by Mike Arnold
Anyone who is familiar with my writings will immediately recognize my proclivity for the use of performance enhancing drugs in sport. Aside from their ability to radically improve the composition and performance of the human body, as a whole they are a fascinating set of compounds, with potential applications extending far beyond our little world of bodybuilding. Yet, for all the wonderful things they can do, they are not without their shortcomings. While this holds true for all PED’s and drugs in general, I want to explore this notion within the context of growth hormone and insulin use in today’s BB’r.
In comparison to AAS, the amount of information available concerning the prevention and treatment of GH & insulin induced side effects is relatively scarce. BB’rs have been left to scavenge for themselves whatever information they can find regarding the safe application of these drugs. This has left many in a precarious situation, afflicted with undiagnosed medical conditions which affect not only their overall health, but their BB’ing progress as well. Up until this point, most of the information available on these two drugs has been tailored towards maximizing their perceived benefits, while many of the associated risk factors have been largely ignored. This is in stark contrast to AAS, which have received a tremendous amount of research in the areas of prevention/treatment.
There is one side effect in particular associated with these drugs which has reached near epidemic proportions, causing it to take precedence over the rest and thereby warranting its own discussion. Not only has it had a significant impact on BB’rs world-wide, but most aren’t even aware the problem exists, let alone taking steps to protect themselves from its ill effects on the body. I am referring to a condition known as insulin resistance. Insulin resistance is defined as a state in which a person’s body tissues have a lowered level of response to insulin. In order to gain a more comprehensive understanding of this issue, I will provide a brief explanation as to how insulin works in the body.
When we eat, juices in the small intestine (pancreatic juice & bile) break down the food into glucose, a simple sugar, which is then diverted into the bloodstream. When the concentration of glucose in the bloodstream exceeds a certain level, the pancreas is stimulated to release insulin into the blood. As the insulin travels through the bloodstream and comes in contact with muscle and fat cells, it attaches itself to the insulin receptor sites on those cells. Once activated, the insulin receptor initiates a series of complex biochemical signals within the cells that allows it to absorb the glucose and convert it to energy. If the pancreas is unable to secrete adequate quantities of insulin and/or the insulin receptors are not operating properly, the cells will be unable to absorb the glucose and blood levels of glucose remain elevated. In the beginning stages of insulin resistance the pancreas increases its production of insulin in an effort to more effectively manage the increased levels of glucose in the blood. As a result, it is not abnormal for those affected by this condition to exhibit high blood sugar levels in tandem with high blood insulin levels (a condition referred to as hyperinsulinemia).
If insulin resistance is not diagnosed and treated, as is often the case with GH & insulin abusing BB’rs, the individual will eventually be exposed to a variety of metabolic dysfunctions associated with or contributing to a broad range of serious health problems, such as increased visceral fat storage, pre-diabetes, high blood pressure, high triglycerides, and lowered LDL. Together, these make up a constellation of health problems normally referred to as Metabolic Syndrome. Unfortunately, this may not be enough to sway the success-minded BB’r away from his destructive habits, as they are frequently (and foolishly) more concerned with their BB’ing progress than their long-term health. However, these individuals should not be deluded into thinking they can simply ignore this problem, while continuing to reap maximum benefit from their BB’ing efforts. No, sir…the negative effects of insulin resistance on muscle growth are well documented. In addition to a reduced capacity to deliver amino acids and glucose into the muscle cell (which can adversely affect growth through several direct and indirect mechanisms), there is a growing body of evidence which suggests that certain, key signaling pathways necessary for the growth process to occur are inhibited by insulin resistance. This alone should be enough to get any BB’rs attention.
Along with steroids, growth hormone and insulin have become staples in the drug-using community, rounding out what have now become known as the “Big-3”. When combined, a synergistic effect is witnessed, allowing the individual to improve not only his growth rate, but his ultimate level of development as well. The allure of this promise is too much for many BB’rs to ignore, so they begin to include these drugs in their program, while frequently following the application guidelines handed down to them by friends or other internet authorities. While the recommendations provided may appear to be sufficient from a results perspective, they most often focus on short-term results, with little to no consideration given to long-term results or health.
