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Metabolic Syndrome 5 Part Deep Dive Part V

<h2 data-mce-style="font-weight: 400;" style="font-weight: 400;">Part 4 – The Mighty Mitochondria – </h2>Mitochondria started off as a small purple bacterium, then they embedded themselves within another cell to symbiotically work together. Over the next billion years those combined cells evolved to form animals and humans. This ancient bacterium is still within us today and continues to create ATP (the energy we use to survive and thrive). The average human cell has between 1000-2000 mitochondria, and some parts of our body that needs the most energy like the brain, retina and our heart contain about 10,000 mitochondria each. In fact, our entire respiratory system, heart, lungs and blood exist to deliver oxygen to our mitochondria so they can make the energy (ATP) that keeps us alive. The most important thing your mitochondria do is extract energy from the food you eat and combine it with oxygen, and make ATP. Our body converts sugar (or sometimes protein) into glucose, or it converts fat into ketone body called beta-hydroxy-butyrate (BHB). Both glucose and BHB can provide carbon and electrons, the raw materials that create energy.Why are we talking about mitochondria you might be asking? Well, Glucose and lipid (fat) metabolism are largely dependent on mitochondria to generate energy in cells. Thereby, when nutrient oxidation is inefficient, the ratio of ATP production/oxygen consumption is low and contribute to mitochondrial disfunction. Mitochondrial dysfunction is a central cause of insulin resistance. We need the mitochondria to be functioning optimally to burn off the fat from the liver and the muscles. Studies have shown that mitochondrial oxidation can predispose someone to ectopic fat accumulation in the liver and the muscles. Gerald Shulman has shown in healthy aging, that mitochondrial function slows, so by the time you are 70-years-old you have a decrease in mitochondrial oxidation by about 30%, compare to a healthy 20-year-old. And this predisposes us to intramyocellular fat accumulation and insulin resistance in the muscles. that’s why as we age, we are more prone to insulin resistance and type 2 diabetes without the presence of obesity. He has also found reduction in mitochondrial oxidation associated with intramyocellular fat accumulation in young lean IR offspring of parents with type 2 diabetes, suggesting there may be a genetic basis for this abnormality.To be metabolically flexible, healthy and have well-functioning mitochondria, we are able to go from burning fat to burning glucose when we need to. To see how this works in practice we can look at the work of Dr. Inigo San Millan, the Director of Exercise Physiology at the University of Colorado and a professional speaker on the topics of sports medicine, metabolic disorders and other types of health and performance issues. His approach is, if he wants to help people with metabolic issues like MtS with the worst functioning mitochondria, he looks at those humans who have the best functioning mitochondria on the planet to see what they are doing and why their mitochondria function so well. And these athletes he looks at are professional cyclists. One way he assesses a client to see how well their mitochondria are function is to measure their fat oxidation rate during exercise, as it provides an indirect method to assess metabolic flexibility. He did a recent study assessing metabolic flexibility in three populations to determine how much fat was oxidised under a given exertion of effort. Fat oxidation ability was significantly higher in professional athletes compared to patients with metabolic syndrome. At rest normal metabolism burns more fat than glucose, and as the intensity of the exercise goes up, we go from burning fat to glucose and lactate levels raise. People who are not metabolically flexible, rely on glucose earlier on in the process.The measurement they use is respiratory exchange rate (RER), at rest in people with normal metabolism their RER remains below 0.7. When 100% of fuel source is glucose the RER is 1.00. Higher RER at low work load, or at rest is a red flag for mitochondrial dysfunction. Metabolically sick people may have their number at 0.9+ while at rest (burning mostly glucose and virtually no fat). <a href="https://peterattiamd.com/inigosanmillan/" data-mce-href="https://peterattiamd.com/inigosanmillan/">(12)</a>﻿ <figure id="figure-4uah2zxgrglo11ckmo"><img id="4uah2zxgrglo11ckmo" src="https://cdn.durable.co/blocks/3bBBEfua0OtWzXMbt2ajPErWrVACCkfL9LUBKKBNRpWWRZi5aYrRhPHqghM7R8iO.png" alt="Athlete vs metabolic syndrome fuel partitioning" class="object-cover bg-gray-100 rounded-sm md:rounded-md lg:rounded-lg" style="aspect-ratio: 16/9; object-position: 35% center;" data-corners="default" data-aspect="16:9" data-caption="PA’s = Professional endurance athlete 	MA’s = Moderately active healthy individuals 	MtS = Metabolic Syndrome 	Here you can see the MtS groups lactate levels 	rose quick from the start and maxed out just 	over 200 Watts. Indicating they went from fat 	oxidation (burning) to glucose oxidation early. 	The pro athlete was still burning mostly fat, 	while the MtS group had maxed out." data-positionx="35%" data-positiony="undefined" data-mce-src="https://cdn.durable.co/blocks/3bBBEfua0OtWzXMbt2ajPErWrVACCkfL9LUBKKBNRpWWRZi5aYrRhPHqghM7R8iO.png" data-mce-style="aspect-ratio: 16/9; object-position: 35% center;"><figcaption class="body-normal text-gray-500 mt-2">PA’s = Professional endurance athlete MA’s = Moderately active healthy individuals MtS = Metabolic Syndrome Here you can see the MtS groups lactate levels rose quick from the start and maxed out just over 200 Watts. Indicating they went from fat oxidation (burning) to glucose oxidation early. The pro athlete was still burning mostly fat, while the MtS group had maxed out. </figcaption></figure><figure id="figure-sgjho1ly6kllo11ffp0"><img id="sgjho1ly6kllo11ffp0" src="https://cdn.durable.co/blocks/15PEwKftwYkPRKerL8XDXurDycLD4iJCWxQMOzToK5svw8wDpap9XL8AmO8Wn7D0.png" alt="fat oxidation and exercise intensity" class="object-cover bg-gray-100 rounded-sm md:rounded-md lg:rounded-lg" style="aspect-ratio: 16/9; object-position: center center;" data-corners="default" data-aspect="16:9" data-caption="This graph shows the same 3 populations, and their fat oxidation levels as the exercise intensifies. Take note of the MtS group and notice how low their fat oxidation is at the start, and how quickly they switch to glucose as fuel." data-positionx="undefined" data-positiony="undefined" data-mce-src="https://cdn.durable.co/blocks/15PEwKftwYkPRKerL8XDXurDycLD4iJCWxQMOzToK5svw8wDpap9XL8AmO8Wn7D0.png" data-mce-style="aspect-ratio: 16/9; object-position: center center;"><figcaption class="body-normal text-gray-500 mt-2">This graph shows the same 3 populations, and their fat oxidation levels as the exercise intensifies. Take note of the MtS group and notice how low their fat oxidation is at the start, and how quickly they switch to glucose as fuel.