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Krista Edwards
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Article:Look beyond the “eat less, exercise more” approach, and learn about hormonal physiology and strategic nutrition.How many times have you trained a client who couldn’t lose weight no matter how hard you trained him or how “clean” he insisted his nutrition was? It’s frustrating for both fitness professional and client when the waistline doesn’tbudge in spite of what seems enough effort. However, the reason belly fat can be so intractable is that it’s as much a hormonal phenomenon as it is a caloric one. In order to understand how to get rid of belly fat, it’s important to factor hormonal physiologyinto the overall equation.This article looks at the many factors involved in stubborn belly fat and offers suggestions on how to help clients reach their goals.Fat and Fat BurningWhen we talk about belly fat, we’re talking not about one thing, but about three things (Ibrahim 2010). Deep fat, called visceral belly fat, lies around the organs under the abdominal muscles, and it can’t be pinched. Superficialsubcutaneous belly fat hangs over the waistline and can be pinched. Deep subcutaneous belly fat is a hybrid of the two. For the purposes of this article, we will focus on visceral and superficial subcutaneous belly fat.Visceral belly fat has greater blood supply, is richer in beta-receptors, is more responsive to cortisol and is less sensitive to insulin than subcutaneous belly fat. All of this means that visceral belly fat is harder to store andeasier to burn (Ibrahim 2010). Subcutaneous belly fat has more alpha-receptors compared with visceral belly fat. This means the subcutaneous fat is less responsive to fat-burning catecholamines and has less blood supply. It is also “colder” fat, which furtherdecreases blood flow. It is far more insulin sensitive and less cortisol reactive—meaning it is easier to store and harder to burn (Ibrahim 2010).Three steps are required to burn fat (Ranallo & Rhodes 199:Release. Fat has to be released from a fat cell. This is called lipolysis.Delivery. Fat then has to travel through the bloodstream and be delivered to a cell that will burn it. Therefore, blood supply to and from fat cells is important.Burning. Finally, fat has to enter the destination cell and be burned. This is called lipid oxidation.It is very important to understand these three steps, which partly explain why visceral fat is usually stored last and burned first and why subcutaneous belly fat can often be so stubborn.Introduction to Hormonal Fat BurningTwo enzymes regulate flux into and out of fat cells: lipoprotein lipase (LPL), which is responsible for fat storage, and hormone-sensitive lipase (HSL), which is involved in fat release (Langfort et al. 2003). Did younotice that the major fat-releasing enzyme is called “hormone-sensitive lipase” and not “calorie-sensitive lipase”? This gives you a hint that calories are not the only factor to consider in belly fat loss.Several different hormones directly or indirectly impact LPL and HSL activity. A few of the most important are insulin, cortisol and the catecholamines (epinephrine and norepinephrine). Estrogen, progesteroneand testosterone play an indirect role as well. Figure 1 shows how the most influential hormones impact LPL and HSL. The “+” sign means the enzyme’s activity is enhanced, while the “-” sign means its activity is repressed.As the chart indicates, insulin enhances LPL activity while sup- pressing HSL activity. This means that as a result of insulin’s effect, fat is more likely to be stored when there is an excess of calories and less likely to be burnedwhen there is a deficit of calories. Cortisol often gets blamed for being the “belly fat hormone,” but hormones don’t behave in isolation. Instead, they are like people and will behave differently depending on who they are “socializing” with. When cortisolis with insulin, for example, cortisol’s action on HSL is blunted, while its effect on LPL is elevated. Insulin and cortisol together are the real hormonal belly fat bullies.Catecholamines are tricky because their impact on fat burning depends on a lesser-known nuance of fat physiology: In and around your fat cells are two types of receptors to which catechol- amines can bind: alpha-receptors, which slowfat release and constrict blood vessels; and beta-receptors, which enhance fat release and open up blood vessels. Both types work via their impact on HSL activity. To keep this straight in your head, remember “A” for alpha and antiburn and “B” for beta andburn.As explained earlier, the location of belly fat makes a difference. Visceral fat is relatively rich in beta-receptors compared with superficial subcutaneous fat, which is richer in alpha-receptors (Ibrahim 2010). As a result, subcutaneousfat is more