by Mike Arnold Before getting into the meat of this thing, let me fill you in on my reasons for writing this article. Just a few hours ago, as
by Mike Arnold
Before getting into the meat of this thing, let me fill you in on my reasons for writing this article. Just a few hours ago, as I was skimming some posts at a popular bodybuilding website, I encountered a thread that was titled “Insulin—New Mike Arnold Protocol, 5X week indefinitely”. After opening the thread I saw that it was in reference to a previous article I had written on insulin, in which I had said it was possible to use insulin 3-5X per week indefinitely, without damaging one’s insulin sensitivity. Although the majority of responders were in agreement, there were a few which strongly opposed my position on this subject.
After seeing what was going on, I got up from the computer for a bit to spend some time with my daughter, but I couldn’t get the thread topic out of my mind. It wasn’t the disagreement that bothered me, but the fact that even after all these years we still have bodybuilders out there who are largely ignorant when it comes to the effects of insulin on the body, and I am not just talking about casual lifters here, but serious competitive bodybuilders who actually use insulin.
Because of this I felt compelled to respond, so after coming back to the thread with the full intention of doing so, I began to type out my post. But what started out as a simple response soon turned into several paragraphs, then a page, then a couple of pages, etc. At that point I decided to do things right and put my thoughts into an article. With that said, what follows is my reply to the claim that insulin cannot be used indefinitely under any circumstances, but that extended breaks must be taken in order for the drug to maintain its effectiveness.
My reponse: “What’s the issue here? From what I have been reading, it is clear that some people believe that insulin cannot be used long-term, but that extended breaks are required in order for the drug to continue providing benefits. Before I go any further, I first need to ask the question “what does it mean to take a “break”? In other words “how long do these breaks have to be? 1 hour, 1 day, 1 week, 1 month, 1 year? What? We’ll get back to that in a minute, but let’s finish laying the groundwork by also asking “why do we need to take breaks”? According to the opposition, the reasons are simple.
Breaks are required to avoid:
A.) Insulin resistance
B.) Fat gain
I can only assume that those who hold this point of view believe that fat gain can be avoided with short-term use, but if one continues using the drug for too long, the body will begin to change the manner in which it processes fat and consequently, begin storing it as adipose tissue rather than using it for energy. Now, it is true that long-term insulin use can potentially lead to fat gain, but the mechanism through which it does so is known as insulin resistance. Knowing this, common sense tells us that if we want to prevent insulin-induced fat gain, we need to keep this metabolic side effect at bay. Insulin resistance is also the reason why the drug can stop working in those who have used it for an extended period of time. Therefore, what we are really looking at here is a singular issue—insulin resistance. But what is insulin resistance and how does it develop? These are pertinent questions which must be answered before one can even begin to come to any sort of accurate conclusion regarding the title question.
In broad terms, insulin resistance can be defined as a subnormal biological response to a given concentration of insulin. In laymen’s terms, the body no longer responds to insulin as well as it should. We normally don’t refer to someone as being “insulin resistant” until the body’s response begins to fall outside the normal range. Clinically speaking, this is when 200 or more units of insulin are required per day, in order to maintain normal blood glucose levels. However, this number is not set in stone, but is just a general guideline. It all depends on the individual’s circumstances.
There are many factors which determine how much insulin someone might need, while still falling within the boundaries of what is considered a normal insulin response. For example, a 6’8, highly active, 300 lb man who needs 5,000 calories per day and a ton of carbs just to maintain his natural bodyweight is going to require a whole lot more insulin than an active, 115 lb elderly lady, even if both have a comparable degree of insulin sensitivity. Regardless, what is important to understand is that insulin resistance is a state in which the body fails to adequately respond to insulin’s signal. This failure can range from minor to severe.