</figcaption></figure>As I mentioned before, skeletal muscle is the first tissue where insulin resistance starts, and about 80% of all the glucose (carbohydrates) that we oxidize in the body after a meal is in skeletal muscle. In well trained athletes, they have 3x-4x the number of mitochondria and each mitochondria are larger compared to the normal individual. Cardio vascular training in a specific range stimulates different pathways for mitochondria biogenesis as well as improves the efficiency of the mitochondria. Inigo says that the best treatment is zone 2 training (cardio training in a specific zone) to adapt and improve mitochondrial function. “What I have been seeing for 25 years, working with elite athletes, is that this [zone 2] is the exercise intensity where I see the biggest improvement in fat burning and the biggest improvement in lactic clearance capacity. Therefore, that means that the mitochondria is where you see the biggest improvement. We also see the biggest improvement in performance.” – Iñigo&nbsp; San Millán, Ph.D.MtS patients utilize more glucose for energy, and they can’t synthesize fatty acids for energy purposes very efficiently, so they rely on glucose at rest more than the average person.Now we are getting somewhere! There is a connection between aerobic fitness levels and training, and mitochondrial function. And we can see that represented in the athlete and the MtS patient and their mitochondrial function. And we know MtS patients have more muscle fat and can’t utilize fat as a fuel and utilize glucose more than an athlete. So, lets look at what a single bout of exercise can do with insulin stimulated muscle glycogen synthesis.<figure id="figure-vlnhreo4hlo11kkwc"><img id="vlnhreo4hlo11kkwc" src="https://cdn.durable.co/blocks/19XIByrJFQqMO1JtGxk44bTSbbl7YpVk7RWtucrqwlPHKTXLg1qbxTSOa5YXbhdW.png" alt="single bout of exercise on insulin stimulated glycogen synthesis" class="object-cover bg-gray-100 rounded-sm md:rounded-md lg:rounded-lg" style="aspect-ratio: 16/9; object-position: center center;" data-corners="default" data-aspect="16:9" data-caption="Gerald Shulman asked the question: “Can we bypass this (transport) abnormality with exercise?” and the answer is yes. As shown here just one bout of 45-min aerobic exercise (three 15 minute sets at 65% of max aerobic capacity, each separated by 5-min of rest) restored the concentration and rate of glycogen synthesis in muscle of insulin-resistant participants to that of the baseline (pre-exercise) level of insulin-sensitive participants. (13) Picture from Gerald Shulman" data-positionx="undefined" data-positiony="undefined" data-mce-src="https://cdn.durable.co/blocks/19XIByrJFQqMO1JtGxk44bTSbbl7YpVk7RWtucrqwlPHKTXLg1qbxTSOa5YXbhdW.png" data-mce-style="aspect-ratio: 16/9; object-position: center center;"><figcaption class="body-normal text-gray-500 mt-2">Gerald Shulman asked the question: “Can we bypass this (transport) abnormality with exercise?” and the answer is yes. As shown here just one bout of 45-min aerobic exercise (three 15 minute sets at 65% of max aerobic capacity, each separated by 5-min of rest) restored the concentration and rate of glycogen synthesis in muscle of insulin-resistant participants to that of the baseline (pre-exercise) level of insulin-sensitive participants. (13) Picture from Gerald Shulman</figcaption></figure>This is an indication of the opening up of the road block. Shulman did another more recent study in a similar population.<a href="https://www.pnas.org/content/108/33/13705.short" data-mce-href="https://www.pnas.org/content/108/33/13705.short">(14)</a> they showed that the same ingested glucose would lead to more glucose deposition as muscle glycogen, and a significant reduction de novo lipogenesis (making fat out of glucose) and a significant reduction in liver triglycerides. A single bout of exercise prior to two carbohydrate-rich meals resulted in an approximately threefold increase in muscle glycogen synthesis and a 30% decrease in de novo lipogenesis in the liver.<figure id="figure-6caxz40gqlo11mxl9"><img id="6caxz40gqlo11mxl9" src="https://cdn.durable.co/blocks/5CtiN8pNCYJ5nuzGoqgDgBOdvmjcnnqHNu757ZqG1K58eCrDO2G6eTL1d3POIxtl.png" alt="exercise can reverse abnormal pattern of carbohydrate storage in insulin resistant individuals" class="object-cover bg-gray-100 rounded-sm md:rounded-md lg:rounded-lg" style="aspect-ratio: 16/9; object-position: center center;" data-corners="default" data-aspect="16:9" data-caption=" This picture shows from the study above, 45-min bout of exercise increases muscle glycogen synthesis, decreases glucose turning to fat and decreases triglycerides. Picture from Gerald Shulman" data-positionx="undefined" data-positiony="undefined" data-mce-src="https://cdn.durable.co/blocks/5CtiN8pNCYJ5nuzGoqgDgBOdvmjcnnqHNu757ZqG1K58eCrDO2G6eTL1d3POIxtl.png" data-mce-style="aspect-ratio: 16/9; object-position: center center;"><figcaption class="body-normal text-gray-500 mt-2">This picture shows from the study above, 45-min bout of exercise increases muscle glycogen synthesis, decreases glucose turning to fat and decreases triglycerides. Picture from Gerald Shulman</figcaption></figure><div>Too finish this article, it is quite exciting to see that aerobic exercise can be a powerful tool in glycaemic control and synthesis in the muscle, and can also start to target the liver in downregulating fat production from glucose and also helps lower triglycerides which is one of the markers for MtS. Also, as Inigo has shown the more we can work on our aerobic fitness, the more we can get our mitochondria functioning better and allowing the insulin resistant person to slowly be able to burn fat for longer. Remember being metabolically flexible is the ability to go from one fuel source to the other with ease. </div>In the next and final article, we will go through some strategies to start reversing MtS and how you can become more metabolically flexible. When you’re more metabolically flexible fat won’t build up in the wrong places, your lipid profile will look better, your blood pressure can even go down to normal, and you can actually start to lose weight! This is exciting, and I hope you’re still reading on and ready to make some life changing choices. <div> </div><div> </div>

