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Stomach Distension: Is Insulin To Blame?
- Updated: August 31, 2015
By Mike Arnold – From the beginning, stomach distension has been synonymous with drug use. Even after 20 years of following this topic, I have yet to see a single distension centered conversation absent of its mention. Although its association with growth hormone was recognized early on, it has only been within the last few years that insulin has been given proper attribution. No longer considered a “GH only” problem, bodybuilders are finally starting to wise up and acknowledge the full gamut of reasons for this unsightly malady.
While most would agree that insulin has played a pretty significant role in the increased size of today’s waistlines, the number of people who understand how it contributes is relatively small, with the majority picking up information via hearsay, rather than acquiring direct knowledge as a result of personal research. This has led many to accept false conclusions as fact and ultimately, it’s been responsible for perpetuating ignorance throughout our community. Fortunately, one need not have a doctorate in endocrinology in order to make sense of this stuff, so with that said, let’s get right to it.
Just like with growth hormone, insulin resistance is the primary mechanism by which insulin causes stomach distension. But before we can understand how one develops this condition, we need to have an understanding of insulin itself. First and foremost, insulin is a transport hormone. It acts as a sort of taxi service, shuttling glucose from the bloodstream to the insulin receptor, which sits on the surface of the cell waiting for insulin to float by. Once this receptor has been activated, Glut-4 (a transporter protein that resides within the cell) is signaled to rise to the cell surface; the job of which is to usher glucose inside the cell, where it can then be used for energy, glycogen replenishment, etc.
When this system stops functioning properly, the individual is said to be insulin resistant. This happens when insulin, after attaching to its receptor, fails to efficiently facilitate Glut-4’s rise to the surface, but how does one become insulin resistant in the first place? Oddly enough, the primary regulator of insulin sensitivity is insulin itself. The more insulin that insulin receptors are exposed to, the less sensitive they become to its signal. Therefore, when we use exogenous insulin, the above normal insulin concentrations lead to a subsequent decrease in sensitivity and the more we use, the worse the problem gets (assuming all other variables remain the same). When sensitivity falls below a certain point, the diagnosis becomes clinical insulin resistance.
Once insulin receptors become resistant to insulin’s effects, they do not immediately regain their sensitivity as soon as insulin levels return to normal, but remain resistant for some time afterward. Because of this, any elevation of blood glucose levels will be met with an increased insulin response. In other words, any time food is consumed, the pancreas will secrete an above normal quantity of insulin in order to maintain normal blood glucose levels. This leads to a viscous cycle, in which the body’s solution to insulin resistance is to produce more of the very hormone responsible for causing the problem in the first place.
OK, we now understand how insulin resistance develops, but how does this condition make the stomach grow? In short, insulin resistance increases visceral fat storage (the fat stored around and inbetween the internal organs) by making glucose more likely to be stored in that region. Here’s how it works. Let’s say you eat some carbohydrates and within 30 minutes, blood glucose levels start to rise. As explained above, the body’s response to this is to release insulin in order normalize blood glucose levels. This newly secreted insulin then circulates through the bloodstream, latching onto glucose and transporting it to muscle cells. Under normal circumstances the muscles will soak up everything they need and if there is any excess, it will be diverted to adipose (fat) tissue to be stored as fat, but this is not what happens in someone who is insulin resistant.
This is because not all insulin dependent tissues become insulin resistant at the same rate. Simply put, some tissues are more “resistant” to becoming insulin resistant, and this is where the problem lies—the order in which these tissues are affected. The fist tissue to be affected is skeletal muscle (technically, it is the liver, but since the liver is not relevant to this discussion, I will bypass it), preventing it from efficiently absorbing nutrients. When this happens the percentage of nutrients being diverted to subcutaneous fat cells rises, resulting in an overall increase in bodyfat. As the problem continues to progress, even subcutaneous fat cells start to become insulin resistant, leaving visceral fat cells as the only viable destination for nutrient delivery. For some reason, visceral fat cells thrive in an insulin resistant environment, continuing to respond to insulin’s signal long after other cells have stopped responding efficiently.
The second mechanism by which insulin causes stomach distension is through mitosis. In short, mitosis is cell division; the process by which a cell splits into two daughter cells, with each one possessing its own nucleus and DNA identical to the parent cell. Mitosis, being the process by which cells regenerate, is responsible for the development and maintenance of our internal organs and other bodily systems. Thus, it is essential to human life. While mitosis is a good thing when properly controlled, it can be problematic when accelerated beyond what is needed.
There are two ways in which insulin can cause mitosis. The first is insulin itself, as insulin is mitogenic by nature. This means it can potentially stimulate cell division in organs such as the intestines, etc. However, this isn’t much of a concern, as insulin is rather limited in this regard. The real problem takes place when a bunch of insulin is dumped into an already insulin resistant body. In short, when insulinemia (abnormally high insulin concentrations) occurs in the setting of insulin resistance, it triggers a series of biochemical events culminating in an enhanced mitogenic response to various growth factors (i.e. IGF-1), thereby accelerating the replication of mitotic cells in our internal organs. To put it another way, insulin can enhance the organ’s responsiveness to IGF-1, making them more likely to grow in the presence of IGF-1. Because of this, any drug which increases IGF-1 levels (ex. growth hormone, exo. insulin, exo. IGF-1) will only make the problem worse.
The final manner in which insulin can cause stomach distension is through water retention. There are two ways that this can happen. One is sodium retention. However, this effect is not confined to a single area of the body, but affects the entire system, leading to an overall increase in water levels. This does not really result in distension, per say, but it can add slight additional girth to the midsection.
A more serious issue is the body’s reaction to surpassing the renal threshold. As noted previously, exogenous insulin abuse can cause insulin resistance, resulting in elevated blood glucose levels. If blood glucose climbs too high, the renal threshold may be reached. At this point the kidneys’ ability to reabsorb glucose is overwhelmed, so in order to prevent a further rise in blood sugar, they begin excreting glucose in the urine. This increases the body’s need for water; a need which is met through increased thirst.
When blood glucose levels are stabilized through the reintroduction of exogenous insulin, water requirements return to normal. However, because the body has become accustomed to dealing with large amounts of glucose on a regular basis, it continues preparing for the next high glucose event by storing water in various tissues, such as those in the stomach. If blood glucose levels remain stable for long enough, the body will eventually realize this and stop storing additional water, but this isn’t what usually happens in those who use insulin for performance enhancement. Most bodybuilders use insulin only part of the time, leaving the body susceptible to hyperglycemia in between insulin injections. Because blood glucose levels continue to fluctuate between the two extremes, the body continues storing water in anticipation of the next high glucose event. The end result is a bigger stomach, with some individuals adding as much as 2-3inches to their waistline over a given period of time.
As you can see, the subject of insulin-induced stomach distension is fairly complex, with each case being the sum total of one or more factors. While all of these can be avoided/minimized through responsible use, many bodybuilders choose to employ this drug in kamikaze fashion, throwing caution to the wind and ultimately paying the price for their stupidity. Unlike many other PED’s, using large doses of insulin indiscriminately provides zero advantage, but will certainly damage one’s physique and health in the process. On the other hand, responsible use holds the potential for improved recovery and growth with minimal risk. As always, know what you’re getting into before you begin and you can avid many of the problems commonly associated with this popular bodybuilding drug.
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