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Damaging the Aesthetic Standard – Stomach Distension – Myth vs Fact Part 1

Stomach Distension

by Mike Arnold

Conflicting Opinions

Beginning in the mid-1990’s, the issue of stomach distension became an area of criticism among traditionalists, with many in the bodybuilding community voicing disapproval over its presence within the upper echelons of the sport. Ever since then various events have continued to transpire, thrusting the issue back into the spotlight and each time, speculation regarding the reasons for its appearance has run rampant.

Most recently, it was Arnold Schwarzenegger who, during an interview with Bob Chicerillo at the annual Arnold Classic, decided to voice his displeasure over the problem. Referring to modern physiques as “bottle-shaped” and ridiculing head judge Jim Manion for his complacency in allowing the sport to depart from traditional aesthetic standards, Arnold’s words were heard loud and clear all around the world. Within one day of his comments making headlines, we started seeing threads pop up all over the place, asking why today’s bodybuilders don’t have the waistlines of yesterday’s champs.

There was no shortage of answers, but just like every other time this question has been raised, there was zero consistency among responders. Even the “authorities” and those with personal experience (i.e. advanced bodybuilders) were posting contradictory information. Of course, if a pro bodybuilder happened to join the discussion and failed to list drugs as the #1 cause of distension in all cases, he was labeled as a liar—acting in his own self-interest by trying to divert attention away from drug use. Without knowing what to think, both fans and aspiring bodybuilders were left to come to their own conclusions, as has been the case for decades now.

There are two primary reasons why so many people still don’t know what to believe even after 20 years of debating the subject. They are: 1) the complexity of the issue and 2) diversity among individuals in terms of causes. Basically, when you have several potential factors that can lead to distension and each case is the sum result of one or more of these factors to various degrees, it becomes impossible to place the blame on any single thing. Furthermore, attempting to diagnose the problem simply by looking at pictures can oftentimes be like trying to diagnose a hair line fracture without an x-ray.

While knowledge and experience can provide us with a pretty good idea of what is going on, we must first sit down with the individual and gather information before being able to come to any concrete conclusions. It is easy to assume that advanced bodybuilders/pros would be educated on this subject, but in many cases their experience is limited only to themselves and perhaps a few others. Therefore, their answer is likely to be based on such, which may or may not reflect someone else’s experience. Furthermore, although it is true that some causes are more prevalent than others, rarely is significant distension attributable to just a single factor.

Now that you know what’s behind all the confusion, let’s take a look at the various causes of stomach distension and the reasons for them, but before we do so it is important to differentiate between off-season and pre-contest (show-ready) bodybuilders. While the potential causes are the same for both, the degree to which each contributes tends to vary based on circumstances. As we proceed through the article, when appropriate, I will make a distinction between those factors which are more or less likely to affect one group of bodybuilders or the other. With that said, here we go.

Growth Hormone

Without a doubt, drugs have shouldered the brunt of the blame for today’s expanding waistlines; to the point where “GH gut” (with the obvious implication that growth hormone is the primary/sole contributor) has become the most common term used to describe this condition. While growth hormone certainly has the potential to cause significant distension through multiple mechanisms (which we will get to in a second), we now know that it is just one part of a greater whole.

The degree to which growth hormone contributes can vary drastically from person to person, with some people experiencing little/no visible effects and others experiencing profound distension. Why such variability among individuals? While it is tempting to point the finger at extreme dosing practices, dosage is really only a predictor, as it increases the likelihood of developing this condition but does not guarantee it. In the absence of other physiological conditions, GH’s ability to cause distension is greatly limited even when utilizing large dosages.

There are two main factors which determine how likely, and to what degree GH contributes to this problem. The first is the body’s sensitivity to insulin. The more sensitive one is to this hormone, the less insulin the pancreas must produce in order to properly regulate blood glucose levels. When insulin sensitivity drops beyond a certain point, the individual is said to be “insulin resistant”, as their insulin receptors are no longer capable of responding to the hormone efficiently. With blood glucose regulation being essential to the maintenance of human life, the body’s reaction to this is to increase insulin output.