Metabolic Syndrome 5 Part Deep Dive Part IV

The clockwork old mechanical  high resolution with words Time for Action

<h2 data-mce-style="font-weight: 400;" style="font-weight: 400;">Part 3 – From metabolically healthy to metabolic syndrome – the mechanics continued</h2>Recapping so far:<ul><li>We start with the physiological cause for insulin resistance in muscle, is that you can’t get glucose into glycogen in the muscle due to a block in the transport part of the process from build-up of fat in the muscle.</li><li>Insulin levels increase to try and cram it in, which increases fat storing hormones and the production of glucose into fat.</li><li>Muscle insulin resistance can lead to fat accumulation in the liver, atherogenic dyslipidaemia (increase in triglycerides, decrease in HDL-C) and fatty liver.</li><li>Insulin resistance in muscle drives glucose to the liver, leading to fat accumulation</li></ul>As for the liver in contrast to the muscle, insulin is not required to stimulate glucose uptake in the liver. <a href="https://peterattiamd.com/geraldshulman/" data-mce-href="https://peterattiamd.com/geraldshulman/" style="font-family: inherit;" data-mce-style="font-family: inherit;">(10)</a>Similar to muscles though, the liver has insulin receptors. Fat in the liver interferes with the signalling, which down regulates glycogen synthesis from the glucose trying to come in, and at the same time because of the liver not receiving the glucose it goes into a process of gluconeogenesis (making glucose from protein or fat).So, now you have a fatty liver from the overflow of insulin resistance in the muscles and the peripheral and this leads to fatty liver and messes with the insulin mechanisms, so glucose can’t get in, so the liver produces more glucose thinking it’s in a starvation mode, increasing blood glucose even more. “When you get both muscle and liver insulin resistance, and increased glucose production by the liver, then something happens to the beta cells (cells in the pancreas that produce insulin) and that’s when things really start to spiral where you have very profound hyperglycaemia (high blood sugar)- fasting and after a meal” Gerald Shulman The next sugar we need to look at also is fructose, which I’m sure you might be aware comes from fruit. But also, normal sugar (Sucrose), the same sugar that is in most processed foods, like soft drinks and candy, is made up from 50% glucose and 50% fructose. It is different from normal carbohydrates which is mostly glucose, fructose is digested differently and is transported to the liver to be processed. The problem here is your liver is the only thing that processes fructose, as where glucose almost every cell in your body can process it. if you take in too much fructose, only your liver can deal with it, and it will tend to make your more insulin resistant. It’s like a 1,2-punch combo.There are also other factors that can contribute to insulin resistance, and they are: <ul><li>Genetic tendencies</li><li>Low Sleep</li><li>Low exercise</li><li>Low sun exposure/vitamin D</li><li>Sedentary behaviour</li><li>Low omega 3</li><li>High omega 6/vegetable oils</li><li>Smoking</li></ul>While insulin resistance is becoming more prevalent nowadays, there is actually an evolutionary explanation for insulin resistance and how it helped us survive starvation.Important organs and systems need glucose to function, like our brain and our central nervous system. In the past, us homosapiens didn’t have a convenient store down the road, we had to hunt and gather for our food. And at times the herd of buffalo might of moved on, or the fruit we’d normally get was out of season, whatever the reason, there were times when we could of gone some time without a real feed, and through evolution from humans all the way to fruit flies, insulin signalling is preserved. This tells us it’s been evolutionary important to spare glucose in times of starvation.When we are in a starvation state, we get an increase of lipolysis (break down of fat) of white fat tissue, which leads to liver fat accumulation, and this fat accumulation is the same as insulin resistance mechanisms and mediates liver insulin resistance and decreases liver glycogen storage and gluconeogenesis (break down of fat and protein to be converted to glucose) increases in the liver. So now we have more glucose available for our central nervous system and our brain.That’s a bit of a, hmm moment, right? So, when we are starving there is an evolutionary natural insulin resistance that occurs to save glucose for our brain and central nervous system. But now we have an overabundance of food available to us. And the western diet of processed and refined foods which makes things easier for us and saves us time, but all the extra calories and specifically refined carbs increase blood glucose. This raises insulin, and if you’re eating these foods all day your insulin levels don’t get a chance to go down. Our cells get jam packed, and insulin keeps trying to jam more in, until we get to the point of insulin resistance, and now our body thinks it’s starving. Yes, both starvation and this toxic environment of overabundance of the wrong foods use the same pathways in opposite directions- promoting disease by doing what they were at one time, was protective. And now they’re being called metabolic syndrome.In the next article we will go through how this broken system can be fixed. Yes, even type 2 diabetes, which was once thought of as being irreversible, can be reversed and has been proven. Once we understand the root cause, we can make changes that really move the dial. This way rather than just getting your blood glucose levels under control we can reverse the process and achieve better markers; like your lipid profile, blood pressure, weight etc.

Metabolic Syndrome 5 Part Deep Dive Part III

gear mechanism in action, highlighted by a colored background.

