By Dan Gwartney, M.D.
A lot has already been said over the last two decades about the decline of symmetry and aesthetics in bodybuilding. Tradition- ally, elite-level bodybuilders were graced with Olympian lines, similar to the figures Michelangelo and other classical artists and sculptors carved and drew in places of worship. These visages were gradually replaced in the late 1980s with more exaggerated physiques, and in some cases big guts!
The Foundation Principles
The big gut has not escaped the notice of the leadership of the IFBB, who in April 2005 posted a mandate dictating a change in judging criteria.1 Recalling the founding principles on which the sport of bodybuilding was created, the IFBB reaffirmed the significance of bal- ance, proportion and classic attributes such as the "V"-taper and a flat, muscu- lar abdomen. The 2005 mandate didn't state what pressures may have incited the de facto change in judging criteria, but noted that distended abdomens and distorted muscles negatively impact symmetry and natural aesthetics, de- tracting from the overall physique.
It's important for competitive body- builders to understand the potential causes for this appearance. There have been numerous message board discus- sions debating the relative contribution of a number of factors, some with merit and others without. Muscle distortion likely refers to the unnatural lumps and bulges appearing in the muscle bellies from the use of inflammatory com- pounds such as Nolotil and synthol.2,3 Injecting these compounds causes the muscle tissue to swell around the area of the injection depot. Done properly, this can lead to significantly enlarged muscle, but poor technique can lead to unsightly lumps, suggesting a golf ball- sized tumor is growing in the deltoid or biceps.
Abdominal distension is a completely separate issue. Younger followers of bodybuilding may not be aware of the classical appearance, which personified the golden era of the sport. Bodybuild- ers used to appear as heavily muscled athletes, gracefully portraying the im- ages adorning Greek temples or the fan-tasy artwork of Boris Vallejo.4 During the later half of the 1980s, changes began to appear in the professional bodybuild- ers' physique.
Gone were the days when the waist- line of a bodybuilder was waspishly tiny, replaced by abdominal girths equaling the titanic proportions of the chest and upper back. Back then, when the tro- phies are handed out and the champions received back-slapping hugs from other competitors, it looked more like a tachi- ai charge in a sumo match. Yet, unlike their sumo counterparts, today's body- builders are extremely lean, even more so than their more aesthetic forebears.
Despite the prodigious guts, which look capable of launching a reptilian creature, like a scene from the movie "Alien," the skin is so thin and subcuta- neous fat so low that muscles, veins and tendons are readily apparent. Those in the know are aware of the direct causes of abdominal distension, while others guess. It's important to dispel irrelevant factors, as they serve only to confuse the issue. The abdominal distension seen in some of today's bodybuilders isn't due to intestinal gas, obesity due to overeat- ing or use of powerlifting movements. Bodybuilders are very sophisticated in regard to diet and it's extremely unlikely that any, let alone every pro, would be downing grams of maltitol or fiber laxatives immediately before walking onstage. As was stated earlier, the body- builders of today have extremely low subcutaneous body fat. The guts of some aren't due to generalized obesity. In the off-season, many of these athletes relax their standards and tend to accumulate body fat, some to the point of obesity, but this isn't a factor onstage during competition.
Causes for the Big Gut
While power movements are still part of the training regimen for many bodybuilders, such moves don't account for the gut. Powerlifters tend to have a more portly appearance, but this is due to higher body fat levels, low aerobic capacity and weakening and/or stretch- ing of the abdominal wall from repeated high intra-abdominal pressure exercises. Powerlifters may also acquire hernias, which can deform the abdominal wall.5 The primary factors leading to the dramatic belly bulging are the abusive levels of GH and insulin use.