Although GH is known to modulate tissue sensitivity to insulin, the sequence of molecular events leading to these changes is poorly understood. Some of the mechanisms by which GH is hypothesized to adversely affect insulin sensitivity are as follows: disruption of carbohydrate and lipid metabolism, direct effects on the insulin receptor, convergence of GH & insulin signals at the post-receptor level, and the increased expression of cellular proteins known to inhibit insulin receptor signaling, among others. While the medical community may still be unclear regarding the exact mechanisms by which GH interferes with tissue sensitivity to insulin, one thing they are 100% sure about is that growth hormone can and does cause a decrease in insulin sensitivity in a dose-dependent manner, which has often lead to full blown insulin resistance at higher dosages.
Inevitably, one of the first questions to be asked is “How much GH can I use without experiencing this problem?” Generally speaking, any dose beyond 3 IU per day can have deleterious effects on insulin sensitivity and as the dose continues to rise, the worse the issue becomes. I realize that most readers would like to me post a graph showing a direct correlation between specific dosages of growth hormone and degrees of insulin resistance/sensitivity, but that is not possible. Not only is there considerable variance in personal response between the different dosages of GH, but there are several other factors which can influence one’s level of sensitivity/resistance. This can drastically affect the outcome, making any type of formalized graph an impossibility. However, for those of you who are wondering if you may have inadvertently exposed yourself to this condition, I will make the following generalized statement. Doses as low as 3IU per day have been show to adversely affect insulin sensitivity, while in my own personal practice I have seen several examples of individuals who at just 5-6 IU per day, have meet the clinical definition of insulin resistance. The official criteria for insulin resistance has been arbitrarily defined as the requirement of 200 or more units of insulin per day to attain glycemic control and to prevent ketosis. However, in order to determine if one is officially insulin resistant, it will typically require the assistance of a physician, who may conduct multiple tests, in addition to gathering personal background and family history information.
In addition to growth hormone, the abuse of exogenous insulin is also a significant risk factor in the development of insulin resistance. Those who use the drug chronically and in high doses are at greatest risk for developing this condition, while even moderate use frequently leads to a measurable decrease in insulin sensitivity. In an effort to minimize the potential for harm, the drug is typically run in cycles or at a reduced frequency. Unlike growth hormone-induced insulin resistance, which is difficult to diagnose without the aid of a physician or glucometer, insulin resistance brought on by exogenous insulin administration provides tell-tale signs of its presence. Chief among them is a diminished response to exogenous insulin administration.
In the beginning stages of insulin resistance, one of the first things most BB’rs notice is a reduced need for food post-injection; it becomes easier to maintain stable levels of blood glucose at an equal dosage. Along with this reduced need for food comes a perceived decrease in effectiveness. It becomes readily apparent that the dose one started with is no longer sufficient for eliciting the massive pumps and extreme increases in muscle fullness initially witnessed. This usually prompts the BB’r to further raise his dose in an effort to compensate for the diminished positive effects.
If this pattern continues to repeat itself, the BB’r will eventually reach a point where a dose previously capable of inducing a dangerous hypoglycemic response will no longer be able to cause a significant alteration in blood glucose levels. Just like with GH, it is impossible to pinpoint a direct correlation between a specific dosing range/ frequency of use and the various degrees of insulin resistance. In fact, this becomes even more difficult with exogenous insulin administration, due to the greater number of variables involved.
With an undeniable connection having been established higher dose growth hormone, insulin use and insulin resistance, the logical solution is to keep our doses below the threshold at which this condition manifests, right? Well, not exactly. This approach might be ideal for those who are primarily interested in preserving their health, but it is far from optimal for those who seek the maximum in muscle mass gains. While insulin resistance is a very real side effect which has the potential to disrupt muscle growth through multiple pathways, the fact remains that the more you use, the better these drugs work…to a point. As the article title suggests, GH and insulin are a true double-edged sword, as they leave the serious, health conscious BB’r in a catch-22 situation, being forced to choose between two extremes. However, it doesn’t have to be this way. As a BB’r in the modern world, you have at your disposal a number of advanced pharmaceutical preparations capable of counteracting many of the negative effects associated with GH & insulin use.