<h2 data-mce-style="font-weight: 400;" style="font-weight: 400;">Part II - From metabolically healthy to metabolic syndrome – the mechanics</h2>As I eluded to before in the previous article, the main issue with Metabolic Syndrome (MtS)/Insulin Resistance (IR) is the dysregulation of insulin. The point I want to make clear right from the get go is, that by the time lab tests pick up that your blood glucose levels aren’t been managed well, and to the point where you have now have type 2 diabetes (T2D) which is classified as “when the body doesn’t produce enough insulin (beta cells in the pancreas are “burnt out”) to function properly, or the body’s cells don’t react to insulin. This means glucose stays in the blood and isn’t used as fuel for energy”. Your insulin levels have been high in the back ground trying to control your blood glucose levels for quite some time, maybe even a decade or more! So, we need to pay more attention to insulin levels a lot earlier and get the right blood tests done, and do something about it.For example, I have a friend who is in his early 50’s and his uncle just passed away from cardio vascular disease and his dad needs a bypass, so he is concerned about his health and his fate. He sent me some blood tests he got done a year ago, he had all the markers for MtS/IR, high triglycerides (TG), lower HDL-C, large amount of belly fat, with a BMI that would classifies him as obese, HBA1C (blood glucose measurement) high, and his TG/HDL-C ratio was above the normal and this marker is a good indicator of insulin resistance. However, his doctor suggested to lose some weight, that he might need to go onto a cholesterol lowering medication and to get a scan to see how his heart is going. This is all great, however when looking through the lens of insulin resistance we might see the results a little different.So, in this article we will discover what metabolic flexibility is, and then look at the mechanisms to which someone would go through to get to metabolic Syndrome/Insulin resistance.Let’s start with the definition again of Metabolic: Relating to the chemical changes in living cells by which energy is provided for vital processes and activities and new material is assimilated.Metabolic flexibility describes the ability to respond or adapt to the changes in metabolic or energy demands. To generate chemical energy and key metabolites either aerobically or by using anaerobic respiration to give it greater versatility and metabolic flexibility to respond and adapt to environmental changes. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5513193/" data-mce-href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5513193/">(8)</a> Said in simpler terms, metabolic flexibility is the ability to switch between burning carbs and burning fat. Someone with great metabolic flexibility can burn carbs when they eat them, they can burn fat when they eat them or in a fasted state. They’re able to switch from carbohydrate metabolism and fat metabolism with relative ease. <a href="https://www.marksdailyapple.com/definitive-guide-to-metabolic-flexibility/" data-mce-href="https://www.marksdailyapple.com/definitive-guide-to-metabolic-flexibility/">(9)</a>The other end of the spectrum of less metabolic flexibility can have consequences like:<ul><li>You get sleepy after eating carbs</li><li>You can’t go five hours between feedings</li><li>You get the midday crash after lunch</li><li>You must snack to sustain your energy levels<ul><li>Fasting is difficult, and if you manage to power through the discomfort, you get worse results than you were expecting (muscle loss, very little fat loss) <a href="https://www.marksdailyapple.com/definitive-guide-to-metabolic-flexibility/" data-mce-href="https://www.marksdailyapple.com/definitive-guide-to-metabolic-flexibility/">(9)</a><div> Now let’s look at the mechanism from flexibility to how you become inflexible and get insulin resistance and metabolic syndrome.</div><div>We will be looking at carbohydrates mainly here as they have the biggest effect on insulin, protein raises insulin a little, and fat raises insulin insignificantly. When we eat carbohydrates that contain glucose or can get broken down into glucose which is most carbohydrates. Processed and refined carbohydrates raise your blood glucose levels the most, this includes things like:<ul><li>White grains which are a refined source of carbs, like breads, pastas and cereals. Baked goods like muffins, cookies, cakes etc.</li><li>Sugar-sweetened drinks like soft drinks, sports drinks and other drinks with added sugar.</li><li>Starchy vegetables have less fibre than other vegetables and raise blood glucose more, and quicker.</li><li>Processed foods can have hidden added sugar like non-dairy milks (which can be very high in sugar), low fat options as more sugar is usually added to add flavour in replace of fat, salad dressing and other packaged foods.</li></ul>When we eat carbs that convert to glucose, our pancreas releases insulin and the glucose then gets stored in skeletal muscles and the liver as stored glycogen to be used as energy when it needs it. In a healthy individual, 80-90% of consumed glucose is stored as glycogen (in muscle and liver). <a href="https://peterattiamd.com/geraldshulman/" data-mce-href="https://peterattiamd.com/geraldshulman/">(10)</a> It also tells the liver to stop gluconeogenesis (the making of new glucose from fat or protein), so, glucose production goes down in the liver.<figure id="figure-tbiff6o7dklo0zjqre"><img id="tbiff6o7dklo0zjqre" class="object-cover bg-gray-100 rounded-sm md:rounded-md lg:rounded-lg" style="aspect-ratio: 16/9; object-position: center center;" src="https://cdn.durable.co/blocks/25zpMb6kjq74oTVWzJufFTltyPwo9DyvvD2EUsdYL2h83gtHQLJO1Zc5QF32fzbC.png" alt="pathogenesis of hyperglycaemia in type 2 diabetes" data-corners="default" data-aspect="16:9" data-caption="Picture from Gerald Shulman" data-positionx="undefined" data-positiony="undefined" data-mce-src="https://cdn.durable.co/blocks/25zpMb6kjq74oTVWzJufFTltyPwo9DyvvD2EUsdYL2h83gtHQLJO1Zc5QF32fzbC.png" data-mce-style="aspect-ratio: 16/9; object-position: center center;"><figcaption class="body-normal text-gray-500 mt-2">Picture from Gerald Shulman</figcaption></figure>If we eat too many carbs that spike our insulin it promotes de novo lipogenesis (converts excess carbohydrates into fatty acids in the form of triglycerides), so triglycerides go up. Insulin also stimulates Lipoprotein lipase (fat storing hormone) thereby increasing circulation of free fatty acids by up to two-fold and facilitating entry of fatty acids into muscle cells<div><a href="https://peterattiamd.com/geraldshulman/" data-mce-href="https://peterattiamd.com/geraldshulman/">.