GH (human growth hormone) was originally provided in very limited sup- ply to dwarf children as it was sourced from the brains of cadavers.6 During the 1970s, advances in genetic engineering allowed for the relatively unlimited pro- duction of growth hormone using recom- binant technology.7 By the late 1980s, GH was readily available and being used by athletes in many sports, including football, cycling and bodybuilding.8 GH was found to be effective in promoting connective tissue health, speeding re- covery, reducing body fat and enhancing anabolic growth. 9
As is the case with most drugs, body- builders applied trial and error to deter- mine the optimal dosing schedule of GH for achieving maximum growth. During this time, endorsements and trophies were won by those who achieved the most exaggerated growth. This system of rewards promoted the use of excessively high doses of GH, upward to 36 interna- tional units (IU) per day.
Despite the relative benefits of extreme muscular growth, bodybuild- ers began to develop adverse side effects. For those familiar with the field of endocrinology, the study of hormones' effects on the body, these side effects were not unexpected. Strange, disfigur- ing growths of the ears, nose and jaw change facial shape; hands and feet enlarge and the abdomen protrudes, being pushed outward by the growth of thoracic (chest) and abdominal (gut) organs. 10, 11
These features are identical to those experienced by people suffering from the disease acromegaly, which is caused by tumors producing high levels of GH in an unregulatedfashion.12 Acromegaly is similar to gigantism, a disease state which begins in childhood, resulting in extreme height and features of acro- megaly. The primary difference is the lack of effect of acromegaly on height, as the growth plates of adults are fused, preventing further height changes.
The question might be raised, "Why use so much GH and could less be used?" It's impossible to say who started using GH, but it's likely the first body- builders mimicked the doses used to treat dwarf children who are very short due to GH deficiency. These children are provided weekly with 0. 3 milligrams per kilogram (2.2 pounds bodyweight); extrapolating those numbers to mas- sive adult bodybuilders' size results in a daily dose of 15–25 IU per day.13
Obviously, some bodybuilders have exceeded even those numbers as the price of GH has dropped with the intro- duction of Asian imports. The high dose of GH is desirable, or was in the days of size for size's sake, because the anabolic effects of GH are dose dependent. The more GH used, the larger the muscles (head, organs, hands and feet) grew.14However, as has been seen onstage and in the clinical realm, exceeding a reasonable dose of GH can lead to problems.
Studies have shown levels as low as six IU per day can lead to early signs of acromegaly, which include physiological changes (insulin resistance) as well as the disfiguring alterations in appear- ance. 15, 16 When GH is low in adults, clini- cal features are noted, including: central (waist) obesity, weak bones, unhealthy cholesterol and fat levels, reduced muscle, decreased exercise tolerance, depression and anxiety.17,18 These features are resolved with GH replace- ment therapy, which can be used safely for years if IGF-1 levels are measured to ensure excess hormone isn't being ad- ministered.18,19 IGF-1 is a protein growth factor, which is produced in response to GH and is responsible for many of its anabolic effects.
Ironically, though GH provides wonderful benefits up to a point, when it's provided beyond what the body can tolerate, it can induce the disfigur- ing changes of acromegaly and lead to the development of the metabolic syndrome. The metabolic syndrome is a collection of risk factors relating to poor health and early death.