Through a combination of drug use and supplementation, as well as the manipulation of insulin type, injection timing, and injection frequency, we are able maintain an acceptable level of insulin sensitivity despite using what most would consider large amounts of these drugs. This enables us to reap maximum benefit from the insulin we put in our body, permitting a reduction in overall dosage without compromising results and sparing our health in the process. In addition, long-term muscle gains are often enhanced, as the BB’r is able to spend more time “on”, due to the body’s improved insulin response.
When it comes to improving insulin sensitivity, no drug has received more attention or acclaim than Glucophage and rightfully so, as it is one of the most effective (and safe) insulin sensitizers on the market. Its relatively inexpensive cost is an additional perk, adding to its overall allure. In my opinion, aside from those using GH and insulin purely for replacement purposes, Glucophage should be a mainstay in the programs of all who use these drugs. For those who seek assurance of its efficacy, they do not have to look any farther than the vast amount of clinical research supporting this drug. Its 1st clinical trial was conducted in 1957, which was subsequently followed by dozens of additional clinical trials spanning the last 5 decades. In the study below, Metformin was compared against a control group and evaluated for its ability to positively affect insulin resistance independent of anthropometric changes.
Metformin and improvement of the hepatic insulin resistance index independent of anthropometric changes.
Gomez-Samano MA, Gulias-Herrero A, Cuevas-Ramos D, Brau-Figueroa H, Mehta R, Vargas-Gutiérrez D, Meza-Arana CE, Nieves-Niebla JM, Vazquez-Hernandez MO.
Source
Department of Internal Medicine, Instituto Nacional de Ciencias [FONT=tahoma, verdana, geneva, lucida, lucida grande, arial, helvetica, sans-serif]Médicas y[/FONT] Nutrición Salvador Zubirán, Mexico City, Mexico.
Abstract
OBJECTIVE:
To determine the change in the hepatic insulin resistance index (HIRI) after metformin treatment.
METHODS:
In this retrospective cohort study, Mexican mestizo patients with a body mass index (BMI) of 25 kg/m (2) or greater were evaluated. Participants were classified into 2 groups: patients who received metformin and patients who did not. Both groups were followed up for a median of 6 months (range, 4-10 months). The HIRI was calculated at baseline and at follow-up in both groups. We evaluated the independent effect of metformin on HIRI after adjustment for the difference in basal and final values (DELTA) of BMI, waist circumference, glucose, and insulin.
RESULTS:
A total of 71 patients were enrolled (51 [72%] female). Forty-one patients received metformin and 30 patients did not. Mean age was 36.3 ± 12.2 years and mean BMI was 42.2 ± 10.7 kg/m (2). After metformin treatment, HIRI significantly decreased from 38 ± 10.7 to 34.7 ± 9.5 (P = .03). In contrast, the control group had a non-significant increase in HIRI (37.6 ± 11.7 to 40.0 ± 14.0, P = .22). Weight significantly decreased in both groups (group 1: 114.6 ± 33.8 kg to 107.6 ± 28.9 kg, P< .01; group 2: 104.8 ± 28.5 kg to 98.9 ± 26.0 kg, P<.01). After BMI adjustment, the total metformin dosage correlated negatively with HIRI (r = -0.36, P = .03). Using a linear regression model (F = 6.0, r2 = 0.37, P = .002) adjusted for DELTA BMI and DELTA waist circumference, the administration of metformin resulted in independent improvement in the HIRI level (standardized β = -0.29, t = -2.0, P = .04). CONCLUSIONS: Metformin improves HIRI independently of anthropometric changes. In persons with elevated HIRI levels, metformin may be considered among the treatment options. In the medical abstract below, we see the authors highlighting the diverse and additional benefits of Metformin:
Metformin: the hidden chronicles of a magic drug.
Mahmood K, Naeem M, Rahimnajjad NA.
Source
Department of Internal Medicine, Dow Medical College, Dow University of Health Sciences, Karachi, Pakistan.
