by Mike Arnold
The issue of insulin sensitivity/resistance has become a hot topic among exogenous insulin users over the last couple years and for good reason; it has a significant effect on not only insulin efficiency and fat cell metabolism, but on overall health. The benefits of increased insulin sensitivity are several-fold and include: improved muscle growth, decreased fat gain/accelerated fat loss, reduced systemic inflammation, diminished beta cell turnover, and a lower risk of developing metabolic disorders such as Type II diabetes and metabolic syndrome, among others.
For a bodybuilder seeking the ultimate physique, the promise of increased muscle mass and reduced bodyfat are strong incentives for learning how to manipulate this powerful hormone to our best advantage. Unfortunately, the act of administering exogenous insulin has an automatic, negative effect on insulin sensitivity, reducing overall insulin efficiency and increasing the likelihood of fat gain. This leaves us in a Catch-22 situation. Do we continue administering exogenous insulin, being content to experience its benefits while begrudgingly accepting its negative effects as part of the package, or is there a better way?
Until recently, most bodybuilders belonged to the former group, tolerating the negative side effects so long as it meant greater recovery and growth. Although the bodybuilders certainly got bigger, they were forced to contend with not only potential health problems, but with distended guts and conditioning issues damaging to the aesthetic standard. Ultimately, despite the increase in overall mass and health issues aside, many felt that the negative effects outweighed the benefits, leaving one to ponder insulin’s role in a bodybuilder’s program.
These days, fewer bodybuilders are willing to just sit back and let the consequences of insulin abuse wreak havoc on their body without any regard for their health, but even for those whose sole concern is muscle gain and fat loss, the more is better approach is far from ideal. Unlike most other PED’s, in which a more is better approach typically yields an increased rate of side effects in tandem with improved results, this is not always the case with insulin. When we over-do insulin without any regard for our body’s built-in feed-back system, it responds to the situation by making the insulin receptors within muscle tissue less sensitive to the effects of insulin, thereby reducing its ability to transport nutrients to the muscle cell and promote growth. The medical term for this is called insulin resistance; a condition that can vary enormously in terms of severity. It would be bad enough if this was all we had to worry about, but it gets worse.
Being that one of insulin’s primary functions is the regulation of blood glucose (i.e. blood sugar), anytime we experience a reduction in sensitivity, the body will automatically require greater amounts of this hormone in order to maintain normal blood glucose concentrations. As insulin resistance worsens, the need for additional insulin continues to rise. This has several negative effects on the body, including reduced muscle growth per IU of insulin administered/produced and undesirable changes in fat cell metabolism. This is because insulin resistance affects muscle cells and fat cells differently. While insulin resistance decreases the ability of insulin to transport nutrients to the muscle cell, it does not inhibit insulin’s ability to store excess calories as bodyfat. Therefore, anytime insulin sensitivity drops, we end up with an unwanted nutrient re-partitioning effect, in which the individual’s nutrient distribution ratio is altered in favor of the fat cell. In other words, the percentage of nutrients being transported to fat cells increases, while the percentage of nutrients being delivered to muscle tissues decreases.
All of these negative effects originate with insulin resistance/reduced insulin sensitivity. Fix that problem and everything else falls into place. Unfortunately, insulin itself is the primary regulator of insulin sensitivity, in that insulin sensitivity is largely determined by our insulin levels. The more insulin that muscle cell insulin receptor comes in contact with, the less sensitive it becomes to its actions. This brings us back to the Catch-22 mentioned above.
What do we do when the drug we are using to achieve a superior growth response is the same drug responsible for causing all of our woes? If the sole goal was to increase insulin sensitivity, then the most obvious solution would be to stop injecting exogenous insulin altogether and follow a keto diet, as this would lead to a massive reduction in overall insulin levels and in return, an equally impressive rise in sensitivity. But we need more than just an increase in insulin sensitivity—we need to increase sensitivity in the face of exogenous insulin use, so that we continue to receive its growth benefits without increasing health risk or impairing fat cell metabolism.
One way to accomplish this is by using insulin sensitizers. These compounds, such as metformin and berberine (there are many others), do exactly what their name implies—they increase insulin sensitivity. The more of these compounds we employ, the more efficient the body becomes at using this hormone. This directly decreases the body’s need for insulin, causing the pancreas to secrete smaller amounts of this hormone. Because insulin is now working more efficiently, we have created an environment in which it’s anabolic and anti-catabolic effects are more pronounced, allowing us to administer smaller dosages without decreasing its muscle building ability, while simultaneously making fat cells less likely to store calories as bodyfat. This is exactly what we want—continued growth, less fat, better health.
However, there is a limit as to how far we can increase sensitivity with insulin sensitizers alone. Sooner or later, we will reach a point where a further increase in sensitivity, assuming all other variables remain constant, is not possible. While one can expect to experience significant increase in sensitivity when employing these compounds, especially when combining several of the most potent ones at optimal dosages, we will eventually research a point of diminishing returns. At this juncture, further improvement necessitates additional supplementation.