The Pathway to Ultimate Size
The central features of the metabolic syndrome are obesity (especially intra- abdominal fat), dangerous cholesterol and fat levels in the blood, fatty buildup in the liver, insulin resistance, high blood pressure, type 2 diabetes and heart attacks. 17 Inflammation has also been suggested to be part of the metabolic syndrome.20 The exceedingly high levels of GH used by some bodybuilders pre- dispose them to symptoms of metabolic syndrome by interfering with the body's ability to respond to insulin.19,21 This leads to elevated levels of both insulin and sugar, causing fat cells to grow, mak- ing it difficult to break down stored fat and get sugar for energy into the muscle cell. The fat-releasing (lipolytic) effect of GH appears to be strong enough to counteract the insulin resistance of fat cells in the subcutaneous layer, but an- other very important reservoir of fat, the visceral fat surrounding the abdominal organs, grows. As the visceral fat deposit enlarges, physiologic changes occur in the body that make the metabolic syndrome more pronounced, worsen heart health and promote cardiovascular disease. 22, 23 These effects compound the heart- altering effect of anabolic steroids and GH, placing many of these bodybuilders at great risk for a heart attack.24,25
Beyond the gut-bulging effect of GH (acting by increasing heart, liver, spleen and intestine size as well as increasing the visceral fat), there's also the effect of insulin. Not only do these bodybuild- ers already have high natural insulin levels due to the GH-induced insulin resistance, but they also administer insulin for its potent anabolic effect.26 Insulin is the primary anabolic hormone of the body, funneling sugar and other nutrients into active tissue and maintain- ing fat stores for periods of starvation. Bodybuilders felt that taking insulin before meals, along with daily GH injec- tions, was the pathway to ultimate size. In a way, they were right, in that the amount of size put on by these athletes was tremendous. Unfortunately, insulin can lead to a severe hypoglycemic reaction, a potentially fatal drop in blood sugar, which hospitalizes many diabetics every year.27 The use of insulin to induce a fatal hypoglycemic event was implicated in the attempted murder case of tycoon Claus von Bulow, whose wife was in coma for over 20 years until she died in 2008.28 Many others have used insulin as a murder weapon, including serial killer William Archerd of California.29
The size insulin puts on a body- builder is not quality size. Muscle growth does occur, especially in the presence of insulin resistance, but fat content is also higher, as is water retention. All fat cells will grow in the presence of insulin, including visceral fat content.30 Bodybuilders can control subcutaneous fat with lipolytic drugs (GH, clenbuterol, etc. ) and water retention with diuretics, but visceral fat is very difficult to combat in the setting of insulin resistance. Given the lack of significant additional mus- cular growth, potential risks and need for additional drugs to counteract the negative effects of insulin, it's falling out of favor.
A big belly— it has a place in the last trimester of a pregnancy, but not onstage in bodybuilding. The introduc- tion of recombinant human growth hormone and a relative abundance of supply make this the drug of choice to support the anabolic effects of steroids and drop body fat to previously unattain- able levels. Unfortunately, the more is better mentality, fueled by the dose- response relationship between GH, IGF-1 and anabolic effects, has led to an epidemic of as many as three unwanted and dangerous side effects. Chronic overdosing of GH may lead to: 1) growth of the organs of the chest and abdomen, causing the "GH gut" look and risking heart failure, 2) facial disfigurement and abnormal growth of the hands, and 3) feet and symptoms of the metabolic syn- drome (vascular disease, diabetes and high blood pressure). Adding insulin to the chemical arsenal increases many of these risks, promotes the growth of the visceral (intra-abdominal) fat, increases water retention and exposes bodybuild- ers to potentially fatal hypoglycemic events.
There really is no place for insulin in a healthy pursuit of bodybuilding. It's a potent anabolic hormone, but its benefits don't outweigh the risks and the side effect of fat storage and water retention also need to be addressed. GH is being used with great benefit in a broad range of people, including athletes. Many of its benefits can be experienced using much more moderate doses of one to five IU per day, six days per week.9,18,31-33 It's impor- tant to monitor IGF-1 levels to ensure the body isn't being overexposed to GH, as each person's need is individualized and may vary over time.32 The benefits of con- nective tissue healing, fat mobilization and augmenting the anabolic effect of exer- cise and steroids can be experienced with these lower and more rational doses.9
■ References:
1. Manion J. IFBB Symmetry Aesthetics Mandate, 2005 April 13.
2. Llewellyn W. Nolotil (metamizol). Anabolics, 2005 Body of Science Publishing, Jupiter, FL;2005:323.
3. Llewelln W. Synthol. Anabolics, 2005 Body of Sci- ence Publishing, Jupiter, FL;2005:324.
4. Vallejo B. Dreams: The art of Boris Vallejo. Thun- der's Mouth Press, ISBN 1560252804;1999.
5. Dickerman RD, Smith A, et al. Umbilical and bilateral inguinal hernias in a veteran powerlifter: is it a pressure-overload syndrome? Clin J Sport Med 2004;Mar;14(2):95-6.