Abstract
Metformin, a biguanide is well known treatment for type 2 diabetes mellitus that has diverse mechanism of actions. Various studies have elucidated the role of this drug in different pathologies. The well-known United Kingdom Prospective Diabetic Study (UKPDS) has observed its survival benefits in a large cohort of individuals. Data has been conclusive that metformin also has beneficial role in lipid disorders as it improves the markers of metabolic syndrome. Studies have also shown the beneficial roles in antipsychotic induced weight gain as well as [FONT=tahoma, verdana, geneva, lucida, lucida grande, arial, helvetica, sans-serif]HIV lipodystrophy syndrome[/FONT]. Evidence is accumulating that metformin also improves the fertility in females with [FONT=tahoma, verdana, geneva, lucida, lucida grande, arial, helvetica, sans-serif]Polycystic Ovarian Syndrome[/FONT] (PCOS). It also delays aging and is effective in aging related disorders and is equally effective in inflammation related disorders at least in different rodent studies. Metformin’s major effect has been shown in various cancers ranging from solid to hematological malignancies. Researchers are working to reveal more benefits of this magic drug but it remains an unexplored territory for the medical community.
While Metformin is recommended as the first-line of defense for those with insulin resistance, there are many other over-the-counter supplements which have been demonstrated to have a significant impact of insulin sensitivity. Here are a few of them: Cinnamon (3-6 grams/day), Banaba leaf (3 grams), Acetic acid (2-4 TB/day), D-Chiro Inositol (1,200 mg/day), and [FONT=tahoma, verdana, geneva, lucida, lucida grande, arial, helvetica, sans-serif]Alpha lipoic acid[/FONT] (600 mcg/day).
Chromium picolinate and fish oil also play a role in the maintenance of healthy blood sugar levels by acting as supporting agents rather than direct insulin sensitizers. Chromium is an essential trace mineral and co-factor in various enzymatic reactions in the body, with one of its tasks being the regulation of blood sugar. However, chromium supplementation will only result in improvement in blood sugar management when trace levels of this trace element are deficient. One should not expect to see any improvement in this area when levels are already satisfactory. In the event that supplementation is desired, a dosage of around 100 mcg per day is sufficient. Fish oil has a similar, indirect impact on blood sugar regulation, but with most Americans lacking in this nutrient, daily supplementation should be considered mandatory. 3-6 grams per day is the generally recommended dosage.
Now that we have addressed the primary problem and explored various avenues of treatment, the question most people want to have answered is…”How do we put this all together into a single, effective program?” In reality, there is no one way to accomplish this, as program set-up should be tailored to the unique circumstances and goals of each individual. This makes crafting a one size fits all master plan impossible. However, I will provide some general guidelines, which can be adjusted from there as needed. Let’s begin by taking a look at prescription supplementation; namely, Glucophage.
According to the drug manufacturer, when used for the treatment of type II diabetes, the daily maximum dose is 2,500 mg. The total daily dose should be split up into 3 equally divided doses, taken with meals. Dosage should be gradually titrated upward in order to avoid potential gastrointestinal upset. The effects of Glucophage are acute, providing a near-maximal effect after the first dose. It can be used temporarily in order to combat the negative effects of insulin resistance causing drugs…or it can be used long-term for the same purpose. In terms of side effects, in very rare cases it can cause a condition known as lactic acidosis, which must be treated immediately (please research this side effect and its related symptoms before use). It can also modestly suppress endogenous testosterone production, which is not a concern of AAS using BB’rs, but would be for those who rely on their natural production to power the muscle growth process.
In addition to the above OTC and prescription supplementation, the BB’r should be mindful to take some time off from his GH and insulin use. Some BB’rs might shun the idea of time off, especially when talking about GH, but this is a mistake, as chronic, long-term GH use results in the build-up of GH anti-bodies, which will greatly decrease the effectiveness of the drug. In essence, it is like you are throwing a portion of your GH in the garbage can and the longer you remain on exogenous GH, the worse the problem will become. By taking a short 4 week break every few months, GH anti-bodies will have time to return to more normal levels; once again enabling the individual to use his GH would good affect.
By taking the time to ensure you maintain an acceptable level of insulin sensitivity, you will enjoy a multitude of benefits. You will look better, feel better, function better, and be healthier. You will get more out of less and save money in the process. You will accelerate fat-loss while significantly reducing your chances of experiencing “GH-insulin gut”. Muscle growth and recovery will be enhanced and your muscles will be tighter & fuller through enhanced glucose transport. The investment is minimal and the application simple. That’s got to be worth looking into, right?
