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Thank you very much Mike for the comprehensive response to your answer I counted the most.I'm sorry, but there is some false information in this thread. Insulin absolutely reduces insulin senstivity. Anyone who has any knowldge of how insulin works knows this. Consider the following...
First of all, it is important to understand that insulin receptor activation is one of the primary mechanisms through which insulin receptors become desensitized...and what activates insulin receptors, you might ask? If you guessed insulin (and to a lesser degree, IGF-1) you are correct!!! Hyperactivation of the insulin receptor is one of the main reasons for the prevalence of insulin resistance in bodybuilding today. Insulin receptors (just like many other types of receptors throughout the body) becomes less sensitive to the effects of their respective binding ligands the more frequently they are activated.
Why do you think keto diets work so wonderfully for restoring insulin senstivity? Because insulin levels are so low. The lower insulin levels fall (resulting in reduced insulin receptor signaling), the greater their senstivity becomes. The greater insulin levels climb (resulting in increased insulin receptor signaling), the less sensitive they become. It is an indisputable fact that hyperinsulinimia is a primary cause of insulin receptor downregulation....and both insulin and growth hormone are quite capable of causing hyperinsulinemia. Insulin does this through direct binding to the IR and GH by way of indirect mechanisms (elevated plasma fatty acid levels, increased IGF-1 levels, etc.). Even a brief look through the literatre (just Google "insulin receptor signaling and insulin resistance" or "insulin resistance and hyperinsulinemia" and you will find tons of scientific literature proving this . This has been known for many decades ago...even a centory ago.
Note: In response to a previous comment, which reads "Why would using insulin make you insulin resistant? That's the literal reason you take the insulin", I will provide the answer. First, let's clarify exactly what insulin resistance is. Quite simply, insulin resistance/decreased insulin sensitivity is a state in which the insulin receptor no longer responds to the actions of insulin as powerfully as it once did/should. While physicians typically won't diagnose someone as "insulin resistant" until their insulin senstivity has decreased to a point where they are clinically pre-diabetic, both insulin resistance and decreased insulin senstivity essentially refer the same thing--insulin receptor downregulation. This usually starts out relatively minor, but can potentially progress to the point of full blown Type II diabetes (again, Type II diabetes is nothing more than a case of severely decreased insulin senstivity).
When insulin senstivity first begins to decrease, the first thing that occurs is a rise in blood glucose levels. Since the regulation of BG levels is absolutely crucial to the maintainance of life, rectifying this issue becomes the body's #1 priority. The body accomplishes this by signaling the pancreas to secrete additional insulin into the bloodstream. This solves the surface issue by restoring a more normal BG level, but it does nothing to resolve the underlying issue (i.e. decreased insulin sensitivity/insulin resistance). If sensitivity continues to worsen, the pancreas will secrete more and more insulin in an attempt to maintain BG levels in an ideal range. However, if the problem progresses beyond a certain point the pancreas will no longer be able to keep up, leading to a further increase in BG levels. At its worst, the beta cells of the pancreas (the cells responsible for making insulin) begin to burnout and die. If this happens, the body's ability to manage BG levels deteriorates even further. After all, if the very cells responsible for making insulin are already incapable of managing BG levels as it is, what do you think will happen when a bunch of them start to die? When this happens, we often see outrageous circulating BG levels.
Fortunately, long before an individual reaches this point, a doctor will prescribe something like metformin. If that isn't sufficient or eventually becomes insufficient due to a continued worsening of insulin sensitivity, other medications are prescibed (usually in tandem with metformin). In the end, if the 1st and 2nd lines of medical defense fail, exogenous insulin is the only option. Exogneous inulin is only employed as a last ditch effort to prevent someone from dying as a result of Type II diabetes induced hyperglycemia. By the time someone is prescribed insulin, their insulin senstivity is so horrible that a multitude of body systems have already been severely affected, leading to numerous health problems. So, as you can see, insulin does NOTHNG to correct insulin resistance/improve insulin senstivity. In this instance, its purpose is soley to manage BG levels, thereby saving the individual from imminent death. Assuming no other steps are taken, such an individual will CONTINUE to maintain horrid insulin senstivity for the rest of their shortened lifespan, while exeriencing all the health problems associated with Type II Diabetes.