6. Preece MA. Diagnosis and treatment of children with growth hormone deficiency. Clin Endocrinol Metab 1982;Mar;11(1):1-24.
7. Jenkins D, Stewart PM. Advances in medical therapy for pituitary disease: treating patients with growth hormone excess and deficiency. J Clin Pharm Ther 1993;Jun;18(3):155-63.
8. Bidlingmaier M, Wu Z, et al. Doping with growth hormone. J Pediatr Endocrinol Metab 2001;Sep- Oct;14(8):1077-83.
9. Doessing S, Kjaer M. Growth hormone and connective tissue in exercise. Scand J Med Sci Sports 2005;Aug;15(4):202-10.
10. Ezzat S. Hepatobiliary and gastrointestinal mani- festations of acromegaly. Dig Dis 1992;10(3):173-80.
11. Colao A, Marzullo P, et al. Prostatic hyperplasia: an unknown feature of acromegaly. J Clin Endocrinol Metab 1998;Mar;83(3):775-9.
12. Ezzat S, Forster MJ, et al. Acromegaly. Clinical and biochemical features in 500 patients. Medicine 1994;Sep;73(5):233-40.
13. Mauras N, Attie KM, et al. High dose recombinant human growth hormone (GH) treatment of GH-deficient patients in puberty increases near-final height: a randomized, multicenter trial. J Clin Endocrinol Metab 2000;Oct;85(10):3653-60.
14. Burgess E, Wanke C. Use of recombinant human growth hormone in HIV-associated lipodystrophy. Curr Opin Infect Dis 2005;Feb;18(1):17-24.
15. Sas T, Mulder P, et al. Carbohydrate metabolism
during long-term growth hormone treatment in children with short stature born small for gestational age. Clin Endocrinol 2001;Feb;54(2):243-51.
16. Jeffcoate W. Growth hormone therapy and its relationship to insulin resistance, glucose intolerance and diabetes mellitus: a review of recent evidence. Drug Saf 2002;25(3):199-212.
17. Johannsson G, Bengtsson BA. Growth hormone and the metabolic syndrome. J Endocrinol Invest 1999;22(5 Suppl):41-6.
18. Cerro AL. Long-term challenges in growth hormone treatment. Horm Res 2004;62 (suppl 4):23-30.
19. Monson JP. Monitoring of insulin-like growth factors during growth hormone treatment: adulthood growth hormone deficiency. Endocr Dev 2005;9:89-99.
20. Esposito K, Giugliano D. The metabolic syndrome and inflammation: association or causation? Nutr Metab Cardiovasc Dis 2004;Oct;14(5):228-32.
21. Takano A, Haruta T, et al. Growth hormone induces cellular insulin resistance by uncoupling phosphati- dylinositol 3-kinase and its downstream signals in 3T3-L1 adipocytes. Diabetes 2001;Aug;50(8):1891-900.
22. Kobayashi H, Nakamura T, et al. Visceral fat ac- cumulation contributes to insulin resistance, small-sized low-density lipoprotein and progression of coronary artery disease in middle-aged non-obese Japanese men. Jpn Circ 2001;Mar;65(3):193-9.
23. Bonora E. Relationship between regional fat distribution and insulin resistance. Int J Obes Relat Metab Disord 2000;Jun;24 Suppl 2:S32-5.
24. Twickler TB, Cramer MJ, et al. Acromegaly and heart failure: revisions of the growth hormone/insulin-like growth factor axis and its relation to the cardiovascular system. Semin Vasc Med 2004;May;4(2):115-20.
25. Urhausen A, Albers T, et al. Are the cardiac effects of anabolic steroid abuse in strength athletes reversible? Heart 2004;May;90(5):496-501.
26. Llewelln W. Insulin. Anabolics, 2005 Body of Sci- ence Publishing, Jupiter, FL;2005:301-3.
27. McCrimmon RJ, Frier BM. Hypoglycemia, the most feared complication of insulin therapy. Diabete Metab 1994;Nov-Dec;20(6):503-12.