One of the side effects of insulin resistance is a heightened propensity for visceral fat (the layer of fat stored inbetween and around the internal organs) storage. The worse insulin sensitivity becomes, the more likely the body is to store fat in this region. Obviously, as visceral fat deposits increase, the larger the midsection is going to become.

The problem with GH is that it directly reduces insulin sensitivity in a dose-dependent manner, directly increasing the likelihood of visceral fat build-up and therefore, stomach distension. However, there is not a direct correlation between a particular GH dose and stomach size, simply because there are so many potential factors involved in insulin sensitivity. For this reason, one person might develop a protruding abdomen at 10 IU of GH, while another may not. Factors such as diet, weight training, cardiovascular exercise, exogenous insulin use, type of insulin used, and supplementation can dramatically impact insulin sensitivity and therefore, the probability of developing visceral fat-induced stomach distension.

The bottom line is that the more insulin sensitive you are, the less likely growth hormone is to affect your waistline. Maintain your insulin sensitivity within a normal range and visceral build-up will not become an issue. Allow your insulin sensitivity to plummet and the risk of developing a problem skyrockets. Be smart. Your GH dose should match your body’s ability to handle it. For a point of reference, doses above 5 IU per day have been shown to result in clinical insulin resistance in normal people. Common sense dictates that if you want to use more than this, you are going to need to take steps to protect yourself.

Once you get up to the 10 IU or more range, implementing as many preventative measures as possible will become a necessity of you want to maintain a normal level of insulin sensitivity. Never sacrifice insulin sensitivity for a higher dose. Doing so will not only increase the size of your waist, but will negatively affect the quality of your musculature through multiple mechanisms (this subject is outside the scope of this article), thereby working against your bodybuilding goals.

The 2nd mechanism by which GH promotes stomach distension is organ growth via IGF-1 elevation. With abundance of IGF-1 receptors in the intestines, liver, and spleen, these organs are at the greatest risk for hypertrophy. The bad part is that one of the main reasons we use GH is to increase IGF-1 levels, as IGF-1 is responsible for the majority of GH’s anabolic effects. For this reason it would be counterproductive, even contradictory, to use GH and then suppress IGF-1 production, unless one was only seeking after its lipolytic effect (i.e. fat loss), but that is one hell of an expensive fat burner.

Although the potential for stomach distension via organ growth and visceral fat build-up are similar, organ growth is usually the lesser contributor. This is because it takes very high doses of GH used over a prolonged period of time in order for organ growth to cause the same degree of distension as that witnessed in someone with severe visceral fat build-up. In other words, most people just don’t have enough money to make organ growth an equal factor.

None the less, GH is fully capable of causing stomach distension through 2 different mechanisms, each of which has considerable potential to grow the waistline. However, the bodybuilding community today is much more educated about the ill effects of growth hormone on metabolic health than it was a few years ago and many are starting to take action to keep these side effects at bay. Well, at least the smart ones are. As always, intelligent application will yield the best results with the least amount of unwanted side effects.


With an undeniable connection between this pancreatic hormone and stomach distension, insulin’s role in the ongoing gut epidemic has been well-noted among both bodybuilders and industry experts alike. However, this has not always been the case, as just a few short years ago GH was considered public enemy number one, with all other factors viewed as minor contributors, at best. These days, insulin appears to have taken GH’s place as da’ gut builder par excellence.

While insulin has certainly played a role in the expansion of modern day waistlines, unlike what some in this community would have you believe, it is far from the only cause. In reality, insulin is very much like growth hormone in that it causes stomach distension to occur through many of the same mechanisms. Here’s how it works. As explained above, growth hormone causes insulin sensitivity to fall, resulting in an increased need for insulin in order to continue managing blood glucose levels. Being that blood sugar regulation is considered a priority over maintaining high levels of insulin sensitivity, insulin output is increased. This state, referred to as insulin resistance, leads to an increase in visceral fat storage.