This is where insulin mimetics come into play. Both sensitizers and mimetics accomplish the same end goal of increasing insulin sensitivity, but they do so through two different mechanisms, allowing us to experience better results than when using either one alone. But, rather than increasing sensitivity directly like insulin sensitizers do, mimetics increase insulin sensitivity indirectly by “mimicking” the actions of insulin in the body. Basically, they act as an insulin replacement, assisting in blood sugar regulation, nutrient transport and doing all the positive things insulin normally does. Because mimetics decrease the body’s need for insulin, endogenous output is reduced, resulting in a concomitant rise in sensitivity.
Whether one uses sensitizers, mimetics, or both, the primary objective is a reduction in endogenous insulin secretion. Since the body cannot remove insulin from the bloodstream once it is present, sensitizers and mimetics do not influence exogenous insulin levels, but as stated above, they can have a profound impact in endogenous production. By lowering endogenous production as much as possible via supplementation, total insulin levels will fall dramatically. So, despite continuing to use substantial dosages of exogenous insulin, total insulin levels, and therefore insulin receptor exposure, will remain moderate, greatly improving insulin sensitivity. This allows us to obtain all the benefits associated with higher insulin levels, but without actually needing to have high insulin levels. We get all the benefits without the side effects.
At this point you may be asking yourself “if mimetics act like insulin in the body, won’t they also impair fat cell metabolism, making me just as likely to store calories as bodyfat? No, and that is the beauty of mimetics. They increase muscle insulin receptor sensitivity, but without negatively affecting the fat cell. Muscle cells are fed, while fat cells are starved. In theory, mimetics should be able to completely replace the need for endogenous insulin, but science has not yet developed a compound capable of doing this. Still, the potential remains.
Let’s look at how a bodybuilder, who we will refer to as John, might use sensitizers and mimetics to help him achieve his goal of enhanced growth and reduced fat gain. On a typical day, John requires roughly 60 IU of endogenous insulin in order to maintain normal blood glucose levels. He has made considerable progress up to this point, but after hearing from fellow gym members how effective insulin is at building muscle mass, he decides to stop at Wal-Mart and pick up a bottle of Novolin-R. After a bit of reading, John settles on a dosage of 30 IU per day, used on training days, which brings his total insulin level up to 90 IU per day. At first, John experiences startling results, gaining both size and bodyweight, but after a little while its once powerful effects begin to wane. His muscles no longer look or feel as full, and while some of the benefits are still present, he cannot deny that it just doesn’t pack the same punch it used to.
At this point John has a choice to make. He can keep things as they are, being content to continue experiencing the same, diminished results. Or, he can increase his insulin dose in order to make up for the decrease in insulin sensitivity. Initially, this will lead to improved results, but after a short time he will end up right back where he was, asking himself the same question—“should I increase the dose or not?” If he does, he will have begun the 1 step forward, ½ step back pattern of use and as it progresses, he will continue getting less and less benefit from each IU of insulin in his body.
John will be able to continue growing with this method, and if he pushes the dose high enough, he will be able to add quite a bit of size, but eventually, even a monstrous dose will provide only relatively mediocre results. What could have been accomplished with much more moderate dosages will now require very large dosages. As an added bonus, he will begin to accumulate unacceptable amounts of bodyfat, probably end up with the classic “slin-gut” (a result of excessive visceral fat storage), and there is a good possibility he will develop pre-diabetes; a condition wholly attributable to insulin resistance.
These are just some of the ill effects John will encounter if he continues increasing his insulin dosage without any regard for his metabolic health—namely, his insulin sensitivity. If John had done things differently from the start, preventing insulin resistance from ever happening in the first place, rather than covering it up, he would have been in a much better position all the way around.
In my opinion, insulin sensitizers and mimetics are among most valuable supplements an insulin user can take. Even for non-insulin users with a normal level of insulin sensitivity, the benefits are virtually identical, but rather than trying to prevent the development of insulin resistance, the individual is simply improving on what he already has. There are also many bodybuilders who, even in the absence of exogenous insulin, suffer from insulin resistance due to the presence of multiple risk factors: high carb diets, growth hormone use (which has been shown to result in clinical insulin resistance at doses as little as 5 IU daily), excessive dietary fat, etc. For those insulin users who are subjected to the full gamut of risk factors, the decision to include sensitizers/mimetics should be an obvious one.
Many have speculated as to why we started seeing so many problems prop up in the 1990’s (the big gut epidemic was by far the most lamented) and as expected, insulin and growth hormone often took the brunt of the blame. The problem with this line of thinking is that it throws the baby out with the bath water. Instead of addressing the underlying problem head-on, insulin and GH were held up as the whipping boys for all our aesthetic woes, when in reality, these hormones are fairly innocuous in this regard. Yes, organ growth is a legitimate concern, but the truth is that it actually accounts for very little of the added girth seen in most of today’s bodybuilders. Therefore, when looking at the issue from a hormonal standpoint, we can see that GH and insulin themselves actually cause very little expansion of the midsection. Rather, it is their accompanying side effects, namely insulin resistance (other side effects play a lesser role), which deserve the lion’s share of the blame.
So, if you want to get big, keep the fat off, minimize damage to your aesthetics, and limit the amount of harm to your health, learning how to use these supplements to your advantage is a great first step towards making that happen. In a future article, I will go over some of the top-rated insulin sensitizers and mimetics on the market today.