28. Dershowitz A. Reversal of fortune: inside the van Bulow case, Random House, New York, ISBN 0394539036;1986.
29. McComb J. California Supreme Court. People v. Archerd, (1970) 3 C3d 615. [Crim. 13053, Cal Sup Ct, Dec 10, 1970].
30. Saiki A, Miyashita Y, et al. Reduction of visceral adiposity after operation in a subject with insulinoma. J Atheroscler Thromb 2004;11(4):209-14.
31. de Boer H, Blok GJ, et al. Changes in subcutaneous and visceral fat mass during growth hormone replace- ment therapy in adult men. Int J Obes Relat Metab Disord 1996;Jun;20(6):580-7.
32. Lustig RH. Optimizing growth hormone efficacy: an evidence-based analysis. Horm Res 2004;62 Suppl 3:93-7.
33. Vigano A, Mora S, et al.
A lot has already been said over the last two decades about the decline of symmetry and aesthetics in bodybuilding. Tradition- ally, elite-level bodybuilders were graced with Olympian lines, similar to the figures Michelangelo and other classical artists and sculptors carved and drew in places of worship. These visages were gradually replaced in the late 1980s with more exaggerated physiques, and in some cases big guts!
The Foundation Principles
The big gut has not escaped the notice of the leadership of the IFBB, who in April 2005 posted a mandate dictating a change in judging criteria.1 Recalling the founding principles on which the sport of bodybuilding was created, the IFBB reaffirmed the significance of bal- ance, proportion and classic attributes such as the "V"-taper and a flat, muscu- lar abdomen. The 2005 mandate didn't state what pressures may have incited the de facto change in judging criteria, but noted that distended abdomens and distorted muscles negatively impact symmetry and natural aesthetics, de- tracting from the overall physique.
It's important for competitive body- builders to understand the potential causes for this appearance. There have been numerous message board discus- sions debating the relative contribution of a number of factors, some with merit and others without. Muscle distortion likely refers to the unnatural lumps and bulges appearing in the muscle bellies from the use of inflammatory com- pounds such as Nolotil and synthol.2,3 Injecting these compounds causes the muscle tissue to swell around the area of the injection depot. Done properly, this can lead to significantly enlarged muscle, but poor technique can lead to unsightly lumps, suggesting a golf ball- sized tumor is growing in the deltoid or biceps.
Abdominal distension is a completely separate issue. Younger followers of bodybuilding may not be aware of the classical appearance, which personified the golden era of the sport. Bodybuild- ers used to appear as heavily muscled athletes, gracefully portraying the im- ages adorning Greek temples or the fan-tasy artwork of Boris Vallejo.4 During the later half of the 1980s, changes began to appear in the professional bodybuild- ers' physique.
Gone were the days when the waist- line of a bodybuilder was waspishly tiny, replaced by abdominal girths equaling the titanic proportions of the chest and upper back. Back then, when the tro- phies are handed out and the champions received back-slapping hugs from other competitors, it looked more like a tachi- ai charge in a sumo match. Yet, unlike their sumo counterparts, today's body- builders are extremely lean, even more so than their more aesthetic forebears.
Despite the prodigious guts, which look capable of launching a reptilian creature, like a scene from the movie "Alien," the skin is so thin and subcuta- neous fat so low that muscles, veins and tendons are readily apparent. Those in the know are aware of the direct causes of abdominal distension, while others guess. It's important to dispel irrelevant factors, as they serve only to confuse the issue. The abdominal distension seen in some of today's bodybuilders isn't due to intestinal gas, obesity due to overeat- ing or use of powerlifting movements. Bodybuilders are very sophisticated in regard to diet and it's extremely unlikely that any, let alone every pro, would be downing grams of maltitol or fiber laxatives immediately before walking onstage. As was stated earlier, the body- builders of today have extremely low subcutaneous body fat. The guts of some aren't due to generalized obesity. In the off-season, many of these athletes relax their standards and tend to accumulate body fat, some to the point of obesity, but this isn't a factor onstage during competition.