(10)</a></div> It’s when the muscle cells start getting fat in them that it impairs the glucose transport into the cells. So now the glucose can’t get into the muscles as well and glucose is still floating around, so more insulin is produced to try and cram it in. <figure id="figure-qc9wmxrh9mlo0zu39g"><img id="qc9wmxrh9mlo0zu39g" src="https://cdn.durable.co/blocks/2eSXAueJ5YeeKBhBA3s25kcMqpTKgcTPl3jA7pVWbkXk7rIdALGeK5IciDE0FUML.png" alt="glucose path with or without insulin resistance" class="object-cover bg-gray-100 rounded-sm md:rounded-md lg:rounded-lg" style="aspect-ratio: 16/9; object-position: undefined undefined;" data-corners="default" data-aspect="16:9" data-caption="In this picture you can see that excess sugar is turned into fat in the form of triglycerides. Lipoprotein Lipase increases due to increase in insulin, increases fatty acid building up in the muscle cell which impairs glucose uptake and glycogen stores in muscle go down. Picture from Gerald Shulman" data-positionx="undefined" data-positiony="undefined" data-mce-src="https://cdn.durable.co/blocks/2eSXAueJ5YeeKBhBA3s25kcMqpTKgcTPl3jA7pVWbkXk7rIdALGeK5IciDE0FUML.png" data-mce-style="aspect-ratio: 16/9; object-position: undefined undefined;"><figcaption class="body-normal text-gray-500 mt-2">In this picture you can see that excess sugar is turned into fat in the form of triglycerides. Lipoprotein Lipase increases due to increase in insulin, increases fatty acid building up in the muscle cell which impairs glucose uptake and glycogen stores in muscle go down. Picture from Gerald Shulman</figcaption></figure><figure><div>As this process happens it causes impairment of mitochondrial (the power plant in every cell that generates most of the chemical energy needed to power the cell) fat oxidation (breaking down of fat), promotes fat accumulation in the liver and increases susceptibility to insulin resistance <a href="https://www.pnas.org/content/104/43/17075.short" data-mce-href="https://www.pnas.org/content/104/43/17075.short">(11)</a></div>So, the first stage of insulin resistance happens when we eat too many carbs that turn to glucose in the blood, which raises insulin levels, to normally store 80-90% of the glucose as glycogen in the muscles and the liver. We normally only need about 5 grams of glucose in the blood at any time, which really isn’t much when you think about it. When insulin runs high for prolonged periods it increases fat storing hormones, increases triglycerides, increases fat to build up in the muscle which defects the glucose transport in the cells and doesn’t let the glucose into the muscle. This will impair our powerplants in our cells to use fat as energy and promotes fat accumulation in the liver.</figure><figure id="figure-de0ubv3amlo0zwtl1"><img id="de0ubv3amlo0zwtl1" class="object-cover bg-gray-100 rounded-sm md:rounded-md lg:rounded-lg" style="aspect-ratio: 16/9; object-position: center center;" src="https://cdn.durable.co/blocks/30CJkqtXJ5yFWkIWU6MZQEh8tNHucWSYN3rgdoDYUZgHdYXZpZQ8i21VCzmVm3XQ.png" alt="metabolic associated fatty liver disease MAFLD" data-corners="default" data-aspect="16:9" data-caption="This picture describes the above process. You can see the yellow dots which are fat accumulating in the muscle and the liver. Fat in the liver will increase the chances of getting Non-Alcoholic Fatty Liver Disease (NAFLD) or what Gerald Schulman calls Metabolic-Associated Fatty Liver Disease (MAFLD) Picture from Gerald Shulman" data-positionx="undefined" data-positiony="undefined" data-mce-src="https://cdn.durable.co/blocks/30CJkqtXJ5yFWkIWU6MZQEh8tNHucWSYN3rgdoDYUZgHdYXZpZQ8i21VCzmVm3XQ.png" data-mce-style="aspect-ratio: 16/9; object-position: center center;"><figcaption class="body-normal text-gray-500 mt-2">This picture describes the above process. You can see the yellow dots which are fat accumulating in the muscle and the liver. Fat in the liver will increase the chances of getting Non-Alcoholic Fatty Liver Disease (NAFLD) or what Gerald Schulman calls Metabolic-Associated Fatty Liver Disease (MAFLD) Picture from Gerald Shulman</figcaption></figure><figure id="figure-ony1kaxi9vlo0zz5mx"><img id="ony1kaxi9vlo0zz5mx" class="object-cover bg-gray-100 rounded-sm md:rounded-md lg:rounded-lg" style="aspect-ratio: 16/9; object-position: center center;" src="https://cdn.durable.co/blocks/24baHqqk8Qu3KHOxFNhXDEKbFZBWtZsmYcvAcgacWE6bvgFn34N0JfviX6FWI4z1.png" alt="muscle and liver glycogen in insulin sensitive and insulin resistance" data-corners="default" data-aspect="16:9" data-caption="Stage 1: Gerald and his team discovered that while insulin-sensitive and insulin-resistant participants were able to store similar amounts of the ingested carbohydrate as liver glycogen, the insulin-resistant participants were able to store much less glycogen in muscle (11) Picture from Gerald Shulm" data-positionx="undefined" data-positiony="undefined" data-mce-src="https://cdn.durable.co/blocks/24baHqqk8Qu3KHOxFNhXDEKbFZBWtZsmYcvAcgacWE6bvgFn34N0JfviX6FWI4z1.png" data-mce-style="aspect-ratio: 16/9; object-position: center center;"><figcaption class="body-normal text-gray-500 mt-2">Stage 1: Gerald and his team discovered that while insulin-sensitive and insulin-resistant participants were able to store similar amounts of the ingested carbohydrate as liver glycogen, the insulin-resistant participants were able to store much less glycogen in muscle (11) Picture from Gerald Shulman</figcaption></figure><figure id="figure-lnv64e9ecclo101l1v"><img id="lnv64e9ecclo101l1v" class="object-cover bg-gray-100 rounded-sm md:rounded-md lg:rounded-lg" style="aspect-ratio: 16/9; object-position: center center;" src="https://cdn.durable.co/blocks/1fYmit0BTCIEzCBDAeF6khwhFe52UbmlEwJE9FtUoa9Do068nUwSqjFR2igTJ1fB.png" alt="liver fat and hepatic de novo lipogenesis" data-corners="default" data-aspect="16:9" data-caption="In this Figure the insulin-resistant participants (yellow) also stored more fat in the liver and synthesized more fat from the ingested glucose (de novo lipogenesis) Picture from Gerald Shulman" data-positionx="undefined" data-positiony="undefined" data-mce-src="https://cdn.durable.co/blocks/1fYmit0BTCIEzCBDAeF6khwhFe52UbmlEwJE9FtUoa9Do068nUwSqjFR2igTJ1fB.png" data-mce-style="aspect-ratio: 16/9; object-position: center center;"><figcaption class="body-normal text-gray-500 mt-2">In this Figure the insulin-resistant participants (yellow) also stored more fat in the liver and synthesized more fat from the ingested glucose (de novo lipogenesis) Picture from Gerald Shulman</figcaption></figure>We might leave it here for this article, as I know there is a lot of information. I hope I have put it in a way that makes it a little easier to understand. On my journey of learning more about chronic diseases and in particular insulin resistance and metabolic syndrome, there is a lot of basic information out there which can leave you asking more questions, then there is the super technical journal articles to sieve through and a few amazing doctors and diabetologists who go into so much detail it’ll make your head spin, I’ve tried to bridge the gap here and paint a picture incorporating the science in an easier to digest way.In the next article we will pick up with stage two and how the liver becomes insulin resistant and how that can affect someone’s health. </div></li></ul></li></ul>