Insulin sensitivity is closely related to insulin resistance, but unlike insulin resistance, it does not possess a positive or negative connotation without context. It is simply the degree to which the body responds to insulin’s signal. The better the body’s response, the more sensitive one is said to be. Therefore, sensitivity can range from excellent to horrible. If someone’s sensitivity is poor, they are generally said to be “insulin resistant”, but how does one become insulin resistant? There are a lot of ways. Certain insulin resistance syndromes, in which auto-antibodies adversely affect insulin receptor function, can cause it, as can rare inherited conditions such as receptor mutations. Glucocorticoid excess, infection, and even obesity can cause/contribute to it. However, in the absence of those factors it is usually caused through insulin receptor over-stimulation. In other words, the more often the insulin receptor is activated via interaction with insulin, the less sensitive it becomes to its effects. This is by far the most common cause of insulin resistance and Type II diabetes in the world and 99% of the time, this is how bodybuilders become insulin resistant as well (IGF-1 is often a huge factor to, especially in bodybuilders, but we will address that later).
OK, that makes sense, but let’s take things one step further and see how the body reacts to this overstimulation. When an insulin receptor is stimulated via interaction with insulin, it signals Glut-4 (an intracellular glucose transporter) to rise to the cell surface, the job of which is to carry the awaiting glucose inside the cell where it can be used for energy, glycogen synthesis, etc. When the receptor is over-stimulated and insulin sensitivity falls, Glut-4’s response to insulin also decreases, causing less Glut-4 to rise to the surface. Since the regulation of blood glucose is one of the body’s top priorities and critical to the maintenance of life, it acts quickly by telling the pancreas to secrete additional insulin. This results in more Glut-4 being called to the surface and the normalization of blood glucose levels. However, as sensitivity continues to worsen, the insulin receptor requires more and more insulin in order to recruit sufficient Glut-4. Eventually, the pancreas can no longer keep up, resulting in chronically elevated blood sugar levels and over time, the development of numerous health problems, such as Type II diabetes.
OK, so we now know that insulin is responsible for causing insulin sensitivity to decline, eventually leading to clinical insulin resistance. However, before we proceed, you need to understand the following very clearly, as it is imperative in understanding why insulin sensitivity can be maintained without extended off-time. The insulin receptor responds to ALL insulin in the same way and to the same degree, regardless of whether it is exogenous or endogenous in nature. In other words, it doesn’t matter if it comes from your pancreas or from a needle. The effect on insulin receptors will be the same (note: there is some debate regarding the effects of the various insulin analogs on sensitivity, but there is no difference between regular human insulin, such as Humulin R/Novolin R, and endogenous insulin) . The insulin receptor only knows how much insulin it is coming in contact with. That’s it. The more insulin it comes in contact with, the less sensitive it becomes, assuming all other variables remain the same.
Fortunately, not all variables need to remain the same. There are many factors which can influence insulin sensitivity and it is through their manipulation that we can potentially negate the negative effects of exogenous insulin use on insulin sensitivity, thereby allowing us to continue using it without extended off-time. Notice I did not say eliminate its negative effect. I said “negate” it. You will not be able to stop exogenous insulin from negatively affecting the insulin receptor, but you can take steps to increase sensitivity through other mechanisms, thereby balancing the good with the bad and negating this unwanted effect. Hence, the need for extended off time is eliminated.
Obviously, there is a limit as to how much exogenous insulin we can use and still maintain a high level of sensitivity, as the available variables can only be manipulated so far in our favor. Still, we can do quite a bit if we know what we’re doing. However, before I continue I want to make it clear that where you start–in terms of insulin sensitivity–will largely determine where you end up. If someone is already insulin resistant, or on the edge of it and decides to begin using exogenous insulin, implementing countermeasures is not going to be enough to move the person into the green. But, for those people who already have good insulin sensitivity, it is easily possible, if the right steps are taken and the drug is not used to excess, to maintain their current level of sensitivity without extended off-time.
This then begs the question “what is considered excessive?” After many years of experience I have found that if exogenous insulin use is administered pre-workout only, 3-5X per week, any decrease in sensitivity will remain minor-moderate, even in the absence of preventative measures. In their presence, this decrease can be prevented in full. Preventative measures include modifications to diet, the addition of cardio, and the inclusion of supplementation. I won’t address diet here, other than to say that it should always be the first place someone looks when attempting to improve insulin sensitivity, as many of the dietary adjustments that assist in this area also result in increased muscle growth, fat loss and improvements in overall metabolic health. So, rather than viewing this type of dietary fine-tuning as a temporary adjustment designed to mitigate a drug-induced side effect, we should view it as a permanent change with long-tem benefits.