stubborn—harder to burn—than visceral fat.Insulin and Belly FatInsulin resistance is a term thrown around a lot, but most people don’t understand what it means. Usually, insulin resistance is synonymous with fat gain; however, insulin resistance is not a global phenomenon in the body.In other words, you can remain sensitive to the action of insulin in one tissue while remaining more resistant in another “depot” (Unnikrishnan 2004). Also, insulin resistance affects different areas of the body in different ways.For example, insulin in the brain has a normal action of suppressing hunger. If you become resistant to insulin’s action in the brain, hunger will increase. Insulin’s net action in muscle cells is to aid muscle growth. It is alsoresponsible for getting fuel into muscle cells. If muscles become resistant to insulin, it leads to muscle loss, less fuel getting into muscle and, therefore, fatigue and poor performance. In the liver, insulin decreases gluconeogenesis (sugar synthesisfrom glycerol and amino acids) andglycogenolysis (the breakdown of stored sugar called glycogen). Insulin resistance in the liver leads to increased sugar production and enhanced glycogen breakdown, which raises blood sugar levels (Lann & LeRoith 2007).When it comes to the brain, muscles and liver, you want the body to be insulin sensitive. Being insulin resistant in these areas makes a person unable to burn fat and sugar or to feel satiated after eating. This is why many obeseclients who are “insulin resistant” in these tissues tend to overeat (because they are hungry all the time) and, at the same time, tend to be malnourished (because fuel can’t get into muscle cells).This discussion is critical to understanding belly fat, because insulin’s effect on fat cells can be counterintuitive if you think of insulin resistance as having the same effect on fat as it has on the brain, muscles and liver. Insulin’snormal action on fat metabolism is to increase the activity of LPL, the major fat-storing enzyme, and to suppress the action of HSL, the prime fat-releasing enzyme. This means insulin’s normal action on fat cells is to make them store and retain more fat. Fromthat perspective, a fat cell resistant to insulin is a good thing. A fat cell that is more sensitive to the action of insulin will be a more greedy and stingy fat cell. A fat cell that is more insulin resistant will be more likely to release fat and less likelyto store it.Visceral belly fat is more resistant to insulin and therefore less likely to be stored and more likely to be burned. Subcutaneous belly fat is more sensitive to insulin and, because of this, more likely to be stored and harder toburn (Ibrahim 2010).Cortisol and Belly FatCortisol is both fat-releasing and fat-storing because it enhances the activity of both LPL and HSL. The net impact of cortisol on belly fat depends on several factors, including how much cortisol is present, for how long, and whatother hormones are with it. High amounts of cortisol present for long periods of time may make people especially prone to accumulating belly fat. This is because of two interesting effects of cortisol, one in the brain and one in the body (Epel et al. 2000;Epel et al. 2001; Kuo et al. 200.In the brain, cortisol impacts hormones that regulate appe- tite. These include neuropeptide Y (NPY), corticotropin-releasing hormone (CRH) and leptin. This is why cortisol is associated with cravings for highly palatablefoods (Epel et al. 2001; Appelhans et al. 2010). Too much cortisol also drives people to eat more of the wrong foods more often, making it far more likely to achieve a calorie surplus and gain fat. Additionally, excess cortisol increases NPY expression in thebody, and this causes smaller, immature fat cells to become larger, mature fat cells. This is not a good thing if you are trying to lose belly fat. There are 400% more cortisol receptors in visceral fat than there are in subcutaneous fat (Epel et al. 2000;Kuo et al. 200. This explains why cortisol may be such an issue for belly fat (Epel et al. 2001).The final thing to know about the relationship between cortisol and belly fat involves an enzyme called11-beta hydroxysteroid dehydrogenase (11 beta HSD). This enzyme generates its own cortisol and is present in high amountsin visceral belly fat. This has profound implications when you understand that chronic cortisol exposure causes more fat accumulation and that this chronic exposure is being generated from the area of accumulation. Visceral belly fat has a parasitic effectin this regard, perpetuating itself at the expense of its host. Another point: Insulin stimulates production of 11 beta HSD (Balachandran et al. 200, so it is not cortisol alone that is to blame for visceral belly fat growth, but rather insulin and cortisoltogether

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