Anyone who is familiar with my writings will immediately recognize my proclivity for the use of performance enhancing drugs in sport. Aside from their ability to radically improve the composition and performance of the human body, as a whole they are a fascinating set of compounds, with potential applications extending far beyond our little world of bodybuilding. Yet, for all the wonderful things they can do, they are not without their shortcomings. While this holds true for all PED’s and drugs in general, I want to explore this notion within the context of growth hormone and insulin use in today’s BB’r.
In comparison to AAS, the amount of information available concerning the prevention and treatment of GH & insulin induced side effects is relatively scarce. BB’rs have been left to scavenge for themselves whatever information they can find regarding the safe application of these drugs. This has left many in a precarious situation, afflicted with undiagnosed medical conditions which affect not only their overall health, but their BB’ing progress as well. Up until this point, most of the information available on these two drugs has been tailored towards maximizing their perceived benefits, while many of the associated risk factors have been largely ignored. This is in stark contrast to AAS, which have received a tremendous amount of research in the areas of prevention/treatment.
There is one side effect in particular associated with these drugs which has reached near epidemic proportions, causing it to take precedence over the rest and thereby warranting its own discussion. Not only has it had a significant impact on BB’rs world-wide, but most aren’t even aware the problem exists, let alone taking steps to protect themselves from its ill effects on the body. I am referring to a condition known as insulin resistance. Insulin resistance is defined as a state in which a person’s body tissues have a lowered level of response to insulin. In order to gain a more comprehensive understanding of this issue, I will provide a brief explanation as to how insulin works in the body.
When we eat, juices in the small intestine (pancreatic juice & bile) break down the food into glucose, a simple sugar, which is then diverted into the bloodstream. When the concentration of glucose in the bloodstream exceeds a certain level, the pancreas is stimulated to release insulin into the blood. As the insulin travels through the bloodstream and comes in contact with muscle and fat cells, it attaches itself to the insulin receptor sites on those cells. Once activated, the insulin receptor initiates a series of complex biochemical signals within the cells that allows it to absorb the glucose and convert it to energy. If the pancreas is unable to secrete adequate quantities of insulin and/or the insulin receptors are not operating properly, the cells will be unable to absorb the glucose and blood levels of glucose remain elevated. In the beginning stages of insulin resistance the pancreas increases its production of insulin in an effort to more effectively manage the increased levels of glucose in the blood. As a result, it is not abnormal for those affected by this condition to exhibit high blood sugar levels in tandem with high blood insulin levels (a condition referred to as hyperinsulinemia).
If insulin resistance is not diagnosed and treated, as is often the case with GH & insulin abusing BB’rs, the individual will eventually be exposed to a variety of metabolic dysfunctions associated with or contributing to a broad range of serious health problems, such as increased visceral fat storage, pre-diabetes, high blood pressure, high triglycerides, and lowered LDL. Together, these make up a constellation of health problems normally referred to as Metabolic Syndrome. Unfortunately, this may not be enough to sway the success-minded BB’r away from his destructive habits, as they are frequently (and foolishly) more concerned with their BB’ing progress than their long-term health. However, these individuals should not be deluded into thinking they can simply ignore this problem, while continuing to reap maximum benefit from their BB’ing efforts. No, sir…the negative effects of insulin resistance on muscle growth are well documented. In addition to a reduced capacity to deliver amino acids and glucose into the muscle cell (which can adversely affect growth through several direct and indirect mechanisms), there is a growing body of evidence which suggests that certain, key signaling pathways necessary for the growth process to occur are inhibited by insulin resistance. This alone should be enough to get any BB’rs attention.
Along with steroids, growth hormone and insulin have become staples in the drug-using community, rounding out what have now become known as the “Big-3”. When combined, a synergistic effect is witnessed, allowing the individual to improve not only his growth rate, but his ultimate level of development as well. The allure of this promise is too much for many BB’rs to ignore, so they begin to include these drugs in their program, while frequently following the application guidelines handed down to them by friends or other internet authorities. While the recommendations provided may appear to be sufficient from a results perspective, they most often focus on short-term results, with little to no consideration given to long-term results or health.