When it comes to supplementation, there are many OTC options which have been clinically shown to provide substantial improvements in insulin sensitivity, some of which are on par with pharmaceutical drugs used to treat diabetes. Berberine appears to be one of the top candidates. In clinical trials, berberine was shown to be as effective as Metformin when compared on a mg per mg basis, and even performed more impressively in certain areas. It also possesses antibacterial, anti-inflammatory, and immune-enhancing properties, but more importantly, it lacks some of the more serious side effects associated with metformin, such as decreased androgen receptor density. Some other non-synthetic insulin sensitizers include bitter melon, Cinnulin-PF, and alpha lipoic acid, to name a few. When combined with an amended diet and some cardio, we can often improve sensitivity beyond what it was before we even started following a pre-workout insulin program.
As you can see, those who believe that insulin use must be interspersed with extended off-time (regardless of the circumstances) lack a basic understanding of how insulin affects the body and therefore, do not understand the problem or how to fix it. Traditional programs, while potentially quite effective in the short-term, were problematic for many reasons; the biggest of which was their failure to adequately balance sensitization with desensitization. In other words, those factors which caused sensitivity to fall outweighed those which caused it to rise. The greater the imbalance, the more necessary off-time becomes. It is only when we have a full understanding of the issues at hand that we become capable of manipulating them in our favor and this is exactly what we accomplish with a properly designed pre-workout plan.
I can’t end this piece without at least touching on growth hormone for a minute. Growth hormone can have a potentially devastating impact on insulin sensitivity; often worse than exogenous insulin. However, the manner in which GH causes insulin resistance isn’t as well understood by the majority, so allow me to elaborate on it for a minute. After we inject GH it makes its way to the liver, where it then binds with GH receptors, triggering an increase in IGF-1 production. This newly released IGF-1 then circulates throughout the body until it comes in contact with insulin receptors, activating them in the same way insulin would, and as you learned from reading the first part of the article, insulin receptor activation is the main pathway through which insulin sensitivity is reduced. However, unlike exogenous insulin, which is typically used intermittently and therefore only stimulates the insulin receptor part of the time, GH use leads to a chronic elevation of IGF-1 levels. As a result, insulin receptors are continually bombarded with IGF-1, overworking the insulin machinery and ultimately down-grading their response to an even greater degree. Exogenous insulin has the same potential for harm, but most people these days have gotten away from the super-heavy use that typified the late 90’s and early-mid 2000’s programs.
Unfortunately, growth hormone has been demonstrated to cause clinical insulin resistance with doses as low as 5 IU daily. So, for those of you who are using even moderate doses of GH on a regular basis, keep in mind that you are already at risk for developing insulin resistance. From a health and insulin sensitivity standpoint, adding exogenous insulin into a program that already includes plenty of GH is like throwing fuel on a fire. Under these circumstances, it is almost impossible to maintain “good” “good” insulin sensitivity. With proper program set-up, most individuals can prevent a good portion of the damage, but this usually doesn’t happen because most people don’t do anything to prevent it.
Back when GH first came on the scene, bodybuilders quickly realized that its use led to increased blood sugar levels. Viewing this as the primary problem, rather than a surface symptom of insulin resistance, they strove not to correct the underlying issue, but to normalize blood sugar levels. This was accomplished by adding exogenous insulin into their programs. While this brought blood glucose concentrations into a normal range, it only served to make the underlying problem worse. As resistance continued to worsen, the solution was to use more insulin. This viscous circle led to more than a few athletes (bodybuilders, strongmen, and powerlifters) becoming diabetic.
Sadly, even today it is not uncommon to see people (including some pro bodybuilders) advocating this same approach, telling GH users that they “must” add insulin into their program in order to manage GH’s negative effect on blood sugar levels. Clearly, this combination is responsible for much of the size increase we have witnessed over the last 25 years, so I am not telling bodybuilders they must abstain, but I am encouraging you to do what you can to keep the underlying problem under control, rather using insulin as a “cure” for GH mediated hyperglycemia. Anyway, that’s it for today.