Causes for the Big Gut
While power movements are still part of the training regimen for many bodybuilders, such moves don't account for the gut. Powerlifters tend to have a more portly appearance, but this is due to higher body fat levels, low aerobic capacity and weakening and/or stretch- ing of the abdominal wall from repeated high intra-abdominal pressure exercises. Powerlifters may also acquire hernias, which can deform the abdominal wall.5 The primary factors leading to the dramatic belly bulging are the abusive levels of GH and insulin use.
GH (human growth hormone) was originally provided in very limited sup- ply to dwarf children as it was sourced from the brains of cadavers.6 During the 1970s, advances in genetic engineering allowed for the relatively unlimited pro- duction of growth hormone using recom- binant technology.7 By the late 1980s, GH was readily available and being used by athletes in many sports, including football, cycling and bodybuilding.8 GH was found to be effective in promoting connective tissue health, speeding re- covery, reducing body fat and enhancing anabolic growth. 9
As is the case with most drugs, body- builders applied trial and error to deter- mine the optimal dosing schedule of GH for achieving maximum growth. During this time, endorsements and trophies were won by those who achieved the most exaggerated growth. This system of rewards promoted the use of excessively high doses of GH, upward to 36 interna- tional units (IU) per day.
Despite the relative benefits of extreme muscular growth, bodybuild- ers began to develop adverse side effects. For those familiar with the field of endocrinology, the study of hormones' effects on the body, these side effects were not unexpected. Strange, disfigur- ing growths of the ears, nose and jaw change facial shape; hands and feet enlarge and the abdomen protrudes, being pushed outward by the growth of thoracic (chest) and abdominal (gut) organs. 10, 11
These features are identical to those experienced by people suffering from the disease acromegaly, which is caused by tumors producing high levels of GH in an unregulatedfashion.12 Acromegaly is similar to gigantism, a disease state which begins in childhood, resulting in extreme height and features of acro- megaly. The primary difference is the lack of effect of acromegaly on height, as the growth plates of adults are fused, preventing further height changes.
The question might be raised, "Why use so much GH and could less be used?" It's impossible to say who started using GH, but it's likely the first body- builders mimicked the doses used to treat dwarf children who are very short due to GH deficiency. These children are provided weekly with 0. 3 milligrams per kilogram (2.2 pounds bodyweight); extrapolating those numbers to mas- sive adult bodybuilders' size results in a daily dose of 15–25 IU per day.13
Obviously, some bodybuilders have exceeded even those numbers as the price of GH has dropped with the intro- duction of Asian imports. The high dose of GH is desirable, or was in the days of size for size's sake, because the anabolic effects of GH are dose dependent. The more GH used, the larger the muscles (head, organs, hands and feet) grew.14However, as has been seen onstage and in the clinical realm, exceeding a reasonable dose of GH can lead to problems.
Studies have shown levels as low as six IU per day can lead to early signs of acromegaly, which include physiological changes (insulin resistance) as well as the disfiguring alterations in appear- ance. 15, 16 When GH is low in adults, clini- cal features are noted, including: central (waist) obesity, weak bones, unhealthy cholesterol and fat levels, reduced muscle, decreased exercise tolerance, depression and anxiety.17,18 These features are resolved with GH replace- ment therapy, which can be used safely for years if IGF-1 levels are measured to ensure excess hormone isn't being ad- ministered.18,19 IGF-1 is a protein growth factor, which is produced in response to GH and is responsible for many of its anabolic effects.
Ironically, though GH provides wonderful benefits up to a point, when it's provided beyond what the body can tolerate, it can induce the disfigur- ing changes of acromegaly and lead to the development of the metabolic syndrome. The metabolic syndrome is a collection of risk factors relating to poor health and early death.