Although GH is known to modulate tissue sensitivity to insulin, the sequence of molecular events leading to these changes is poorly understood. Some of the mechanisms by which GH is hypothesized to adversely affect insulin sensitivity are as follows: disruption of carbohydrate and lipid metabolism, direct effects on the insulin receptor, convergence of GH & insulin signals at the post-receptor level, and the increased expression of cellular proteins known to inhibit insulin receptor signaling, among others. While the medical community may still be unclear regarding the exact mechanisms by which GH interferes with tissue sensitivity to insulin, one thing they are 100% sure about is that growth hormone can and does cause a decrease in insulin sensitivity in a dose-dependent manner, which has often lead to full blown insulin resistance at higher dosages.
Inevitably, one of the first questions to be asked is “How much GH can I use without experiencing this problem?” Generally speaking, any dose beyond 3 IU per day can have deleterious effects on insulin sensitivity and as the dose continues to rise, the worse the issue becomes. I realize that most readers would like to me post a graph showing a direct correlation between specific dosages of growth hormone and degrees of insulin resistance/sensitivity, but that is not possible. Not only is there considerable variance in personal response between the different dosages of GH, but there are several other factors which can influence one’s level of sensitivity/resistance. This can drastically affect the outcome, making any type of formalized graph an impossibility. However, for those of you who are wondering if you may have inadvertently exposed yourself to this condition, I will make the following generalized statement. Doses as low as 3IU per day have been show to adversely affect insulin sensitivity, while in my own personal practice I have seen several examples of individuals who at just 5-6 IU per day, have meet the clinical definition of insulin resistance. The official criteria for insulin resistance has been arbitrarily defined as the requirement of 200 or more units of insulin per day to attain glycemic control and to prevent ketosis. However, in order to determine if one is officially insulin resistant, it will typically require the assistance of a physician, who may conduct multiple tests, in addition to gathering personal background and family history information.
In addition to growth hormone, the abuse of exogenous insulin is also a significant risk factor in the development of insulin resistance. Those who use the drug chronically and in high doses are at greatest risk for developing this condition, while even moderate use frequently leads to a measurable decrease in insulin sensitivity. In an effort to minimize the potential for harm, the drug is typically run in cycles or at a reduced frequency. Unlike growth hormone-induced insulin resistance, which is difficult to diagnose without the aid of a physician or glucometer, insulin resistance brought on by exogenous insulin administration provides tell-tale signs of its presence. Chief among them is a diminished response to exogenous insulin administration.
In the beginning stages of insulin resistance, one of the first things most BB’rs notice is a reduced need for food post-injection; it becomes easier to maintain stable levels of blood glucose at an equal dosage. Along with this reduced need for food comes a perceived decrease in effectiveness. It becomes readily apparent that the dose one started with is no longer sufficient for eliciting the massive pumps and extreme increases in muscle fullness initially witnessed. This usually prompts the BB’r to further raise his dose in an effort to compensate for the diminished positive effects.
If this pattern continues to repeat itself, the BB’r will eventually reach a point where a dose previously capable of inducing a dangerous hypoglycemic response will no longer be able to cause a significant alteration in blood glucose levels. Just like with GH, it is impossible to pinpoint a direct correlation between a specific dosing range/ frequency of use and the various degrees of insulin resistance. In fact, this becomes even more difficult with exogenous insulin administration, due to the greater number of variables involved.
With an undeniable connection having been established higher dose growth hormone, insulin use and insulin resistance, the logical solution is to keep our doses below the threshold at which this condition manifests, right? Well, not exactly. This approach might be ideal for those who are primarily interested in preserving their health, but it is far from optimal for those who seek the maximum in muscle mass gains. While insulin resistance is a very real side effect which has the potential to disrupt muscle growth through multiple pathways, the fact remains that the more you use, the better these drugs work…to a point. As the article title suggests, GH and insulin are a true double-edged sword, as they leave the serious, health conscious BB’r in a catch-22 situation, being forced to choose between two extremes. However, it doesn’t have to be this way. As a BB’r in the modern world, you have at your disposal a number of advanced pharmaceutical preparations capable of counteracting many of the negative effects associated with GH & insulin use.