Metabolic Syndrome 5 Part Deep Dive  part II

Weight loss, junk food, overweight, dieting concept. Unknown woman trying to button tight shirt on obese belly, close up

<h2 data-mce-style="font-weight: 400;" style="font-weight: 400;">Part 1 - What is Metabolic Syndrome and Stats –</h2> Metabolic Syndrome may be the most common and serious condition you’ve never heard of. And research shows that it’s on the rise! It is also been called syndrome X and insulin resistance syndromeIn this 5-part series of articles I will go through what it is, the stats, risk factors and what we can do to stay healthy and fight off this disorder which can lead to some of the deadliest diseases. Once we can understand what metabolic syndrome is, what causes it, and what we can actually do to reduce the risk factors that contribute, you become empowered that the control is in your hands and you don’t have to be a victim to it. There can be genetic factors that play into Metabolic Syndrome, but this doesn’t’ have to mean you will get it. All your genetic factors are, are switches, and the way we flick the switch one way to go down the path or not, is based on your epigenetics which is the lifestyle you choose which will or won’t flick these switches. More on that later.So, what is it? Let’s break it down, according to Merriam-Webster:Metabolic: Relating to the chemical changes in living cells by which energy is provided for vital processes and activities and new material is assimilated. Syndrome: A group of signs and symptoms that occur together and characterize a particular abnormality or condition.Back in the 1980’s Gerald M Reaven, MD discovered from a lot of research, that if you had some specific measurements in the body together it meant something, and he called it metabolic syndrome. And he said if you have 3 or more on the list below you had metabolic syndrome:<ol><li>Low HDL (good) cholesterol</li><li>High blood triglycerides</li><li>Large waist measurement</li><li>Elevated blood pressure</li><li>High blood sugars</li></ol>While having any of the components of metabolic syndrome above can cause health problems on their own, having a combination of them powerfully increases the risk for most other modern-day chronic inflammatory diseases like:<ul><li>Obesity</li><li>Gout</li><li>Cancer</li><li>Stroke</li><li>Atherosclerosis</li><li>Coronary Heart Disease</li><li>Type 2 Diabetes<ul><li>Alzheimer’s</li><li>Fatty Liver disease</li><li>Asthma</li></ul></li></ul>While there is a high correlation of being overweight and obese with metabolic syndrome, not everyone who has metabolic syndrome is overweight or obese. But there is a higher prediction of metabolic syndrome. Compared with men with&nbsp;BMI&nbsp;18.5–20.9 kg/m2, the odds of the&nbsp;metabolic syndrome&nbsp;were 2.97 (95% CI 1.24–7.15) for men with&nbsp;BMI&nbsp;21–22.9 kg/m2, 4.95 (2.13–11.54) for men with&nbsp;BMI&nbsp;23–24.9 kg/m2, and 9.88 (4.29–22.75) for men with&nbsp;BMI25–26.9 kg/m2 . Individuals in the upper normal-weight and slightly overweight BMI range have a relatively high prevalence and are at increased risk of having metabolic syndrome.&nbsp;<a href="https://care.diabetesjournals.org/content/27/9/2222" data-mce-href="https://care.diabetesjournals.org/content/27/9/2222">(1)</a>-People with metabolic syndrome have 2 to 3 times the risk of having&nbsp;<a href="https://www.healthdirect.gov.au/heart-attack" data-mce-href="https://www.healthdirect.gov.au/heart-attack">heart attack</a>&nbsp;and&nbsp;<a href="https://www.healthdirect.gov.au/stroke" data-mce-href="https://www.healthdirect.gov.au/stroke">stroke</a>,&nbsp;<a href="https://www.healthdirect.gov.au/diabetes-types" data-mce-href="https://www.healthdirect.gov.au/diabetes-types">type 2 diabetes</a>&nbsp;or&nbsp;<a href="https://www.healthdirect.gov.au/chronic-kidney-disease" data-mce-href="https://www.healthdirect.gov.au/chronic-kidney-disease">chronic kidney disease</a>&nbsp;than people without the condition. - Metabolic syndrome affects about 20% to 30% of adults in Australia but can also affect children and adolescents. - About 25% of people globally have&nbsp;non-alcoholic fatty liver disease&nbsp;(NAFLD), and over 80 million Americans have NAFLD - Over 100 million people have either pre-diabetes and diabetes (<a href="https://www.cdc.gov/media/releases/2017/p0718-diabetes-report.html" data-mce-href="https://www.cdc.gov/media/releases/2017/p0718-diabetes-report.html">2017</a>)OK, hopefully by now I have your attention, Especially if we look at the risk factors that contribute to metabolic syndrome (MtS) and we can see how prevalent it is within our community. For example: <a href="https://www.aihw.gov.au/reports/biomedical-risk-factors/risk-factors-to-health/contents/abnormal-blood-lipids-dyslipidaemia" data-mce-href="https://www.aihw.gov.au/reports/biomedical-risk-factors/risk-factors-to-health/contents/abnormal-blood-lipids-dyslipidaemia">(2)</a> - Almost 2 in 3 Australian adults (63%) had abnormal blood lipids in 2011-12 - Almost 2 in 3 Australian adults (63%) were overweight or obese in 2014-15, similar to 2011-12 - 1 in 3 Australian adults (33%) have high levels of LDL cholesterol (LDL-C) - Almost 1 in 4 (23%) have low levels of HDL-C - 1 in 7 (14%) have high levels of Triglycerides - It has been shown that the simple measurement of waist circumference is highly correlated with insulin resistance (IR) in a group of Caucasian, healthy adult men. which reflects underlying visceral adiposity (fat around the organs) and correlates with IR. <a href="https://www.diabetesonthenet.com/resources/details/waist-circumference-a-predictive-tool-for-insulin-resistance" data-mce-href="https://www.diabetesonthenet.com/resources/details/waist-circumference-a-predictive-tool-for-insulin-resistance">(3)</a>Next time you’re out have a look and see how many people walking around have large bellies or better known as the beer belly. A lot of these people, and you see it more in men, might look lean enough in the rest of the body compared to the beer belly, this is a worrying sign of IR/MtS.