The Pathway to Ultimate Size
The central features of the metabolic syndrome are obesity (especially intra- abdominal fat), dangerous cholesterol and fat levels in the blood, fatty buildup in the liver, insulin resistance, high blood pressure, type 2 diabetes and heart attacks. 17 Inflammation has also been suggested to be part of the metabolic syndrome.20 The exceedingly high levels of GH used by some bodybuilders pre- dispose them to symptoms of metabolic syndrome by interfering with the body's ability to respond to insulin.19,21 This leads to elevated levels of both insulin and sugar, causing fat cells to grow, mak- ing it difficult to break down stored fat and get sugar for energy into the muscle cell. The fat-releasing (lipolytic) effect of GH appears to be strong enough to counteract the insulin resistance of fat cells in the subcutaneous layer, but an- other very important reservoir of fat, the visceral fat surrounding the abdominal organs, grows. As the visceral fat deposit enlarges, physiologic changes occur in the body that make the metabolic syndrome more pronounced, worsen heart health and promote cardiovascular disease. 22, 23 These effects compound the heart- altering effect of anabolic steroids and GH, placing many of these bodybuilders at great risk for a heart attack.24,25
Beyond the gut-bulging effect of GH (acting by increasing heart, liver, spleen and intestine size as well as increasing the visceral fat), there's also the effect of insulin. Not only do these bodybuild- ers already have high natural insulin levels due to the GH-induced insulin resistance, but they also administer insulin for its potent anabolic effect.26 Insulin is the primary anabolic hormone of the body, funneling sugar and other nutrients into active tissue and maintain- ing fat stores for periods of starvation. Bodybuilders felt that taking insulin before meals, along with daily GH injec- tions, was the pathway to ultimate size. In a way, they were right, in that the amount of size put on by these athletes was tremendous. Unfortunately, insulin can lead to a severe hypoglycemic reaction, a potentially fatal drop in blood sugar, which hospitalizes many diabetics every year.27 The use of insulin to induce a fatal hypoglycemic event was implicated in the attempted murder case of tycoon Claus von Bulow, whose wife was in coma for over 20 years until she died in 2008.28 Many others have used insulin as a murder weapon, including serial killer William Archerd of California.29
The size insulin puts on a body- builder is not quality size. Muscle growth does occur, especially in the presence of insulin resistance, but fat content is also higher, as is water retention. All fat cells will grow in the presence of insulin, including visceral fat content.30 Bodybuilders can control subcutaneous fat with lipolytic drugs (GH, clenbuterol, etc. ) and water retention with diuretics, but visceral fat is very difficult to combat in the setting of insulin resistance. Given the lack of significant additional mus- cular growth, potential risks and need for additional drugs to counteract the negative effects of insulin, it's falling out of favor.
A big belly— it has a place in the last trimester of a pregnancy, but not onstage in bodybuilding. The introduc- tion of recombinant human growth hormone and a relative abundance of supply make this the drug of choice to support the anabolic effects of steroids and drop body fat to previously unattain- able levels. Unfortunately, the more is better mentality, fueled by the dose- response relationship between GH, IGF-1 and anabolic effects, has led to an epidemic of as many as three unwanted and dangerous side effects. Chronic overdosing of GH may lead to: 1) growth of the organs of the chest and abdomen, causing the "GH gut" look and risking heart failure, 2) facial disfigurement and abnormal growth of the hands, and 3) feet and symptoms of the metabolic syn- drome (vascular disease, diabetes and high blood pressure). Adding insulin to the chemical arsenal increases many of these risks, promotes the growth of the visceral (intra-abdominal) fat, increases water retention and exposes bodybuild- ers to potentially fatal hypoglycemic events.
There really is no place for insulin in a healthy pursuit of bodybuilding. It's a potent anabolic hormone, but its benefits don't outweigh the risks and the side effect of fat storage and water retention also need to be addressed. GH is being used with great benefit in a broad range of people, including athletes. Many of its benefits can be experienced using much more moderate doses of one to five IU per day, six days per week.9,18,31-33 It's impor- tant to monitor IGF-1 levels to ensure the body isn't being overexposed to GH, as each person's need is individualized and may vary over time.32 The benefits of con- nective tissue healing, fat mobilization and augmenting the anabolic effect of exer- cise and steroids can be experienced with these lower and more rational doses.9
■ References:
