complex interactions between the epigenome, transcriptome, genome, and metabolic health. Longitudinal studies, ideally spanning multiple generations, are essential to establishing causal relationships. We can expect more such studies in the future, but this will take time.
While animal studies continue to demonstrate an effect of early life nutritional exposure on the epigenome and metabolic health of the offspring, human data are still limited. However, recent studies have provided clear�evidence that exposure to suboptimal nutrition during specific periods of prenatal development is associated with methylation changes in the offspring and therefore have the potential to influence adult phenotype. Animal studies will be important to verify human findings in a more controlled setting, help determine whether the identified methylation changes have any impact on metabolic health, and unravel the mechanisms underlying this intergenerational/transgenerational epigenetic regulation. The identification of causal mechanisms underlying metabolic memory responses, the mode of transmission of the phenotypic effects into successive generations, the degree of impact and stability of the transmitted trait, and the identification of an overarching and unifying evolutionary context also remain important questions to be addressed. The latter is often encapsulated by the predictive adaptive response hypothesis, i.e., a response to a future anticipated environment that increases fitness of the population. However, this hypothesis has increasingly been questioned as there is limited evidence for increased fitness later in life .
In summary, outcomes are promising, as the epigenetic changes are linked with adult metabolic health and they act as a mediator between altered prenatal nutrition and subsequent increased risk of poor metabolic health outcomes. New epigenetic marks have been identified that are associated with measures of metabolic health. Integration of different layers of genomic information has added further support to causal relationships, and there have been further studies showing effects of pre- and postnatal environment on the epigenome and health. While many important questions remain, recent methodological advances have enabled the types of large-scale population-based studies that will be required to address the knowledge gaps. The next decade promises to be a period of major activity in this important research area.
Susan J. van Dijk1, Ross L. Tellam2, Janna L. Morrison3, Beverly S. Muhlhausler4,5� and Peter L. Molloy1*�
The authors declare that they have no competing interests.
All authors contributed to the drafting and critical revision of the manuscript, and all authors read and approved the final manuscript.
Beverly S. Muhlhausler and Peter L. Molloy are joint last authors.
This work has been supported by a grant from the Science and Industry Endowment Fund (Grant RP03-064). JLM and BSM are supported by the National Health and Medical Research Council Career Development Fellowships (JLM, APP1066916; BSM, APP1004211). We thank Lance Macaulay and Sue Mitchell for critical reading and comments on the manuscript.
1CSIRO Food and Nutrition Flagship, PO Box 52, North Ryde, NSW 1670, Australia. 2CSIRO Agriculture Flagship, 306 Carmody Road, St Lucia, QLD 4067, Australia. 3Early Origins of Adult Health Research Group, School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, GPO Box 2471, Adelaide, SA 5001, Australia�4FOODplus Research Centre, Waite Campus, The University of Adelaide, PMB 1, Glen Osmond, SA 5064, Australia. 5Women�s and Children�s Health Research Institute, 72 King William Road, North Adelaide, SA 5006, Australia.
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