Through a combination of drug use and supplementation, as well as the manipulation of insulin type, injection timing, and injection frequency, we are able maintain an acceptable level of insulin sensitivity despite using what most would consider large amounts of these drugs. This enables us to reap maximum benefit from the insulin we put in our body, permitting a reduction in overall dosage without compromising results and sparing our health in the process. In addition, long-term muscle gains are often enhanced, as the BB’r is able to spend more time “on”, due to the body’s improved insulin response.
When it comes to improving insulin sensitivity, no drug has received more attention or acclaim than Glucophage and rightfully so, as it is one of the most effective (and safe) insulin sensitizers on the market. Its relatively inexpensive cost is an additional perk, adding to its overall allure. In my opinion, aside from those using GH and insulin purely for replacement purposes, Glucophage should be a mainstay in the programs of all who use these drugs. For those who seek assurance of its efficacy, they do not have to look any farther than the vast amount of clinical research supporting this drug. Its 1st clinical trial was conducted in 1957, which was subsequently followed by dozens of additional clinical trials spanning the last 5 decades. In the study below, Metformin was compared against a control group and evaluated for its ability to positively affect insulin resistance independent of anthropometric changes.
Metformin and improvement of the hepatic insulin resistance index independent of anthropometric changes.
Gomez-Samano MA, Gulias-Herrero A, Cuevas-Ramos D, Brau-Figueroa H, Mehta R, Vargas-Gutiérrez D, Meza-Arana CE, Nieves-Niebla JM, Vazquez-Hernandez MO.
Source
Department of Internal Medicine, Instituto Nacional de Ciencias [FONT=tahoma, verdana, geneva, lucida, lucida grande, arial, helvetica, sans-serif]Médicas y[/FONT] Nutrición Salvador Zubirán, Mexico City, Mexico.
Abstract
OBJECTIVE:
To determine the change in the hepatic insulin resistance index (HIRI) after metformin treatment.
METHODS:
In this retrospective cohort study, Mexican mestizo patients with a body mass index (BMI) of 25 kg/m (2) or greater were evaluated. Participants were classified into 2 groups: patients who received metformin and patients who did not. Both groups were followed up for a median of 6 months (range, 4-10 months). The HIRI was calculated at baseline and at follow-up in both groups. We evaluated the independent effect of metformin on HIRI after adjustment for the difference in basal and final values (DELTA) of BMI, waist circumference, glucose, and insulin.
RESULTS:
A total of 71 patients were enrolled (51 [72%] female). Forty-one patients received metformin and 30 patients did not. Mean age was 36.3 ± 12.2 years and mean BMI was 42.2 ± 10.7 kg/m (2). After metformin treatment, HIRI significantly decreased from 38 ± 10.7 to 34.7 ± 9.5 (P = .03). In contrast, the control group had a non-significant increase in HIRI (37.6 ± 11.7 to 40.0 ± 14.0, P = .22). Weight significantly decreased in both groups (group 1: 114.6 ± 33.8 kg to 107.6 ± 28.9 kg, P< .01; group 2: 104.8 ± 28.5 kg to 98.9 ± 26.0 kg, P<.01). After BMI adjustment, the total metformin dosage correlated negatively with HIRI (r = -0.36, P = .03). Using a linear regression model (F = 6.0, r2 = 0.37, P = .002) adjusted for DELTA BMI and DELTA waist circumference, the administration of metformin resulted in independent improvement in the HIRI level (standardized β = -0.29, t = -2.0, P = .04). CONCLUSIONS: Metformin improves HIRI independently of anthropometric changes. In persons with elevated HIRI levels, metformin may be considered among the treatment options. In the medical abstract below, we see the authors highlighting the diverse and additional benefits of Metformin:
Metformin: the hidden chronicles of a magic drug.
Mahmood K, Naeem M, Rahimnajjad NA.
Source
Department of Internal Medicine, Dow Medical College, Dow University of Health Sciences, Karachi, Pakistan.