In addition to growth hormone’s direct effect on insulin sensitivity, it also indirectly affects sensitivity through a 2nd mechanism—elevated insulin levels. In other words, the body’s solution to GH-mediated insulin resistance is to produce more of the very hormone which causes insulin resistance. If you are wondering how insulin reduces insulin sensitivity, the explanation is simple. You see, insulin does not transport nutrients into muscle cells. Rather, it acts more like a taxi, picking up nutrients on the roadside (bloodstream) and bringing them to their destination (muscle cell), but stopping short of entering the building. Once insulin reaches its receptor site, it signals another transporter called Glut-4 (which resides inside the muscle cell) to rise to the cell surface. The job of Glut-4 is to shuttle nutrients inside of the cell, where they can then be used for energy, stored as glycogen, etc.

However, just like with the HPTA, the insulin-glucagon loop is regulated by negative feedback. In laymen’s terms, the more insulin that insulin receptors come in contact with, the less sensitive they becomes to insulin’s signal. So, when a bodybuilder uses exogenous insulin in the face of GH-induced insulin resistance, he adds insult to injury by heaping even more insulin onto an already insensitive receptor. Aside from the associated metabolic consequences, what do you think all that insulin is going to do? Since it is no longer being efficiently utilized by muscle cells, it is going to travel straight to fat cells, including visceral fat cells, stimulating glucose uptake and making one’s gut even bigger.

It gets worse. Growth hormone and insulin also have a synergistic effect, with each one potentiating the negative effects of the other. As you now know, insulin shuttles nutrients to both muscle cells and fat cells all over the body, including both regular fat cells and visceral fat cells. Under normal circumstances, muscles cells are prioritized in terms of nutrient delivery.

Only after the muscles cells have soaked up all the nutrients they need is the excess transported to adipose tissue, where it is then stored as fat. However, when we become insulin resistant, the muscle cells are the first to be affected, preventing them from efficiently absorbing nutrients. When this happens the percentage of nutrients being diverted to fat cells rises, causing an overall increase in bodyfat. But as insulin resistance continues to worsen, even normal fat cells start to become resistant to insulin’s effects, leaving visceral fat cells as the only easy target. For some reason, visceral fat cells thrive in an insulin resistant environment, continuing to respond to insulin quite well long after other cells have stopped responding efficiently.

The second mechanism by which insulin increases waist size (and another example of GH and insulin working synergitically) is through its mitogenic effect. Mitosis is basically cell division, in which a cell splits in order to form two daughter cells, each of which have the same chromosome profile as the parent nucleus. Not all cells in the body are mitotic. For example, muscle cells are not considered to be mitotic, while cancer cells are. This is why doctors sometimes advise prostate cancer patients to discontinue using TRT, as DHT (a testosterone metabolite) can cause prostate cancer cells to grow, accelerating the cancer’s progression.

Insulin is mitogenic, meaning it can potentially activate the splitting of mitotic cells. Unfortunately, insulinemia in the setting of insulin resistance (such as that promoted by GH and exogenous insulin usage) triggers a series of biochemical events culminating in an enhanced mitogenic response to various growth factors (i.e. IGF-1), thereby accelerating growth in mitotic cells, such as those found in the organs. To put it another way, insulin enhances the organ’s responsiveness to IGF-1, making them even more likely to cause gut growth.

Lastly, insulin interferes with electrolyte balance by increasing sodium retention, the end result of which is water retention. This water retention does not occur just under the skin, but everywhere within the body, including the midsection. Many people tend to notice swelling in the abdomen after an injection, especially with regular use. Although this effect is temporary and will dissipate upon discontinuation, it is still part of the equation as long as insulin remains in the program.

This is why the GH & insulin combo has caught so much flak—because it really does have the “potential” (keyword is potential) to blow out the midsection. However, given the amount of information currently available on the subject, someone has to be a total moron to allow this to happen to themselves. At extreme doses, there is going to be at least some ill effect no matter what is done, but as long as the individual makes sure to implement as many insulin sensitizing measures as possible, one can still use extremely effective dosages while greatly reducing, and possibly preventing visible changes in waist circumference.

Stay tuned for Part 2…

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