<figure id="figure-tf5qho2xhdlo0z372m"><img id="tf5qho2xhdlo0z372m" src="https://cdn.durable.co/blocks/5kxCBh67JBy9Ci3N66NrH0YpeGfpkVDPvkSqnU3sPSj9fXNKq9GJd7mxhTg5kZZO.png" alt="Insulin resistance and disease" class="object-cover bg-gray-100 rounded-sm md:rounded-md lg:rounded-lg" style="aspect-ratio: 16/9; object-position: 0% center;" data-corners="default" data-aspect="16:9" data-caption="In this study, they divided the volunteers into three equal-sized groups based on their degree of insulin resistance. Group I had the lowest level of insulin resistance, group II had an intermediate level, and group III had the highest level. The following graph illustrates the number of people who were diagnosed with disease (and/or died) in each group over the course of the study: Including hypertension, coronary heart disease, stroke, type 2 diabetes, and cancer. (20)" data-positionx="0%" data-positiony="undefined" data-mce-src="https://cdn.durable.co/blocks/5kxCBh67JBy9Ci3N66NrH0YpeGfpkVDPvkSqnU3sPSj9fXNKq9GJd7mxhTg5kZZO.png" data-mce-style="aspect-ratio: 16/9; object-position: 0% center;"><figcaption class="body-normal text-gray-500 mt-2">In this study, they divided the volunteers into three equal-sized groups based on their degree of insulin resistance. Group I had the lowest level of insulin resistance, group II had an intermediate level, and group III had the highest level. The following graph illustrates the number of people who were diagnosed with disease (and/or died) in each group over the course of the study: Including hypertension, coronary heart disease, stroke, type 2 diabetes, and cancer. (20)</figcaption></figure>As Metabolic Syndrome is a combination of factors there isn’t just 1 blood test or 1 sign that you have it. As it is still being understood and realising the prevalence of it, your doctor may miss seeing the pieces come together to create this disorder or might not get enough information to make a decision.So, what should you look for to see if you have metabolic syndrome/insulin resistance?&nbsp;<h3 data-mce-style="font-weight: 400;" style="font-weight: 400;">&nbsp; &nbsp;Usual Markers:</h3>-Central or abdominal Obesity -&nbsp;&nbsp;&nbsp;&nbsp; -Men – greater than 101.6cm&nbsp;&nbsp;&nbsp;&nbsp; -Women – greater than 88.9cm-Triglycerides - greater than or equal to 150 milligrams per &nbsp; &nbsp; &nbsp; &nbsp;decilitre of blood (mg/dL)-HDL Cholesterol - &nbsp;&nbsp;&nbsp;&nbsp; -Men – Less than 40 mg/dL&nbsp;&nbsp;&nbsp;&nbsp; -Women – Less than 50 mg/dL- blood pressure - greater than or equal to 130/85 millimetres of &nbsp; &nbsp; mercury (mmHg)- Fasting glucose - greater than or equal to 100mg/dL<h2 data-mce-style="font-weight: 400;" style="font-weight: 400;">Some other really good markers to take into account as proxies for insulin resistance:</h2><ul><li>Total Cholesterol/HDL cholesterol - 5:1 is considered good a higher ratio increases risk</li><li>Triglycerides/HDL-C – this marker should be below 2</li><li>LPIR - scores range from 0-100 and the higher the score indicates greater IR. According to new research, the recently developed lipoprotein insulin resistance (LPIR) score can identify type 2 diabetes (T2D) risk years before glycaemic abnormalities are clinically detected.</li><li>GGT – in the range of 0 to 30 IU/L are normal. Anything above 30 IU/L could be a sign that your liver isn't working the way it should. (more on liver function and IR later) <a href="https://labtestsonline.org/tests/gamma-glutamyl-transferase-ggt" data-mce-href="https://labtestsonline.org/tests/gamma-glutamyl-transferase-ggt">(3)</a></li><li>Ferritin – The normal range is 25-155 microgram/L in menstruating adult females, and 40-260 microgram/L in&nbsp;adult males. Serum&nbsp;ferritin(SF) has been positively associated with&nbsp;insulin resistance&nbsp;and the metabolic syndrome in whites without&nbsp;diabetes <a href="https://www.mayoclinic.org/tests-procedures/ferritin-test/about/pac-20384928" data-mce-href="https://www.mayoclinic.org/tests-procedures/ferritin-test/about/pac-20384928">(4)</a></li><li>Fasted insulin – less than 25 mlU/L</li><li>HOMA IR - HOMA-IR &gt;3.80 as “high” having clear correlates of insulin resistance Homeostatic model assessment (HOMA) is a method for assessing β-cell function and insulin resistance (IR) from basal (fasting) glucose and insulin <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3114864/" data-mce-href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3114864/">(5)</a></li><li>OGTT – 54mg/dL – 138mg/dL is normal glucose levels at 2-hour point above 140mg/dL is considered prediabetic.</li><li>OGTT (insulin) – Below 30 mlU/L is good, above 40 mlU/L is concerning. When you get an Oral glucose tolerance test (OGTT) also ask for your insulin level at the 2-hour point. (this isn’t normally done but will give you earlier detection that something may be going wrong, more on this to come)</li><li>Leptin – For men with a BMI of 22, values need to be between 0.7 and 5.3 ng/mL and for women values need to be between 3.3 and 18.3 ng/mL. Higher readings can raise concerns. It is secreted by adipocytes (fat cells) and binds to the hypothalamic leptin receptor (Ob-R) to enhance metabolism and reduce appetite, thereby increasing energy expenditure and decreasing energy intake. Glucocorticoids and insulin act on adipocytes to increase leptin expression. It is associated with obesity, since a higher adipose tissue mass results in elevated leptin levels. It is also significantly associated with BMI Insulin and HOMA index. <a href="https://www.hindawi.com/journals/ije/2015/534320/" data-mce-href="https://www.hindawi.com/journals/ije/2015/534320/">(6)</a></li><li>Adiponectin- For men ranges are 2-26 ug/mL and for women ranges are 4-37 ug/mL. Lower scores are a sign for concern. Adiponectin level negatively correlates with cardiovascular and metabolic disorders. Adiponectin in the plasma correlate inversely with adiposity and directly with insulin sensitivity. <a href="https://www.hindawi.com/journals/ije/2015/534320/" data-mce-href="https://www.hindawi.com/journals/ije/2015/534320/">(7)</a> </li></ul>As you can see metabolic syndrome/insulin resistance can affect a lot of different systems in the body, and when you can assess these areas through different blood tests you can see where on a scale you are. As eventually if untreated MtS/IR can transform into full blown type 2 diabetes, which then carries its own risk for other deadly diseases. In the next article we will walk through some of the mechanisms of how insulin should work, and when it starts to get out of balance, the path that it takes, and the consequences that lead to MtS/IR.