Abstract
Metformin, a biguanide is well known treatment for type 2 diabetes mellitus that has diverse mechanism of actions. Various studies have elucidated the role of this drug in different pathologies. The well-known United Kingdom Prospective Diabetic Study (UKPDS) has observed its survival benefits in a large cohort of individuals. Data has been conclusive that metformin also has beneficial role in lipid disorders as it improves the markers of metabolic syndrome. Studies have also shown the beneficial roles in antipsychotic induced weight gain as well as [FONT=tahoma, verdana, geneva, lucida, lucida grande, arial, helvetica, sans-serif]HIV lipodystrophy syndrome[/FONT]. Evidence is accumulating that metformin also improves the fertility in females with [FONT=tahoma, verdana, geneva, lucida, lucida grande, arial, helvetica, sans-serif]Polycystic Ovarian Syndrome[/FONT] (PCOS). It also delays aging and is effective in aging related disorders and is equally effective in inflammation related disorders at least in different rodent studies. Metformin’s major effect has been shown in various cancers ranging from solid to hematological malignancies. Researchers are working to reveal more benefits of this magic drug but it remains an unexplored territory for the medical community.
While Metformin is recommended as the first-line of defense for those with insulin resistance, there are many other over-the-counter supplements which have been demonstrated to have a significant impact of insulin sensitivity. Here are a few of them: Cinnamon (3-6 grams/day), Banaba leaf (3 grams), Acetic acid (2-4 TB/day), D-Chiro Inositol (1,200 mg/day), and [FONT=tahoma, verdana, geneva, lucida, lucida grande, arial, helvetica, sans-serif]Alpha lipoic acid[/FONT] (600 mcg/day).
Chromium picolinate and fish oil also play a role in the maintenance of healthy blood sugar levels by acting as supporting agents rather than direct insulin sensitizers. Chromium is an essential trace mineral and co-factor in various enzymatic reactions in the body, with one of its tasks being the regulation of blood sugar. However, chromium supplementation will only result in improvement in blood sugar management when trace levels of this trace element are deficient. One should not expect to see any improvement in this area when levels are already satisfactory. In the event that supplementation is desired, a dosage of around 100 mcg per day is sufficient. Fish oil has a similar, indirect impact on blood sugar regulation, but with most Americans lacking in this nutrient, daily supplementation should be considered mandatory. 3-6 grams per day is the generally recommended dosage.
Now that we have addressed the primary problem and explored various avenues of treatment, the question most people want to have answered is…”How do we put this all together into a single, effective program?” In reality, there is no one way to accomplish this, as program set-up should be tailored to the unique circumstances and goals of each individual. This makes crafting a one size fits all master plan impossible. However, I will provide some general guidelines, which can be adjusted from there as needed. Let’s begin by taking a look at prescription supplementation; namely, Glucophage.
According to the drug manufacturer, when used for the treatment of type II diabetes, the daily maximum dose is 2,500 mg. The total daily dose should be split up into 3 equally divided doses, taken with meals. Dosage should be gradually titrated upward in order to avoid potential gastrointestinal upset. The effects of Glucophage are acute, providing a near-maximal effect after the first dose. It can be used temporarily in order to combat the negative effects of insulin resistance causing drugs…or it can be used long-term for the same purpose. In terms of side effects, in very rare cases it can cause a condition known as lactic acidosis, which must be treated immediately (please research this side effect and its related symptoms before use). It can also modestly suppress endogenous testosterone production, which is not a concern of AAS using BB’rs, but would be for those who rely on their natural production to power the muscle growth process.
In addition to the above OTC and prescription supplementation, the BB’r should be mindful to take some time off from his GH and insulin use. Some BB’rs might shun the idea of time off, especially when talking about GH, but this is a mistake, as chronic, long-term GH use results in the build-up of GH anti-bodies, which will greatly decrease the effectiveness of the drug. In essence, it is like you are throwing a portion of your GH in the garbage can and the longer you remain on exogenous GH, the worse the problem will become. By taking a short 4 week break every few months, GH anti-bodies will have time to return to more normal levels; once again enabling the individual to use his GH would good affect.
By taking the time to ensure you maintain an acceptable level of insulin sensitivity, you will enjoy a multitude of benefits. You will look better, feel better, function better, and be healthier. You will get more out of less and save money in the process. You will accelerate fat-loss while significantly reducing your chances of experiencing “GH-insulin gut”. Muscle growth and recovery will be enhanced and your muscles will be tighter & fuller through enhanced glucose transport. The investment is minimal and the application simple. That’s got to be worth looking into, right?