Now that we've established the above, there are few ways you can use Lantus--some good, some bad. Let's break down the various programs:
* Extended Use, Low Dose
* Extended Use, High Dose
* Intermittent Use, Low dose
* Intermittent Use, High dose
Extended Use, Low Dose: It makes no sense, as you will only be replacing your body's own endogeous production with lantus. Remember, the main reason exogneous insulin provides its benefits is because insulin levels reach supraphysiological levels. If insulin levels never really go above normal (which is what occurs with low dose Lantus), what benefit do you expect to receive? The reason low dose lantus doesn't result in suprephyiological levels of insulin is because it releases so slowly. Therefore, when supplemtning with low doses of lantus, you are really just using it as a substitution for your body's own insulin. You're not getting anthing extra.
Note: I see some potential applications with this method in those who are suffering from beta cell burnout, but this does not apply to healthy bodybuilders with good insulin sensitivity.
Extended Use, High Dose: Stupid. Sure, it will lead to rapid intial weight gain, but the resulting decrease in insulin senstivity will be extreme. When employed over the long-term, such programs will lead to pre-diabetes/Type II dibates...and as we should all know by now, this does NOT lead to a better physique. I am not gong to go into all the ways in which insulin resistance ruins the physique (shape, health AND eventually size), as it is outside the scope of this post, but if you want to know what your ultimate lot is if you choose to go down this road, look no further than pictures of Dave Palumbo or Greg Kovacs towards the end of their careers. This is what happens when severe long-term insulin resistance remains unchecked. Remember, things didn't start out this way for them. In the beginning things seemed great. They just seemed to get bigger, but the consequences of their actions reared their ugly heads over time. Why do you think Dave (whom I like) espouses keto dieting so much these days...and perpetually follows a keto diet himself (because he scared the shit out of himself after he saw what uncontrolled insulin resistance does to the body and health). If you want to build the best physique possible and fullfill your true potential, don't even consider this approach. You will not be a better bodybuilder. Too many guys in the 90's and early 2000's did this and destroyed their physiques (growth hormone just made things worse).
Intermittent Use, Low Dose: While I don't have any issue with this from a health standpoint, you run into the same problem as above. Once again, you will just be replacing your body's own natural production of insulin with LANTUS.
Intermittent Use, High Dose: This can work very well while minimizing insulin resistance. I recommend a 1-2X day per week approach at high doses, either with weak bodyparts, or, if the individual needs overall mass, on the days he trains his largest bodyparts. By simultaneously implementing steps to maintain insulin senstivity (e.g. berberine, GW, cardio, eating a clean diet low in simple sugars and removing unecessary, excess dietary fat, etc.) one can greatly reduce or even completely offset the decrease in insulin senstivity that accompanies large dose intermittent insulin usage. One other option is to use high dose Lantus daily for 1-2 weeks during a blast, while simultaneously taking steps to maintain/improve insulin senstivity. If sensitivity is still a bit low after the blast, continue utilizings the insulin sensitizing methods mentioned above until senstivity is fully restored. It shouldn't take long--1 week or so--if you previously had good insulin senstivity. Truth be told, some people should always be taking these steps. Things such as berbrine, cardio and optimal diets (I am a huge proponent of GW for improving insulin senstivity and overall metabolic health) are of paramount importance for enhanced bodybuilders attempting to maximize their development, especially if GH is part of their program.
With the high dose in mind for a 290-300 pound weight and 8-9% bf bodybuilder, what dose do you mean? 100iu? and if I would like to use 1-2x a week a high dose for, say, 10 weeks, would you also note the days on which lantus gives a higher dose of gh? and do these days make high carbohydrates and avoid as much extra fats as possible?