1. Manion J. IFBB Symmetry Aesthetics Mandate, 2005 April 13.
2. Llewellyn W. Nolotil (metamizol). Anabolics, 2005 Body of Science Publishing, Jupiter, FL;2005:323.
3. Llewelln W. Synthol. Anabolics, 2005 Body of Sci- ence Publishing, Jupiter, FL;2005:324.
4. Vallejo B. Dreams: The art of Boris Vallejo. Thun- der's Mouth Press, ISBN 1560252804;1999.
5. Dickerman RD, Smith A, et al. Umbilical and bilateral inguinal hernias in a veteran powerlifter: is it a pressure-overload syndrome? Clin J Sport Med 2004;Mar;14(2):95-6.
6. Preece MA. Diagnosis and treatment of children with growth hormone deficiency. Clin Endocrinol Metab 1982;Mar;11(1):1-24.
7. Jenkins D, Stewart PM. Advances in medical therapy for pituitary disease: treating patients with growth hormone excess and deficiency. J Clin Pharm Ther 1993;Jun;18(3):155-63.
8. Bidlingmaier M, Wu Z, et al. Doping with growth hormone. J Pediatr Endocrinol Metab 2001;Sep- Oct;14(8):1077-83.
9. Doessing S, Kjaer M. Growth hormone and connective tissue in exercise. Scand J Med Sci Sports 2005;Aug;15(4):202-10.
10. Ezzat S. Hepatobiliary and gastrointestinal mani- festations of acromegaly. Dig Dis 1992;10(3):173-80.
11. Colao A, Marzullo P, et al. Prostatic hyperplasia: an unknown feature of acromegaly. J Clin Endocrinol Metab 1998;Mar;83(3):775-9.
12. Ezzat S, Forster MJ, et al. Acromegaly. Clinical and biochemical features in 500 patients. Medicine 1994;Sep;73(5):233-40.
13. Mauras N, Attie KM, et al. High dose recombinant human growth hormone (GH) treatment of GH-deficient patients in puberty increases near-final height: a randomized, multicenter trial. J Clin Endocrinol Metab 2000;Oct;85(10):3653-60.
14. Burgess E, Wanke C. Use of recombinant human growth hormone in HIV-associated lipodystrophy. Curr Opin Infect Dis 2005;Feb;18(1):17-24.
15. Sas T, Mulder P, et al. Carbohydrate metabolism
during long-term growth hormone treatment in children with short stature born small for gestational age. Clin Endocrinol 2001;Feb;54(2):243-51.
16. Jeffcoate W. Growth hormone therapy and its relationship to insulin resistance, glucose intolerance and diabetes mellitus: a review of recent evidence. Drug Saf 2002;25(3):199-212.
17. Johannsson G, Bengtsson BA. Growth hormone and the metabolic syndrome. J Endocrinol Invest 1999;22(5 Suppl):41-6.
18. Cerro AL. Long-term challenges in growth hormone treatment. Horm Res 2004;62 (suppl 4):23-30.
19. Monson JP. Monitoring of insulin-like growth factors during growth hormone treatment: adulthood growth hormone deficiency. Endocr Dev 2005;9:89-99.
20. Esposito K, Giugliano D. The metabolic syndrome and inflammation: association or causation? Nutr Metab Cardiovasc Dis 2004;Oct;14(5):228-32.
21. Takano A, Haruta T, et al. Growth hormone induces cellular insulin resistance by uncoupling phosphati- dylinositol 3-kinase and its downstream signals in 3T3-L1 adipocytes. Diabetes 2001;Aug;50(8):1891-900.
22. Kobayashi H, Nakamura T, et al. Visceral fat ac- cumulation contributes to insulin resistance, small-sized low-density lipoprotein and progression of coronary artery disease in middle-aged non-obese Japanese men. Jpn Circ 2001;Mar;65(3):193-9.
23. Bonora E. Relationship between regional fat distribution and insulin resistance. Int J Obes Relat Metab Disord 2000;Jun;24 Suppl 2:S32-5.
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