Metabolic Syndrome 5 Part Deep Dive Part I

<h2>Tips for Controlling Your Blood Sugar</h2>Managing blood sugar levels is essential for individuals with diabetes or those at risk of developing the condition. By controlling your blood sugar, you can prevent complications and maintain overall health. Here are five tips to help you keep your blood sugar levels in check:<h3>1. Eat a Balanced Diet</h3>A well-balanced diet plays a crucial role in managing blood sugar levels. Focus on consuming a variety of nutrient-rich foods, including &nbsp;lean proteins, fruits, and vegetables. Limit your intake of processed foods, sugary snacks, and beverages. Incorporate foods with a low glycemic index, such as beans, lentils, and leafy greens, to help stabilize blood sugar levels.<figure id="figure-e0pe13aq6lo0wzd3a"><img id="e0pe13aq6lo0wzd3a" src="https://images.unsplash.com/photo-1618897996318-5a901fa6ca71?crop=entropy&amp;cs=tinysrgb&amp;fit=max&amp;fm=jpg&amp;ixid=M3wyNjI5NjF8MHwxfHNlYXJjaHwyM3x8aGVhbHRoeSUyMGRpZXR8ZW58MHx8fHwxNjk3OTQ1NjE5fDA&amp;ixlib=rb-4.0.3&amp;q=80&amp;w=1080" alt="healthy diet" class="object-cover bg-gray-100" style="aspect-ratio: 16/9;" data-mce-src="https://images.unsplash.com/photo-1618897996318-5a901fa6ca71?crop=entropy&amp;cs=tinysrgb&amp;fit=max&amp;fm=jpg&amp;ixid=M3wyNjI5NjF8MHwxfHNlYXJjaHwyM3x8aGVhbHRoeSUyMGRpZXR8ZW58MHx8fHwxNjk3OTQ1NjE5fDA&amp;ixlib=rb-4.0.3&amp;q=80&amp;w=1080" data-mce-style="aspect-ratio: 16/9;"></figure><h3>2. Monitor Carbohydrate Intake</h3>Carbohydrates have the most significant impact on blood sugar levels. Be mindful of the type and amount of carbs you consume. Opt for complex carbohydrates that are high in fiber as they will be released into your blood a lot slower. Never drink your carbs, as most the fiber is removed in juices and soft drinks so it will spike your blood glucose a lot quicker.<h3>3. Engage in Regular Physical Activity</h3>Exercise is not only beneficial for weight management but also helps regulate blood sugar levels. Engaging in regular physical activity can improve insulin sensitivity, allowing your body to use glucose more effectively. Aim for at least 150 minutes of moderate-intensity aerobic exercise, such as brisk walking or cycling, each week. Don't forget to consult your healthcare provider before starting any new exercise routine. Your muscles are your biggest sink for glucose and when you exercise your muscles gobble them up as fuel.<figure id="figure-7jcjjzjjalo0wzewv"><img id="7jcjjzjjalo0wzewv" src="https://images.unsplash.com/photo-1571019613454-1cb2f99b2d8b?crop=entropy&amp;cs=tinysrgb&amp;fit=max&amp;fm=jpg&amp;ixid=M3wyNjI5NjF8MHwxfHNlYXJjaHwyNHx8ZXhlcmNpc2UlMjByb3V0aW5lfGVufDB8fHx8MTY5Nzk0NTYyMXww&amp;ixlib=rb-4.0.3&amp;q=80&amp;w=1080" alt="exercise routine" class="object-cover bg-gray-100" style="aspect-ratio: 16/9;" data-mce-src="https://images.unsplash.com/photo-1571019613454-1cb2f99b2d8b?crop=entropy&amp;cs=tinysrgb&amp;fit=max&amp;fm=jpg&amp;ixid=M3wyNjI5NjF8MHwxfHNlYXJjaHwyNHx8ZXhlcmNpc2UlMjByb3V0aW5lfGVufDB8fHx8MTY5Nzk0NTYyMXww&amp;ixlib=rb-4.0.3&amp;q=80&amp;w=1080" data-mce-style="aspect-ratio: 16/9;"></figure><h3>4. Stay Hydrated</h3>Proper hydration is essential for maintaining healthy blood sugar levels. Drinking an adequate amount of water throughout the day can help prevent dehydration, which can lead to elevated blood sugar levels. Limit your intake of sugary beverages, as they can cause blood sugar spikes. Carry a water bottle with you to remind yourself to stay hydrated.<h3>5. Manage Stress Levels</h3>Stress can have a significant impact on blood sugar levels. When you're stressed, your body produces hormones that can cause your blood sugar to rise. Find healthy ways to manage stress, such as practicing relaxation techniques, engaging in hobbies, or seeking support from friends and family. Prioritize self-care and make time for activities that help you unwind.<figure id="figure-ny920v6ac8lo0wzgk0"><img id="ny920v6ac8lo0wzgk0" src="https://images.unsplash.com/photo-1533537841959-705741f3d3a5?crop=entropy&amp;cs=tinysrgb&amp;fit=max&amp;fm=jpg&amp;ixid=M3wyNjI5NjF8MHwxfHNlYXJjaHwyMHx8c3RyZXNzJTIwbWFuYWdlbWVudHxlbnwwfHx8fDE2OTc5NDU2MjN8MA&amp;ixlib=rb-4.0.3&amp;q=80&amp;w=1080" alt="stress management" class="object-cover bg-gray-100" style="aspect-ratio: 16/9;" data-mce-src="https://images.unsplash.com/photo-1533537841959-705741f3d3a5?crop=entropy&amp;cs=tinysrgb&amp;fit=max&amp;fm=jpg&amp;ixid=M3wyNjI5NjF8MHwxfHNlYXJjaHwyMHx8c3RyZXNzJTIwbWFuYWdlbWVudHxlbnwwfHx8fDE2OTc5NDU2MjN8MA&amp;ixlib=rb-4.0.3&amp;q=80&amp;w=1080" data-mce-style="aspect-ratio: 16/9;"></figure><h3>Conclusion&nbsp;</h3>By following these tips, you can take control of your blood sugar levels and reduce the risk of complications associated with diabetes. Remember to consult with your healthcare provider for personalized advice and guidance tailored to your specific needs. With proper management, you can lead a healthy and fulfilling life.

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Metabolic Syndrome 5 Part Deep Dive Part V

Metabolic Syndrome 5 Part Deep Dive Part IV

Metabolic Syndrome 5 Part Deep Dive Part III

Metabolic Syndrome 5 Part Deep Dive part II

Metabolic Syndrome 5 Part Deep Dive Part I

5 tips for controlling your blood sugar